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hematoma, mass lesion NASOPHARYNGEAL AND OROPHARYNGEAL Adenotonsillar hypertrophy Macroglossia Cystic hygroma Velopharyngeal flap repair Cleft palate repair Pharyngeal mass lesion CRANIOFACIAL Micrognathiaretrognathia Midface hypoplasia (e.g., trisomy 21, Crouzon disease, Apert syndrome) Mandibular hypoplasia (Pierre Robin, Treacher Collins, Cornelia de Lange syndromes) Craniofacial trauma Skeletal and storage diseases Achondroplasia Storage diseases (e.g., glycogen; Hunter, Hurler syndromes) Table 31.3 Basic Principles of Healthy Sleep for Adolescents 1. Wake up and go to bed at about the same time every night. Bedtime and wake up time should not differ from school to nonschool nights by more than approximately 1 hr. 2. Avoid sleeping in on weekends to catch up on sleep. This makes it more likely that you will have problems falling asleep. 3. If you take naps, they should be short (no more than 1 hr) and scheduled in the early to mid afternoon. However, if you have a problem with falling asleep at night, napping during the day may make it worse and should be avoided. 4. Spend time outside every day. Exposure to sunlight helps to keep your bodys internal clock on track. 5. Exercise regularly. Exercise may help you fall asleep and sleep more deeply. 6. Use your bed for sleeping only. Dont study, read, listen to music, or watch television on your bed. 7. Make the 30 60 min before bedtime a quiet or wind down time. Relaxing, calm, enjoyable activities, such as reading a book or listening to calm music, help your body and mind slow down enough to let you get to sleep. Dont study, watch excitingscary movies, exercise, or get involved in energizing activities just before bed. 8. Eat regular meals, and dont go to bed hungry. A light snack before bed is a good idea; eating a full meal within 1 hr before bed is not. 9. Avoid eating or drinking products containing caffeine from dinnertime to bedtime. These include caffeinated sodas, coffee, tea, and chocolate. 10. Do not use alcohol. Alcohol disrupts sleep and may cause you to awaken throughout the night. 11. Smoking (e.g., cigarettes) disturbs sleep. Although you should not smoke at all, if you do, do not smoke at least 2 hr before bed. 12. Do not use sleeping pills, melatonin, or other nonprescription sleep aids to help you sleep unless specifically recommended by your doctor. These can be dangerous, and the sleep problems often return when you stop taking the medicine. Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. Chapter 31 u Sleep Medicine 207 metabolic and cardiovascular complications of SDB, such as insulin resistance and systemic hypertension. Morbidly obese children are also at increased risk for postoperative complications as well as residual OSA after adenotonsillectomy. Epidemiology Overall prevalence of parent reported snoring in the pediatric popula tion is approximately 8; always snoring is reported in 1.56, and often snoring in 315. When
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defined by parent reported symptoms, the prevalence of OSA is 411. The prevalence of pediatric OSA as documented by overnight sleep studies using ventilatory monitor ing procedures (e.g., in lab polysomnography, home studies) is 14 overall, with a reported range of 0.113. Prevalence is also affected by the demographic characteristics such as age (increased prevalence between 2 and 8 years), gender (more common in males, especially after puberty), ethnicity (increased prevalence in African American and Asian children), history of prematurity, and family history of OSA. Pathogenesis The upregulation of inflammatory pathways, as indicated by an increase in peripheral markers of inflammation (e.g., C reactive pro tein, interleukins), appears to be linked to metabolic dysfunction (e.g., insulin resistance, dyslipidemia, alterations in neurohormone levels such as leptin) in both obese and nonobese children with OSA. Sys temic inflammation and arousal mediated increases in sympathetic autonomic nervous system activity with altered vasomotor tone may be key contributors to increased cardiovascular risk due to alterations in vascular endothelium in both adults and children with OSA. Other potential mechanisms that may mediate cardiovascular sequelae in adults and children with OSA include elevated systemic blood pres sure and ventricular dysfunction. Mechanical stress on the upper air way induced by chronic snoring may also result in both local mucosal inflammation of adenotonsillar tissues and subsequent upregulation of inflammatory molecules, most notably leukotrienes. One of the primary mechanisms by which OSA is believed to exert negative influences on cognitive function appears to involve repeated episodic arousals from sleep leading to sleep fragmentation and sleepi ness. Equally important, intermittent hypoxia may lead directly to systemic inflammatory vascular changes in the brain. Levels of inflam matory markers such as C reactive protein and interleukin 6 are elevated in children with OSA and are also associated with cognitive dysfunction. Clinical Manifestations The clinical manifestations of OSA may be divided into sleep related and daytime symptoms. The most common nocturnal manifestations of OSA in children and adolescents are loud, frequent, and disruptive snoring; breathing pauses; choking or gasping arousals; restless sleep; and nocturnal diaphoresis. Many children who snore do not have OSA, but few children with OSA do not snore (caregivers may not be aware of snoring in older children and adolescents). Children, like adults, tend to have more frequent and more severe obstructive events in REM sleep and when sleeping in the supine position. Children with OSA may adopt unusual sleeping positions, keeping their necks hyperex tended to maintain airway patency. Frequent arousals associated with obstruction may result in nocturnal awakenings but are more likely to cause fragmented sleep. Daytime symptoms of OSA include mouth breathing and dry mouth, chronic nasal congestion or rhinorrhea, hyponasal speech, morning headaches, difficulty swallowing, and poor appetite. Children with OSA may have secondary enuresis, postulated to result from the disruption of the normal nocturnal pattern of atrial natriuretic pep tide secretion by changes in intrathoracic pressure associated with OSA. Partial arousal parasomnias (sleepwalking and sleep terrors) may occur more frequently in children with OSA, related
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to the frequent associated arousals and an increased percentage of SWS. One of the most important but frequently overlooked sequelae of OSA in children is the effect on mood, behavior, learning, and aca demic functioning. The neurobehavioral consequences of OSA in children include daytime sleepiness with drowsiness, difficulty in morning waking, and unplanned napping or dozing off during activi ties, although evidence of frank hypersomnolence tends to be less common in children compared to adults with OSA (except in very obese children or those with severe disease). Mood changes include increased irritability, mood instability and emotional dysregulation, low frustration tolerance, and depression or anxiety. Behavioral issues include both internalizing (i.e., increased somatic complaints and social withdrawal) and externalizing behaviors, including aggression, impulsivity, hyperactivity, oppositional behavior, and conduct prob lems. There is substantial overlap between the clinical impairments associated with OSA and the diagnostic criteria for ADHD, including inattention, poor concentration, and distractibility (see Chapter 50). Many of the studies that have looked at changes in behavior and neuropsychologic functioning in children after treatment (usually ade notonsillectomy) for OSA have found significant improvement in out comes, both short term and long term, including daytime sleepiness, mood, behavior, academics, and quality of life. However, most studies failed to find a dose dependent relationship between OSA in children and specific neurobehavioral neurocognitive deficits, suggesting that other factors may influence neurocognitive outcomes, including indi vidual genetic susceptibility, racialethnic background, environmental influences (e.g., passive smoking exposure), and comorbid conditions, such as obesity, shortened sleep duration, and other sleep disorders. Diagnosis The 2012 revised American Academy of Pediatrics clinical practice guidelines provide excellent information for the evaluation and man agement of uncomplicated childhood OSA (Table 31.5). No physical examination findings are truly pathognomonic for OSA, and most healthy children with OSA appear normal; however, certain physical examination findings may suggest OSA. Growth parameters may be abnormal (obesity, or less frequently, failure to thrive), and there may be evidence of chronic nasal obstruction (hyponasal speech, mouth breathing, septal deviation) and signs of atopic disease (i.e., allergic shiners). Oropharyngeal examination may reveal enlarged tonsils, excess soft tissue in the posterior pharynx, and a narrowed posterior pharyngeal space, as well as craniofacial features associated with an increased risk of obstruction including adenoidal facies with open mouth posture and longasymmetric face, midface hypoplasia, retrog nathia and micrognathia, forward head posture (best appreciated by inspection of the frontal and lateral facial profile), and teeth crowding, narrow arched palate, and tongue tie (short frenulum). In severe cases the child may have evidence of pulmonary hypertension, right sided heart failure, and cor pulmonale; systemic hypertension may occur, especially in obese children. Because no combination of clinical history and physical findings can accurately predict which children with snoring have OSA, the gold standard for diagnosing OSA remains an in lab overnight PSG. Over night PSG is a technician supervised, monitored study that documents physiologic variables during sleep; sleep staging, arousal measurement, cardiovascular parameters, and body movements (electroencepha lography EEG, electrooculography, chin and leg electromyography
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EMG, electrocardiogram, body position sensors, and video record ing), and a combination of breathing monitors (oronasal thermal sen sor and nasal air pressure transducer for airflow), chestabdominal monitors (e.g., inductance plethysmography for respiratory effort, pulse oximeter for O2 saturation, end tidal or transcutaneous CO2 for CO2 retention, snore microphone). The PSG parameter most often used in evaluating for sleep disordered breathing is the apnea hypopnea index (AHI), which indicates the number of apneic and hypopneic (both obstructive and central) events per hour of sleep. There are no universally accepted PSG normal reference values or parameters for diagnosing OSA in children, and it is still unclear which parameters best predict morbidity. Normal preschool and school age children generally have a total AHI 1.5 (obstructive AHI 1), and this is the most widely used cutoff value for OSA in children 12 years old; in older adolescents the adult cutoff of an AHI 5 is generally used. When AHI is between one and five obstructive events per hour, assessment of Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. 208 Part II u Growth, Development, and Behavior additional PSG parameters (e.g., elevated CO2 indicating obstructive hypoventilation, O2 desaturation, respiratory related arousals), clini cal judgment regarding risk factors for SDB, presence and severity of clinical symptoms, and evidence of daytime sequelae should determine further management. Treatment No universally accepted guidelines exist regarding the indications for treatment of pediatric SDB, including primary snoring and OSA. Rec ommendations largely emphasize weighing what is known about the potential cardiovascular, metabolic, and neurocognitive sequelae of SDB in children in combination with the individual healthcare profes sionals clinical judgment. The decision of whether and how to treat OSA specifically in children depends on several parameters, including severity (nocturnal symptoms, daytime sequelae, sleep study results), duration of disease, and individual patient variables such as age, comorbid conditions, and underlying etiologic factors. In the case of moderate (AHI 5 10) to severe (AHI 10) disease, the decision to treat is usually straightforward, and most pediatric sleep experts recom mend that any child with AHI 5 should be treated. However, a large randomized trial of early adenotonsillectomy vs watchful waiting with supportive care demonstrated that 46 of the control group children normalized on PSG (vs 79 of early adenotonsillectomy group) during the 7 month observation period. In addition, it is worth emphasizing that the child with habitual snoring (3week) but without polysom nographic evidence of OSA may also experience adverse neurobehav ioral and neurocognitive outcomes; ongoing studies are examining whether these children may benefit from more aggressive treatment such as adenotonsillectomy. In the majority of cases of pediatric OSA, adenotonsillectomy is the first line treatment in any child with significant adenotonsillar hyper trophy, even in the presence of additional risk factors such as obesity. Adenotonsillectomy (or adenotonsillotomy, which is considered a less invasive procedure and may be
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indicated in some children) in uncom plicated cases generally (7090 of children) results in complete reso lution of symptoms; regrowth of adenoidal tissue after surgical removal occurs in some cases. Groups considered at high risk include young children (3 years) as well as those with severe OSA documented by PSG, significant clinical sequelae of OSA (e.g., failure to thrive), or associated medical conditions, such as craniofacial syndromes, morbid obesity, and hypotonia. All patients should be reevaluated postopera tively to determine whether additional evaluation, a repeat PSG, and treatment are required. The American Academy of Sleep Medicine rec ommends that in high risk groups (children with obesity, craniofacial anomalies, Down syndrome, or moderate severe OSA) or in children with continued symptoms of OSA, a follow up sleep study about 6 weeks after adenotonsillectomy is indicated. Also, a number of studies have suggested that children who are underweight, normal weight, or overweightobese at baseline all tend to gain weight after adenotonsil lectomy, and thus clinical vigilance is required during follow up. It should be noted that in cases of residual OSA postadenotonsil lectomy, additional diagnostic evaluation to identify other sites of obstruction may be necessary to more specifically tailor treatment. An example of this type of advanced diagnostic tool is drug induced sleep Table 31.5 American Academy of Pediatrics Clinical Practice Guideline: Diagnosis and Management of Childhood Obstructive Sleep Apnea Syndrome Key Action Statement 1: Screening for OSA As part of routine health maintenance visits, clinicians should inquire whether the child or adolescent snores. If the answer is affirmative or if a child or adolescent presents with signs or symptoms of OSA, clinicians should perform a more focused evaluation. (Evidence Quality: Grade B; Recommendation Strength: Recommendation.) Key Action Statement 2A: Polysomnography If a child or adolescent snores on a regular basis and has any of the complaints or findings of OSA, clinicians should either (1) obtain a polysomnogram (Evidence Quality: Grade A; Recommendation Strength: Recommendation) or (2) refer the patient to a sleep specialist or otolaryngologist for a more extensive evaluation. (Evidence Quality: Grade D; Recommendation Strength: Option.) Key Action Statement 2B: Alternative Testing If polysomnography is not available, clinicians may order alternative diagnostic tests, such as nocturnal video recording, nocturnal oximetry, daytime nap polysomnography, or ambulatory polysomnography. (Evidence Quality: Grade C; Recommendation Strength: Option.) Key Action Statement 3: Adenotonsillectomy If a child is determined to have OSA, has a clinical examination consistent with adenotonsillar hypertrophy, and does not have a contraindication to surgery, the clinician should recommend adenotonsillectomy as the first line of treatment. If the child has OSA but does not have adenotonsillar hypertrophy, other treatment should be considered (see Key Action Statement 6). Clinical judgment is required to determine the benefits of adenotonsillectomy compared with other treatments in obese children with varying degrees of adenotonsillar hypertrophy. (Evidence Quality: Grade B; Recommendation Strength: Recommendation.) Key Action Statement 4: High Risk Patients Undergoing Adenotonsillectomy Clinicians should monitor high risk patients undergoing adenotonsillectomy as inpatients postoperatively. (Evidence Quality: Grade B; Recommendation Strength:
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Recommendation.) Key Action Statement 5: Reevaluation Clinicians should clinically reassess all patients with OSA for persisting signs and symptoms after therapy to determine whether further treatment is required. (Evidence Quality: Grade B; Recommendation Strength: Recommendation.) Key Action Statement 5B: Reevaluation of High Risk Patients Clinicians should reevaluate high risk patients for persistent OSA after adenotonsillectomy, including those who had a significantly abnormal baseline polysomnogram, have sequelae of OSA, are obese, or remain symptomatic after treatment, with an objective test (see Key Action Statement 2), or refer such patients to a sleep specialist. (Evidence Quality: Grade B; Recommendation Strength: Recommendation.) Key Action Statement 6: CPAP Clinicians should refer patients for CPAP management if symptomssigns or objective evidence of OSA persists after adenotonsillectomy or if adenotonsillectomy is not performed. (Evidence Quality: Grade B; Recommendation Strength: Recommendation.) Key Action Statement 7: Weight Loss Clinicians should recommend weight loss in addition to other therapy if a childadolescent with OSA is overweight or obese. (Evidence Quality: Grade C; Recommendation Strength: Recommendation.) Key Action Statement 8: Intranasal Corticosteroids Clinicians may prescribe topical intranasal corticosteroids for children with mild OSA in whom adenotonsillectomy is contraindicated or for children with mild postoperative OSA. (Evidence Quality: Grade B; Recommendation Strength: Option.) CPAP, Continuous Positive Airway Pressure; OSA, obstructive sleep apnea. Adapted from Marcus CL, Brooks LJ, Draper KA, et al. Diagnosis and management of childhood obstructive sleep apnea syndrome. Pediatrics. 2012;130:576584. Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. Chapter 31 u Sleep Medicine 209 endoscopy (DISE), a powerful method for studying the airway in a sleeping patient in real time. DISE provides direct visualization of the spontaneously breathing airway under light anesthesia and facilitates identification of obstructive lesions. Site of obstruction with potential surgical corrections include lingual (resection) tonsils, tongue base (reductions), turbinate (reduction), and supraglottoplasty. Additional treatment measures that may be appropriate include weight loss, positional therapy (attaching a firm object, such as a tennis ball, to the back of a sleep garment to prevent the child from sleeping in the supine position), and aggressive treatment of additional risk factors when present, such as asthma, seasonal allergies, and gas troesophageal reflux. Evidence suggests that intranasal corticosteroids and leukotriene inhibitors may be helpful in reducing upper airway inflammation in mild OSA. Other surgical procedures (e.g., uvulopha ryngopalatoplasty) and maxillofacial surgery (e.g., mandibular distrac tion osteogenesis) are seldom performed in children. Oral appliances, such as mandibular advancing devices and palatal expanders, may be considered in select cases, particularly in those children with craniofa cial risk factors as mentioned earlier, and consultation with a pediatric dentist or orthodontist is recommended. Neuromuscular reeducation or repatterning of the oral and facial muscles with exercises to address abnormal tongue position and low upper airway tone (i.e., myofunc tional therapy) have been shown to be beneficial in addressing pedi atric OSA as well as alleviating chewing and swallowing
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problems in children able to cooperate with the behavioral program. Continuous or bilevel positive airway pressure (CPAP or BiPAP) is the most common treatment for OSA in adults and can be used suc cessfully in children and adolescents. Positive airway pressure (PAP) may be recommended if removing the adenoids and tonsils is not indi cated, if there is residual disease following adenotonsillectomy, or if there are major risk factors not amenable to surgery (obesity, hypoto nia). PAP delivers humidified, warmed air through an interface (mask, nasal pillows) that, under pressure, effectively splints the upper airway open. Optimal pressure settings (that abolish or significantly reduce obstructive respiratory events without increasing arousals or central apneas) are determined in the sleep lab during a full night PAP titration. Careful attention should be paid to education of the child and family, and desensitization protocols should usually be implemented to increase the likelihood of adherence. Efficacy studies at the cur rent pressure and retitrations should be conducted periodically with long term use (at least annually) or in association with significant weight changes or resurgence of SDB symptoms. High flow nasal can nula therapy may be another approach. A novel treatment for OSA in adults is hypoglossal nerve stimulation; case series suggest this may be an effective treatment in selected pediatric cases, especially in children with Down syndrome. Parasomnias Parasomnias are episodic nocturnal behaviors that often involve cog nitive disorientation and autonomic and skeletal muscle disturbance. Parasomnias may be further characterized as occurring primarily dur ing non REM sleep (partial arousal parasomnias) or in association with REM sleep, including nightmares, hypnogogic hallucinations, and sleep paralysis; other common parasomnias include sleep talking and hypnic jerks or sleep starts. Etiology Partial arousal parasomnias represent a dissociated sleepwake state, the neurobiology of which remains unclear, although genetic factors and an intrinsic oscillation of subcortical cortical arousal with sleep have been proposed. These episodic events, which include sleepwalk ing, sleep terrors, and confusional arousals, are more common in preschool and school age children because of the relatively higher percentage of SWS in younger children. Partial arousal parasomnias typically occur when SWS predominates, in the first third of the night. In contrast, nightmares, which are much more common than partial arousal parasomnias but are often confused with them, tend to be con centrated in the last third of the night, when REM sleep is most promi nent. Any factor associated with an increase in the relative percentage of SWS (certain medications, previous sleep restriction) may increase the frequency of events in a predisposed child. There appears to be a genetic predisposition for both sleepwalking and sleep terrors. Partial arousal parasomnias may also be difficult to distinguish from noctur nal seizures. Table 31.6 summarizes similarities and differences among these nocturnal arousal events. Epidemiology Many children sleepwalk on at least one occasion; the lifetime prevalence by age 10 years is 13. Sleepwalking (somnambu lism) may persist into adulthood, with the prevalence in adults of Table 31.6 Key Similarities and Differentiating Features Between NonREM
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and REM Parasomnias as Well as Nocturnal Seizures CONFUSIONAL AROUSALS SLEEP TERRORS SLEEPWALKING NIGHTMARES NOCTURNAL SEIZURES Time Early Early Early mid Late Any Sleep stage SWA SWA SWA REM Any EEG discharges Scream Autonomic activation Motor activity Awakens Duration (min) 0.5 10; more gradual offset 1 10; more gradual offset 2 30; more gradual offset 3 20 5 15; abrupt onset and offset Postevent confusion Age Child Child Child Child, young adult Adolescent, young adult Genetics Organic CNS lesion CNS, Central nervous system; EEG, electroencephalogram; REM, rapid eye movement; SWA, slow wave arousal. From Avidan A, Kaplish N. The parasomnias: epidemiology, clinical features and diagnostic approach. Clin Chest Med. 2010;31:353370. Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. 210 Part II u Growth, Development, and Behavior approximately 4. The prevalence is approximately 10 times greater in children with a family history of sleepwalking. The peak prev alence of sleep terrors (or night terrors) is 34 at age 1 5 years, decreasing to 10 by age 7; the age at onset is usually between 4 and 12 years. Because of the common genetic predisposition, the likelihood of developing sleepwalking after age 5 is almost twofold higher in children with a history of sleep terrors. Although sleep terrors can occur at any age from infancy through adulthood, most individuals outgrow sleep terrors by adolescence. Confusional arousals may be accompanied by (and often precede in onset) epi sodes sleepwalking and sleep terrors; prevalence rates have been estimated at 15 in children age 3 13 years. Clinical Manifestations The partial arousal parasomnias have several features in common. Because they typically occur at the transition out of deep sleep or SWS, partial arousal parasomnias have clinical features of both the awake (ambulation, vocalizations) and the sleeping (high arousal threshold, unresponsiveness to environment) states, usually with amnesia for the events. External (noise) or internal (obstruction) factors may trigger events in some individuals. The duration is typi cally a few minutes (sleep terrors) up to 30 40 minutes (confusional arousals). Sleep terrors are sudden in onset and characteristically involve a high degree of autonomic arousal (tachycardia, diapho resis, dilated pupils). Confusional arousals typically arise more gradually from sleep, may involve thrashing around, mumbling, and other vocalizations, but usually not displacement from bed, and are often accompanied by slow mentation, disorientation, and confusion on forced arousal from SWS or on waking in the morn ing. Sleepwalking may be associated with safety concerns (e.g., fall ing out of windows, wandering outside). The childs avoidance of, or increased agitation with, comforting by parents or prolongation of events by attempts at awakening are also common to all partial arousal parasomnias. Treatment Management of partial arousal parasomnias involves some combi nation of parental education and reassurance, healthy sleep prac tices, and avoidance of exacerbating factors such as sleep restriction and caffeine. Particularly in the case of
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sleepwalking, it is important to institute safety precautions such as use of gates in doorways and at the top of staircases, locking of outside doors and windows, and installation of parent notification systems such as bedroom door alarms. Scheduled awakening is a behavioral intervention that involves having the parent wake the child 15 30 minutes before the time of night that the first parasomnia episode typically occurs and is most likely to be successful in situations where partial arousal epi sodes occur on a nightly basis. Pharmacotherapy is rarely necessary but may be indicated in cases of frequent or severe episodes despite nonpharmacologic interventions and absence of treatable underly ing sleep disorders exacerbating partial arousal parasomnias such as OSA or periodic limb movement disorder (PLMD), high risk of injury, violent behavior, or serious disruption to the family. The primary pharmacologic agents used are potent SWS suppressants, primarily benzodiazepines and tricyclic antidepressants. Sleep Related Movement Disorders: Restless Legs SyndromePeriodic Limb Movement Disorder, Restless Sleep Disorder, and Rhythmic Movement Disorder Although some of these sleep disorders share common features (e.g., movements of specific body parts such as extremities vs whole body movements) and pathogenesis (e.g., iron deficiency), each has a dis tinctive set of diagnostic criteria, epidemiology and clinical manage ment, and may differ in the degree of disruption to sleep quality and quantity and related daytime consequences. Although most of these sleep related movement disorders do not require overnight polysomnographic evaluation for diagnosis (PLMD is a notable exception), a videotaped episode by caregivers in the home setting can prove very valuable in helping to differentiate sleep related movements from nocturnal seizures. Such sleep related seizures usu ally arise from the frontal andor temporal lobes. Ambulatory EEG, in patient video EEG monitoring and overnight video PSG with chin and leg EMG recording may be necessary to establish a diagnosis of a sleep related movement disorder. Restless Legs SyndromePeriodic Limb Movement Disorder Restless legs syndrome (RLS), also termed Willis Ekbom disease, is a primary disorder of the CNS sensorimotor network characterized by an almost irresistible urge to move the legs, often accompanied by uncomfortable sensations in the lower extremities. Both the urge to move and the sensations are usually worse at rest and in the evening and are at least partially relieved by movement, including walking, stretching, and rubbing, but only if the motion continues. RLS is a clinical diagnosis that is based on the presence of these key symptoms (Table 31.7). PLMD is characterized by periodic, repetitive, brief (0.5 10 seconds), and highly stereotyped limb jerks typically occurring at 20 40 second intervals. These movements occur primarily during sleep, usually occur in the legs, and frequently consist of rhythmic extension of the big toe and dorsiflexion at the ankle. Although there may be clinical complaints of kicking movements in sleep or restless sleep, the diagnosis of periodic limb movements (PLMs) requires overnight PSG to document the characteristic limb move ments with anterior tibialis EMG leads. However, like adults, chil dren also show
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considerable individual night to night variability of PLMs, and a single night PSG may not always reflect the true severity. Etiology RLS has a clear genetic component, with a sixfold to sevenfold increase in prevalence in first degree relatives of RLS patients. The mode of inheritance is complex, and several genetic loci have been identified (MEIS1, BTBD9, MAP2K5). Low serum iron levels (even without anemia) in both adults and children may be an important etiologic factor for the presence and severity of both RLS symptoms and PLMs. As a marker of decreased iron stores, serum ferritin levels in both children and adults with RLS are frequently low (50 gmL). The postulated underlying mechanism is related to the role of iron as a cofactor in tyrosine hydroxylation, a rate limiting step in dopamine Table 31.7 Diagnostic Criteria for Restless Legs Syndrome A. An urge to move legs, usually accompanied by or in response to uncomfortable and unpleasant sensations in the legs, characterized by the following: 1. The urge to move the legs begins or worsens during periods of rest or inactivity. 2. The urge to move the legs is partially or totally relieved by movement. 3. The urge to move the legs is worse in the evening or at night than during the day, or occurs only in the evening or at night. B. The symptoms in Criterion A occur at least 3 times per week and have persisted for at least 3 mo. C. The symptoms in Criterion A are accompanied by significant distress or impairment in social, occupational, educational, academic, behavioral, or other important areas of functioning. D. The symptoms in Criterion A are not attributable to another mental disorder or medical condition (e.g., arthritis, leg edema, peripheral ischemia, leg cramps) and are not better explained by a behavioral condition (e.g., positional discomfort, habitual foot tapping). E. The symptoms are not attributable to the physiologic effects of a drug or abuse or medication (e.g., akathisia). From American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 5th ed, Arlington, VA: American Psychiatric Association; 2013. p 410. Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. Chapter 31 u Sleep Medicine 211 synthesis; in turn, dopaminergic dysfunction has been implicated, particularly in the genesis of the sensory component of RLS, as well as in PLMD. Certain medical conditions, including diabetes mel litus, end stage renal disease, cancer, idiopathic juvenile arthritis, hypothyroidism, and pregnancy, may also be associated with RLS PLMD, as are specific medications (e.g., antidepressants, including tricyclic antidepressants, and selective serotonin reuptake inhibitors (SSRIs), such as fluoxetine, first generation sedating antihistamines, and dopamine receptor antagonists, such as Compazine and meto clopramide), as well as caffeine. Epidemiology Survey studies estimate the prevalence rates of RLS in the pediat ric population as between 1 and 6; approximately 2 of 8 17 year olds meet the criteria
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for definite RLS. Prevalence rates of PLMs 5 per hour in clinical populations of children referred for sleep stud ies range from 527; in survey studies of PLM symptoms, rates are 812. About 40 of adults with RLS have symptoms before age 20 years; 20 report symptoms before age 10. Familial cases usually have a younger age of onset. Several studies in referral populations have found that PLMs occur in as many as 25 of children diagnosed with ADHD. Clinical Manifestations In addition to the urge to move the legs and the sensory component (paresthesia like, tingling, burning, itching, crawling), most RLS episodes are initiated or exacerbated by rest or inactivity, such as lying in bed to fall asleep or riding in a car for prolonged periods. Children may describe the sensory symptoms as a funny feeling, tickling, hurting, or pain or bugs, spiders, ants, or goosebumps in the legs. Sometimes, the child may draw pins, needles, tiny sand particles, and bugs over his or her legs when asked to depict the symptoms. An informal suggested clinical immobilization test (SCIT) (i.e., If I asked you to lie perfectly still sitting on your bed at bedtime, would you be able to do it?) can be helpful in elicit ing RLS complaints. A unique feature of RLS is that the timing of symptoms also appears to have a circadian component, in that they often peak in the evening hours. Some children may complain of growing pains, although this is considered a nonspecific feature. Because RLS symptoms are usually worse in the evening, bedtime struggles and difficulty falling asleep are two of the most common presenting complaints. In contrast to patients with RLS, individuals with PLMs are usually unaware of these movements, but children may complain of morning muscle pain or fatigue; these movements may result in arousals during sleep and consequent significant sleep disruption. Parents of children with RLSPLMD may report that their child is a restless sleeper and kicks a bed partner. The differential diagnosis includes growing pains, leg cramps, neu ropathy, arthritis, myalgias, nerve compression (leg fell asleep), and dopamine antagonistassociated akathisia. Treatment Because of the frequent co occurrence and overlap in underlying pathophysiology and risk factors for RLS and PLMD, management strategies for both disorders are similar. The clinical decision to treat RLS and PLMs is based on the severity of symptoms, sleep distur bances, and effect on daytime functioning. An acronym that summa rizes the management approach for RLSPLMD in children is AIMS. This includes the following: u Avoidance of drugssubstances which may exacerbate RLSPLMD (including caffeine, nicotine, alcohol) u Iron supplementation u Muscles: increased physical activity, massage, application of heat cold, muscle relaxation and biofeedback u Sleep: regular and adequate sleep Treatment with iron supplementation is indicated if serum fer ritin is 50 ngmL. Administration of oral supplements for ferritin levels 75 100 gL, at least in adults, are likely ineffective because of low absorption. It should be kept in mind that ferritin is an acute phase
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reactant and thus may be falsely elevated (i.e., normal) in the setting of a concomitant illness. In addition, the ferritin level should be drawn, if possible, in the early morning after avoiding a dinner with a high iron content (e.g., red meat) on the previous eve ning. A typical iron regimen is ferrous fumarate or sulfate as an oral tablet or liquid: 3 6 mgkg of elemental ironday 3 months with 200 mg vitamin C on an empty stomach while avoiding calcium containing foods that may slow absorption. Ferritin levels should be repeated after 3 months to assess response and avoid iron overload. If ferritin levels are very low or levels fail to improve after treatment with iron, these children may require referral to hematology for evalu ation of their iron deficiency (e.g., occult blood loss, malabsorption). Although pediatric data regarding IV iron for RLSPLMD are largely lacking, there are studies examining the role of IV iron therapy (e.g., ferric carboxymaltose, iron dextran) in the treatment of severe iron deficiency or with iron malabsorption in adults. Potential advantages of IV therapy include rapid response and avoidance of malabsorption tolerancecompliance issues. Treatment with pharmacologic agents may be indicated in children with moderate severe RLS symptoms and PLMD, who did not respond to the previously mentioned measures. Currently, there are no Food and Drug Administration (FDA) approved pharmacologic agents for RLSPLMD in children. Dopaminergic medication is considered the first line of treatment for RLS in adults. Other classes of medications used to treat PLSPLMD include agonists, opiates, benzodiazepines, and bupropion. Restless Sleep Disorder Restless sleep disorder (RSD) has both clinical and PSG features distinct from RLS and PLMD. Clinical descriptors include a com plaint of restless sleep typically reported by a parent, caregiver, or bedpartner; the visible body movements, involving large muscle groups of the whole body, all four limbs, arms, legs, or head during sleep, may be characterized further as frequent repositioning dis ruption of the bedsheets, falling out of bed and being found in a completely different position compared to the position in which they fell asleep. Diagnostic criteria also include objective documen tation on videography of increased levels of nocturnal activity and gross body movements with a total movement index during sleep that exceeds five per hour of sleep. RSD has also been found to be associated with low serum iron levels with symptomatic improve ment following iron supplementation. Sleep related rhythmic movements, including head banging, body rocking, and head rolling, are characterized by repetitive, stereotyped, and rhythmic movements or behaviors that involve large muscle groups. These behaviors typically occur with the transition to sleep at bedtime, but also at nap times and after nighttime arousals. Children are thought to engage in these behaviors as a means of soothing them selves to (or back to) sleep. These behaviors are very common, with about two thirds of all infants having some type, typically beginning before 12 months and usually disappearing by preschool age. In most cases, rhythmic movement behaviors are
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benign, because sleep is not significantly disrupted, and associated significant injury is rare; how ever, these behaviors can potentially affect the sleep of a family member room sharing andor caregivers in nearby sleeping spaces. In addition, caregivers are often concerned about these behaviors as potentially being harmful to the child or possibly indicative of an underlying neu rologic or neurodevelopmental disorder (e.g., autism). However, these behaviors typically occur in normally developing children and in the majority of cases do not indicate some underlying neurologic or psy chologic problem. Usually, the most important aspect in management of sleep related rhythmic movements is reassurance to the family that this behavior is normal, common, benign, and self limited. Safety may be an important concern, and appropriate measures such as tighten ing of crib bolts and guardrails on the bed should be taken to prevent injury; noise dampening measures such as moving the bed away from adjoining walls may be helpful. If there are concerns about an associ ated sleep disorder, seizure disorder, or risk of injury referral to a sleep specialist may be considered. Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. 212 Part II u Growth, Development, and Behavior Central Disorders of Hypersomnolence: Narcolepsy type 1, Narcolepsy type 2, Idiopathic Hypersomnia Hypersomnia is a clinical term that is used to describe a group of dis orders characterized by recurrent episodes of EDS, reduced baseline alertness, andor prolonged nighttime sleep periods that interfere with normal daily functioning (Table 31.8). The many potential causes of EDS can be broadly grouped as extrinsic (e.g., secondary to insuf ficient andor fragmented sleep) or intrinsic (e.g., resulting from an increased need for sleep). Narcolepsy Narcolepsy is a chronic, lifelong CNS disorder, typically presenting in adolescence and early adulthood, characterized by profound daytime sleepiness resulting in significant functional impairment. More than half of patients with narcolepsy also present with cataplexy (type 1 narcolepsy), defined as the sudden, brief, partial, or complete loss of skeletal muscle tone, typically triggered by strong emotion (e.g., laughter, surprise, anger), with retained consciousness. Other symp toms frequently associated with narcolepsy, including hypnogogic hypnopompic (immediately before falling asleepawakening) visual, auditory, or perceptual hallucinations, and sleep paralysis, may be conceptualized as representing the intrusion of REM related phe nomena (dream mentation, loss of motor tone) into the waking state. Other REM related features include observance of eye movements and twitches at sleep onset and vivid dreams. Somewhat paradoxi cally, increased sleep fragmentation is a common feature. Rapid weight gain, especially near symptom onset, may be observed, and young children with narcolepsy have been reported to develop preco cious puberty. Etiology The genesis of narcolepsy with cataplexy (type 1) is thought to be related to a specific deficit in the hypothalamic orexinhypocretin neu rotransmitter system involving the selective loss of cells that secrete hypocretinorexin in the lateral hypothalamus. Hypocretin neurons
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stimulate a range of wake promoting neurons in the brainstem, hypo thalamus, and cortex and basal forebrain that produce neurochemicals to sustain the wake state and prevent lapses into sleep. The development of narcolepsy may involve autoimmune mecha nisms, possibly triggered by streptococcal, influenza virus, H1N1, and other viral infections, likely in combination with a genetic predisposition and environmental factors. A 12 13fold increase in narcolepsy type 1 cases, especially in children, was reported in parts of Europe in 2009 2010 following immunization with the AS03 adjuvanted H1N1 influenza vaccine. Human leukocyte antigen testing also shows a strong associa tion with narcolepsy; the majority of individuals with this antigen (25 of the general population) do not have narcolepsy, but most (90) patients with narcolepsy with cataplexy are HLA DQB10602positive. Patients with narcolepsy without cataplexy (type 2) are increasingly thought to have a significantly different underlying pathophysiology; they are much less likely to be HLA DQB10602positive (450), and cerebrospinal fluid (CSF) hypocretin levels are normal in most patients. Although most cases of narcolepsy are considered idiopathic (auto immune), secondary narcolepsy can be caused by lesions to the pos terior hypothalamus induced by traumatic brain injury, tumor, stroke, and neuroinflammatory processes such as poststreptococcal pediatric autoimmune neuropsychiatric disorder associated with streptococ cal infection (PANDAS; see Chapter 229), as well as by neurogenetic diseases such as Prader Willi syndrome (Chapter 99.7), Niemann Pick type C (Chapter 106.4), myotonic dystrophy (Chapter 649.6), Angelman syndrome, autosomal dominant cerebellar ataxia deafness narcolepsy (ADCA DN), Moebius syndrome, and Norrie disease. Epidemiology Narcolepsy is a rare disorder with a prevalence of approximately 1 in 2000 with equal sex distribution; however, specific countries (e.g., Japan) appear to have relatively higher prevalence rates. The risk of developing narcolepsy with cataplexy in a first degree relative of a nar coleptic patient is estimated at 12. This represents an increase of 10 40fold compared to the general population, but the risk remains very low, reinforcing the likely role for other etiologic factors. Clinical Manifestations and Diagnosis The typical onset of symptoms of narcolepsy is in adolescence and early adulthood, although symptoms may initially present in school age and even younger children. The early manifestations of narcolepsy are often ignored, misinterpreted, or misdiagnosed as other medical, neurologic, or psychiatric conditions, and the appropriate diagnosis is frequently delayed for years. The onset may be abrupt or slowly progressive. Table 31.8 Diagnostic Criteria for Narcolepsy A. Recurrent periods of an irrepressible need to sleep, lapsing into sleep, or napping occurring within the same day. These must have been occurring at least 3 times per week over the past 3 mo. B. The presence of at least one of the following: 1. Episodes of cataplexy, defined as either (a) or (b), occurring at least a few times per month: a. In individuals with long standing disease, brief (seconds to minutes) episodes of sudden bilateral loss of muscle tone with maintained consciousness that are precipitated by laughter or joking. b. In children or individuals within 6 mo
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of onset, spontaneous grimaces or jaw opening episodes with tongue thrusting or a global hypotonia, without any obvious emotional triggers. 2. Hypocretin deficiency, as measured using CSF hypocretin 1 immunoreactivity values (less than or equal to one third of values obtained in healthy subjects tested using the same assay, or 110 pgmL). Low CSF levels of hypocretin 1 must not be observed in the context of acute brain injury, inflammation, or infection. 3. Nocturnal sleep polysomnography showing REM sleep latency 15 min, or a multiple sleep latency test showing a mean sleep latency 8 min and two or more sleep onset REM periods. Specify whether: Narcolepsy without cataplexy but with hypocretin deficiency: Criterion B requirements of low CSF hypocretin 1 levels and positive polysomnographymultiple sleep latency test are met, but no cataplexy is present (Criterion B1 not met). Narcolepsy with cataplexy but without hypocretin deficiency: In this rare subtype (5 of narcolepsy cases), Criterion B requirements of cataplexy and positive polysomnographymultiple sleep latency test are met, but CSF hypocretin 1 levels are normal (Criterion B2 not met). Autosomal dominant cerebellar ataxia, deafness, and narcolepsy: This subtype is caused by exon 21 DNA (cytosine 5) methyltransferase 1 mutations and is characterized by late onset (age 30 40 yr) narcolepsy (with low or intermediate CSF hypocretin 1 levels), deafness, cerebellar ataxia, and eventually dementia. Autosomal dominant narcolepsy, obesity, and type 2 diabetes: Narcolepsy, obesity, and type 2 diabetes are low; CSF hypocretin 1 levels have been described in rare cases and are associated with a mutation in the myelin oligodendrocyte glycoprotein gene. Narcolepsy without cataplexy but with hypocretin deficiency: This subtype is for narcolepsy that develops secondary to medical conditions that cause infectious (e.g., Whipple disease, sarcoidosis), traumatic, or tumoral destruction of hypocretin neurons. Severity: Mild: Infrequent cataplexy (less than once per week), need for naps only once or twice per day, and less disturbed nocturnal sleep. Moderate: Cataplexy once daily or every few days, disturbed nocturnal sleep and need for multiple naps daily. Severe: Drug resistant cataplexy with multiple attacks daily, nearly constant sleepiness, and disturbed nocturnal sleep (i.e., movements, insomnia, and vivid dreaming). CSF, Cerebrospinal fluid; REM, rapid eye movement. From American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, 5th ed, Arlington, VA: American Psychiatric Association; 2013. pp 372373. Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. Chapter 31 u Sleep Medicine 213 The most prominent clinical manifestation of narcolepsy is pro found daytime sleepiness, characterized by both an increased baseline level of daytime drowsiness and the repeated occurrence of sudden and unpredictable sleep episodes. These sleep attacks are often described as irresistible, in that the child or adolescent is unable to stay awake despite considerable effort and occur even in the context of normally stimulating activities (e.g., during meals, in conversation). Very brief (several seconds) sleep attacks may also occur in
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which the individ ual may stare off, appear unresponsive, or continue to engage in an ongoing activity (automatic behavior). EDS may also be manifested by increased nighttime sleep needs and extreme difficulty waking in the morning or after a nap. Cataplexy is considered virtually pathognomonic for narcolepsy but can develop several years after the onset of EDS. Manifestations are trig gered by strong positive (laughing, joy) or negative (fright, anger, frus tration) emotions and predominantly include facial slackening, head nodding, jaw dropping, and less often, knees buckling or complete col lapse with falling to the ground. The cataplectic attacks are typically brief (seconds to minutes), the patient is awake and aware, and episodes are fully reversible, with complete recovery of normal tone when the epi sode ends. A form of cataplexy unique to children known as cataplec tic facies is characterized by prolonged tongue protrusion, ptosis, slack jaw, slurred speech, grimacing, and gait instability. Additionally, children may have positive motor phenomenon similar to dyskinesias or motor tics, with repetitive grimacing and tongue thrusting. The cataplectic attacks are typically brief (seconds to minutes) but in children may last for hours or days (status cataplecticus). The differential diagnosis of cataplexy includes syncope, seizures, cataplexy like episodes in KCNA1 pathologic variants (ataxia myokymia syndrome), hyperekplexia, hypo and hyperkalemic periodic paralysis syndromes, and pseudocataplexy. Hypnogogichypnopompic hallucinations usually involve vivid visual but also auditory and sometimes tactile sensory experiences during transitions between sleep and wakefulness, either at sleep off set (hypnopompic) or sleep onset (hypnogogic). Sleep paralysis is the inability to move or speak for a few seconds or minutes at sleep onset or offset and often accompanies the hallucinations. Other symptoms associated with narcolepsy include disrupted nocturnal sleep, impaired cognition, inattention and ADHD like symptoms, and behavioral and mood dysregulation. Several pediatric screening questionnaires for EDS, including the modified Epworth Sleepiness Scale, help to guide the need for further evaluation in clinical practice when faced with the presenting com plaint of daytime sleepiness. Physical examination should include a detailed neurologic assessment. Overnight PSG and a multiple sleep latency test (MSLT) are strongly recommended components in the evaluation of a patient with profound unexplained daytime sleepiness or suspected narcolepsy. The purpose of the overnight PSG is to evalu ate for primary sleep disorders (e.g., OSA) that may cause EDS. The MSLT involves a series of five opportunities to nap (20 min long), dur ing which patients with narcolepsy demonstrate a pathologically short ened mean sleep onset latency (8 minutes, typically 5 minutes) as well as at least two periods of REM sleep occurring immediately after sleep onset. Alternatively, a diagnosis of type 1 narcolepsy can be made by findings of low CSF hypocretin 1 concentration (typically 110 pg mL) with a standardized assay. Treatment In general, the management of pediatric narcolepsy is best done in con junction with a pediatric sleep specialist. An individualized narcolepsy treatment plan usually involves education, good sleep hygiene, behav ioral changes, and medication. Scheduled naps during the day are often
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helpful. Wake promoting medications such as modafinil or armodafinil may be prescribed to control the EDS, although these are not approved for use in children by the U.S. FDA, and potential side effects include rare reports of Stevens Johnson syndrome and reduced efficacy of hormone based contraceptives. Psychostimulants are approved for ADHD in children and can be used for EDS; side effects include appetite suppression, mood lability, and cardiovascular effects. Antidepressants (serotonin reuptake inhibitors, tricyclic antidepressants, venlafaxine) may be used to reduce cataplexy. Sodium oxybate, which is approved for use in children, is a unique drug that appears to have a positive impact on daytime sleepiness, cataplexy, and nocturnal sleep disruption; reported side effects include dizziness, weight loss, enuresis, exacerba tion of OSA, depression, and risk of respiratory depression, especially when combined with CNS depressants, including alcohol. Pitolisant has a novel mechanism as a histamine (H3) receptor agonist and has been shown to improve cataplexy and EDS in adult patients with narcolepsy. Preliminary results in children have been encouraging. Solriamfetol, a norepinephrine dopamine reuptake inhibitor, is another alertness enhancing drug recently approved in adults. The goal for the child should be to allow the fullest possible return of normal functioning in school, at home, and in social situations. Idiopathic Hypersomnia Idiopathic hypersomnia (IH) is a central sleep disorder, presenting in adolescence and young adults, characterized by chronic and EDS, but without cataplexy or REM sleep intrusions. Patients typically present with prolonged nocturnal sleep duration and severe sleep inertia, making it difficult to arouse from nocturnal sleep or day time naps. Patients often report transient periods of confusion and sleep drunkenness on awakening, sleep paralysis, and hypnagogic hallucinations. Unlike patients with narcolepsy, daytime naps tend to be long (more than 1 hour) and unrefreshing. The prevalence in the general population is not known because of challenges with diagnos tic evaluation, but is estimated to be approximately 20 50 cases per million. The pathogenesis also is not well understood; however, some cases were documented to be precipitated by viral illnesses, suggest ing a possible autoimmune process. A diagnosis of IH requires daily periods of irrepressible need to sleep or daytime lapses into sleep for at least 3 months, absence of cataplexy, and exclusion of other causes including insufficient sleep. Diagnosis is made by PSG followed by an MSLT showing mean sleep latency of 8 minutes and less than two sleep onset REM periods (SOREMPs) on MSLT or no SOREMPs if the REM sleep latency preceding PSG is 15 minutes or less. When the mean sleep latency on the MSLT is 8 minutes, a 24hour PSG or 2week actigraphy to ensure a total 24hour sleep time 660 minutes is needed. Treatment is mostly derived from experience with medi cations to treat EDS in narcolepsy. Wakeful promoting medications such as modafinil, armodafinil, methylphenidate, amphetamines, and oxybate are treatment options. Behavior modifications such as sched uled naps are not generally helpful. Kleine Levin syndrome (KLS) may mimic IH and manifests with recurrent episodes of hypersomnia
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(Table 31.9). KLS may resolve over time; some reports support the use of parenteral steroids during an episode. Table 31.9 Diagnostic Criteria for Kleine Levin Syndrome CRITERIA AE MUST BE MET A. The patient experiences at least two recurrent episodes of excessive sleepiness and sleep duration, each persisting for 2 days to 5 weeks. B. Episodes recur usually more than once a year and at least once every 18 months. C. The patient has normal alertness, cognitive function, behavior, and mood between episodes. D. The patient must demonstrate at least one of the following during episodes: E. Cognitive dysfunction. F. Altered perception. G. Eating disorder (anorexia or hyperphagia). H. Disinhibited behavior (such as hypersexuality). I. The hypersomnolence and related symptoms are not better explained by another sleep disorder, other medical, neurologic, or psychiatric disorder (especially bipolar disorder), or use of drugs or medications. From Afolabi Brown O, Mason II TBA. Kleine Levin syndrome. Pediatr Respir Rev. 2018;25:913, Table 1, p 10. Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. 214 Part II u Growth, Development, and Behavior Delayed SleepWake Phase Disorder Delayed sleepwake phase disorder (DSWPD), a circadian rhythm disorder, involves a significant, persistent, and intractable phase shift in sleepwake schedule (later sleep onset and wake time) that con flicts with the individuals normal school, work, and lifestyle demands. DSWPD may occur at any age but is most common in adolescents and young adults. Etiology Individuals with DSPD may start out as night owls; that is, they have an underlying biologic predispositioncircadian based eve ningness chronotype that results in a propensity for staying up relatively late at night and sleeping until late in the morning or early afternoon, and in extreme cases, a complete day night reversal. Although these patients struggle to get up in time for school or work, they usually revert to their preferred sleep schedule on week ends, holidays, and summer vacations. The underlying pathophysi ology of DSWPD is still unknown, although some theorize that it involves an intrinsic abnormality in the circadian oscillators that govern the timing of the sleep period. Epidemiology Studies indicate that the prevalence of DSWPD may be as high as 716 in adolescents and young adults. Clinical Manifestations The most common clinical presentation of DSWPD is sleep initiation insomnia when the individual attempts to fall asleep at a socially acceptable desired bedtime and experiences very delayed sleep onset (often after 1 2 am), accompanied by daytime sleepiness. Patients may also report extreme difficulty arising in the morning even for desired activities, with pronounced confusion on waking (sleep inertia), and caregivers often complain of the need for multiple reminders or even the complete failure to awaken the adolescent in time to attend school. Sleep maintenance is gener ally not problematic, and no sleep onset insomnia is experienced if bedtime coincides with the preferred sleep onset time. Patients
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may also develop secondary psychophysiologic insomnia as a result of spending prolonged time in bed attempting to fall asleep. School tardiness and frequent absenteeism with a decline in academic performance often occur, and there may be school related disci plinary action (i.e., suspension, truancy label) or a need to justify home based schoolingtutoring that motivate families to seek help. It is important to recognize that there may also be issues related to family dynamics and comorbid anxiety, depression, or learning disabilities that provide a motivation to avoid attending school and perpetuate the sleep schedule problems, as well as reducing adher ence to interventions. Treatment The treatment of DSWPD usually has three components, all directed toward the goals of shifting the sleepwake schedule to an earlier, more desirable time and maintaining the new schedule. The initial step involves shifting the sleepwake schedule to the desired earlier times, usually with gradual (i.e., in 15 30 minute increments every few days) alternating advancement of rise time in the morning and bedtime in the evening. More significant phase delays (i.e., larger difference between current sleep onset and desired bedtime) may require chronotherapy, which involves delaying bedtime and wake time by 2 3 hours every 24 hours forward around the clock until the target bedtime is reached. Because melatonin secretion is highly sensitive to light, exposure to light in the morning (either natu ral light or a light box, which typically produces light at around 10,000 lux) and avoidance of evening light exposure (especially from screens emitting predominantly blue light, such as computers and laptops) are often beneficial. Exogenous oral melatonin supple mentation may also be used; larger, mildly sedating doses (5 mg) are typically given 30 minutes before bedtime, but some studies have suggested that physiologic doses of oral melatonin (0.3 0.5 mg) administered in the afternoon or early evening (5 7 hours before the habitual sleep onset time or 2 hours before the desired bedtime) may be more effective in advancing the sleep phase. SLEEP HEALTH SUPERVISION It is especially important for pediatricians to screen for and rec ognize sleep disorders in children and adolescents during routine healthcare encounters. The well child visit is an opportunity to edu cate parents about normal sleep and to teach strategies to prevent sleep problems from developing (primary prevention) or becoming chronic, if problems already exist (secondary prevention). Develop mentally appropriate screening for sleep disturbances should take place in the context of every well child visit and should include a range of potential sleep problems; Table 31.10 outlines a simple sleep screening algorithm called the BEARS. Because parents may not always be aware of sleep problems, especially in older children and adolescents, it is also important to question the child directly about sleep concerns. The recognition and evaluation of sleep problems in children require both an understanding of the association between sleep disturbances and daytime consequences (e.g., irritability, inat tention, poor impulse control) knowledge of risk factors for the wide variety of sleep disorders (e.g., obesity, positive
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family history, medications), and familiarity with the developmentally appropriate differential diagnoses of common presenting sleep complaints (dif ficulty initiating and maintaining sleep, episodic nocturnal events). An assessment of sleep patterns and possible sleep problems should be part of the initial evaluation of every child presenting with behavioral or academic problems, especially ADHD. Effective preventive measures include educating parents of newborns about normal sleep amounts and patterns. The ability to regulate sleep begins to develop in the first 8 12 weeks of life. Thus it is important to recommend that parents put their 2 4 month old infants to bed drowsy but awake if they want to avoid dependence on parental presence at sleep onset and foster the infants ability to self soothe. Other important sleep issues include discussing the importance of regular bedtimes, bedtime routines, and transitional objects for toddlers, and providing parents and children with basic information about healthy sleep practices, recom mended sleep amounts at different ages, and signs that a child is not get ting sufficient sleep. The cultural and family context within which sleep problems in children occur should be considered. For example, bed sharing of infants and parents is a common and accepted practice in many racialethnic groups, and these families may not share the goal of independent self soothing in young infants. Anticipatory guidance needs to balance cultural awareness with the critical importance of safe sleep conditions in sudden infant death syndrome preven tion (i.e., sleeping in the supine position, avoidance of bed sharing but encouragement of room sharing in the first year of life) (see Chapter 423). On the other hand, the institution of cosleeping by parents as an attempt to address a childs underlying sleep problem (so called reactive cosleeping), rather than as a conscious family decision, is likely to yield only a temporary respite from the prob lem and may set the stage for more significant sleep issues. EVALUATION OF PEDIATRIC SLEEP PROBLEMS The clinical evaluation of a child presenting with a sleep problem involves obtaining a careful medical history to assess for potential medical causes of sleep disturbances, such as allergies, concomitant medications, and acute or chronic pain conditions. A developmental history is important because of the increased risk of sleep problems in children with neurodevelopmental disorders. Assessment of the childs current level of functioning (school, home) is a key part of evaluating possible mood, behavioral, and neurocognitive sequelae of sleep problems. Current sleep patterns, including the usual sleep duration and sleepwake schedule, are often best assessed with a sleep diary, in which a parent (or adolescent) records daily sleep behaviors for an extended period (1 2 weeks). A review of sleep habits, such as bedtime routines, daily caffeine intake, and the Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. Chapter 31 u Sleep Medicine 215 sleeping environment (e.g., temperature, noise level), may reveal
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environmental factors that contribute to the sleep problems. Noc turnal symptoms that may be indicative of a medically based sleep disorder, such as OSA (loud snoring, choking or gasping, sweating) or PLMs (restless sleep, repetitive kicking movements), should be elicited. Home video recording may be helpful in the evaluation of potential parasomnia episodes and the assessment of snoring and increased work of breathing in children with OSA. An overnight sleep study (PSG) is not routinely warranted in the evaluation of a child with sleep problems unless there are symptoms suggestive of OSA or PLMs, unusual features of episodic nocturnal events, or unexplained daytime sleepiness. Visit Elsevier eBooks at eBooks.Health.Elsevier.com for Bibliography. Table 31.10 BEARS Sleep Screening Algorithm The BEARS instrument is divided into five major sleep domains, providing a comprehensive screen for the major sleep disorders affecting children 2 18 yr old. Each sleep domain has a set of age appropriate trigger questions for use in the clinical interview. B Bedtime problems E Excessive daytime sleepiness A Awakenings during the night R Regularity and duration of sleep S Snoring DEVELOPMENTALLY APPROPRIATE TRIGGER QUESTIONS TODDLER, PRESCHOOL (2 5 YR) SCHOOL AGE (6 12 YR) ADOLESCENT (13 18 YR) 1. Bedtime problems Does your child have any problems going to bed? Falling asleep? Does your child have any problems at bedtime? (P) Do you any problems going to bed? (C) Do you have any problems falling asleep at bedtime? (C) 2. Excessive daytime sleepiness Does your child seem overtired or sleepy a lot during the day? Does your child still take naps? Does your child have difficulty waking in the morning, seem sleepy during the day, or take naps? (P) Do you feel tired a lot? (C) Do you feel sleepy a lot during the day? In school? While driving? (C) 3. Awakenings during the night Does your child wake up a lot at night? Does your child seem to wake up a lot at night? Any sleepwalking or nightmares? (P) Do you wake up a lot at night? Do you have trouble getting back to sleep? (C) Do you wake up a lot at night? Do you have trouble getting back to sleep? (C) 4. Regularity and duration of sleep Does your child have a regular bedtime and wake time? What are they? What time does your child go to bed and get up on school days? Weekends? Do you think your child is getting enough sleep? (P) What time do you usually go to bed on school nights? Weekends? How much sleep do you usually get? (C) 5. Snoring Does your child snore a lot or have difficulty breathing at night? Does your child have loud or nightly snoring or any breathing difficulties at night? (P) Does your teenager snore loudly or nightly? (P) C, Child; P, parent. Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All
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rights reserved. 216 PART III Behavioral and Psychiatric Disorders It is estimated that 20 of children living in the United States experi ence a mental illness in a given year; mental illness is more prevalent than leukemia, diabetes, and AIDS combined. More money is spent on mental disorders than on any other childhood illness, including asthma, trauma, and infectious diseases. Although nearly one in five youths suffers from a psychiatric disorder, 7585 do not receive specialty mental health services; rather most services are delivered in nonspecialty sectors (primary care, schools, child welfare, juvenile jus tice), where mental health expertise may be limited. Untreated or inad equately treated psychiatric disorders persist over decades, become increasingly intractable to treatment, impair adherence to medical treatment regimens, and incur progressively greater social, educa tional, and economic consequences over time. AIMS OF PSYCHOSOCIAL ASSESSMENT IN THE PEDIATRIC SETTING A psychosocial assessment in the pediatric setting should determine whether there are signs and symptoms of cognitive, developmental, emotional, behavioral, or social difficulties and characterize those signs and symptoms sufficiently to determine their appropriate management. The focus of the assessment varies with the nature of the presenting problem and the clinical setting. Under emergency circumstances, the focus may be limited to an assessment of dangerousness to self or oth ers for the purpose of determining the safest level of care. In routine circumstances (well child visits), the focus may be broader, involving a screen for symptoms, distress, and functional impairment in the major psychosocial domains. The challenge for the pediatric practitioner will be to determine as accurately as possible whether the presenting signs and symptoms are likely to meet criteria for a psychiatric disorder and whether the severity and complexity of the disorder suggest referral to a mental health specialist or management in the primary care setting. PRESENTING PROBLEMS Infants may come to clinical attention because of problems with eating andor sleep regulation, concerns about failure to gain weight, poor social responsiveness, limited vocalization, apathy or disinterest, and response to strangers that is excessively fearful or overly familiar. Psy chiatric disorders most commonly diagnosed during this period are rumination and reactive attachment disorders. Toddlers are assessed for concerns about sleep problems, lan guage delay, motor hyperactivity, extreme misbehavior, extreme shyness, inflexible adherence to routines, difficulty separating from parents, struggles over toilet training, dietary issues, and testing lim its. Developmental delays and more subtle physiologic, sensory, and motor processing problems can be presented as concerns. Problems with goodness of fit between the childs temperament and the par ents expectations can create relationship difficulties that also require assessment (see Chapter 19). Mental health disorders most commonly diagnosed during this period are developmental delays, autism spec trum disorder (ASD) and reactive attachment disorders. Presenting problems in preschoolers include elimination difficul ties, sibling jealousy, difficulty forming friendships, self destructive impulsiveness, multiple fears, nightmares, refusal to follow directions, rigidity, somatization, speech that is difficult to understand, and tem per tantrums. Mental health disorders most commonly diagnosed in this period are ASD, communication,
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oppositional, attention deficit hyperactivity (ADHD), anxiety (separation, selective mutism), reactive attachment, and sleep disorders. Older children are brought to clinical attention because of concerns about angry or sad mood, bed wetting, overactivity, impulsiveness, distractibility, learning problems, arguing, defiance, nightmares, school refusal, bullying or being bullied, worries and fears, somatization, com munication problems, tics, and withdrawal or isolation. Mental health disorders most commonly diagnosed during this period are ADHD, oppositional, anxiety (phobias), elimination, somatic symptom, spe cific learning, and tic disorders. Adolescents are assessed for concerns about the family situation, experimentation with sexuality and drugs, delinquency and gang involvement, friendship patterns, issues of independence, identity formation, self esteem, and morality. Mental health disorders most often diagnosed during this period are anxiety (panic, social anxiety), depressive, bipolar, psychotic, obsessive compulsive, impulse control, conduct, substance related, and eating disorders. GENERAL PRINCIPLES OF THE PSYCHOSOCIAL INTERVIEW Psychosocial interviewing in the context of a routine pediatric visit requires adequate time and privacy. The purpose of this line of inquiry should be explained to the child and parents (to make sure things are going OK at home, at school, and with friends), along with the limits of confidentiality. Thereafter, the first goal of the interview is to build rapport with both the child and the parents (see Chapters 18 and 34 for further discussion of strategies for engaging families). With the parents, this rapport is grounded in respect for the parents knowledge of their child, their role as the central influence in their childs life, and their desire to make a better life for their child. Parents often feel anxious or guilty because they believe that problems a child is experiencing imply that their parenting skills are inadequate. Parents experiences of their own childhood influence the meaning a parent places on a childs feelings and behavior. A good working alliance allows mutual discovery of the past as it is active in the present and permits potential distortions to be modified more readily. Developmentally appropriate overtures can facilitate rapport with the child. Examples include playing peek a boo with an infant, racing toy cars with a preschooler, commenting on sports with a child who is wearing a baseball cap, and discussing music with a teenager who is wearing a rock band T shirt. After an overture with the child, it is helpful to begin with family centered interviewing, in which the parent is invited to present any psychosocial concerns (learning, feelings, behavior, peer relationships) about the child. With adolescent patients, it is important to conduct a separate interview to give the adolescent an opportunity to confirm or refute the parents presentation and to present the problem from his or her perspective. Following the familys undirected presentation of the primary problem, it is important to shift to direct questioning to clarify the duration, frequency, and severity of symptoms, associated distress or functional impairment, and the developmental and environmental context in which the symptoms occur. Because of the high degree of comorbidity of psychosocial prob lems in children, after
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eliciting the presenting problem, the pediatric practitioner should then briefly screen for problems in all the major Chapter 32 Psychosocial Assessment and Psychiatric Diagnostic Evaluation Heather J. Walter Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. Chapter 32 u Psychosocial Assessment and Psychiatric Diagnostic Evaluation 217 developmentally appropriate categories of cognitive, developmental, emotional, behavioral, and social disturbance, including problems with mood, anxiety, attention, behavior, substance use, eating, elimina tion, social relatedness, language, and learning. This can be preceded by a transition statement such as, Now Id like to ask about some other issues that I discuss with all parents and kids. Have there been any problems with attention, learning, behavior, sad mood etc. A useful guide for this area of inquiry is provided by the 11 Action Signs (Table 32.1), designed to give frontline clinicians the tools needed to recognize early symptoms of mental disorders. Functional impairment can be assessed by inquiring about symptoms and function in the major life domains, including home and family, school, peers, and community. These domains are included in the HEADSS (Home, Education, Activities, Drugs, Sexuality, SuicideDepression) Interview Guide, often used in the screening of adolescents (Table 32.2). The nature and severity of the presenting problem(s) can be fur ther characterized through a standardized self , parent , or teacher informant symptom rating scale; Table 32.3 lists selected scales in the public domain. A rating scale is a type of measure that provides a relatively rapid assessment of a specific construct with an easily derived numerical score that is readily interpreted. The use of symptom rating scales can ensure efficient, systematic coverage of relevant symptoms, quantify symptom severity, and document a baseline against which treatment effects can be measured. Functional impairment also can be assessed with self and other reported rating scales. Clinical experience and methodologic studies suggest that parents and teachers are more likely than the child to report externalizing problems (disruptive, impulsive, overactive, or antisocial behavior). Children may be more likely to report anxious or depressive feel ings, including suicidal thoughts and acts, of which the parents may be unaware. Discrepancies across informants are common and can shed light on whether the symptoms are pervasive or contextual. Although concerns have been raised about childrens competence as self reporters (because of limitations in linguistic skills, self reflection, emotional awareness, ability to monitor behavior, thoughts, and feel ings, tendency toward social desirability), children and adolescents can both be reliable and valid self reporters. Pediatric practitioners are encouraged to become familiar with the psychometric characteristics and appropriate use of at least one gen eral (broad band) psychosocial screening instrument, such as the Strengths and Difficulties Questionnaire (SDQ) or the Pediatric Symp tom Checklist (PSC) to identify potential mental health problems. If the clinical interview or broad band symptom rating scale suggests difficulties in one or more specific symptom areas, the
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clinician can follow with a psychometrically sound, corresponding narrow band http:www.sdqinfo.orgpysdqinfob0.py. http:www.brightfutures.orgmentalhealthpdfprofessionalspedsymptonchklst.pdf. instrument, such as the Vanderbilt ADHD Diagnostic Rating Scale or Swanson Nolan and Pelham (SNAP) IV 26 for attention and behav ior problems; the Center for Epidemiological Studies Depression Scale for Children (CES DC), Mood and Feelings Questionnaire (MFQ), or Patient Health Questionnaire 9 (PHQ 9) for depression; or the Screen for Child Anxiety Related Emotional Disorders (SCARED) or the Gener alized Anxiety Disorder 7 (GAD 7) for anxiety. Children and adolescents scoring above focused symptom rating scale cutpoints in most cases should undergo a mental health assess ment, because scores above cutpoints are highly correlated with clini cally significant psychiatric disorders. Youths scoring just below or only slightly above cutpoints may be appropriate for preventive intervention (anticipatory guidance) in the pediatric primary care setting. Youths scoring moderately above cutpoints for disorders commonly present ing in pediatric primary care (e.g., anxiety, depression, ADHD) may be appropriate for treatment in primary care. Youths scoring greatly above cutpoints for anxiety, depression, and ADHD, or youths presenting with symptoms of psychiatric disorders nearly always characterized by severity and complexity (e.g., bipolar, psychotic, obsessive compulsive, Table 32.1 Mental Health Action Signs Feeling very sad or withdrawn for more than 2 weeks Seriously trying to harm or kill yourself, or making plans to do so Sudden overwhelming fear for no reason, sometimes with a racing heart or fast breathing Involvement in many fights, using a weapon, or wanting to badly hurt others Severe out of control behavior that can hurt yourself or others Not eating, throwing up, or using laxatives to make yourself lose weight Intense worries or fears that get in the way of your daily activities Extreme difficulty in concentrating or staying still that puts you in physical danger or causes school failure Repeated use of drugs or alcohol Severe mood swings that cause problems in relationships Drastic changes in your behavior or personality From The Action Signs Project. Center for the Advancement of Childrens Mental Health at Columbia University. Table 32.2 HEADSS Screening Interview for Taking a Rapid Psychosocial History PARENT INTERVIEW Home How well does the family get along with each other? Education How well does your child do in school? Activities What does your child like to do? Does your child do anything that has you really concerned? How does your child get along with peers? Drugs Has your child used drugs or alcohol? Sexuality Are there any issues regarding sexuality or sexual activity that are of concern to you? SuicideDepression Has your child ever been treated for an emotional problem? Has your child ever intentionally tried to hurt himherself or made threats to others? ADOLESCENT INTERVIEW Home How do you get along with your parents? Education How do you like school and your teachers? How well do you do in school? Activities Do you have a best friend or group of good friends? What do you like to do? Drugs Have you used drugs or alcohol? Sexuality
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Are there any issues regarding sexuality or sexual activity that are of concern to you? SuicideDepression Everyone feels sad or angry some of the time. How about you? Did you ever feel so upset that you wished you were not alive or so angry you wanted to hurt someone else badly? HEADSS, Home, Education, Activities, Drugs, Sexuality, SuicideDepression. From Cohen E, MacKenzie RG, Yates GL. HEADSS, a psychosocial risk assessment instrument: implications for designing effective intervention programs for runaway youth. J Adolesc Health. 1991;12:539544. Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. 218 Part III u Behavioral and Psychiatric Disorders posttraumatic stress, eating) may be most appropriate for treatment in specialty care. The safety of the child in the context of the home and commu nity is of paramount importance. The interview should sensitively assess whether the child has been exposed to any frightening events, including abuse, neglect, bullying, marital discord, or domestic or community violence; whether the child shows any indication of dangerousness to self or others or a severely altered mental status (psychosis, intoxication, delirium, rage, hopelessness); or whether the child (if age appropriate) has been involved in any risky behav ior, including running away, staying out without permission, tru ancy, gang involvement, experimentation with substances, and unprotected sexual encounters. The interview also should assess the capacity of the parents to adequately provide for the childs physi cal, emotional, and social needs or whether parental capacity has been diminished by psychiatric disorder, family dysfunction, or the sequelae of disadvantaged socioeconomic status. Any indications of threats to the childs safety should be immediately followed by thor ough assessment and protective action. DIAGNOSIS There is variability in the level of confidence pediatric practitio ners perceive in diagnosing mental health problems in children and adolescents in accordance with Diagnostic and Statistical Manual of Mental Disorders (DSM) criteria. Pediatric practitioners who have familiarity with psychiatric diagnostic criteria may feel confident diagnosing certain disorders, particularly the more common neuro developmental, elimination, and eating disorders (ADHD, anxiety, autism spectrum, tics, enuresis, encopresis, anorexia). The disor ders about which some pediatric practitioners might have less diag nostic confidence include the disruptiveimpulse controlconduct, anxiety, depressive, bipolar, psychotic, obsessive compulsive, trauma related, somatic symptom, and substance related disorders. Pediatric practitioners may prefer to use the unspecified diagno sis option in the context of diagnostic uncertainty until clarification is achieved, often through consultation with or referral to a mental health clinician. While focusing on the specific psychiatric manifestations and their appropriate treatment, the practitioner must also take into consideration secondary etiologies (systemic illnesses, substance and medication use Tables 32.4 and 32.5) producing psychiatric symptoms. Disease specific therapy combined with psychopharma cology is often necessary when a systemic disorder is identified. PSYCHIATRIC DIAGNOSTIC EVALUATION The objectives of the psychiatric diagnostic evaluation of the child and adolescent, generally conducted by a behavioral health specialist,
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are to determine whether psychopathology or developmental risk is pres ent and if so, to establish an explanatory formulation and a differen tial diagnosis, and to determine whether treatment is indicated and, if so, to develop a treatment plan and facilitate the parents and childs involvement in the plan. The aims of the diagnostic evaluation are to clarify the reasons for the referral, to obtain an accurate accounting of the childs developmental functioning and the nature and extent of the childs psychosocial difficulties, functional impairment, and subjective distress, and to identify potential individual, family, or environmental factors that might account for, influence, or ameliorate these difficul ties. The issues relevant to diagnosis and treatment planning can span genetic, constitutional, and temperamental factors, individual psy chodynamics, cognitive, language, and social skills, family patterns of interaction and child rearing practices, and community, school, and socioeconomic influences. Table 32.3 Selected List of Mental Health Rating Scales in the Public Domain INSTRUMENTS FOR AGES (YR) INFORMANT: NUMBER OF ITEMS TIME TO COMPLETE (MIN) AVAILABLE AT BROAD BANDGENERALIZED Pediatric Symptom Checklist (PSC) 4 18 Parent: 35, 17 Youth: 35, 17 5 10 https:www.massgeneral.orgpsychiatrytre atments and servicespediatric symptom checklist Strengths and Difficulties Questionnaire (SDQ) 4 18 Parent, Teacher, Child: 25 5 https:www.sdqinfo.org NARROW BANDFOCUSED Anxiety Self Report for Childhood Anxiety Related Emotional Disorders (SCARED) 8 18 Parent, Child: 41 5 https:www.pediatricbipolar.pitt.eduresour cesinstruments Generalized Anxiety Disorder 7 (GAD 7) 12 18 Youth: 7 1 https:www.phqscreeners.com Attention and Behavior Vanderbilt ADHD Diagnostic Rating Scale 6 12 Parent: 55 Teacher: 43 10 https:www.nichq.orgresourcenichq vanderbilt assessment scales Swanson Nolan and Pelham (SNAP) IV 26 6 18 Parent and Teacher: 26 5 http:www.shared care.cafilesScoringfor SNAPIVGuide26 item.pdf Autism Modified Checklist for Autism in Toddlers (M CHAT) 16 30 mo Parent: 23 5 10 https:mchatscreen.com Depression Center for Epidemiological Studies Depression Scale for Children (CES DC) 6 18 Child: 20 5 https:www.brightfutures.orgmentalhealth pdfprofessionalsbridgescesdc.pdf Mood and Feelings Questionnaire (MFQ) 7 18 Parent: 34 Child: 33 5 https:devepi.duhs.duke.edumeasurest he mood and feelings questionnaire mfq Patient Health Questionnaire9 (PHQ 9) 1213 9 5 https:www.phqscreeners.com ADHD, Attention deficithyperactivity disorder. Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. Chapter 32 u Psychosocial Assessment and Psychiatric Diagnostic Evaluation 219 Table 32.4 Medical (Secondary) and Psychiatric (Primary) Causes of Psychosis andor Depression CATEGORY DISORDERS Psychiatric Schizophrenia Schizoaffective Schizophreniform Brief psychotic Major depression Bipolar Postpartum Head trauma Traumatic brain injury Subdural hematoma Infectious Viral infectionsencephalitides (HIV infection encephalopathy, herpes encephalitis, cytomegalo virus, Epstein Barr virus, COVID 19) Lyme disease Cerebral malaria Endocarditis Neurosyphilis Whipple disease Inflammatory Autoimmune encephalitis: NMDAR, limbic, others (see Table 32.5) Systemic lupus erythematosus Sjgren syndrome Hashimoto encephalopathy (steroid responsive encephalopathy associated with autoimmune thyroiditis SREAT) Sydenham chorea Sarcoidosis Celiac disease Neoplastic Primary or secondary cerebral neoplasm Paraneoplastic encephalitis: ovarian teratoma associated autoimmune encephalitis Systemic neoplasm Pheochromocytoma Endocrine or acquired metabolic Hepatic encephalopathy Uremic encephalopathy Hypohyperparathyroidism Hypohyperthyroidism Addison disease Cushing disease Vitamin
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deficiency: vitamin B12, folate, niacin, vitamin C, thiamine Gastric bypassassociated nutritional deficiencies Hypoglycemia Hyponatremia Vascular Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) Other vasculitis syndromes Stroke Degenerative Idiopathic basal ganglia calcifications, Fahr disease Neuroacanthocytosis Neurodegeneration with brain iron accumulation (NBIA) Tuberous sclerosis Huntington disease Corticobasal ganglionic degeneration Multisystem atrophy, striatonigral degeneration, olivopontocerebellar atrophy Demyelinating, dysmyelinating Multiple sclerosis Acute disseminated encephalomyelitis Adrenoleukodystrophy Metachromatic leukodystrophy Inherited metabolic Wilson disease Posterior horn syndrome Tay Sachs disease (adult onset) Neuronal ceroid lipofuscinosis Niemann Pick disease type C Acute intermittent porphyria Mitochondrial encephalopathy, lactic acidosis, and stroke like episodes (MELAS) CATEGORY DISORDERS Mitochondrial neurogastrointestinal encephalopathy (MNGIE) Cerebrotendinous xanthomatosis Homocystinuria Ornithine transcarbamylase deficiency Phenylketonuria Syndromes Williams Prader Willi Marfan Fragile X Deletion 22q11.2 Rapid onset obesity with hypothalamic dysfunction, hypoventilation, autonomic dysregulation (ROHHAD) Klinefelter Epilepsy Ictal Interictal Postictal Postepilepsy surgery Lafora progressive myoclonic epilepsy Complex partial (temporal lobe) Substance induced (medications) Analgesics Acyclovir Androgens (anabolic steroids) Antiarrhythmics Anticonvulsants Anticholinergics Antihypertensives Antineoplastic agents Blocking agents Cefepime Clarithromycin Cyclosporine Dextromethorphan Dopamine agonists Ketamine Fluoroquinolones Metronidazole Sulfamethoxazole trimethoprim Oral contraceptives Sedativeshypnotics Selective serotonin reuptake inhibitors (SSRIs) (serotonin syndrome) Steroids Substance induced Alcohol Amphetamines Cocaine LSD Marijuana and synthetic cannabinoids Methylenedioxymethamphetamine (MDMA, Ecstasy) Phencyclidine Mescaline Psilocybins (mushrooms) Drug withdrawal syndromes Alcohol Barbiturates Benzodiazepines Amphetamines SSRIs Toxins Heavy metals: lead, mercury, arsenic Carbon monoxide Inhalants Organophosphates St. Johns wort Other Normal pressure hydrocephalus Ionizing radiation Decompression sickness Narcolepsy From Byrne R, Elsner G, Beattie A. Emotional and behavioral symptoms. In Kliegman RM, Toth H, Bordini BJ, Basel D (eds): Nelson Pediatric Symptom Based Diagnosis: Common Diseases and their Mimics, 2nd ed. Philadelphia: Elsevier, 2023. Table 31.4, p. 514515. Inherited metabolic (contd) Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. 220 Part III u Behavioral and Psychiatric Disorders Table 32.5 Antigenic Targets in Autoimmune Encephalitis with Associated Psychiatric Features COMMONLY TARGETED ANTIGENS ANTIGEN DESCRIPTION OR EPITOPE MAIN ENCEPHALOPATHY SYNDROME AND PSYCHIATRIC FEATURES OTHER ASSOCIATED NEUROLOGIC DISORDERS MAIN PSYCHIATRIC FEATURES NMDAR Ligand gated ion channel Encephalopathy (frequently extralimbic manifestation) Postherpes simplex encephalitis relapse with chorea; pediatric dyskinetic encephalitis lethargica; idiopathic epilepsy; immunotherapy responsive dementia Anxiety, agitation, bizarre behavior, catatonia, delusional or paranoid thoughts, and visual or auditory hallucinations; also movement disorder, seizures, autonomic instability LGI1 VGKC associated and AMPAR associated secreted molecule Limbic encephalitis with or without faciobrachial dystonic seizures; prominent hyponatremia Morvan syndrome, neuromyotonia, epilepsy, REM sleep behavior disorder; rarely isolated movement disorder (parkinsonism, dystonia, chorea) Confusion, hallucinations, depression CASPR2 VGKC associated adhesion molecule Morvan syndrome: peripheral nerve hyperexcitability, autonomic instability, encephalopathy Limbic encephalitis, neuromyotonia, epilepsy; rarely isolated movement disorder (chorea, myoclonus) Confusion, hallucinations, agitation, delusions AMPAR Ligand gated ion channel Limbic encephalitis NA Personality change, psychosis, apathy, agitation, confabulation GABAAR Ligand gated ion channel Limbic encephalitis with refractory seizures Varied presentations Confusion, anxiety, affective changes (including depression), hallucinations, catatonia GABABR Ligand gated ion channel Limbic encephalitis with refractory status epilepticus Opsoclonus myoclonus;
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cerebellar ataxia; PERM Psychosis, agitation, catatonia Hu Intracellular RNA binding protein Limbic encephalitis or limbic encephalomyelitis occurring with small cell lung cancer Painful sensory neuropathy; cerebellar ataxia Confusion, depression, less commonly hallucinations Ma2 Intracellular protein involved in mRNA processing or biogenesis Limbic encephalitis occurring with testicular germ cell tumors; REM sleep disorder is common; frequent short term memory problems Visual dysfunction, gait disturbance, hypokinesia Confusion and anxiety, including obsessions and compulsions D2R Metabotropic receptor So called basal ganglia encephalitis with prominent movement disorder (i.e., dystonia, parkinsonism, chorea, tics) Sydenham chorea, PANDAS Agitation, depression, psychosis, emotional lability DPPX Auxiliary subunit of Kv4.2 potassium channels Limbic encephalitis with enteropathy PERM Amnesia, delirium, psychosis, depression MGluR5 Metabotropic glutamate receptor So called Ophelia syndrome: limbic encephalitis in association with Hodgkin lymphoma Paraneoplastic limbic encephalitis without lymphoma, or nonparaneoplastic limbic encephalitis; immunotherapy responsive prosopagnosia Depression, anxiety, delusions, visual and auditory hallucinations, personality change, anterograde amnesia GFAP Intracellular (cytosolic) glial intermediate filament protein Corticosteroid responsive meningoencephalitis or encephalitis, with or without myelitis; presents with subacute onset of memory loss and confusion NA Occurred in 29 in one study but not described in detail; psychosis and behavioral changes reported AMPAR, Amino 3 hydroxy 5 methyl 4 isoxazolepropionic acid receptor; CASPR2, contactin associated protein like 2; D2R, dopamine receptor D2; DPPX, dipeptidyl peptidase like protein 6; GABAAR, aminobutyric acid type A receptor; GABABR, aminobutyric acid type B receptor; GFAP, glial fibrillary acidic protein; LGI1, leucine rich glioma inactivated 1; MGluR5, metabotropic glutamate receptor 5; NA, not applicable; NMDAR, N methyl d aspartate receptor; PANDAS, pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections; PERM, progressive encephalomyelitis with rigidity and myoclonus; REM, rapid eye movement; VGKC, voltage gated potassium channel. Modified from Pollak TA, Lennox BR, Muller S, et al. Autoimmune psychosis: an international consensus on an approach to the diagnosis and management of psychosis of suspected autoimmune origin. Lancet Psychiatry. 2020;7(1):93108. Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. Chapter 32 u Psychosocial Assessment and Psychiatric Diagnostic Evaluation 221 The focus of the evaluation is developmental; it seeks to describe the childs functioning in various realms and to assess the childs adaptation in these areas relative to that expected for the childs age and phase of development. The developmental perspec tive extends beyond current difficulties to vulnerabilities that can affect future development and as such are important targets for preventive intervention. Vulnerabilities may include subthreshold or subsyndromal difficulties that, especially when manifold, often are accompanied by significant distress or impairment and as such are important as potential harbingers of future problems. Throughout the assessment, the clinician focuses on identify ing a realistic balance of vulnerabilities and strengths in the child, in the parents, and in the parentchild interactions. From this strength based approach, over time a hopeful family narrative is co constructed to frame the childs current developmental progress and predict the childs
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ongoing progress within the scope of current risk and protective factors. As described earlier a psychiatric assessment conducted by a pediatric primary care practitioner generally will be a brief psy chosocial assessment focused on obtaining sufficient information to triage the case to the appropriate level of care. A brief assess ment can comprise both administration of a focused (narrow band) symptom rating scale to assess symptom severity and a focused clinical interview. The focused clinical interview can comprise four dimensions: history (onset, duration, response to prior treatment, family history), severity (as derived from the focused rating scale and verbal query about the degree of distress andor impairment associated with the symptoms), complexity (brief review of psy chiatric comorbidities and medical or social complexities), and safety (ascertainment of imminent and substantial risk of harm). With this information, the pediatrician can provisionally diagnose the case and triage the case to primary care (for preventive inter vention or treatment of mild to moderate presentations of common disorders e.g., ADHD, anxiety, depression), or to specialty behav ioral healthcare (for severe presentations of these disorders or for other psychiatric disorders nearly always characterized by severity and complexity). In the specialty care setting, although the scope of the evaluation will vary with the clinical setting (e.g., emergency room vs medical floor vs psychiatric clinic), a comprehensive psychiatric diagnos tic evaluation typically has 12 major components: u Presenting problem(s) and the context in which they occur u Review of psychiatric symptoms u History of psychiatric treatment u Medical history u Developmental history u Educational history u Family history u Mental status examination u Biopsychosocial clinical formulation u DSM, Fifth Edition (DSM 5) diagnosis u Risk assessment u Treatment plan For infants and young children, the presenting problem and his torical information is derived from parents and other informants. As children mature, they become increasingly important con tributors to the information base, and they become the primary source of information in later adolescence. Information relevant to formulation and differential diagnosis is derived in multiple ways, including directive and nondirective questioning, interactive play, and observation of the child alone and together with the caregiver(s). The explication of the presenting problem(s) includes infor mation about onset, duration, frequency, setting, and severity of symptoms, associated distress andor functional impairment, and predisposing, precipitating, perpetuating, and ameliorating contex tual factors. The symptom review assesses potential comorbidity in the major domains of child and adolescent psychopathology. The history of psychiatric treatment includes gathering information about prior emergency mental health assessments, psychiatric hos pitalizations, day treatment, psychotherapy, pharmacotherapy, and nontraditional treatments. The medical history includes information about the source of primary care, the frequency of health supervision, past and current medical illnesses and treatments, and the youth and familys history of adherence to medical treatment. A systematic review of organ or functional systems facilitates the identification of abnormalities that require investigation or monitoring by the pediatric practitioner, as well as the identification of cautionary factors related to the prescrip tion of psychotropic medication. The developmental
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history includes information about the circumstances of conception, pregnancy, or adoption, pre , peri , or postnatal insults, attachment and tempera ment, cognitive, motor, linguistic, emotional, social, and moral devel opment, health habits, sexuality, substance use (as age appropriate), coping and defensive structure, future orientation, and perceived strengths. The educational history includes schools attended, typi cal grades, attendance, behavior, classroom accommodations, special education services, disciplinary actions, social relationships, extracur ricular activities, and barriers to learning. The family history assesses family composition, sociodemographic and neighborhood character istics, domiciliary arrangements, parenting capacities, family function, medicalpsychiatric histories of family members, and culturalreligious affiliations. The mental status examination assesses appearance, relatedness, cognition, communication, mood, affective expression, behavior, memory, orientation, and perception. The comprehensive psychiatric evaluation culminates in a biopsy chosocial formulation, diagnosis, and risk assessment. The biopsy chosocial formulation is derived from an assessment of vulnerabilities and strengths in the biologic, psychologic, and social domains and serves to identify targets for intervention and treatment. In the bio logic domain, major vulnerabilities include a family history of psychi atric disorder as well as a personal history of pre , peri , or postnatal insults, cognitive or linguistic impairments, chronic physical illness, and a difficult temperament. In the psychologic domain, major vul nerabilities include failure to achieve developmental tasks, unre solved unconscious conflicts, and maladaptive coping and defensive styles. In the social domain, major vulnerabilities include parental incapacity, unskilled parenting, family dysfunction, social isolation, inadequate school setting, absence of supportive community struc tures, and sociodemographic disadvantage. Major strengths include cognitive and linguistic capability, physical health and vigor, stable, moderate temperamental characteristics, and stable supportive par enting, family, peer, and community structures. The biopsychosocial formulation can be organized to reflect predisposing, precipitating, perpetuating, and protective (ameliorating) factors (the 4 Ps) influ encing the development of the observed psychopathology. The diagnosis is made in accordance with the nomenclature in DSM 5. This nomenclature categorizes cross sectional phenom enology into discrete clinical syndromes and seeks to improve diagnostic accuracy at the expense of theories of causation. By DSM 5 convention, if diagnostic criteria are met, the diagnosis is given (except where hierarchical rules apply); consequently, psychi atric comorbidity is a common occurrence. The risk assessment includes a careful assessment of risk status, including suicidality, homicidality, assaultiveness, self injuriousness, acute mental status changes, and involvement in risky behavior or situations. The comprehensive psychiatric diagnostic evaluation culmi nates in a treatment plan that brings the broad array of targeted interventions to the service of the child. Diagnoses drive the choice of evidence based psychotherapeutic and psychopharmacologic treatments. The formulation drives the selection of interventions targeted at biologic, psychologic, and social vulnerabilities and strengths. Many of these treatments and interventions are described in the succeeding chapters. Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. 222 Part III u Behavioral and Psychiatric Disorders SPECIAL CONSIDERATIONS IN THE
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DIAGNOSTIC EVALUATION OF INFANTS AND YOUNG CHILDREN Evaluation of infants and young children with challenging behaviors includes the domains of physiology, temperament, language and motor development, affective behavior, social behavior, and communication. Although much of the information in these domains will be derived from parent report, much also can be gleaned from nonverbal behavior and observation of the parentchild interaction. Observations should include predominant affective tone of parent and child (positive, negative, apa thetic), involvement in the situation (curiosity, disinterest), social respon siveness (mutuality of gaze, auditory responsiveness), and reactions to transitions (including separation). A screen for maternal depression is critical at this stage, as is an assess ment of the mothers (or other caregivers) ability to respond rapidly on a contingent basis to the childs expressed needs, regulate the childs rapid shifts of emotion and behavior, and provide a stimulus shelter to prevent the child from being overwhelmed. Standardized screening instruments (Ages and Stages Questionnaires, Brief Infant Toddler Social Emotional Assessment, Early Childhood Screening Assessment, Modified Checklist for Autism in Toddlers, Par ents Evaluation of Developmental Status, and Survey of Well being of Young Children) designed for this age group can be helpful in systematiz ing the evaluation. In addition, the Infant, Toddler and Preschool Mental Status Exam (ITP MSE) is a reference tool that describes how traditional categories of the mental status examination can be adapted to observa tions of young children. Additional categories, including sensory and state regulation, have been added that reflect important areas of development in young children. Diagnostic systems that are more age appropriate than DSM 5 have been developed for infants and young children. These systems include the Research Diagnostic CriteriaPreschool Age (RDC PA) and Zero to Three Diagnostic Classification of Mental Health and Developmen tal Disorders of Infancy and Early Childhood Revised (DC: 0 3R). The DC: 0 3R includes a relationship classification that assesses the range of interactional adaptation in each parentchild relationship and regu lation disorders of sensory processing that identify a range of consti tutionally and maturationally based sensory reactivity patterns, motor patterns, and behavior patterns that together can dysregulate a child internally and impact the childs interactions with caregivers. Visit Elsevier eBooks at eBooks.Health.Elsevier.com for Bibliography. See http:www.medicalhomeportal.orgclinical practicescreening and preventionmaternal depression for several examples. Psychopharmacology is the first line treatment for several child and adolescent mental health disorders (e.g., attention deficithyperactiv ity ADHD, schizophrenia spectrum, and bipolar disorders) and is used adjunctively with psychosocial treatments for other disorders (or comorbid conditions), including anxiety, depressive, autism spectrum, trauma related, and obsessive compulsive disorders. Before prescribing a psychotropic medication, primary care practitioners (PCPs) should review full prescribing information for each medication (in package inserts or at reliable websites such as the National Institutes of Health DailyMed) to obtain complete and up to date information about indi cations, contraindications, warnings, interactions, and precautions. https:dailymed.nlm.nih.govdailymedindex.cfm. Chapter 33 Psychopharmacology David R. DeMaso and Heather J. Walter It is helpful for PCPs to be guided by principles for effective use of psychotropic medications
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in their medication assessment and manage ment (Table 33.1). These principles involve a series of interconnected steps, including conducting a focused behavioral health assessment, establishing target symptom(s) and appropriate level of care, deciding on a medication and a monitoring plan, obtaining treatment assent consent, and implementing treatment. In following this approach, PCPs are well positioned to provide safe and effective first line psy chopharmacology for common mental health conditions (e.g., ADHD, anxiety, depression) with moderate symptom presentations. Severe complex presentations likely are better served through consultation with andor referral to a behavioral health specialist. Questions remain about the quality of the evidence supporting the use of many psychotropic medications in children and adolescents. In general, cognitive, emotional, and behavioral symptoms are targets for medication treatment when (1) there is no or insufficient response to available evidence based psychosocial interventions, (2) the patients symptoms are severe and the patient is experiencing significant distress or functional impairment, andor (3) the patients symptoms convey significant risk of harm. Common target symptoms include agita tion, aggression, anxiety, depression, mania, hyperactivity, inattention, impulsivity, obsessions, compulsions, and psychosis (Table 33.2). All these symptoms can be quantitatively measured with standardized rat ing scales to establish baseline symptom severity and facilitate treating to target. STIMULANTS AND OTHER ADHD MEDICATIONS Stimulants are sympathomimetic drugs that act both in the central ner vous system (CNS) and peripherally by enhancing dopaminergic and noradrenergic transmission (Table 33.3). Strong evidence (approxi mate effect size 1.00, large) exists for the effectiveness of these medi cations for the treatment of ADHD (Chapter 50); stimulants also are effective for the management of aggression. In some cases, stimulants have been used as monotherapy for fatigue or malaise associated with chronic physical illnesses. No major differences in efficacy or tolerability have been found between different classes of stimulants, and no consistent patient pro file identifies those who will respond preferentially to one class over another. The most common (generally dose dependent) side effects of stimulants include headache, stomachache, appetite suppression, weight loss, blood pressure (BP) and heart rate increases, and delayed sleep onset. Less common side effects include irritability (more promi nent in younger children), aggression, social withdrawal, and rarely, hallucinations (visual or tactile). Stimulants have been associated with elevations in mean BP (5 mm Hg) and pulse (10 beatsmin); a subset of individuals (510) may have greater increases. The rate of sudden death in pediatric patients taking stimulants is comparable to children in the general population; the hazard ratio for serious cardiovascular (CV) events is 0.75 (although up to a twofold increase in risk could not be ruled out). Moreover, a case series analysis of children with a CV incident and treatment with methylphenidate demonstrated an increased risk of arrhythmia (inci dence rate ratio, 1.61) that was highest in the presence of congenital heart disease. The U.S. Food and Drug Administration (FDA) recom mends that stimulants should be avoided in the presence of structural cardiac abnormalities (e.g., postoperative tetralogy of Fallot, coronary artery abnormalities, subaortic stenosis, hypertrophic
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cardiomyopa thy) and patient symptoms (syncope, palpitations, arrhythmias) or family history (e.g., unexplained sudden death) suggestive of CV dis ease. In these circumstances, cardiology consultation is recommended before prescribing. Routine electrocardiograms (ECGs) are not recom mended in the absence of cardiac risk factors. The adrenergic agents clonidine and guanfacine are presynap tic adrenergic agonists that appear to stimulate inhibitory presynaptic autoreceptors in the CNS (see Table 33.3). The extended release formu lations of both agents have FDA approval for ADHD. The extended release formulation of guanfacine has strong evidence (approximate effect size 0.80, large) for the monotherapy of ADHD. Extended release guanfacine also has moderate evidence for effective treatment Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. Chapter 33 u Psychopharmacology 223 Table 33.1 Principles for Effective Use of Psychotropic Medications Identify potential target symptoms using broad mental health screening instruments (e.g., Pediatric Symptom Checklist PSC 17) Conduct focused behavioral health (BH) assessment to establish target symptoms and appropriate level of care Focused symptom rating scales, e.g., Patient Health Questionnaire 9 (PHQ 9) Mood and Feelings Questionnaire (MFQ) Screen for Child Anxiety Related Disorders (SCARED) Generalized Anxiety Disorder 7 (GAD 7) Vanderbilt ADHD Diagnostic Rating Scales Swanson Nolan and Pelham IV 26 (SNAP IV 26) Focused clinical interview to determine symptom history, severity (from focused rating scale score), complexity (psychiatric comorbidities, medical or psychosocial complexity), and safety (imminent risk of substantial harm) If insufficient information is available to render a precise diagnosis for a symptom cluster, consider applying Unspecified Diagnostic and Statistical Manual of Mental Disorders 5 (DSM 5) psychiatric diagnosis Rule out alternative explanations (medical, medication, substance, or developmental masqueraders) for target symptoms (may require specialty referral) Establish appropriate level of care based upon findings from focused BH assessment Subclinical to mild presentation: triage to brief preventive intervention (e.g., anticipatory guidance) Moderate presentation: triage to primary care for basic psychopharmacology andor brief psychosocial intervention Severe presentation: triage to specialty behavioral healthcare for comprehensive diagnostic evaluation, advanced psychopharmacology, andor specialized psychotherapy Rule out relative or absolute contraindications to medication use, e.g., Medical conditions Drug interactions Inability to monitor (e.g., unreliable parentguardian, patient residing out of town) Concern about drug diversion in the context of substance abuse or antisocial behavior Counsel about factors potentially contributing to symptom presentation or affecting response to medication Inadequate nutrition, physical activity, sleep, recreation, stress management; substance use Consider response to previous medication trials Favorable and adverse effects Develop comprehensive treatment plan as indicated Psychotherapy andor medication Home andor school interventions Obtain informed consent from parentguardian and assent from patient Nature of the condition needing treatment Nature and purpose of proposed treatment and the probability that it will succeed Risks and benefits of the proposed treatment Alternatives to the proposed treatment, and their attendant risks and benefits Prognosis with and without the proposed treatment Select evidence based medication and prescribe
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an adequate dose for an adequate duration; whenever possible, U.S. Food and Drug Administration (FDA) approved medications for the given indication should be prioritized Titrate to effective tolerated dose within established dosage range Consider the period of time needed for each medication to achieve maximum effect Start low, go slow Explain details of medication management Name of medication When to administer Who should administer (e.g., parent, older teen) How to administer (e.g., with food, swallowed whole) Time to onset Duration of action How to store medication Review of side effects and what to do if each should occur How response to medication will be monitored (e.g., focused symptom rating scales, heightweight, pulseblood pressure, side effect checks) Special safety instructions (e.g., suicidal thoughts, severe agitation) What the next step will be if medication is ineffective or not tolerated How long medication likely will need to be taken if effective Consider providing parent with standardized Medication Guide, such as those found at https:dailymed.nlm.nih.govdailymedindex.cfm Monitor medication compliance and physicallaboratory parameters as indicated Monitor response to treatment Periodic readministration of focused symptom rating scale(s); adjust dose as indicated to achieve remission Taper and discontinue ineffective medication before substituting alternative medication, or have clear rationale for using medication combinations Plan for medication discontinuation after symptom free and high functioning interval of ADHD with comorbid oppositional defiant disorder (ODD), favor ably affecting both symptom clusters, as well as for the treatment of agitation in autism. Sedation, somnolence, headache, abdominal pain, hypotension, bra dycardia, cardiac conduction abnormalities, dry mouth, depression, and confusion are potential side effects of clonidine and guanfacine. Abrupt withdrawal can result in rebound hypertension; overdose can result in bradycardia and hypotension leading to hospitalization or death. Atomoxetine is a selective inhibitor of presynaptic norepinephrine reuptake that increases dopamine and norepinephrine in the prefrontal cortex (see Table 33.3). It is less effective for the treatment of ADHD (approximate effect size 0.60, medium) than stimulants, but atomoxetine has a longer duration of action (approximately 24 hours). Atomoxetine can have an onset of action within 1 2 weeks of starting treatment, but there is an incrementally increasing response for up to 4 6 weeks or longer. Common side effects include nausea, headache, abdominal pain, insomnia, somnolence, erectile dysfunction, irritability, fatigue, Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. 224 Part III u Behavioral and Psychiatric Disorders decreased appetite, weight loss, and dizziness, along with nonclinical increases in heart rate and BP. Potential serious neuropsychiatric reac tions include psychosis, mania, panic attacks, aggressive behavior, depression, seizures, and suicidal thinking. Atomoxetine carries an FDA warning regarding the risk of suicidal thinking and the need to monitor this closely. Atomoxetine also has been associated with rare hepatotoxic ity and should be discontinued in patients with jaundice or laboratory evidence of liver injury, and should not be restarted. Because of the risk of sudden death,
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atomoxetine generally should be avoided in youth with known serious structural cardiac abnormalities, cardiomyopathy, heart rhythm abnormalities, or other serious cardiac problems. Viloxazine is a second selective norepinephrine reuptake inhibitor that was approved for ADHD by the FDA in 2021. It has once daily dos ing, reaches steady state by day 2, and has a similar side effect profile to atomoxetine (including FDA warnings on suicidality and increases in heart rate and blood pressure). ANTIDEPRESSANTS Antidepressant drugs act on presynaptic and postsynaptic receptors affecting the release and reuptake of brain neurotransmitters, including norepinephrine, serotonin, and dopamine (Table 33.4). There is mod erate evidence for the effectiveness of antidepressant medications in the treatment of anxiety and obsessive compulsive disorders (approxi mate effect size 0.70, medium) and weaker evidence for the treatment of depressive disorders (approximate effect size 0.30, small). Suicidal thoughts have been reported during treatment with all antidepressants. The overall risk difference of suicidal thoughtsbehaviors across ran domized controlled trials (RCTs) of all antidepressants and all indica tions has been reported as 0.7, corresponding to a number needed to harm of 143. All antidepressants carry an FDA warning for suicidality; careful monitoring is recommended during the initial stages of treat ment and following dose adjustments. The selective serotonin reuptake inhibitor (SSRI) fluoxetine out performs all other antidepressants (both SSRI and non SSRI) studied and is the only SSRI separating from placebo in studies of depressed preadolescents. Side effects to SSRIs generally manifest in the first few weeks of treatment, and many will resolve with time. More common side effects include nausea, irritability, insomnia, appetite changes, weight lossgain, headaches, dry mouth, dizziness, bruxism, diapho resis, tremors, akathisia, and restlessness. A small proportion of youth taking SSRIs, particularly younger children, develop behavioral acti vation (motor or mental restlessness, increased impulsivity, disin hibited behavior, talkativeness, insomnia) that can be confused with mania, but the activation symptoms typically resolve when the dose is decreased or the medication discontinued. Because the likelihood of activation events has been associated with higher antidepressant plasma levels, slow up titration and close monitoring (particularly in younger children) is warranted and underscores the importance of educating parentsguardians and patients in advance about this poten tial side effect. Sexual side effects are common, including decreased libido, anor gasmia, and erectile dysfunction. There is an increased risk of bleeding, especially when used with aspirin or nonsteroidal antiinflammatory drugs (NSAIDs). SSRIs can be associated with abnormal heart rhythms, and cita lopram causes dose dependent QT interval prolongation, contrain dicating doses 40 mgday. Patients with diabetes may experience hypoglycemia during SSRI treatment and hyperglycemia on discontin uation. Discontinuation symptoms (e.g., dysphoric mood, irritability, agitation, dizziness, sensory disturbances, anxiety, confusion, head ache, lethargy, emotional lability, insomnia, hypomania) are common with short acting SSRIs (sertraline, citalopram, escitalopram), leading to a recommendation for divided doses if these medications are used at higher doses and graduated reduction if discontinued. Serotonin syndrome results from excessive agonism of the CNS and peripheral nervous system serotonergic receptors and can be caused
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by prescribing multiple serotonergic medications concomitantly (Chap ter 94). Symptoms can arise within 24 48 hours and are characterized by mental status changes (confusion, agitation, anxiety), neuromus cular hyperactivity (tremors, clonus, hyperreflexia, muscle rigidity), and autonomic hyperactivity (hypertension, tachycardia, arrhythmias, tachypnea, diaphoresis, shivering, vomiting, diarrhea). Advanced symptoms include fever, seizures, arrhythmias, and unconsciousness, which can lead to fatalities. Treatment is hospital based and includes discontinuation of all serotonergic agents and supportive care with con tinuous cardiac monitoring. Monoamine oxidase inhibitors (MAOIs) play a role in most cases of serotonin syndrome and should be avoided in combination with any other serotonergic drug, including another MAOI. Moreover, caution should be exercised when combining two or more non MAOI serotonergic drugs, including antidepressants, opi oids and other pain medications, stimulants, coughcoldallergy medi cations, and other over the counter products. Caution entails starting the second non MAOI serotonergic drug at a low dose, increasing the dose slowly, and monitoring for symptoms, especially in the first 24 48 hours after dosage changes. Adolescents should be informed that cer tain recreational drugs (e.g., dextromethorphan, ecstasy) are highly serotonergic and can cause serious interactions with antidepressants. The non SSRI antidepressants include duloxetine, venlafaxine, bupropion, and mirtazapine (see Table 33.4). These medications all lack rigorous evidence to support their effectiveness in children and adolescents and as such should not be considered first line options. Duloxetine and venlafaxine are serotonin norepinephrine reup take inhibitors (SNRIs). Duloxetine has FDA approval for treatment of generalized anxiety disorder in children and adolescents but typi cally is not as effective for anxiety as the SSRIs. Studies of duloxetine for depression in youth have been negative. There is some evidence in adults that duloxetine can be useful for fibromyalgia and chronic mus culoskeletal pain, an effect that has also been observed in children and adolescents. Common side effects of duloxetine include nausea, diar rhea, decreased weight, and dizziness. Increases in heart rate and BP have been noted; BP should be monitored at each visit and with each dosage change. In addition, there have been reports of hepatic failure, sometimes fatal; duloxetine should be discontinued and not resumed in patients who develop jaundice or other evidence of liver dysfunc tion. Duloxetine also has been associated with severe skin reactions (erythema multiforme and Stevens Johnson syndrome). Table 33.2 Target Symptom Approach to Psychopharmacologic Management TARGET SYMPTOM MEDICATION CONSIDERATIONS Aggression Stimulant Agonist Antipsychotic (only if aggression is severe or dangerous) Agitation Antipsychotic (only if agitation is severe or dangerous) Anxiolytic Anxiety Antidepressant Anxiolytic (only for acute situational anxiety) Depression Antidepressant Hyperactivity, inattention, impulsivity Stimulant Agonist Selective norepinephrine reuptake inhibitor Mania Antipsychotic Lithium Obsessions, compulsions Antidepressant Psychosis Antipsychotic Tics Agonist Antipsychotic (only if tics are severe disabling) Adapted from Shaw RJ, DeMaso DR. Clinical Manual of Pediatric Consultation Liaison Psychiatry. Washington, DC: American Psychiatric Press, 2020: 443. Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc.
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All rights reserved. Chapter 33 u Psychopharmacology 225 Table 33.3 Select Medications for Attention DeficitHyperactivity Disorder Symptoms GENERIC BRAND (HOW SUPPLIED) DURATION OF ACTION FDA APPROVED (AGE RANGE IN YEARS) TARGET SYMPTOMS SUGGESTED DAILY STARTING DOSE (MG) USUAL DAILY THERAPEUTIC DOSAGE RANGE (MG) Methylphenidate Concerta (18, 27, 36, 54 mg caps) 12 hr ADHD (6) Inattention Hyperactivity Impulsivity 18 Age 6 12: 18 54; Age 12: 18 72 Dexmethylphenidate Focalin XR (5, 10, 15, 20 mg caps) 10 12 hr ADHD (6) Inattention Hyperactivity Impulsivity 5 5 30 Serdexmethylphenidate dexmethylphenidate Azstarys (26.1 mg5.2 mg, 39.2 mg7.8 mg, 52.3 mg10.4 mg) 12 hr ADHD (6) Inattention Hyperactivity Impulsivity 26.1 5.2 26.1 5.252.310.4 Methylphenidate suspension, extended release Quillivant XR (25 mg5 mL) 12 hr ADHD (6) Inattention Hyperactivity Impulsivity 10 10 60 Dextroamphetamine amphetamine Adderall XR (5, 10, 15, 20, 25, 30 mg caps) 12 hr ADHD (6) Inattention Hyperactivity Impulsivity 2.5 5 5 30 Lisdexamfetamine Vyvanse (10, 20, 30, 40, 50, 60, 70 mg caps; 10, 20, 30, 40, 50, 60 mg chewable tabs) 12 14 hr ADHD (6) Inattention Hyperactivity Impulsivity 10 10 70 Amphetamine suspension extended release Dyanavel XR (2.5mL) 13 hr ADHD (6) Inattention Hyperactivity Impulsivity 2.5 5 2.5 20 Methylphenidate Metadate CD (10, 20, 30, 40, 60 mg caps) 8 hr ADHD (6) Inattention Hyperactivity Impulsivity 10 10 60 Methylphenidate Ritalin LA (10, 20, 30, 40 mg caps) 8 hr ADHD (6) Inattention Hyperactivity Impulsivity 10 10 60 Dextroamphetamine Dexedrine Spansule (5, 10, 15 mg spansules) 6 8 hr ADHD (6) Inattention Hyperactivity Impulsivity 5 540 Dexmethylphenidate Focalin (2.5, 5, 10 mg tabs) 4 5 hr ADHD (6) Inattention Hyperactivity Impulsivity 2.5 5 5 20 Methylphenidate Ritalin (5, 10, 20 mg tabs) 4 hr ADHD (6) Inattention Hyperactivity Impulsivity 2.5 5 5 60 Methylphenidate Methylin (5 mg5 mL, 10 mg5 mL) 4 hr ADHD (6) Inattention Hyperactivity Impulsivity 2.5 5 5 60 Dextroamphetamine amphetamine Adderall (5, 10, 15, 20, 30 mg tabs) 4 5 hr ADHD (3) Inattention Hyperactivity Impulsivity Age 3 5: 2.5 Age 6: 5 Age 6 12: 5 30; Age 12: 5 40 Continued Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. 226 Part III u Behavioral and Psychiatric Disorders Bupropion, a norepinephrine dopamine reuptake inhibitor (NDRI), appears to have an indirect mixed agonist effect on norepi nephrine and dopamine transmission. No rigorous studies of bupro pion for anxiety or depression have been conducted with children or adolescents, although some evidence suggests that bupropion may be effective for smoking cessation and ADHD in youth. Common side effects include irritability, nausea, anorexia, headache, and insomnia. Dose related seizures (0.1 risk at 300 mgday and 0.4 risk at 400 mgday) have occurred with bupropion, so it is contraindicated in those with epilepsy, eating disorders, or at risk for seizures. Venlafaxine has only negative trials for the treatment of depression in
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children and adolescents but does have some favorable evidence for the treatment of anxiety. Side effects are similar to SSRIs, including hypertension, irritability, insomnia, headaches, anorexia, nervousness, and dizziness, and dropout rates are high in clinical trials of venlafax ine. BP should be monitored at each visit and with each dosage change. Discontinuation symptoms are more pronounced with venlafaxine than the other non SSRI antidepressants. In addition, suicidal thinking and agitation may be more common with venlafaxine than with other antidepressants, requiring close monitoring. In light of the substantial adverse effects, venlafaxine likely should be considered to be a third line medication. Mirtazapine is both a noradrenergic and a specific serotonergic antidepressant. Mirtazapine has only negative trials for the treat ment of depression in youth and has no rigorous evidence of effec tiveness for any other child or adolescent psychiatric disorder. Mirtazapine is associated with a risk for substantial weight gain and, more rarely, hypotension, elevated liver enzymes, agranulocytosis, and QT prolongation. Although its sedating properties have led to its adjunctive use for insomnia in adults with depressiveanxiety disorders, there is no evidence for use of mirtazapine in childhood sleep disorders. The tricyclic antidepressants (TCAs) have mixed mechanisms of action; for example, clomipramine is primarily serotonergic, and imip ramine is both noradrenergic and serotonergic. With the advent of the SSRIs, the lack of efficacy studies, particularly in depression, and more serious side effects, the use of TCAs in children and adolescents has substantially declined. Clomipramine has been used in the treatment of obsessive compulsive disorder (see Table 33.4). TCAs also have been used for neuropathic pain. TCAs cause both blood pressure and heart rate increases and are class I antiarrhythmics with quinidinelike prop erties that are potentially fatal in overdose. Anticholinergic symptoms (e.g., dry mouth, blurred vision, constipation) are the most common side effects. Anxiolytic agents, including lorazepam, clonazepam, and hydroxy zine, have been effectively used for the short term relief of the symp toms of acute anxiety (see Table 33.4). They are less effective as chronic (4 months) anxiolytic medications, particularly when used as mono therapy. Chronic use carries a significant risk of physical and psycho logic dependence. ANTIPSYCHOTICS Based on their mechanism of action, antipsychotic medications can be divided into first generation (blocking dopamine D2 receptors) and second generation (mixed dopaminergic and serotonergic antago nists) agents (Table 33.5). The second generation antipsychotics (SGAs) have relatively strong antagonistic interactions with 5 HT2 receptors and perhaps more variable activity at central adrenergic, cholinergic, and hista minic sites, which might account for the varying side effects, particu larly metabolic, noted among these agents. The SGAs have moderate evidence for the treatment of agitation in autism and for the treatment of schizophrenia, bipolar disorder, and aggression. Haloperidol is a Table 33.3 Select Medications for Attention DeficitHyperactivity Disorder Symptomscontd GENERIC BRAND (HOW SUPPLIED) DURATION OF ACTION FDA APPROVED (AGE RANGE IN YEARS) TARGET SYMPTOMS SUGGESTED DAILY STARTING DOSE (MG) USUAL DAILY THERAPEUTIC DOSAGE RANGE (MG) Dextroamphetamine Dexedrine (5, 10, 15, mg caps) 4
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hr ADHD (3) Inattention Hyperactivity Impulsivity Age 3 5: 2.5 Age 6: 5 5 40 Atomoxetine Strattera (10, 18, 25, 40, 60, 80, 100 mg caps) 24 hr ADHD (6) Inattention Hyperactivity Impulsivity 70 kg: 0.5 mgkgday 70 kg: 40 70 kg: 0.5 1.2 mgkgday 70 kg: 40 100 Viloxazine Qelbree (100, 150, 200 mg ER caps) 24 hr ADHD (6) Inattention Hyperactivity Impulsivity Age 6 11: 100 Age 12: 200 Age 6 11: 100 400 Age 11: 200 400 Clonidine Kapvay (0.1 mg tabs) 12 hr ADHD (6) Inattention Hyperactivity Impulsivity 0.05 2540kg: 0.050.2 4145kg: 0.050.3 45kg: 0.050.4 Guanfacine Intuniv (1, 2, 3, 4 mg tabs) 24 hr ADHD (6) Inattention Hyperactivity Impulsivity 1 2540kg: 12 4145kg: 13 45kg: 14 Clonidine Catapres (0.1, 0.2, 0.3 mg tabs) 4 hr None Inattention Hyperactivity Impulsivity 0.05 25 40 kg: 0.05 0.2 41 45 kg: 0.05 0.3 45 kg: 0.05 0.4 Guanfacine Tenex (1, 2 mg tabs) 6 hr None Inattention Hyperactivity Impulsivity 0.5 25 40 kg: 0.5 2 mg 41 45 kg: 0.5 3 mg 45 kg: 0.5 4 mg Doses shown in table may exceed maximum recommended dose for some children. Capsule contents may be sprinkled on soft food. ADHD, Attention deficithyperactivity disorder; FDA, U.S. Food and Drug Administration. Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. Chapter 33 u Psychopharmacology 227 high potency first generation antipsychotic that is most commonly used in treatment of agitation and schizophrenia. The antipsychotic agents have significant side effects, including sedation, extrapyramidal symptoms, hyperprolactinemia, anticho linergic, seizures, orthostasis, CV effects, weight gain, hyperlip idemia, metabolic syndrome, glucose abnormalities, hematologic effects (e.g., leukopenia, neutropenia), and elevated liver transami nases (Table 33.6). They have an FDA warning for increased risk of diabetes. Youth appear to be more sensitive to sedation, extra pyramidal side effects (except akathisia), withdrawal dyskinesia, prolactin abnormalities, weight gain, hepatotoxicity, and metabolic abnormalities. The development of diabetes or tardive dyskinesia appears less prevalent than in adults, although this may be a func tion of short follow up periods because these side effects may not emerge until adulthood. The management of adverse effects should be proactive with base line assessment and ongoing monitoring (Table 33.7). Abnormal movements (dystonia, akathisia, tardive dyskinesia) need periodic assessment using a standardized instrument such as the Abnormal Involuntary Movement Scale (AIMS). The need for antiparkinsonian agents may be a consideration, particularly for patients at risk for acute dystonia or who have a previous history of dystonic reactions. CV effects include prolongation of the QTc interval, tachycardia, orthostatic hypertension, and pericarditis. In patients with a per sonal or family history of cardiac abnormalities, including syncope, palpitations, arrhythmias, or sudden unexplained death, a baseline ECG with subsequent monitoring should be considered, along with cardiology consultation before prescribing. Alternative pharma cology should be considered if the resting heart rate exceeds 130 beatsmin, or the PR, QRS,
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and QTc exceed 200, 120, and 460 msec, respectively. The cytochrome P450 (CYP) enzymes metabolize the antipsychot ics and as such necessitate that the PCP and psychiatrist are alert for potential drug drug interactions that may impact the serum levels of all patient medications. CYP3A4 is mainly relevant to lurasidone, quetiapine, olanzapine, and haloperidol, whereas CYP2D6 predomi nately clears aripiprazole and risperidone. Asenapine is metabolized by CYP1A2 as well as direct glucuronidation by UGT1A4. Because 10 of paliperidone undergoes CYP first pass metabolism, there is a lower likelihood of drug drug interactions. Primary prevention strategies to manage weight and metabolic dys function include educating the youth and family about healthy lifestyle behaviors and selecting an agent that has the lowest likelihood of impacting metabolic status. Secondary strategies would include intensifying healthy lifestyle instructions, consideration of switch ing agents, and a weight loss treatment program. Consideration Table 33.4 Select Medications for Depression and Anxiety in Children and Adolescents GENERIC BRAND (HOW SUPPLIED) FDA APPROVED (AGE RANGE IN YEARS) TARGET SYMPTOMS SUGGESTED DAILY STARTING DOSE (MG) USUAL DAILY THERAPEUTIC DOSAGE RANGE (MG) Citalopram Celexa (10, 20, 40 mg tabs) None Depression Anxiety Obsessions Compulsions Age 612: 10 Age 1317: 20 10 40 Escitalopram Lexapro (5, 10, 20 mg tabs) Depression (12 17) Anxiety (717) Depression Anxiety Obsessions Compulsions 10 5 20 Fluoxetine Prozac (10, 20, 40, 60 mg tabs) Depression (8 17) OCD (7 17) Depression Anxiety Obsessions Compulsions Age 6 12: 10 Age 13 17: 20 Depression: 10 20 Anxiety, OCD: 10 60 Sertraline Zoloft (25, 50, 100 mg tabs) OCD (6 17) Depression Anxiety Obsessions Compulsions Age 6 12: 12.5 25 Age 13 17: 25 50 25200 Duloxetine Cymbalta (20, 30, 60 mg tabs) Anxiety (7 17) Depression Anxiety 30 30 60 Venlafaxine Effexor XR (37.5, 75, 150 mg caps) None Depression Anxiety 37.5 37.5 225 Bupropion Wellbutrin XL (150, 300 mg tabs) None Depression 150 150 300 Mirtazapine Remeron (15, 30, 45 mg tabs) None Depression 7.5 7.5 45 Clomipramine Anafranil (25, 50, 75 mg caps) OCD (10 17) Obsessions Compulsions 25 25 200 Lorazepam Ativan (0.5, 1, 2 mg tabs) None Acute anxiety 0.5 0.5 2 Clonazepam Klonopin (0.5, 1, 2 mg tabs) None Panic 0.5 0.5 1 Hydroxyzine Vistaril (25, 50 mg caps) Anxiety Acute anxiety Age 12: 12.525 Age 12: 2550 Age 12: 2550 Age 12: 50100 Doses shown in table may exceed maximum recommended dose for some children. Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. 228 Part III u Behavioral and Psychiatric Disorders of weight management interventions and increased monitoring of blood glucose and lipid levels should be implemented if weight gain exceeds the 90th percentile of body mass index (BMI) for age, or a change of 5 BMI units in youth who were obese at the initiation of treatment. Tertiary strategies, where diabetes, hypertension, obe sity, or
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another metabolic abnormality has occurred, require more intensive weight reduction interventions, changing medication, and consultation with a medical subspecialist. Metformin has been found to be an effective treatment for antipsychoticinduced weight gain in children with autism spectrum disorder. Extrapyramidal adverse effects are generally dose and titration ratedependent and may respond to dose or titration rate reductions. More disabling effects may benefit from adjunctive treatment (e.g., anticholinergics, antihistamines). Neuroleptic malignant syndrome is a rare, potentially fatal reaction that can occur during antipsychotic therapy (see Chapter 94). The syndrome generally manifests with fever, muscle rigidity, autonomic instability, and delirium. It is associated with elevated serum creatine phosphokinase levels, a metabolic acidosis, and high end tidal CO2 excretion. It has been estimated to occur in 0.21 of patients treated with dopamine blocking agents. Malnutrition and dehydration in the context of an organic brain syndrome and simultaneous treatment with lithium and antipsychotic agents (par ticularly haloperidol) can increase the risk. Mortality rates may be as high as 2030 as a result of dehydration, aspiration, kidney fail ure, and respiratory collapse. Differential diagnosis of neuroleptic malignant syndrome includes infections, heat stroke, malignant hyperthermia, lethal catatonia, agitated delirium, thyrotoxico sis, serotonin syndrome, drug withdrawal, and anticholinergic or amphetamine, ecstasy, and salicylate toxicity. MOOD STABILIZERS Because of their limited evidence of effectiveness and concerns about safety, mood stabilizing medications (see Table 33.5) have limited use in the treatment of child and adolescent psychiatric disorders. For the treatment of bipolar mania in adolescents, antipsychotics are consid ered first line therapy. Of the mood stabilizers, lithium alone has rigorous support for the treatment of bipolar mania. Lithiums mechanism of action is not well understood; proposed theories relate to neurotransmission, endocrine effects, circadian rhythm, and cellular processes. Com mon side effects include polyuria and polydipsia, hypothyroidism, Table 33.5 Select Medications for Psychosis, Mania, Irritability, Agitation, Aggression, and Tourette Disorder in Children and Adolescents GENERIC (BRAND) FDA APPROVED (AGE RANGE IN YEARS) TARGET SYMPTOMS SUGGESTED DAILY STARTING DOSE USUAL DAILY THERAPEUTIC DOSAGE RANGE (MG) Aripiprazole Abilify Bipolar (10 17) Schizophrenia (13 17) Irritability in autism (6 17) Tourette (6 17) Mania Psychosis Irritability Aggression Agitation Vocalmotor tics Bipolar, schizophrenia: 2 Autism: 2 Tourette: 2 Bipolar, schizophrenia: 10 30 Autism: 5 15 Tourette: 5 20 Olanzapine Zyprexa Available in dissolvable and IM prep Bipolar (13 17) Schizophrenia (13 17) Mania Psychosis Agitation 2.5 2.5 20 Quetiapine Seroquel Bipolar (10 17) Schizophrenia (13 17) Mania Psychosis Agitation 25 mg bid Bipolar: 400 600 Schizophrenia: 400 800 Risperidone Risperdal Available in liquid and dissolvable prep Bipolar (10 17) Schizophrenia (13 17) Irritability in autism (5 17) Mania Psychosis Irritability Aggression Agitation Bipolar, schizophrenia: 0.5 Autism: 20 kg: 0.25 20 kg: 0.5 Bipolar, schizophrenia: 1 6 Autism: 0.5 3 Paliperidone Invega Available in IM prep Schizophrenia (12 17) Psychosis 3 51 kg: 3 6 51 kg: 3 12 Lurasidone Latuda Schizophrenia (13 17) Depressive episodes with Bipolar (13 17) Psychosis Schizophrenia: 40 Bipolar: 20 Schizophrenia: 40 80 Bipolar: 20 80 Asenapine Saphris Bipolar (10 17)
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Mania Psychosis 2.5 twice daily 5 20 Haloperidol Haldol Available in liquid and IM prep Psychosis Severe behavioral disorders Agitation (3 17) Tourette disorder Mania Psychosis Irritability Aggression Agitation Vocalmotor tics 0.05 mgkgday 0.05 0.15 mgkgday Lithium carbonate Available in liquid prep Bipolar (12 17) Mania Acute mania: 1800 mgday Target level: 1.0 1.5 mEqL Long term control: 900 1200 mgday Target level: 0.6 1.2 mEqL Doses shown in table may exceed maximum recommended dose for some children. Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. Chapter 33 u Psychopharmacology 229 hyperparathyroidism, weight gain, nausea, abdominal pain, diar rhea, acne, and CNS symptoms (sedation, tremor, somnolence, memory impairment). Periodic monitoring of lithium levels along with thyroid and renal function is needed. Lithium serum levels of 0.8 1.2 mEqL are targeted for acute episodes, and levels of 0.6 0.9 mEqL are targeted for maintenance therapy. Acute overdose (level 1.5 mEqL) manifests with neurologic symptoms (e.g., tremor, ataxia, nystagmus, hyperreflexia, myoclonus, slurred speech, delirium, coma, seizures) and altered renal function. Toxicity is enhanced when dehydrated or with drugs that affect renal function, such as NSAIDs or angiotensin converting enzyme (ACE) inhibi tors. Neuroleptic malignant syndrome has been reported in patients concurrently taking antipsychotic drugs and lithium. MEDICATION USE IN PHYSICAL ILLNESS There are special considerations in the use of psychotropic medications with physically ill children. Between 80 and 95 of most psychotropic medications are protein bound; the exceptions are lithium (0), methyl phenidate (1030), and venlafaxine (2530). As a result, psychotro pic levels may be directly affected because albumin binding is reduced in many physical illnesses. Metabolism is primarily through the liver and gastrointestinal (GI) tract, with excretion via the kidney. Therefore dosages may need to be adjusted in children with hepatic or renal impairment. Hepatic Disease In general, it is necessary to use lower doses of medications for patients with hepatic disease. Initial dosing of medications should Table 33.6 Relative Side Effects for Select Antipsychotic Medications ADVERSE EFFECT ARIPIPRAZOLE ABILIFY OLANZAPINE ZYPREXA QUETIAPINE SEROQUEL RISPERIDONE RISPERDAL PALIPERIDONE INVEGA LURASIDONE LATUDA HALOPERIDOL HALDOL Akathisia Parkinsonism Dystonia Tardive dyskinesia Hyperprolactinemia Anticholinergic Seizures Orthostasis QT interval Weight gain Hyperlipidemia Glucose abnormalities Sedation Seldom; sometimes; often. Adapted from Keepers GA, Fochtmann LJ, Anzia JM, et al. The American Psychiatric Association Practice Guideline for the Treatment of Patients With Schizophrenia. Am J Psychiatry. 2020;177(9):868872. Table 33.7 Metabolic Monitoring Parameters Based on ADAAPA Consensus Guidelines BASELINE WEEK 4 WEEK 8 WEEK 12 EVERY 3 MO THEREAFTER ANNUALLY Medical history X X X Body mass index X X X X X X Waist circumference X X X Blood pressure X X X Fasting glucose and Hemoglobin A1c X X X Fasting lipid panel X X X Personalfamily history of obesity, hypertension, and cardiovascular disease. From American Diabetes Association. American Psychiatric Association; American Association of Clinical Endocrinologists; North American Association for the Study
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of Obesity. Consensus development conference on antipsychotic drugs and obesity and diabetes. Diabetes Care. 2004;27(2):596601. Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. 230 Part III u Behavioral and Psychiatric Disorders be reduced, and titration should proceed slowly. In acute hepatitis, there is generally no need to modify dosing because metabolism is only minimally altered. In chronic hepatitis and cirrhosis, hepato cytes are destroyed, and doses may need to be modified. In steady state situations, changes in protein binding can result in elevated unbound medication, resulting in increased drug action even in the presence of normal serum drug concentrations. Albu min and 1 glycoproteins produced in the liver may be reduced with infectious and inflammatory hepatic disease, whereas surgery, trauma, and cirrhosis may result in elevated protein levels. Because it is often difficult to predict changes in protein binding, it is important to maintain attention to the clinical effects of psy chotropic medications and not rely exclusively on serum drug concentrations. Medications with high baseline rates of liver clearance (e.g., haloper idol, sertraline, venlafaxine) are significantly affected by hepatic dis ease. For drugs that have significant hepatic metabolism, intravenous (IV) administration may be preferred because parenteral administra tion avoids first pass liver metabolic effects, and the dosing and action of parenteral medications are similar to those in patients with normal hepatic function. Gastrointestinal Disease GI disease primary affects drug absorption. Examples that impact absorption include conditions affecting GI motility, surgical alterations of the GI tract, short bowel syndrome, or celiac disease. Any condition that diverts blood away from the GI tract (e.g., congestive heart failure, shock) may also reduce absorption. Psychotropic medications have the potential to cause GI side effects. Medications with anticholinergic side effects can slow GI motility, affecting absorption and causing constipation. SSRIs increase gastric motility and can cause diarrhea. SSRIs can increase the risk of GI bleed ing, especially when administered with NSAIDs. Extended release or controlled release preparations of medications can reduce GI side effects, particularly where gastric distress is related to rapid increases in plasma drug concentrations. Using extended release medication preparations may reduce these side effects. Renal Disease In general, initial dosages of medication should be reduced or dos ing intervals lengthened in renal failure. The rule of two thirds is that dosages should be reduced by one third of the normal dosage for a patient with renal insufficiency. However, most psychotropic medications, with the exceptions of lithium and gabapentin, do not require significant dosing adjustments in kidney failure. It is important to monitor serum concentrations in renal insufficiency, particularly for medications with a narrow therapeutic index. Cyclosporine can elevate serum lithium levels by decreasing lithium excretion. Although TCAs have been largely supplanted by SSRIs, patients with kidney failure and those on dialysis appear to be more sensitive to their side effects, possibly because of the accumulation of
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hydroxylated tricyclic metabolites. Because most psychotropic medications are highly protein bound, they are not significantly cleared by dialysis. Lithium is essentially completely removed by dialysis, and the common practice is to admin ister lithium after dialysis. Patients on dialysis often have significant fluid shifts and are at risk for dehydration, with neuroleptic malignant syndrome more likely in these situations. Cardiac Disease Antipsychotics, TCAs, and citalopram (40 mgday) can lead to prolongation of the QTc interval, with increased risk of ventricular tachycardia and ventricular fibrillation, particularly in patients with structural heart disease. Patients with a baseline QTc interval of 440 msec should be particularly considered at risk. The normal QTc value in children is 400 msec (25 30 msec). A QTc value that exceeds 2 standard deviations (SDs; 450 460 msec) is considered too long and may be associated with increased mortality. An increase in the QTc from a baseline of 60 msec is also associated with increased mortality. There is increased risk of morbidity and mortality in patients with preexisting cardiac conduction problems. Patients with Wolff Parkinson White syndrome who have a short PR interval (0.12 sec) and widened QRS interval associated with paroxysmal tachy cardia are at high risk for life threatening ventricular tachycardia that may be exacerbated by the use of antipsychotics, TCAs, and citalopram. Respiratory Disease Anxiolytic agents can increase the risk of respiratory suppression in patients with pulmonary disease. SSRIs are the first line medications to consider in treating disabling anxiety. Possible airway compromise caused by acute laryngospasm should be considered when dopamine blocking antipsychotic agents are used. Neurologic Disease Psychotropic medications can be used safely with epilepsy following consideration of potential interactions among the medication, the seizure disorder, and the anticonvulsant. Any behavioral toxicity of anticonvulsants used either alone or in combination should be consid ered before proceeding with psychotropic treatment. Simplification of combination anticonvulsant therapy or a change to another agent can result in a reduction of behavioral or emotional symptoms and obviate the need for psychotropic intervention. Clomipramine and bupropion possess significant seizure inducing properties and should be avoided when the risk of seizures is present. Principles for Psychotropic Prescribing in Primary Care In the context of a severe and prolonged shortage of child and adolescent psychiatrists (CAPs), PCPs are increasingly managing behavioral health conditions in primary care. The principles for effective use of psychotropic medications outlined in the begin ning of this chapter can be used by PCPs to guide their medica tion assessment and management (see Table 33.1). This approach emphasizes baseline assessment with standardized symptom rat ing scales to identify target symptoms and their level of severity, prioritizing FDA approved medications for the target symptom and patient age range, adherence to recommendations regard ing therapeutic dosage ranges, using a follow up symptom rating scale assessment to monitor medication response, continuing the medication trial for sufficient duration, and switching to an alter native FDA approved medication if the first medication trial is ineffective. PCPs can access support for psychotropic prescribing through
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the development of collaborative relationships with CAPs who can pro vide timely consultation for questionsadvice; interim management until stable; and ongoing care for patients with severe, complex, unsafe, or treatment refractory conditions. Ideally, consultation with a CAP should occur if one is considering using psychotropic medications with very young children, multiple psychotropic medi cations, medication doses outside of therapeutic range, or non FDA approved medications. Visit Elsevier eBooks at eBooks.Health.Elsevier.com for Bibliography. Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. Chapter 34 u Psychotherapy 231 PSYCHOTHERAPY Psychotherapy is the first line treatment for many child and adoles cent psychiatric disorders (e.g., posttraumatic stress disorder PTSD, depression, anxiety, behavior, substance related) because for these disorders, psychotherapy produces outcomes greater than or equal to pharmacotherapy, with less risk of harm. Even with disorders (e.g., schizophrenia, bipolar disorder, attention deficithyperactivity disor der ADHD) for which medication is typically the first line treatment, adjunctive psychotherapy can convey additional benefit. Psychotherapy is moderately effective in reducing psychiatric symp tomatology and achieving remission of illness. In a 2017 multilevel meta analysis of almost 500 randomized trials over 5 decades, there was a 63 probability that a youth receiving psychotherapy fared bet ter than a youth in a control condition. Effects varied across multiple moderators. The mean posttreatment and follow up effect sizes were highest for anxiety, followed by behaviorconduct, ADHD, and depres sion, and lowest for multiple concurrent comorbidities. Effect sizes var ied according to outcome measure informant, with youth and parents generally reporting larger effects than teachers. A variety of psychotherapeutic modalities have been developed, with varying levels of effectiveness (Table 34.1). Differences between thera peutic approaches may be less pronounced in practice than in theory. The quality of the therapist patient alliance is consistently one of the most important predictors of treatment outcome. A positive working relationship, expecting change to occur, facing problems assertively, increasing mastery, and attributing change to the participation in the therapy have all been associated with effective therapy, irrespective of the specific psychotherapeutic modality. All psychotherapy interventions involve a series of interconnected steps, including performing an assessment, constructing working diagno ses and an explanatory formulation, deciding on treatment and a moni toring plan, obtaining treatment assentconsent, implementing treatment, terminating treatment, and following for symptom recurrence. Psycho therapists ideally develop a treatment plan by combining evidence based therapies with clinical judgment and patientfamily preference to collab oratively arrive at a specific intervention plan for the individual patient. Behavior Therapy Behavior therapy is based on both classic (Pavlovian) and operant (Skinnerian) conditioning. Both approaches address the antecedent stimuli and consequent outcomes of problematic thoughts or behav iors. The treatment begins with a behavioral assessment along with a functional analysis of the setting, immediately preceding events, and real world outcomes of the behavior to identify the settings in which the behavior occurs andor the reason the child
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engages in the behavior. Often the function of problematic behavior is to gain access to atten tion or a tangible item the child wants or to avoid a task or stressful situation. The goal is to teach the child a more adaptive response using tools such as positive and negative reinforcement; social and tangible rewards; response costconsequences; shaping, modeling, and prompt ing; systematic desensitization; and aversive conditioning. Behavior therapy has shown particular effectiveness with opposi tional behavior, obsessive compulsive, autism spectrum disorder, and substance use disorders, and ADHD. Cognitive Behavioral Therapy Cognitive behavioral therapy (CBT) is based on social and cognitive learning theories and extends behavior therapy to address the influence of cognitive processes on behavior. CBT is a short term, problem and goal oriented treatment centered on correcting problematic patterns in thinking and behavior that lead to emotional difficulties and functional impairments. The CBT therapist seeks to help the patient identify and change cognitive distortions (e.g., learned helplessness, irrational fears); identify and incrementally approach aversive situations; and identify and practice distress reducing behavior. Self monitoring (daily thought records), self instruction (brief sentences asserting thoughts that are comforting and adaptive), and self reinforcement (rewarding oneself for adaptive behaviors) are key tools used to facili tate achievement of the CBT goals. CBT has good quality evidence for the treatment of anxiety, obsessive compulsive disorder (OCD), behavior disorders, substance abuse, and insomnia, and fair evidence for the treatment of depres sion. For many childhood psychiatric disorders, CBT alone provides outcomes comparable to psychotropic medication alone, and the com bination of both may convey additional benefit in symptom and harm reduction. Modified versions of CBT have shown applicability to the treatment of other disorders. Trauma Focused Cognitive Behavioral Therapy Trauma focused cognitive behavioral therapy (TF CBT) is designed to process and master the psychologic, behavioral, and physiologic con sequences of a specific traumatic experience. It involves a combina tion of education about the broad effects of trauma exposure; teaching effective relaxation, affective modulation, and cognitive coping and processing skills; creating a trauma narrative to foster understanding; mastering trauma reminders; enhancing future safety and develop ment; and teaching parents how to support youth with trauma expo sure. TF CBT is considered the first line treatment for PTSD. Dialectical Behavioral Therapy Dialectical behavioral therapy (DBT) is a modality targeted at emo tional and behavioral dysregulation by synthesizing or integrating the seemingly opposite strategies of acceptance and change. Dialectic con flicts (wanting to die vs wanting to live) often exist in the same patient. The four skills modulesmindfulness (the practice of being fully aware and present in the moment), distress tolerance (how to tol erate emotional pain), interpersonal effectiveness (how to maintain self respect and effective communication in relationships with oth ers), and emotion regulation (how to manage complex emotions) are balanced in terms of acceptance and change. The treatment targets, in order of priority within a given session, are life threatening behaviors, such as suicidal and self injurious behaviors or communica tions; therapy interfering behaviors,
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such as coming late to sessions, canceling appointments, and being uncollaborative in working toward treatment goals; quality of life behaviors, including relationship and occupational problems and financial crises; and skills acquisition to help patients achieve their goals. DBT has good quality evidence for self injurious thoughts and behaviors and has shown promise for the treatment of bipolar disorder and other manifestations of emotional behavioral dysregulation. Interpersonal Psychotherapy Interpersonal psychotherapy (IPT) focuses on resolving interpersonal difficulties that lead to psychologic distress and maladaptive behaviors. Patients are viewed as having strengths and vulnerabilities that deter mine the manner in which they cope with or respond to an interper sonal crisis (stressor). The main goals of IPT include expanding social support, decreasing interpersonal stress, enhancing the processing of emotions, and improving social functioning within significant rela tionships. The interpersonal inventory, a detailed review of the patients significant relationships, both current and past, with their emotional valence, leads to a formulation linking the interpersonal situations to the emotionalbehavior symptoms. Various techniques (linking emo tionsbehaviors to interpersonal events, communication and problem solving training, perspective taking, role adaptation) are utilized to resolve interpersonal difficulties. IPT is a well established treatment for adolescent depression. Chapter 34 Psychotherapy Erica H. Lee, Keneisha R. Sinclair McBride, David R. DeMaso, and Heather J. Walter Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. 232 Part III u Behavioral and Psychiatric Disorders Psychodynamic Psychotherapy At the core of psychodynamic psychotherapy lies a dynamic interac tion between different dimensions of the mind, conscious and uncon scious. This approach is based on the belief that much of ones mental activity occurs outside ones awareness. The patient is often unaware of internal conflicts because threatening or painful emotions, impulses, and memories are repressed to avoid experiencing psychologic pain. Behavior is then controlled by what the patient does not know about himself or herself. Therapy objectives are to increase self understanding and acceptance of painful conflicting feelings, and to develop realistic relationships between self and others. A fundamental difference of this modality is its nondirective approach to allow a patients characteris tic patterns of thinking and behavior to emerge over time. The rela tionship between the patient and the therapist can play a key role in identifying these patterns, as they are recapitulated in the therapeutic environment. The therapist can then analyze and interpret the manifest pattern so that self understanding and a corrective emotional experi ence can be fostered. Psychodynamic psychotherapy has shown applicability for the treatment of self injurious thoughts and behaviors as well as anxiety, Table 34.1 Effective Psychotherapies for Specific Behavioral Health Disorders DISORDER WELL ESTABLISHED PROBABLY EFFICACIOUS Anorexia Family therapy: behavioral Family therapy: systemic Individual psychodynamic psychotherapy Anxiety, children under 8 Family based CBT Group parent CBT group child CBT Anxiety CBT parent component medication Family psychoeducation Parentchild CBT Relaxation, assertiveness training Attention deficithyperactivity BPT
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Behavioral classroom management Behavioral peer interventions Organization (executive function) training Combined training interventions Autism Individual, comprehensive ABA Teacher implemented focused ABA DSP Individual, focused (communication) ABA DSP Focused DSP parent training Behavior, child Group BPT Individual BPT with child component Modifications of Group BPT Individual BPT alone or with other modifications Self directed parent behavior therapy Group child behavior therapy teacher training Individual child behavior therapy parent component Groupindividual child centered play therapy Behavior, adolescent Behavioral therapy CBT family therapy CBT Bipolar Family skill building psychoeducation DBT Depression, child None None Depression, adolescent Individualgroup CBT Individual IPT Group IPT Obsessive compulsive Family focused CBT Individual CBT Posttraumatic stress Individualgroup trauma focused CBT parent component Group CBT parent component EMDR Substance use Individualgroupfamily CBT MET Family based treatment, ecologic CBT MET Family based treatment, behavioral Motivational interviewingMET Family based treatment, ecologic contingency management Family based treatment, behavioral, ecologic, contingency management MET MET CBT contingency management Self injurious thoughts and behaviors DBT adolescents (deliberate self harm, suicidal ideation) DBTadolescents (nonsuicidal self injury, suicide attempt) Individualfamily CBT (suicide attempt) Family therapy (suicide attempt) Interpersonal therapyadolescents (suicidal ideation) Individual psychodynamic therapy (deliberate self harm) Parent training (self injurious thoughts and behaviors (suicidal and nonsuicidal) Two or more consistent randomized controlled trials demonstrating superiority of treatment over control groups; conducted by independent investigators working at different research settings. Same as in the previous footnote, but lacking independent investigator criterion. Modifications of Group Behavioral Parent Training that are probably efficacious include adding child components or family problem solving strategies CBT, Cognitive behavioral therapy; BPT, behavioral parent training; ABA, applied behavioral analysis; DSP, developmental social pragmatic; DBT, dialectical behavioral therapy; IPT, interpersonal psychotherapy; EMDR, eye movement desensitization and reprocessing; MET, motivational enhancement treatment. Adapted from Society of Clinical Child and Adolescent Psychology. Concerns, symptoms and disorders. https:effectivechildtherapy.orgconcerns symptoms disorders. Accessed July 13, 2021. Criteria derived from Southam Gerow MA, Prinstein MJ. Evidence base updates: The evolution of the evaluation of psychological treatments for children and adolescents. J Clin Child Adol Psychol. 2014;43(1):16. Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. Chapter 34 u Psychotherapy 233 depression, and maladaptive aspects of personality. Brief, time limited psychodynamic psychotherapy can be appropriate for youth who are in acute situational distress. Long term therapy can be appropriate when the biologic or social factors destabilizing the childs adaptation and development are chronic, or the psychologic difficulties are complex, or if entrenched conflicts and developmental interferences are present. Supportive Psychotherapy Supportive psychotherapy aims to minimize levels of emotional distress through the provision of individual and contextual support. The goal is to reduce symptoms, and treatment is focused on the here and now. The therapist is active and helpful in providing the patient with symp tomatic relief by helping the patient to contain and manage anxiety, sadness, and anger. The therapist provides support and encouragement (coaching) to bolster
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a patients existing coping mechanisms, facili tates problem solving, and provides social and instrumental support for ameliorating or lessening contextual precipitants. CBT informed techniques are often combined with supportive psychotherapy. Proba bly the most common psychotherapy employed by therapists, support ive psychotherapy has shown comparable results to CBT in a number of research studies, particularly those targeting depression. Family Therapy The core premise in family therapy is that dysfunctional family inter action patterns precipitate andor perpetuate an individuals emotional or behavioral difficulties. Family dysfunction can take a variety of forms, including enmeshment, disengagement, role reversal or confu sion, and maladaptive communication patterns. Family therapy begins with an assessment of the family system, including observing patterns of interaction; assessing family beliefs and the meanings attached to behaviors; defining social and cultural contexts; exploring the pre senting problem in the context of individual and family development; assessing the familys style of dealing with problems; and identifying family strengths and weaknesses. Family therapy techniques are drawn from two major theoretical models: structural and behavioral. Structural family therapy develops structures believed to foster well functioning families, including clear and flexible boundaries between individuals, well defined roles, and an appropriate balance between closeness and independence. Behavioral family therapy focuses on behavioral sequences that occur in daily life and attempts to interrupt unhelpful behavioral patterns and strengthen positive behavioral patterns through effective communication and problem solving. Family therapy has shown established applicability in anorexia ner vosa, behavior problems, and substance use and may be a promising treatment for depression and bipolar disorder. Parenting Interventions See Chapters 20 and 42 for more details. Parenting interventions seek to improve both the parentchild rela tionship and parenting skills using the principles of behavior therapy previously described. These interventions can be provided in individual or group therapy formats. Core relationship recommendations include spending quality time with the child to foster a strong parentchild bond, increasing positive verbal interaction, showing physical affec tion, and engaging in child directed play. Core parenting skills include increasing reinforcement of positive behaviors; decreasing reinforce ment of negative behaviors; ignoring merely annoying behaviors; applying logical consequences for dangerousdestructive behaviors; and making parental responses predictable, contingent, and immedi ate. Parenting interventions have shown applicability for behavior dis orders and ADHD. Common Elements of Evidence Based Psychotherapies A major challenge for the practitioner is selecting the right interven tion for the right person in the right setting, and delivering the intervention in the right way (to meet the needs of patients and families). This challenge has led to an interest in identifying common practice elements across efficacious evidence based therapies that could be matched in a flexible way to patients of a certain age, gender, and raceethnicity who have certain psychiatric disorders. Table 34.2 provides the major practice elements for three of the most common child and adolescent psychiatric disorders: anxiety, depression, and disruptive behaviors. These practice elements, when made available to patients with psychiatric disorders in a system of care, are estimated to be relevant to approximately
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two thirds of the patients. Six of the practice elementspsychoeducation of the parent, problem solving skills, relaxation skills, self monitoring, cognitivecoping skills, and psychoeducation of the childare applicable to all three disorders and as such could be considered core competencies for both mental health specialists as well as primary care practitioners (PCPs) inter ested in delivering brief psychotherapeutic interventions in the con text of anticipatory guidance (see Discussion of Common Factors in Chapter 18). Psychoeducation is the education of the parent and child about the cause, course, prognosis, and treatment of the disorder. Problem solv ing includes techniques, discussions, or activities designed to bring about solutions to targeted problems, with the intention of imparting skills for how to approach and solve future problems in a similar man ner. Relaxation includes techniques designed to create and maintain the physiologic relaxation response. Self monitoring is the repeated measurement of a target emotional or behavioral metric by the child or parent to establish goals for treatment and monitor progress toward mastery. Cognitivecoping skills consist of techniques designed to alter interpretations of events through examination of the childs reported thoughts, accompanied by exercises designed to test the validity of the reported thoughts. Modular Therapy Packages Of considerable importance to day to day clinical work is the manner in which common therapy practice elements are selected, sequenced, repeated, or selectively applied. This coordination of psychothera peutic elements is particularly relevant for patients presenting with multiple concurrent psychiatric disorders whose primary concern may shift between sessions. The Modular Approach to Therapy for Children (MATCH) is a multi disorder intervention system that incorporates treatment procedures (practice elements) and treatment logic (coor dination) corresponding to efficacious interventions for childhood anxiety, depression, traumatic stress, and behavior problems, with modifications to allow the system to operate as a single protocol. Com pared with standard manualized treatments for individual disorders and with usual care, the modular package outperformed both compar ators on multiple clinical and service outcome measures when assessed over a 2 year period, although additional, independently derived evi dence is needed to determine the conditions under which it is most effective and categorize this treatment approach as well established. Treatment Engagement Interventions Treatment engagement is conceptualized as a multidimensional construct targeting cognitive, attendance, and adherence domains. Research has identified several key factors addressing these domains that are associated with treatment engagement: accessibility promo tion, psychoeducation about services, appointment reminders, assess ment of treatment barriers, patient assessment, setting of positive expectations, modeling, homework assignments, rapport building, cultural acknowledgement, and goal setting (Table 34.3). To promote treatment engagement, the first 10 of these factors can be addressed by the PCP and the medical home team as soon as a mental health prob lem is identified that would benefit from treatment (see Chapter 18 for further discussion). Psychotherapy in the Medical Home Recognizing that up to one half of visits to PCPs involve a mental health problem and that an estimated one fifth of pediatric patients have a functionally impairing psychiatric disorder,
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in the context of limited access to specialty mental health services in community or hospital settings a number of models have been developed to deliver Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. 234 Part III u Behavioral and Psychiatric Disorders psychotherapy in primary care. Two prominent models, both origi nally developed for adult populations, are collaborative care and pri mary care behavioral health. Collaborative care, which spans a spectrum ranging from coor dinated to co located to integrated, provides mental healthcare for patients through a collaboration between mental health specialists and PCPs. In integrated collaborative care, patients mental health problems are managed in the medical home setting by an inter disciplinary care team of PCPs, mental health clinicians, and care coordinators supported by a consulting psychiatrist. The PCP is the team captain; the mental health clinician maintains a popu lation registry, provides brief, focused psychosocial interventions, and monitors treatment response; the care coordinator facilitates external referrals; and the consulting psychiatrist provides input regarding evidence based psychiatric diagnosis and treatment. The four critical elements of integrated collaborative care are that it is team driven, population focused, measurement guided, and evidence based. These elements guide a treatment approach in which the patient perceives a seamless integration of medical and mental healthcare. In children and adolescents, randomized controlled trials (RCTs) have shown that integrated collaborative care for child behavior prob lems, adolescent depression, and adolescent substance use is associ ated with more favorable treatment adherence, symptom reduction, disorder remission, and consumer satisfaction outcomes than usual care, with or without specialty referral. In a meta analysis of collabora tive care RCTs, larger effects were observed for treatment trials target ing diagnoses and elevated symptoms relative to prevention trials and for mental health diagnoses relative to substance related diagnosis, as well as for integrated models relative to other types of collaborative mental healthcare. Primary care behavioral health employs a mental health clini cian (psychologist, social worker, mental health counselor) in the primary care setting to provide focused assessment of patients with mental health, health behavior, and substance use problems, and short term therapy as well as healthmental health promo tion and prevention interventions. Mental health clinicians typi cally collaborate with PCPs to develop treatment plans, monitor patient progress, and flexibly provide care to meet patients chang ing needs. The model uses a wide net approach aimed at serving the entire primary care population, with emphasis on brief, focused interventions. The results of brief interventions, particularly applicable to the fast paced medical home setting, are encouraging. Interventions lasting only one session, particularly those utilizing CBT techniques, can be effective for mild presentations of multiple child psychiatric disorders, particularly anxiety and behavior problems in children (vs adolescents). These interventions can greatly expand capacity to Table 34.2 Practice Elements in Interventions for Three Common Child and Adolescent Psychiatric Disorders ANXIETY DISORDERS
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DEPRESSION DISRUPTIVE BEHAVIOR Directed play X Limit setting X Time out X Cost response X Activity scheduling X Maintenance X X Skill building X Social skills training X X Therapist praiserewards X Natural and logical consequences X X Communication skills X X Assertiveness training X Parent monitoring X X Modeling X Ignoring X X Parent praise X X Problem solving X X X Parent coping X X Psychoeducation, parent X X X Relaxation X X X Tangible rewards X X Self monitoring X X X Cognitivecoping X X X Psychoeducation, child X X X Exposure X Adapted from Chorpita BF, Daleiden EL, Weisz JR. Identifying and selecting the common elements of evidence based interventions: a distillation and matching model. Ment Health Serv Res. 2005;7(1):520. Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. Chapter 35 u Somatic Symptom and Related Disorders 235 provide mental health support to those patients with emerging mild mental health problems, with the goal of preventing escalation into full blown psychiatric disorders if problems are left untreated. Visit Elsevier eBooks at eBooks.Health.Elsevier.com for Bibliography. Table 34.3 Selected Psychotherapy Engagement Elements ELEMENT DEFINITION Accessibility promotion Any strategy used to make services convenient and accessible to proactively encourage and increase participation in treatment; e.g., hiring a co located therapist or referring to a local community based therapist with whom the practice has an ongoing collaborative relationship Psychoeducation about services Provision of information about services or the service delivery system; e.g., type of therapy being recommended, information about the therapist, session frequency and duration Appointment reminders Providing information about the day, time, and location of the therapy office for the initial appointment via mail, text, phone, email, etc., to increase session attendance Assessment of treatment barriers Discussion to elicit and identify barriers that hinder participation in treatment; e.g., transportation, scheduling, childcare, previous experiences with therapy, stigma Assessment Measurement of the patients strengths needs through a variety of methods; e.g., mental health screening instruments, interviews, recorded reviews during which the referring practitioner can motivate treatment engagement Modeling Demonstration of a desired behavior to promote imitation and performance of that behavior by client Expectation setting Instillation of hope regarding the efficacy of therapy and the patients ability to participate successfully in treatment Homework assignment Therapeutic tasks given to the patient to complete outside the therapy session to reinforce or facilitate knowledge or skills that are consistent with the treatment plan Goal setting Selection of a therapeutic goal for the purpose of making a plan to achieve that goal Rapport building Strategies used to strengthen the relationship between therapist and patient Cultural acknowledgment Exploration of an individuals culture; e.g., raceethnicity, age, sexual orientation, gender identity Adapted from Lindsey MA, Brandt NE, Becker KD, et al. Identifying the common elements of treatment engagement interventions in childrens mental health services. Clin Child Fam Psychol Rev. 2014;17(3):283298; Becker KD, Lee
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BR, Daleiden EL, Lindsey M, Brandt NE, Chorpita BF. The common elements of engagement in childrens mental health services: which elements for which outcomes?. J Clin Child Adolesc Psychol. 2015;44(1):3043; and Becker KD, Boustani M, Gellatly R, Chorpita BF. Forty Years of Engagement Research in Childrens Mental Health Services: Multidimensional Measurement and Practice Elements. J Clin Child Adolesc Psychol. 2018;47(1):123. Chapter 35 Somatic Symptom and Related Disorders David R. DeMaso Table 35.1 DSM 5 Diagnostic Criteria for Somatic Symptom Disorder A. One or more somatic symptoms that are distressing or result in significant disruption of daily life. B. Excessive thoughts, feelings, or behaviors related to the somatic symptoms or associated health concerns, as manifested by at least one of the following: 1. Disproportionate and persistent thoughts about the seriousness of ones symptoms. 2. Persistent high level of anxiety about health and symptoms. 3. Excessive time and energy devoted to these symptoms or health concerns. C. Although any one somatic symptom may not be continuously present, the state of being symptomatic is persistent (typically 6 mo). Specify if: With predominant pain (previously known as pain disorder in DSM IV TR): for individuals whose somatic symptoms predominantly involve pain. Persistent: A persistent course is characterized by severe symptoms, marked impairment, and long duration (6 mo). From the Diagnostic and Statistical Manual of Mental Disorders, 5th ed. p 311. Copyright 2013. American Psychiatric Association. Medically unexplained physical symptoms are common in children and adolescents. Although frequently chronic and disabling, these symptoms do not often result in referrals for mental health assess ment and treatment (see Chapter 212). The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM 5) somatic symp tom and related disorders (SSRDs) are those conditions in which the physical symptoms are unexplained or for which the patients response to the underlying medical condition is disproportionate and debilitating. The SSRDs include somatic symptom disorder (Table 35.1), con version disorder (Table 35.2), factitious disorders (Table 35.3), illness anxiety disorder (Table 35.4), and other specifiedunspecified somatic symptom disorders (Table 35.5), as well as psychologic factors affect ing other medical conditions (Table 35.6). With the exception of illness anxiety disorder (with high level of anxiety about health in the absence of significant somatic symptoms) and psychologic factors affecting other medical conditions (with psychologic andor behavioral factors adversely affect a pediatric condition), SSRDs are classified on the basis of physical symptoms associated with clinically significant distress and impairment, with or without the presence of a diagnosed medical condition. Most patients with SSRDs are seen by primary care practitioners or by pediatric subspecialists, who may make specialty specific diagnoses such as visceral hyperalgesia, chronic fatigue syndrome, psychogenic syncope, or noncardiac chest pain. Even within psychiatry, SSRDs are variously referred to as functional or psychosomatic disorders or as medically unexplained symptoms. The nosologic heterogeneity across the pediatric subspecialties contributes to the varying diagnostic labels. There is a significant overlap in the symptoms and presentation of patients with somatic symptoms who have received different diag noses from
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different specialties. Moreover, SSRDs share similarities Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. 236 Part III u Behavioral and Psychiatric Disorders Table 35.2 DSM 5 Diagnostic Criteria for Conversion Disorder or Functional Neurologic Symptom Disorder A. One or more symptoms of altered voluntary motor or sensory function. B. Clinical findings provide evidence of incompatibility between the symptom and recognized neurologic or medical conditions. C. The symptom is not better explained by another medical or mental disorder. D. The symptom causes clinically significant distress or impairment in social, occupational, or other important areas of functioning or warrants medical evaluation. Specify symptom type: weakness or paralysis, abnormal movements, swallowing symptoms, speech symptom, attacksseizures, anesthesiasensory loss, special sensory symptom (e.g., visual, olfactory, hearing), or mixed symptoms. From the Diagnostic and Statistical Manual of Mental Disorders, 5th ed. p 318. Copyright 2013. American Psychiatric Association. Table 35.3 DSM 5 Diagnostic Criteria for Factitious Disorders FACTITIOUS DISORDER IMPOSED ON SELF A. Falsification of physical or psychologic signs or symptoms, or induction of injury or disease, associated with identified deception. B. The individual presents himself or herself to others as ill, impaired, or injured. C. The deceptive behavior is evident even in the absence of obvious external rewards. D. The behavior is not better explained by another mental disorder, such as delusional disorder or another psychotic disorder. Specify if: single episode or recurrent episodes. FACTITIOUS DISORDER IMPOSED ON ANOTHER (PREVIOUSLY FACTITIOUS DISORDER BY PROXY) A. Falsification of physical or psychologic signs or symptoms, or induction of injury or disease, in another, associated with identified deception. B. The individual presents another individual (victim) to others as ill, impaired, or injured. C. The deceptive behavior is evident even in the absence of obvious external rewards. D. The behavior is not better explained by another mental disorder, such as delusional disorder or another psychotic disorder. Note: The perpetrator, not the victim, receives this diagnosis. Specify if: single episode or recurrent episodes. From the Diagnostic and Statistical Manual of Mental Disorders, 5th ed. p 324. Copyright 2013. American Psychiatric Association. Table 35.4 DSM 5 Diagnostic Criteria for Illness Anxiety Disorder A. Preoccupation with having or acquiring a serious illness. B. Somatic symptoms are not present, or, if present, are only mild in intensity. If another medical condition is present or there is a high risk for developing a medical condition (e.g., strong family history is present), the preoccupation is clearly excessive or disproportionate. C. There is a high level of anxiety about health, and the individual is easily alarmed about personal health status. D. The individual performs excessive health related behaviors (e.g., repeatedly checks his or her body for signs of illness) or exhibits maladaptive avoidance (e.g., avoids doctor appointments and hospitals). E. Illness preoccupation has been present for at least 6 months, but the specific illness that is feared may change over
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that time. F. The illness related preoccupation is not better explained by another mental disorder. Specify whether: care seeking type or care avoidant type. From the Diagnostic and Statistical Manual of Mental Disorders, 5th ed. p 315. Copyright 2013. American Psychiatric Association. Table 35.5 DSM 5 Diagnostic Criteria for Other Specified Unspecified Somatic Symptom and Related Disorders OTHER SPECIFIED This category applies to presentations in which symptoms characteristic of a somatic symptom and related disorder that cause clinically significant distress or impairment in social, occupational, or other important areas of functioning predominate but do not meet full criteria for any of the disorders in the somatic symptom and related disorders diagnostic class. Examples of presentations that can be specified using the other specified designation include the following: 1. Brief somatic symptom disorder: duration of symptoms is 6 mo. 2. Brief illness anxiety disorder: duration of symptoms is 6 mo. 3. Illness anxiety disorder without excessive health related behaviors: Criterion D for illness anxiety disorder is not met (see Table 35.4). 4. Pseudocyesis: a false belief of being pregnant that is associated with objective signs and reported symptoms of pregnancy. UNSPECIFIED This category applies to presentations in which symptoms characteristic of a somatic symptom and related disorder that cause clinically significant distress or impairment in functioning predominate but do not meet criteria for any of the other disorders in the somatic symptom and related disorders diagnostic class. From the Diagnostic and Statistical Manual of Mental Disorders, 5th ed. p 327. Copyright 2013. American Psychiatric Association. in etiology, pathophysiology, neurobiology, psychologic mechanisms, patient characteristics, and management and treatment response, which is indicative of a single spectrum of somatic disorders. It is helpful for all healthcare providers to avoid the dichotomy of approaching illness using a medical model in which diseases are con sidered physically or psychologically based. In contrast, a developmen tal biopsychosocial continuum of disease better characterizes these illnesses as occurring across a spectrum ranging from a predominantly biologic to a predominantly psychosocial etiology. Indeed, there is a neurobiologic component to the related functional neurologic disor ders, especially related to pain symptoms (see Chapters 212 and 389). SOMATIZATION The term somatization is defined as a pattern of seeking medical help for physical symptoms that cannot be fully explained by pathophysi ologic mechanisms but are nevertheless attributed to physical dis ease by the sufferer. It has been described as the propensity to express psychologic distress through somatic complaints. It is thought to occur universally in young children (but occurs in every age group) who have not yet developed the cognitive and a linguistic skill needed to compre hend and communicate their feelings. Between 10 and 30 of children worldwide experience physical symptoms that are seemingly unexplained by a physical illness, with recurrent somatic complaints generally falling into cardiovascular, gas trointestinal, pain, and pseudoneurologic symptom clusters (Chapter 212). The prevalence of somatization is roughly equal among school age males and females with a rise in adolescence, at which point somatic complaints in females
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are five times greater than those in males. Youth with a history of somatization are more likely to experience emotional behavioral difficulties, be absent from school, and perform poorly academically. There are high rates of anxiety and depressive disorders in youth with SSRDs. Youth with conversion disorder, specifically Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. Chapter 35 u Somatic Symptom and Related Disorders 237 nonepileptic seizures, have increased rates of comorbid psychopathol ogy including internalizing disorders and posttraumatic stress disor ders. Somatization is common in cultures that accept physical illness but not psychologic symptoms as a reason for disability. RISK FACTORS FOR SOMATIZATION Genetic and biologic factors, stressful life events, personality traits and coping styles, cognitive and learning difficulties, learned complaints, family factors, and sociocultural background are potential risk factors that have been associated with pediatric somatization. Genetic and Biologic Factors Somatization clusters in families with increased rates in first degree relatives of patients with SSRDs. The concordance rates for somatiza tion approximate 29 in monozygotic twin studies. Genetic factors have been hypothesized to contribute to the development of person ality traits that may predispose to somatization when combined with environmental factors. Neuroimaging studies have found neuronal areas (premotor and supplementary motor cortexes, the middle frontal gyrus, the anterior cingulate cortex, the insula, and the posterior cin gulate cortex) to differ between patients with SSRDs. Stressful Life Events Stressful life events, including childhood trauma, physicalsexual abuse, bullying, and exposure to natural disasters have all been associ ated with somatization. Youth with SSRDs have shown high rates of comorbid anxiety, suicidal histories, family psychiatric histories, bully ing, learning difficulties, and significant life events. Personality Traits and Coping Styles Somatization has been postulated to occur in patients who are unable to verbalize emotional distress and instead use physical symptoms as a means of expression. Physical symptoms have been called a form of body language for children who have difficulty expressing emotions verbally. Examples include individuals who have difficul ties with disclosing traumatic events and high achieving children who cannot admit they are under too much pressure. Alexithymia has been used to describe individuals with somatic concerns who do not have a verbal vocabulary to describe their feelings. Somatic complaints have also been linked to somatosensory amplification, which is the tendency to experience normal somatic sensations as intense, noxious and disturbing. When present, patients are hypervigilant to their own bodily sensations, overreact to these sen sations, and interpret them as indicating physical illness. Cognitive and Learning Difficulties Children with difficulties learning and using academic skills, particu larly in the context of high parental expectations, are associated with increased rates of somatization. Compared with unaffected siblings, youth with functional neurologic disorders have been found to score lower on tests of full scale IQ, vocabulary level, and mathematics as well as to have more learning difficulties. Between 40
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and 60 of patients with psychogenic nonepileptic seizures are reported to have learning and subtle language problems. Learned Complaints In operant conditioning learning, attention and sympathy from others andor decrease in responsibilities (secondary gain) can reinforce somatic complaints. If somatic symptoms are reinforced (i.e., increased parental attention andor avoidance of unpleasant school pressures) early in the course of an SSRD the likelihood increases that the somatic complaints will become more ingrained and less amenable to change. Social learning theory suggests that somatic symptoms may be a result of modeling or observational learning within the family. Family members with similar physical complaints (symptom model) are commonly found in SSRDs. Family Factors In family systems theory, somatization can serve the function of draw ing attention away from other areas of tension with a family. It has been suggested that children in families with significant conflict may develop somatic complaints as a mechanism to avoid any emotional expression that may exacerbate family conflict. Sociocultural Background SSRDs have been reported to be more common in rural areas and among individuals of lower socioeconomic status. Spells or visions are common aspects of culturally sanctioned religious and healing rituals, and falling down with loss or alteration in consciousness is a feature in a variety of culture specific syndromes. ASSESSMENT The diagnosis of SSRD must be based on the presence of somatic symptoms that are distressing andor result in significant impairment of daily life. These somatic symptoms must be accompanied by exces sive thoughts, feelings, and behaviors related to these symptoms and or associated health concerns. SSRDs are not diagnoses of exclusion; the mere absence of a medical explanation is insufficient to make the diagnosis. The assessment of suspected SSRDs should include an assessment of biologic, psychologic, social, and developmental realms, both separately and in relation to each other. A collaborative healthcare approach between pediatric practitioners and mental health clinicians is indicated to ensure that all realms are considered in the assessment of medically unexplained physical symptoms (Table 35.7) Medical Assessment A comprehensive medical workup to rule out serious physical illness is necessary, but must be carefully balanced with efforts to avoid unnec essary and potentially harmful tests and procedures. Certain medical conditions are notoriously overlooked and should be carefully consid ered as part of the diagnostic workup for problematic somatic symp toms (Table 35.8). The presence of a medical condition does not exclude the possibility of somatization playing an important role in the presentation. Somatic symp toms early in a disease course that can be directly attributed to a specific physical illness (e.g., acute respiratory illness) may evolve into psycho logically based symptoms, particularly in situations where the patient may experience benefit from adopting the sick role. Symptoms may not fol low known physiologic principles or anatomic patterns and may respond to suggestion or placebo. Physical findings may occur secondary to the effects of the SSRD, especially when chronic or severe (e.g., decondition ing, disuse atrophy from prolonged immobilization, nutritional deficiency, gastroparesis and constipation from chronic
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poor oral intake). Table 35.6 DSM 5 Diagnostic Criteria for Psychologic Factors Affecting Other Medical Conditions A. A medical symptom or condition (other than a mental disorder) is present. B. Psychologic or behavioral factors adversely affect the medical condition in one of the following ways: 1. The factors have influenced the course of the medical condition, as shown by a close temporal association between the psychologic factors and the development or exacerbation of, or delayed recovery from, the medical condition. 2. The factors interfere with the treatment of the medical condition (e.g., poor adherence). 3. The factors constitute additional well established health risks for the individual. 4. The factors influence the underlying pathophysiology, precipitating or exacerbating symptoms or necessitating medical attention. C. The psychologic and behavioral factors in Criterion B are not better explained by another mental disorder (e.g., panic disorder, major depressive disorder, posttraumatic stress disorder). Specify if: mild, moderate, severe, or extreme. From the Diagnostic and Statistical Manual of Mental Disorders, 5th ed. p 322. Copyright 2013. American Psychiatric Association. Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. 238 Part III u Behavioral and Psychiatric Disorders Psychosocial Assessment If somatization is suspected, a mental health consultation should be included early in the diagnostic workup. This can be a difficult step for many families given their belief that there is a medical cause for their childs problem. A common response is for the family to react adversely and think that their childs symptoms are not being taken seriously. It is helpful for the pediatric practitioner to frame the consultation as a routine part of the medical workup as well as an opportunity to assess the level of stress connected with the current physical symptoms. The practitioner can communicate that the mental health consultation will be used to gain a more complete understanding of the origins of their childs distress, what perpetuates it, and which treatments are likely to be most effective. The mental health assessment should include a careful assessment of psychosocial stressors, comorbid depression or anxiety disorders, indi vidual and family histories of somatization, the presence of a model of illness behavior, and evidence of secondary gain resulting from the symptoms. The assessment should provide the pediatric practitioner(s) with a biopsychosocial explanation of the childs symptoms (diagnosis and formulation), which will inform the development of a comprehen sive biopsychosocial management plan. Differential Diagnoses The primary differential diagnosis is between an SSRD and a physical illness. Importantly, however, these disorders are not mutually exclu sive and often coexist. Depressive and anxiety disorders frequently include the presence of physical symptoms, which tend to remit with treatment of the primary depressive or anxiety symptoms, and which appear distinct from physical complaints seen in SSRDs. Distinguish ing features of other physical complaint disorders are noted in Table 35.9. Chronic pain syndromes may be caused by fibromyalgia
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and small fiber autonomic neuropathy and complex regional pain syn drome (see Chapter 211). MANAGEMENT Effective management of SSRDs begins with the development of a posi tive working relationship between the patient, family, pediatric practi tioner, and mental health clinician based on a shared understanding of the diagnosis, formulation, and a management plan that generally incorporates a number of different treatment modalities. The formulation of the problem is the crucial first step. Patients and their families routinely present with the belief that their symptoms are caused by a medical illness alone. This view needs to be reframed from this narrow medical model view to a comprehensive biopsycho social understanding. With the completion of medical and psychoso cial assessments, a joint meeting of the pediatric practitioner(s) and Table 35.7 Key Elements to Consider in the Psychiatric Assessment of Somatic Symptoms and Related Disorders in Children and Adolescents MEDICAL FINDINGS SUGGESTIVE OF SSRDS Absence of findings despite thorough medical workup Lack of electrical evidence on video electroencephalographic monitoring Inconsistent findings on examination Sensory changes inconsistent with anatomic distribution (e.g., splitting at the midline, loss of sensation of entire face but not scalp, discrepancy between pain and temperature sensation, absence of Romberg sign) Absence of functional impairment despite claims of profound weakness (e.g., impairment of fine motor function on testing, yet able to dress and undress) Face hand test (deflecting falling arm from face) Hoover sign (patient pushes down with paretic leg when attempting to raise unaffected leg and fails to press down with unaffected leg when raising paretic leg) Astasia abasia (staggering gait, momentarily balancing, but never actually falling) Dragging a weak leg as though it were a totally lifeless object instead of circumduction of the leg Psychogenic deafness responding to unexpected words or noises Tunnel vision Movement disorder with normal concurrent electroencephalogram Symptoms suggestive of conversion seizures (see Table 634.3). Increased symptoms in the presence of family or medical staff Periods of normal function when distracted Temporal relationship between onset of symptom and psychosocial stressor PSYCHIATRIC FINDINGS SUGGESTIVE OF SSRDS Excessive thoughts, feelings, or behaviors related to the somatic symptoms or associated health concerns Co occurring psychiatric disorder Learning difficulties and academic failure Stressful life events (including childhood trauma and bullying) Symptom model(s) FAMILY BELIEFS REGARDING SOMATIC SYMPTOMS Belief in a single undiagnosed primary medical cause Investment in further medical workup Fear about serious medical illness Belief in the role of environmental triggers Belief in the role of psychologic factors Beliefs regarding symptom management Awareness of nonpharmacologic approaches Belief that the child should rest and be excused from usual responsibilities FAMILY MEDICAL HISTORY Family history of unexplained somatic symptoms Pattern of reinforcement of illness behavior in the family IMPACT OF SOMATIC SYMPTOMS Emotional (e.g., depressionanxiety vs la belle indiffrence) Family (e.g., disruption of work schedule, impact on marital relationship, impact on distraction from family conflict) Social and peer relationships Academic (e.g., absenteeism, placement in home teaching) REINFORCEMENT OF SOMATIC SYMPTOMS Reinforcement by parents Medical journals and diaries of symptoms kept by
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parents Parent home from work Increased attention from familyfriends Increased attention from medical providers Avoidance of school, social, or athletic stressor SSRD, Somatic symptoms and related disorder. From Shaw RJ, DeMaso DR. Clinical Manual of Pediatric Consultation Liaison Psychiatry. American Psychiatric Press; 2020:250252. Table 35.8 Selected Medical Conditions to Consider in the Differential Diagnosis of Youth Presenting with Disabling Somatic Symptoms AIDS Acquired myopathies Acute intermittent porphyria Angina Autoinflammatory (recurrent fever) syndromes Basal ganglia disease Brain tumors Cardiac arrhythmias Chronic systemic infections Ehlers Danlos syndrome Fabry disease Gaucher disease Guillain Barr syndrome Hereditary neuropathies Hereditary angioedema Hyperparathyroidism Hyperthyroidism Juvenile idiopathic arthritis Lyme disease Migraine headaches Mitochondrial disorders Multiple sclerosis Myasthenia gravis Narcolepsy Optic neuritis Periodic paralysis Postural orthostatic hypertension syndrome Polymyositis Seizure disorders Small fiber neuropathy Superior mesenteric artery syndrome Systemic lupus erythematosus Modified from Shaw RJ, DeMaso DR. Clinical Manual of Pediatric Consultation Liaison Psychiatry. American Psychiatric Press; 2020:248. Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. Chapter 35 u Somatic Symptom and Related Disorders 239 mental health clinician (as well as any involved pediatric specialists) should be arranged to reach and ensure a consensus on the diagnosis and treatment plan and facilitate adequate and consistent communica tion among all providers. The next step is an informing conference or meeting that includes both the managing pediatric practitioner and the family. It is important in this meeting that this practitioner present the medical and psychosocial findings together to the patient and the family in a supportive and nonjudgmental manner. If patients and their families believe that the practitioner understands and empathizes with the degree of distress the somatic symptoms have produced, then they are more likely to be active participants in treatment. Depending on the comfort and expertise of the pediatric practitioner and the sever ity of the SSRD, the mental health clinician may or may not elect to attend this meeting. After complete medical investigations yield no unifying results, labeling the symptoms as psychiatric may be problematic because it can shift the search for the cause onto family functioning, resulting in children and parents feeling blamed for the symptoms. The goal is to avoid such labeling and instead help the family move toward an under standing of the mind body connection and to shift their approach from searching for the cause of the symptoms to increasing child functioning. Providing mind body examples, such as facial flushing when embar rassed, hand shaking when frightened, or phantom limb pain, will help the patient and family understand how the brain may produce physical symptoms. Treatment With child and family acceptance of a biopsychosocial understanding, an integrated medical and psychosocial treatment approach focused on the development and implementation a treatment plan to improve the patients functioning, and not a continued search for a cause of the pre senting symptoms, can be implemented. It is helpful to establish
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real istic goals that emphasize improvements in functioning rather than the illusion that the symptoms can be completely removed. Those patients with mild moderate presentations can be treated effectively in the pri mary or specialty pediatric care setting with appropriate mental health follow up, whereas those with severe presentations and high complex ity are better managed in the psychiatry specialty care setting. Role of the Pediatric Practitioner The pediatric practitioner serves an important role in providing ongoing monitoring and treatment for possible physical illness in addition to the recommended mental health interventions. Frequent, brief, and ongoing pediatric visits can be scheduled as a means of helping avoid unneces sary medical investigations and procedures. This arrangement permits the patient to receive attention from their pediatric practitioner without having to develop somatic symptoms. Furthermore it may reassure the family that the team is continuing to monitor for symptoms that would require further evaluation and helps ensure that any further medical evaluation is directed by a clinician knowledgeable about the previous symptoms and evaluations. It is generally more helpful for the practitio ner to attend to a patients anxiety in relation to their physical symptoms rather than the symptoms themselves. This approach has been shown to reduce overall healthcare utilization and to improve patient satisfaction. Using Rehabilitation Approach A rehabilitative approach acknowledges the reality of the symptoms, emphasizes the necessary involvement of mind and body in the recovery process, and shifts the focus from cure to return to normal function ing while allowing youth to save face through the promotion of physi cal recovery as the primary goal. A rehabilitative approach includes the use of intensive physical and occupational therapy that emphasizes the recovery of function. This approach can be combined with a behavioral modification program, with incentives for improvements in functioning, while removing secondary gain for illness behavior. In severely disabled patients, it may be preferable to recommend admission to an inpatient medical psychiatric treatment program that specializes in SSRDs. Another useful option to consider is that of day treatment or partial hospitalization programs. Multidisciplinary inpa tient rehabilitation programs have much to offer these patients because they are designed to support both physical and psychologic recovery. Families are generally reassured that multidisciplinary staff can con tinue to monitor physical symptoms, thus ensuring that any missed diagnoses will be recognized quickly. Youth with a high level of impairment often miss a significant amount of school. Communication with the school is often crucial in coordinating a successful reintegration. In addition to discussions with the school guidance counselor andor nurse, a letter for the school providing education and recommended approaches for the patients symptoms can be beneficial. These interventions can be formalized by having the school work with the family to develop either a 504 plan for accommodations needed in regular education settings, or an indi vidualized educational plan (IEP) if the child needs special education services. Ongoing communication between the school and the pediat ric practitioner for monitoring of further symptoms is recommended. Table
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35.9 Features of Conditions Characterized by Patients Physical Complaints ILLNESS ANXIETY DISORDER SOMATIC SYMPTOM DISORDER CONVERSION DISORDER FUNCTIONAL NEUROLOGIC DISORDER Presenting complaint Primary concern is the development of a serious illnessdoes not require specific symptoms Primary concern is a specific symptom; generally presents with a more specific physical complaint There are no objective physical findings other than those related to deconditioning Presents with new onset neurologic or physical symptom; patient may or may not be concerned about this new symptom Medical correlation to complaint Generally present with more vague complaints than a specific symptom; not usually explained by medical workup In the presence of a known disease, the complaint does not correlate to the natural history of the disorder in severity, duration, or dysfunction Patient can have a medical explanation for their symptom; however, the worry about the seriousness of the symptom is disproportionate or excessive Physical and neurologic findings do not correlate with patients presentation Neurologic manifestations involve aspects of CNS where voluntary control is exercised Course of disease Often associated with other anxiety disorders; can be chronic Chronic; rarely remits Generally acute onset; can recur with same or different presenting symptom(s) CNS, Central nervous system Modified from Byrne R, Elsner G, Beattie A. Emotional and behavioral symptoms. In: Kliegman RM, Toth H, Bordini BJ, Basel D, eds. Nelson Pediatric Symptom Based Diagnosis: Common Diseases and their Mimics. 2nd ed. Elsevier; 2023:Table 31.14, p. 530. Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. 240 Part III u Behavioral and Psychiatric Disorders Psychotherapy and Psychopharmacology Meta analyses have shown that psychologic treatments improve symp tom load, disability, and school attendance in youth suffering from various somatic symptoms including functional abdominal symptoms, fatigue, tension type headache, and musculoskeletal pain. Cognitive behavioral therapy (CBT) interventions modify symptom experi ence and restore central nervous system abnormalities associated with functional impairment. CBT techniques (e.g., relaxation training, biofeedback, hypnosis) can be used to teach patients the control they can have over certain physiologic processes, such as autonomic system activity. Cognitive restructuring is effective in addressing and altering dysfunctional thoughts regarding symptoms and their implications for functioning. Treatments that encourage active coping strategies and emotional expression and modulation are helpful in reducing symp toms and improving functioning. Modifying parental response pat terns that are overprotective and potentially reinforcing (e.g., allowing the child to sleep late or to stay home from school in response to symp toms) help to decrease disability. Psychopharmacologic treatment may be considered when psychi atric comorbidities are present, specifically, depressive and anxiety disorders. A combination of pharmacotherapy, physical therapy, and psychologic interventions in multicomponent management programs has been shown to be effective. Visit Elsevier eBooks at eBooks.Health.Elsevier.com for Bibliography. 36.1 Rumination Disorder Chase B. Samsel, Heather J. Walter, and David R. DeMaso Rumination disorder is the repeated regurgitation of food, in which the regurgitated food may be
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rechewed, reswallowed, or spit out, for a period of at least 1 month following a period of normal func tioning. Regurgitation is typically frequent and daily; it does not occur during sleep. It is not caused by an associated gastrointestinal illness or other medical conditions (e.g., gastroesophageal reflux, pyloric stenosis). It does not occur exclusively during the course of anorexia nervosa, bulimia nervosa, binge eating disorder, or avoid antrestrictive food intake disorder. If the symptoms occur in the context of an intellectual or other neurodevelopmental disorder, the symptoms must be sufficiently severe to warrant additional clinical attention. Weight loss and failure to make expected weight are common fea tures in infants with rumination disorder. Infants may display a char acteristic position of straining and arching the back with the head held back while making sucking movements with their tongue. In infants and older individuals with intellectual disability, the rumina tion behavior may appear to have a self soothing or self stimulating function. Malnutrition may occur in older children and adults, Chapter 36 Rumination and Pica Chase B. Samsel, Heather J. Walter, and David R. DeMaso particularly when the regurgitation is associated with restricted food intake (which may be designed to avoid regurgitation in front of oth ers). They may attempt to hide the regurgitation behavior or avoid eating among others. EPIDEMIOLOGY Originally thought of as a disorder predominantly seen in infants and those with intellectual disability, rumination disorder has also been recognized in healthy individuals across the life span and can be overlooked in adolescents. In otherwise healthy children, rumi nation disorder typically appears in the first year of life, generally between ages 3 and 12 months. The disorder can have an episodic course or can occur continuously until treatment is initiated. In infants the disorder frequently remits spontaneously but can be protracted with problematic and even life threatening malnutri tion. Additional complications related to the secondary effects of malnutrition include growth delay and negative effects on develop ment and learning potential. ETIOLOGY AND DIFFERENTIAL DIAGNOSIS Risk factors for rumination disorder in infants and young children include a disturbed relationship with primary caregivers, lack of an appropriately stimulating environment, neglect, stressful life situations, learned behavior reinforced by pleasurable sensations, distraction from negative emotions, and inadvertent reinforce ment (attention) from primary caregivers. Risk factors for rumina tion disorder in adolescents include similar early childhood factors along with female gender and comorbid anxiety and depression. The differential diagnosis includes congenital gastrointestinal system anomalies, pyloric stenosis, Sandifer syndrome, gastroparesis, hiatal hernia, increased intracranial pressure, diencephalic tumors, adrenal insufficiency, and inborn errors of metabolism. Older children and adults with anorexia nervosa or bulimia nervosa may also engage in regurgitation because of concerns about weight gain. The diagnosis of rumination disorder is appropriate only when the severity of the dis turbance exceeds that routinely associated with a concurrent physical illness or mental disorder. TREATMENT The first step in treatment begins with a behavioral analysis to deter mine whether the disorder serves a self stimulation purpose
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andor is socially motivated. The behavior may begin as self stimulation, but it subsequently becomes reinforced and maintained by the social atten tion given to the behavior. The central focus of behavioral treatment is to reinforce correct eating behavior while minimizing attention to rumination. Diaphragmatic breathing and postprandial gum chewing, when used as a competing response, have been shown to be helpful. Aversive conditioning techniques (e.g., withdrawal of positive atten tion, introducing bittersour flavors when regurgitating) are consid ered when a childs health is jeopardized but can be more reasonable and useful in adolescents. Additional techniques shown to be useful in adolescents include reswallowing all regurgitation, use of paradoxical intention, and guided progressive food trials. Successful behavioral treatment requires the childs primary caregivers to be involved in the intervention. The caretakers need education and counseling on responding adaptively to the childs behavior as well as altering any maladaptive responses. No current evidence supports a psychopharmacologic intervention for rumina tion disorder. In more severe or intractable cases (e.g., severe dehy dration, malnutrition), an intensive integrated medical behavioral treatment program on a medical or medical psychiatric unit may be necessary. Visit Elsevier eBooks at eBooks.Health.Elsevier.com for Bibliography. Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. Chapter 37 u Motor Disorders and Habits 241 36.2 Pica Chase B. Samsel, Heather J. Walter, and David R. DeMaso Pica involves the persistent eating of nonnutritive, nonfood sub stances (e.g., paper, soap, plaster, charcoal, clay, wool, ashes, paint, earth) over a period of at least 1 month. The eating behavior is inap propriate to the developmental level (e.g., the normal mouthing and tasting of objects in infants and toddlers), and therefore a minimum age of 2 years is suggested. The eating behavior is not part of a cul turally supported or socially normative practice. A diagnosis of pica may be assigned in the presence of any other feeding and eating disorder. EPIDEMIOLOGY Pica can occur throughout life but occurs most frequently in child hood. It is more common in those with intellectual disability and autism spectrum disorders, and to a lesser degree in obsessive compulsive and schizophrenic disorders. The prevalence of pica is unclear, although it appears to increase with the severity of an intel lectual disability. It usually remits in childhood but can continue into adolescence and adulthood. Geophagia (eating earth) is asso ciated with pregnancy and is not seen as abnormal in some cultures (e.g., rural or preindustrial societies in parts of Africa and India). Children with pica are at increased risk for lead poisoning, iron deficiency anemia, mechanical bowel problems, intestinal obstruc tion, intestinal perforations, dental injury, and parasitic infections. Pica can be fatal based on substances ingested. ETIOLOGY AND DIFFERENTIAL DIAGNOSIS Numerous etiologies have been proposed but not proved, ranging from psychosocial causes to physical ones. They include nutritional deficiencies (e.g., iron, zinc, calcium), low socioeconomic
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factors (e.g., lead paint exposure), child abuse and neglect, family disorga nization (e.g., poor supervision), mental disorder, learned behavior, underlying (but undetermined) biochemical disorder, and cultural and familial factors. The differential diagnosis includes anorexia nervosa, factitious disorder, and nonsuicidal self injury. A sepa rate diagnosis of pica should be made only if the eating behavior is sufficiently severe enough to warrant additional clinical attention. TREATMENT Combined behavioral, social, and medical approaches are gener ally indicated for pica. Assessment for neglect and family supervi sion combined with psychiatric assessment for concurrent mental disorders and developmental delay are important in developing an effective intervention strategy for pica. Behavioral interventions, particularly applied behavioral analysis in patients with intellectual disability or autism spectrum disorders, are increasingly found to be helpful. The sequelae related to an ingested item can require spe cific treatment (e.g., lead toxicity, iron deficiency anemia, parasitic infestation). Ingestion of hair can require medical or surgical inter vention for a gastric bezoar. Visit Elsevier eBooks at eBooks.Health.Elsevier.com for Bibliography. Motor disorders are interrelated sets of psychiatric symptoms charac terized by abnormal motor movements and associated phenomena. In the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM 5), they include tic, stereotypic movement, and developmental coordination disorders. Tic disorders (Tourette, persistent motor or vocal tic, provisional tic, other specifiedunspecified tic) and stereo typic movement disorders (SMDs) are addressed in this chapter. Hab its present as repetitive and often problematic motor behaviors (e.g., thumb sucking, nail biting, teeth grinding). When the problems cause significant distress or impairment they are discussed as body focused repetitive behavior disorder in the Obsessive Compulsive and Related Disorders section of DSM 5. 37.1 Tic Disorders Jung Won Kim, Heather J. Walter, and David R. DeMaso Tourette disorder (TD), persistent (chronic) motor or vocal tic dis order (PTD), and provisional tic disorders are characterized by invol untary, rapid, repetitive, and single or multiple motor andor vocal phonic tics that wax and wane in frequency but have persisted for 1 year since the first tic onset (1 year for provisional tic disorder) (Table 37.1). PTD is differentiated from TD in that PTD is limited to either motor or vocal tics (not both), whereas TD has both motor and vocal tics at some point in the illness (although not necessarily concur rently). The tic disorders are hierarchical in order (i.e., TD followed by PTD followed by provisional tic disorder), such that once a tic disorder at one level of the hierarchy is diagnosed, a lower hierarchy diagnosis cannot be made. Other specifiedunspecified tic disorders are pre sentations in which symptoms characteristic of a tic disorder that cause significant distress or impairment predominate but do not meet the full criteria for a tic or other neurodevelopmental disorder. DESCRIPTION Tics are sudden, rapid, recurrent, nonrhythmic motor movements or vocalizations. Simple motor tics (e.g., eye blinking, neck jerking, shoul der shrugging, extension of the extremities) are fast, brief movements involving one or a few muscle groups. Complex motor tics involve sequentially andor simultaneously
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produced, relatively coordinated movements that can seem purposeful (e.g., brushing back ones hair bangs, tapping the foot, imitating someone elses movement echo praxia, or making a sexual or obscene gesture copropraxia). Simple vocal tics (e.g., throat clearing, sniffing, coughing) are solitary, mean ingless sounds and noises. Complex vocal tics involve recognizable word or utterances (e.g., partial words syllables, words out of context, obscenities or slurs coprolalia, repeating ones own sounds or words palilalia, or repeating the last heard word or phrase echolalia). Chapter 37 Motor Disorders and Habits Jung Won Kim, Heather J. Walter, and David R. DeMaso Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. 242 Part III u Behavioral and Psychiatric Disorders Table 37.1 DSM 5 Diagnostic Criteria for Tic Disorders TOURETTE DISORDER A. Both multiple motor and one or more vocal tics have been present at some time during the illness, although not necessarily concurrently. B. The tics may wax and wane in frequency but have persisted for 1 year since first tic onset. C. Onset is before age 18 years. D. The disturbance is not attributable to the physiologic effects of a substance (e.g., cocaine) or another medical condition (e.g., Huntington disease, postviral encephalitis). PERSISTENT (CHRONIC) MOTOR OR VOCAL TIC DISORDER A. Single or multiple motor or vocal tics have been present during the illness, but not both motor and vocal. B. The tics may wax and wane in frequency but have persisted for 1 year since first tic onset. C. Onset is before age 18 years. D. The disturbance is not attributable to the physiologic effects of a substance (e.g., cocaine) or another medical condition (e.g., Huntington disease, postviral encephalitis). E. Criteria have never been met for Tourette disorder. Specify if: With motor tics only With vocal tics only PROVISIONAL TIC DISORDER A. Single or multiple motor andor vocal tics. B. The tics have been present for 1 year since first tic onset. C. Onset is before age 18 years. D. The disturbance is not attributable to the physiologic effects of a substance (e.g., cocaine) or another medical condition (e.g., Huntington disease, postviral encephalitis). E. Criteria have never been met for Tourette disorder or persistent (chronic) motor or vocal tic disorder. Note: A tic is a sudden, rapid, recurrent, nonrhythmic motor movement or vocalization. Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, 5th ed. p 81. Copyright 2013. American Psychiatric Association. All Rights Reserved. Sensory phenomena (premonitory urges) that precede and trigger the urge to tic have been described. Individuals with tics can suppress them for varying periods of time, particularly when external demands exert their influence, when deeply engaged in a focused task or activity, or during sleep. Tics are often suggestible and are worsened by anxi ety, excitement, or exhaustion. Parents have described increasing fre quency of tics at the end of the
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day. CLINICAL COURSE Onset of tics is typically between ages 4 and 6 years. The frequency of tics tends to wax and wane with peak tic severity between ages 10 and 12 years and marked attenuation of tic severity in most individuals (65) by age 18 20 years. A small percentage will have worsening tics into adulthood. New onset of tics in adulthood is very rare and most often is associated with exposure to drugs or insults to the central ner vous system. Tics manifest similarly in all age groups, with changes in affected muscle groups and vocalizations that occur over time. Some individuals may have tic free periods of weeks to months. EPIDEMIOLOGY Prevalence rates for all tics range from 618 for males and 311 for females, with the rate of TD alone estimated as 0.8. In general, PTDTD has a male preponderance with a gender ratio varying from 2:1 to 4:1. DIFFERENTIAL DIAGNOSIS The differential diagnosis includes other repetitive movements of childhood (Table 37.2). Tics may be difficult to differentiate from ste reotypies. Although stereotypies may resemble tics, stereotypies are typically rhythmic movements and do not demonstrate the change in body location or movement type over time that is typical of tics. Compulsions may be difficult to differentiate from tics when tics have premonitory urges. Tics should be differentiated from a variety of developmental and benign movement disorders (e.g., benign parox ysmal torticollis, Sandifer syndrome, benign jitteriness of newborns, shuddering attacks). Although tics may present in various neurologic illnesses (e.g., Wilson disease, neuroacanthocytosis, Huntington syn drome, various frontal subcortical brain lesions), it is rare for tics to be the only manifestation of these disorders (Table 37.3). Individuals presenting with tics in the context of declining motor or cognitive function should be referred for neurologic assessment. Substancesmedications that are reported to worsen tics include selec tive serotonin reuptake inhibitors (SSRIs), lamotrigine, and cocaine. If tics develop in close temporal relationship to the use of a substance or medication and then remit when use of the substance is discontinued, a causal relationship is possible. Stimulants do not commonly increase tics. COMORBIDITIES Comorbid psychiatric disorders are common, often with both patient and family viewing the accompanying condition as more problem atic than the tics. There is a bidirectional association between PTD TD (especially TD) and obsessive compulsive disorder (OCD), with 2060 of TD patients meeting OCD criteria and 2040 of OCD patients reporting tics (Fig. 37.1). Attention deficithyperactivity dis order (ADHD) occurs in approximately 50 of all childhood PTD TD, but estimates in clinically referred patients suggest much higher rates (6080). PTDTD is often accompanied by behavior problems, including poor frustration tolerance, temper outbursts, and oppo sitionality. Learning disabilities have been found in 20 of these patients. Concurrent anxiety and depression have also been observed. Some patients with PTDTD will display symptoms of autism spec trum disorder (ASD); careful assessment is required to determine which disorder is primary. ETIOLOGY Tics are proposed to be the result of dysfunctional corticostriatal thalamocortical motor
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pathways in the basal ganglia, striatum, and frontal lobes associated with abnormalities in the dopamine, serotonin, and norepinephrine neurotransmitter systems. Male predominance in PTDTD may be attributable to influences of sex hormones on the neu rodevelopment of these motor pathways, as reflected by the effects of antiandrogens in the treatment of TD. Family studies suggest a 10 100fold increased risk of PTDTD among first degree relatives compared to rates in the general popula tion. Twin studies also support a genetic link, with approximately 80 of monozygotic twins and 30 of dizygotic twins showing concordance for PTDTD. Candidate gene association and nonparametric linkage studies have not identified specific susceptibility genes for PTDTD. Autoimmune mediated mechanisms have been hypothesized as having a potential etiologic role in some tic disorders. The pediatric autoimmune neuropsychiatric disorder associated with streptococ cal infection (PANDAS) designation describes cases of acute child hood onset of OCD andor tics following a streptococcal infection. Pediatric acute onset neuropsychiatric syndrome (PANS) describes a subtype of acute childhood onset OCD (tics are not a required fea ture) in which a link to a prior streptococcal infection is not evident, suggesting that other infectious agents may be responsible. In addition to a diagnosis of OCD and tics, children with PANSPANDAS may potentially have separation anxiety, nightmares, personality change, oppositional behaviors, and deterioration in math skills and handwrit ing. Although some studies suggest a prior history of infections may increase the risk for developing tic disorder, this remains controversial. Premorbid stress has been hypothesized to act as a sensitizing agent in the pathogenesis of TD among susceptible individuals by affecting stress responsive biologic systems such as the hypothalamic pituitary adrenal axis. Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. Chapter 37 u Motor Disorders and Habits 243 SEQUELAE Many individuals with mild to moderate tics express minimal to no distress or functional impairment and may even be unaware of their tics. Even individuals with moderate to severe tics can experience minimal functional impairment, but psychologic distress may occur. Infrequently, the presence of tics can lead to social isolation, social victimization, inability to work or attend school, or impaired quality of life. TDPTD is associated with increased risk of suicide. Suicidal behavior should be monitored, particularly in those with persistent tics, history of suicide attempts, and psychiatric comorbidities. SCREENING Pediatric practitioners should routinely screen for unusual movements (e.g., sudden twitches or jerks, eye blinking, neck twisting, muscle tight ening, shoulder shrugging, or involuntary gestures) or vocalizations (e.g., utter involuntary sounds, like grunts, yelps, squeaks, or throat clears). Often families are unaware that frequent sniffing, coughing, or blinking may be indicative of tics, attributing these behaviors to medi cal problems (e.g., allergies, visual problems). A careful assessment of the timing, triggers, and specific characteristics may differentiate tics from other medical problems. If differentiation is difficult, a referral to a pediatric
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specialist in the affected system is warranted. ASSESSMENT If the screening suggests the presence of a tic disorder, a more com prehensive evaluation should ensue, including the age of onset, types of tics, tic frequency, alleviating and aggravating factors, and a family history of tics. Parent rating scales specific for tics (e.g., the Motor Tic, Obsessions and Compulsions, Vocal Tic Evaluation Survey MOVES and Autism Tics, ADHD and other Comorbidities inven tory (A TAC) can supplement the assessment. For clinician rated tic severity, the most comprehensive, reliable, and valid instrument is the Yale Global Tic Severity Scale (YGTSS), though its relatively long administration makes routine use in clinical practice problematic (https:candapediatricmedicalhomes.files.wordpress.com201702 yale global tic severity scale.pdf). A medical workup should be considered for new onset tics, par ticularly for presentations characterized by sudden onset, atypi cality, or mental status abnormalities. Basic laboratory measures (hemogram, renalhepatic function panel, thyroid panel, and fer ritin, along with urine drug screen for adolescents) should be con sidered. For new, sudden onset, or severe symptom exacerbation, pediatric practitioners may assess for concurrent acute infection (e.g., culture, rapid viral tests). Electroencephalography and brain imaging are not routinely recommended for isolated tics and should be reserved for patients with other neurologic findings that might suggest an autoimmune encephalitis syndrome (limbic encepha litis). Comorbid psychiatric disorders (e.g., OCD, ADHD, ASD) should be investigated. TREATMENT The decision to treat tics is made with the child and family based on the level of impairment and distress caused by the tics. If tics are mild in severity, the pediatric practitioner can provide the family with educa tion, often with no need for further intervention. Patient and family education should include common symptom presentations, implications of concurrent conditions, course and prog nosis, and treatment options (including no treatment). The patients typical exacerbating and alleviating factors should be outlined. Pedi atric practitioners can also direct the patient and family to infor mational websites, including the Tourette Association of America (www.tourette.org). Almost 75 of children with TDPTD receive some form of class room accommodation (e.g., directions to ignore tics and permission to leave the room as needed). The accommodations may need to be formalized in an individualized education plan (IEP) if a child needs special education services or a 504 plan if the child just needs accom modations in the regular classroom. Table 37.2 Repetitive Movements of Childhood MOVEMENT DESCRIPTION TYPICAL DISORDERS WHERE PRESENT Tics Sudden rapid, recurrent, nonrhythmic, stereotyped, vocalization or motor movement Transient tics, Tourette disorder, persistent tic disorder Dystonia Involuntary, sustained, or intermittent muscle contractions that cause twisting and repetitive movements, abnormal postures, or both DYT1 gene, Wilson disease, myoclonic dystonia, extra pyramidal symptoms caused by dopamine blocking agents Chorea Involuntary, random, quick, jerking movements, most often of the proximal extremities, that flow from joint to joint. Movements are abrupt, nonrepetitive, and arrhythmic and have variable frequency and intensity Sydenham chorea, Huntington chorea Stereotypies Stereotyped, rhythmic, repetitive movements or patterns of speech, with lack of variation over time Autism, stereotypic movement
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disorder, intellectual disability Compulsions A repetitive, excessive, meaningless activity or mental exercise that a person performs in an attempt to avoid distress or worry Obsessive compulsive disorder, anorexia, body dysmorphic disorder, trichotillomania, excoriation disorder Myoclonus Shocklike involuntary muscle jerk that may affect a single body region, one side of the body, or the entire body; may occur as a single jerk or repetitive jerks Hiccups, hypnic jerks, Lennox Gastaut syndrome, juvenile myoclonic epilepsy, mitochondrial encephalopathies, metabolic disorders Akathisia Unpleasant sensations of inner restlessness, often prompting movements in an effort to reduce the sensations Extrapyramidal adverse effects from dopamine blocking agents; anxiety Volitional behaviors Behavior that may be impulsive or caused by boredom, such as tapping peers or making sounds (animal noises) Attention deficithyperactivity disorder, oppositional defiant disorder, sensory integration disorders Adapted from Murphy TK, Lewin AB, Storch EA, Stock S. American Academy of Child and Adolescent Psychiatry (AACAP) Committee on Quality Issues (CQI). Practice parameter for the assessment and treatment of children and adolescents with tic disorders. J Am Acad Child Adolesc Psychiatry. 2013;52(12):13411359. Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. 244 Part III u Behavioral and Psychiatric Disorders Referral to a behavioral treatment specialist should be considered when tics are distressing or functionally impairing. The behavioral interventions with the strongest empirical support are habit reversal therapy (HRT) and comprehensive behavioral intervention for tics (CBIT). The basic components of HRT include premonitory urge awareness training and building a competing response to the urge to tic (Table 37.4). Based on HRT, CBIT additionally includes relaxation training and a functional intervention designed to mitigate against tic generating situations. A course of HRTCBIT treatment typically takes several months or 8 10 sessions. CBIT has been found to reduce significantly the severity of tics compared to education and supportive therapy. Medications should be considered when the tics are causing severe impairment in the quality of life or when psychiatric comorbidities are present. The only U.S. Food and Drug Administration (FDA) approved medications to treat TD in children and adolescents are two first generation antipsychotics (haloperidol, pimozide) and one second generation antipsychotic (aripiprazole). Agonists (clonidine, guanfacine) are also considered as first line agents because of their more favorable side effect profile compared with the antipsychotic medications (see Chapter 33). Youths with tic disorders may benefit from SSRIs for the treat ment of comorbid obsessive compulsive, anxiety, or depressive disorders. Augmentation of SSRIs with an atypical antipsychotic has been a consideration in patients with concurrent tic disorders and OCD responding poorly to an SSRI alone. The presence of tics does not preclude the use of stimulants to address comorbid ADHD. Treatment of tics and comorbid ADHD with a combina tion of agonists and stimulants (e.g., clonidine with methylphe nidate) decreases tics. Close clinical monitoring is required for possible exacerbation of tics during stimulant treatment. Anger and rage outbursts are
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common particularly among youth with severe tics (up to 80 in clinically referred samples). Behavioral therapies (cognitive behavioral therapy CBT, parent management training; see Chapter 34) that address anger management may be useful. A systematic review indicated high confidence of efficacy for CBIT; moderate confidence for medications, such as haloperidol, risperidone, aripiprazole, clonidine; and low confidence for medi cations, such as ziprasidone, guanfacine, and topiramate. No evi dence exists to differentiate the effectiveness of HRTCBIT alone vs combined with pharmacotherapy as tic disorder treatment options. There is no rigorous scientific evidence to support the use of deep brain stimulation, repetitive magnetic stimulation, or dietary sup plements in the treatment of TD or PTD. In severe presentations, pediatric practitioners should consider seeking consultations from andor making referrals to pediatric tic disorder specialists (i.e., behavioral psychologist, pediatric neurol ogist, developmental behavioral pediatrician, or child and adoles cent psychiatrist) in determining a treatment regimen. Table 37.3 Etiology of Tics PRIMARY CAUSES Sporadic Transient motor or phonic (1 year), chronic motor or phonic tics (1 year), adult onset recurrent) tics, Tourette disorder, primary dystonia Inherited Tourette disorder, Huntington disease, primary dystonia, neuroacanthocytosis syndromes, neurodegeneration with brain iron accumulation (type 1) (pantothenate kinase associated neurodegeneration), tuberous sclerosis, Wilson disease, Duchenne muscular dystrophy SECONDARY CAUSES Infections Encephalitis, Creutzfeldt Jakob disease, neurosyphilis, Sydenham chorea, PANS Drugs Amphetamines, methylphenidate, levodopa, cocaine, carbamazepine, phenytoin, phenobarbital, lamotrigine, antipsychotics, and other dopamine receptor blocking drugs Toxins Carbon monoxide, wasp venom Developmental Static encephalopathy, intellectual disability syndromes, chromosomal abnormalities, autistic spectrum disorders Chromosomal Disorders Down syndrome, Klinefelter syndrome, XYY karyotype, fragile X, triple X, and 9p mosaicism, partial trisomy 16, 9p monosomy, citrullinemia, Beckwith Wiedemann syndrome Other Causes Head trauma, stroke, cardiopulmonary bypass with hypothermia, neurocutaneous syndromes, schizophrenia, neurodegenerative diseases RELATED DISORDERS Stereotypieshabitsmannerisms Self injurious behaviors Motor restlessness Akathisia Compulsions Hyperekplexia Jumping Frenchman (startle response) PANS, Pediatric acute neuropsychiatric syndrome. Modified from Jankovic J. Differential diagnosis and etiology of tics. In: Cohen DJ, Goetz, CG, Jankovic J, eds. Tourette Syndrome. Lippincott Williams Wilkins, 2001:Table 2.2, p. 18. Attention deficit hyperactivity disorder Obsessive compulsive disorder Tourette disorder plus Pure Tourette disorder Impulse control disordersDepression Fig. 37.1 Schematic representation of the behavioral spectrum in Tourette disorder. The size of each area is proportional to the estimated prevalence of the symptoms; the background color intensity is propor tional to the complexity of the clinical presentation. (From Cavanna AE, Seri S. Tourettes syndrome. BMJ. 2013;347:f4964.) Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. Chapter 37 u Motor Disorders and Habits 245 37.2 Stereotypic Movement Disorder Jung Won Kim, Heather J. Walter, and David R. DeMaso Stereotypic movement disorder (SMD) is defined in DSM 5 as a neurodevelopmental disorder characterized by repetitive, seemingly driven, and apparently purposeless motor behavior (stereotypy) that interferes with social, academic, or other activities and may result in self injury. The onset of SMD is the early
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developmental period (often before age 3 years), and the symptoms are not attributable to the physiologic effects of a substance or neurologic condition and are not better explained by another neurodevelopmental or men tal disorder. The disorder is considered mild if symptoms are easily suppressed by sensory stimulation or distraction, and severe if con tinuous monitoring and protective measures are required to prevent serious injury, with moderate falling between mild and severe. DESCRIPTION Examples of stereotypic movements include hand shaking or wav ing, body rocking, head banging, self biting, and hitting ones own body. The presentation depends on the nature of the stereotypic movement and level of the childs awareness of the behavior. Among typically developing children, the repetitive movements may be stopped when attention is directed to the movements or when the child is distracted from performing them. Among youth with intellectual disability, the behaviors may be less responsive to such efforts. Each individual presents with their own uniquely patterned behavior. Stereotypic movements may occur many times during a day, lasting a few seconds to several minutes or longer. The behav iors may occur in multiple contexts, including when the individual is excited, stressed, fatigued, or bored. CLINICAL COURSE Stereotypic movements typically begin before age 3 years. In those who develop complex motor stereotypies, the great majority exhibit these symptoms before 24 months. In most typically developing youth, these movements resolve over time. Among those with intellectual disability, the stereotyped behaviors may persist for years, although the pattern may change over time. EPIDEMIOLOGY Simple stereotypic movements are common in typically develop ing young children. Some children may bang their head on their mattress as they are falling asleep or may sit and rock when bored or overstimulated. Self injurious habits, such as self biting or head banging, can occur in up to 25 of typically developing toddlers (often during tantrums), but they are almost invariably associated with developmental delay in youth older than 5 years. Complex ste reotypic movements are much less common (approximately 34). Between 4 and 16 of patients with intellectual disability engage in stereotypic movements. COMORBIDITY Stereotypic movements are a common manifestation of a variety of neurogenetic disorders, such as Lesch Nyhan, Rett, fragile X, Cornelia de Lange, and Smith Magenis syndromes. DIFFERENTIAL DIAGNOSIS According to DSM 5, stereotypic movements must be differentiated from normal development, ASDs, tic disorders, OCDs, and other neurologicmedical conditions. Simple stereotypic movements occurring in the context of typical development usually resolve with age. Stereotypic movements may be a presenting symptom of ASD, but SMD does not include the deficits in the social communication characteristic of ASD. When ASD is present, SMD is diagnosed only when there is self injury or when the stereotypic behaviors are suf ficiently severe to become a focus of treatment. Typically, SMD has an earlier age of onset than the tic disorders. SMD is distinguished from OCD by the absence of obsessions as well as the nature of the repetitive behaviors, which in OCD are purposeful (e.g.,
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in response to obsessions). The diagnosis of stereotypic movements requires the exclusion of mannerisms, paroxysmal dyskinesias, and benign hereditary chorea. A neurologic history and examination are required to assess features suggestive of other disorders, such as myoclonus, dystonia, and chorea. ETIOLOGY There is a possible evolutionary link between repetitive abnormal grooming like behaviors and early human experience with adver sity. Brain regions implicated in this model (e.g., amygdala, hip pocampus) are those involved in navigating human experience through unpredictable, anxiety provoked emotional states, as well as regions (e.g., nucleus accumbens) related to pleasure and reward seeking. The latter involves the hypothesis that individuals expe rience some level of gratification from performing the stereotypic behavior. Social isolation with insufficient stimulation (e.g., severe neglect) is a risk factor for self stimulation that may progress into stereo typies, particularly repetitive rocking or spinning. Environmental stress may trigger stereotypic behaviors. Repetitive self injurious behavior may be a behavioral phenotype in neurogenetic syndromes (e.g., Lesch Nyhan, Rett, and Cornelia de Lange syndromes). Lower cognitive functioning is also linked to greater risk of stereotypic behaviors. TREATMENT The initial approach to mild stereotypy is for the primary caretak ers to ignore the undesired behavior, encourage substitute behavior, and not convey worry to their child. These behaviors may disappear with time and elimination of attention in young children. How ever, in children with intellectual disability or ASDs, stereotypies may be more refractory to treatment than in typically developing children and may necessitate referral to a behavioral psychologist, developmental behavioral pediatrician, or child and adolescent psy chiatrist for behavioral andor psychopharmacologic management. The pediatric practitioner should consider and rule out neglect of the child, which can be associated with repetitive rocking, spinning, or other stereotypic movements. Behavior therapy is the mainstay of treatment, using a variety of strategies, including habit reversal, relaxation training, self monitoring, contingency management, competing responses, and negative practice. The environment should also be modified to reduce risk of injury to those engaging in self injurious behavior. Atypical antipsychotic medications may be helpful in reducing ste reotypic movements in youth with ASD. Patients with anxiety and obsessive compulsive behaviors treated with SSRIs may show improve ment in their stereotypic movements. HABITS Habits involve an action or pattern of behavior that is repeated often. Habits are common in childhood and range from usually benign and transient behaviors (e.g., thumb sucking, nail biting) to more problematic (e.g., trichotillomania, bruxism). In DSM 5, habits are not included as a diagnostic category because they are not viewed as disorders causing clinically significant distress or impair ment in functioning. When they do cause distress or impairment or are associated with repeated attempts by the individual to stop the behavior they are discussed as body focused repetitive behavior disorder. HRT has been effective as a first line treatment approach (see Table 37.4). Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier
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Inc. All rights reserved. 246 Part III u Behavioral and Psychiatric Disorders Thumb Sucking Thumb sucking is common in infancy and occurring in as many as 25 of children age 2 years and 15 of children age 5 years. Thumb sucking beyond 5 years of age may be associated with sequelae (e.g., paronychia, anterior open bite). As with other rhythmic patterns of behavior, thumb sucking is self soothing. Basic behavioral manage ment, including encouraging parents to ignore thumb sucking and instead focus on praising the child for substitute behaviors, is often an effective treatment. Simple reminders and reinforcers can also be considered; giving the child a sticker or other reward for each block of time that they do not thumb suck. In rare cases, mechani cal devices placed on the thumb or in the mouth to prevent thumb sucking or noxious agents (bitter salves) placed on the thumb may be part of the treatment plan. Bruxism Bruxism or teeth grinding is common (530 of children), can begin in the first 5 years of life, and may be associated with daytime anxiety. Persistent bruxism can manifest as muscular or temporomandibular joint pain. Untreated bruxism can cause problems with dental occlu sion. Helping the child find ways to reduce anxiety might relieve the problem; bedtime can be made more relaxing by reading or talking with the child and allowing the child to discuss fears. Praise and other emotional support are useful. Persistent bruxism requires referral to a dentist given the risk for dental occlusion. Visit Elsevier eBooks at eBooks.Health.Elsevier.com for Bibliography. Table 37.4 Components of Habit Reversal Training INCREASE INDIVIDUALS AWARENESS OF HABIT Response descriptionhave individual describe behavior to therapist in detail while reenacting the behavior and looking in a mirror. Response detectioninform individual of each occurrence of the behavior until each occurrence is detected without assistance. Early warninghave individual practice identifying earliest signs of the target behavior. Situation awarenesshave individual describe all situations in which the target behavior is likely to occur. TEACH COMPETING RESPONSE TO HABIT The competing response must result in isometric contraction of muscles involved in the habit, be capable of being maintained for 3 min, and be socially inconspicuous and compatible with normal ongoing activities but incompatible with the habit (e.g., clenching ones fist, grasping and clenching an object). For vocal tics and stuttering, deep relaxed breathing with a slight exhale before speech has been used as the competing response. SUSTAIN COMPLIANCE Habit inconvenience reviewhave individual review in detail all problems associated with target behavior. Social support procedurefamily members and friends provide high levels of praise when a habit free period is noted. Public displayindividual demonstrates to others that he or she can control the target behavior in situations in which the behavior occurred in the past. FACILITATE GENERALIZATIONSYMBOLIC REHEARSAL PROCEDURE For each situation identified in situation awareness procedure, individual imagines himself or herself beginning the target behavior but stopping and engaging in the competing response. From Carey WB, Crocker AC, Coleman WL, et al., eds. Developmental
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Behavioral Pediatrics. 4th ed. Philadelphia: Saunders; 2009:639. Anxiety is not necessarily pathologic, is seen across the life span, and can be adaptive (e.g., the anxiety one might feel during life threatening situations). It has both a cognitive behavioral component, expressed in worrying and wariness, and a physiologic component, mediated by the autonomic nervous system. Anxiety is characterized as pathologic (e.g., a disorder) when it becomes disabling, interferes with social interac tions, or derails normal development. Anxiety disorders are some of the most common psychiatric disor ders in childhood. The point prevalence worldwide is nearly 7, and the estimated lifetime prevalence in the United States is approximately 2030. Anxiety disorders are often comorbid with other psychiatric and medical disorders, and they can have physical manifestations, such as weight loss, palpitations, tremors, muscle cramps, paresthesias, hyper reflexia, and abdominal distress (Table 38.1). Although onset can be acute, the course is generally chronic with periods of fluctuating severity. The potential consequences of untreated anxiety include impairments in social, educational, and overall functioning. Because anxiety is both a normal phenomenon and, when highly activated, strongly associated with impairment, the clinician is tasked with differentiating between normal anxiety and abnormal anxiety across development (Fig. 38.1). The median age of onset is 11 years. However, there are known peri ods of typical onset during specific developmental phases for both nor mal and pathologic anxiety. Normal stranger anxiety begins around 7 9 months of age. Preschoolers typically have specific fears related to the dark, animals, and imaginary situations. Separation anxiety can occur during the preschool years. Although most school aged children abandon the imaginary fears of early childhood, some replace them with fears of bodily harm or other worries, reaching the level of a spe cific phobia (Table 38.2). Some characteristics of obsessive compulsive disorder (OCD) can be considered typical in early school ages, but OCD often has its onset in the midschool aged years (Table 38.3). Social anxiety occurs in later grade school ages and early adolescence (Table 38.4) as the value of peer relationships increases. Generalized anxiety, panic, and agoraphobia tend to occur during the teen and young adult years (Tables 38.5 to 38.7). Genetic or temperamental factors contribute more to the develop ment of some anxiety disorders, whereas environmental factors are closely linked to the cause of others. Specifically, behavioral inhibition (sensitivity to novel stimuli) appears to be a heritable tendency and is linked with social phobia, generalized anxiety, and selective mutism. OCD and other disorders associated with OCD like behaviors, such as Tourette syndrome and other tic disorders, tend to have high genetic risk as well (see Chapter 37.1). Environmental factors, such as parent infant attachment and exposure to trauma, contribute more to sepa ration anxiety disorder and posttraumatic stress disorder (PTSD) (Table 38.8). Parental anxiety disorder is associated with an increased risk of anxiety disorder in offspring. Chapter 38 Anxiety Disorders, Obsessive Compulsive Disorder, and Post traumatic Stress Disorder Rosa K. Kim Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California
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from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. Chapter 38 u Anxiety Disorders, Obsessive Compulsive Disorder, and Post traumatic Stress Disorder 247 Table 38.1 Mental and Somatic Disorders that are Frequently Comorbid or Difficult to Distinguish in Anxiety Disorder EXAMPLES OF OVERLAPPING SYMPTOMS KEY CLINICAL INSIGHTS TO RECOGNIZE MENTAL DISORDERS Major depressive disorder Fatigue, anxiety, worry, or agitation Major depressive disorder is the highest comorbidity in anxiety disorder and associated with higher severity, suicidality, disability and chronicity; clinicians must comprehensively assess because major depressive disorder comorbidity requires more intensive pharmacologic treatment and a different form of psychotherapy treatment (e.g., cognitive behavioral therapy for depression rather than for anxiety disorder) Bipolar disorder Agitation, irritability, or racing thoughts Anxiety is often present in bipolar disorder and is associated with rapid cycling; targeting anxiety could aid in mood stabilization; bipolar disorder requires focus on mood stabilization and considerate use of medication, which could induce mania (especially antidepressants) Obsessive compulsive disorder Extreme worry or inability to relax People who have obsessive compulsive disorder engage in ritualistic, repetitive behavior to deal with their fears, which is absent in anxiety disorder; these people often realize that their behavior is irrational and inappropriate Posttraumatic stress disorder Avoidance, hyperarousal, or anxiety laden intrusive memories The intense experience of anxiety in posttraumatic stress disorder is specifically in response to a psychologic trauma (e.g., abuse, war, or accident); specific psychotherapies focused on the trauma associated with the posttraumatic stress disorder should be used Health anxiety (hypochondriasis) Anxiety or worry from bodily responses Anxiety is specifically related to preoccupation with having or acquiring a serious, undiagnosed medical illness Substance use (e.g., illicit drugs, alcohol, or benzodiazepines) disorder Tremor, sweating, palpitations, or panic attacks (during withdrawal or in some cases intoxication) When suspected, clinicians should conduct a psychiatric interview of substance use disorders, with potential breath, urine, or plasma drug screening; comorbidity of alcohol or benzodiazepine abuse with anxiety disorder is considerable SOMATIC DISORDERS Cardiac disease Chest pain or palpitations (which is also common in panic disorder) Clinical evaluation, including electrocardiogram, assessment of plasma troponin concentration, or Holter monitoring Thyroid disease (e.g., hyperthyroidism) Palpitations, tremor, panic attacks, or persistent anxiety Laboratory assessment of plasma thyroid stimulating hormone Respiratory disease (e.g., asthma) Shortness of breath Clinical evaluation with a pulmonary function test Pheochromocytoma or other disorders that result in sudden blood pressure increase Panic attacks or bodily sensations Blood pressure monitoring over 24 hr or hormone assessment (e.g., in blood or urine) Epilepsy Anxiety symptoms as part of aura or start of seizure Clinical evaluation or neurologic referral when the causes of symptoms are unclear In previous classifications of the Diagnostic and Statistical Manual of Mental Disorders and International Classification of Diseases, these disorders were included in the classification of anxiety disorders. In current classifications (e.g., the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders and the 11th edition of the International Classification of
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Diseases), they are integrated in different classifications. From Penninx BWJH, Pine DS, Holmes EA, Reif A. Anxiety disorders. Lancet. 2021;397:914926:Table 2, p. 917. Separation N or m at iv e fe ar s Dying and death of others Thunder, lightning, fire, water, darkness, nightmares, animals, imaginary creatures Fear of negative evaluation School anxiety, performance anxiety Germs, getting ill, natural Peer rejection AdolescenceSchool ageChildhood Age (years) 12630 Infancy and toddlerhood disasters, traumatic events, harm to self or others Stranger shyness Fig. 38.1 Normative fears throughout childhood and adolescence. (From Craske MG, Stein MB. Anxiety. Lancet. 2016;38810063:30483059.) Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. 248 Part III u Behavioral and Psychiatric Disorders Table 38.2 DSM 5 Diagnostic Criteria for Specific Phobia A. Marked fear or anxiety about a specific object or situation (e.g., flying, heights, animals, receiving an injection, seeing blood). Note: In children, the fear or anxiety may be expressed by crying, tantrums, freezing, or clinging. B. The phobic object or situation almost always provokes immediate fear or anxiety. C. The phobic object or situation is actively avoided or endured with intense fear or anxiety. D. The fear or anxiety is out of proportion to the actual danger posed by the specific object or situation and to the sociocultural context. E. The fear, anxiety, or avoidance is persistent, typically lasting for 6 mo or more. F. The fear, anxiety, or avoidance causes clinically significant distress or impairment in social, occupational, or other important areas of functioning. G. The disturbance is not better explained by the symptoms of another mental disorder, including fear, anxiety, and avoidance or situations associated with panic like symptoms or other incapacitating symptoms (as in agoraphobia); objects or situations related to obsessions (as in obsessive compulsive disorder); remainders of traumatic events (as in posttraumatic stress disorder); separation from home or attachment figures (as in separation anxiety disorder); or social situations (as in social anxiety disorder). Specify if: Code based on the phobic stimulus: Animal (e.g., spiders, insects, dogs). Natural environment (e.g., heights, storms, water). Blood injection injury (e.g., needles, invasive medical procedures). Situational (e.g., airplanes, elevators, enclosed places). Other (e.g., situations that may lead to choking or vomiting; in children, e.g., loud sounds or costumed characters). From the Diagnostic and Statistical Manual of Mental Disorders, 5th ed. pp 197198. Copyright 2013. American Psychiatric Association. Table 38.3 DSM 5 Diagnostic Criteria for Obsessive Compulsive Disorder A. Presence of obsessions, compulsions, or both: Obsessions are defined by (1) and (2): 1. Recurrent and persistent thoughts, urges, or images that are experienced, at some time during the disturbance, as intrusive and unwanted, and that in most individuals cause marked anxiety or distress. 2. The individual attempts to ignore or suppress such thoughts, urges, or images, or to neutralize them with some other thought or action (i.e., by performing a compulsion). Compulsions are defined by
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(1) and (2): 1. Repetitive behaviors (e.g., handwashing, ordering, checking) or mental acts (e.g., praying, counting, repeating words silently) that the individual feels driven to perform in response to an obsession or according to rules that must be applied rigidly. 2. The behaviors or mental acts are aimed at preventing or reducing anxiety or distress, or preventing some dreaded event or situation; however, these behaviors or mental acts are not connected in a realistic way with what they are designed to neutralize or prevent, or are clearly excessive. B. The obsessions or compulsions are time consuming (e.g., take more than 1 hrday) or cause clinically significant distress or impairment in social, occupational, or other important areas of functioning. C. The obsessive compulsive symptoms are not attributable to the physiologic effects of a substance (e.g., a drug of abuse, a medication) or another medical condition. D. The disturbance is not better explained by the symptoms of another mental disorder (e.g., excessive worries, as in generalized anxiety disorder; preoccupation with appearance, as in body dysmorphic disorder; difficulty discarding or parting with possessions, as in hoarding disorder; hair pulling, as in trichotillomania hair pulling disorder; skin picking, as in excoriation skin picking disorder; stereotypies, as in stereotypic movement disorder; ritualized eating disorder, as in eating disorders; preoccupation with substances or gambling, as in substance related and addictive disorders; preoccupation with having an illness, as in illness anxiety disorder; sexual urges or fantasies, as in paraphilic disorders; impulses, as in disruptive, impulse control, and conduct disorders; guilty ruminations, as in schizophrenia spectrum and other psychotic disorders; or repetitive patterns of behavior, as in autism spectrum disorder). Specify if: With good or fair insight: The individual recognizes that obsessive compulsive disorder beliefs are definitely or probably not true or that they may or may not be true. With poor insight: The individual thinks obsessive compulsive disorder beliefs are probably true. With absent insightdelusional beliefs: The individual is completely convinced that obsessive compulsive disorder beliefs are true. Specify if: Tic related: The individual has a current or past history of a tic disorder. From the Diagnostic and Statistical Manual of Mental Disorders, 5th ed. p 237. Copyright 2013. American Psychiatric Association. Table 38.4 DSM 5 Diagnostic Criteria for Social Anxiety Disorder (Social Phobia) A. Marked fear or anxiety about one or more social situations in which the individual is exposed to possible scrutiny by others. Examples include social interactions (e.g., having a conversation, meeting unfamiliar people), being observed (e.g., eating or drinking), and performing in front of others (e.g., giving a speech). B. The individual fears that he or she will act in a way or show anxiety symptoms that will be negatively evaluated (i.e., will be humiliating or embarrassing; will lead to rejection or offend others). C. The social situations almost always provoke fear or anxiety. Note: In children, the fear or anxiety may be expressed by crying, tantrums, freezing, clinging, shrinking, or failing to speak in social situations. D. The social situations are avoided
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or endured with intense fear or anxiety. E. The fear or anxiety is out of proportion to the actual threat posed by the social situation and to the sociocultural context. F. The fear, anxiety, or avoidance is persistent, typically lasting for 6 mo or more. G. The fear, anxiety, or avoidance causes clinically significant distress or impairment in social, occupational, or other important areas of functioning. H. The fear, anxiety, or avoidance is not attributable to the physiologic effects of a substance (e.g., a drug of abuse, a medication) or another medical condition. I. The fear, anxiety, or avoidance is not better explained by the symptoms of another mental disorder, such as panic disorder, body dysmorphic disorder, or autism spectrum disorder. J. If another medical condition (e.g., Parkinson disease, obesity, disfigurement from burns or injury) is present, the anxiety or avoidance is clearly unrelated or is excessive. Specify if: Performance only: If the fear is restricted to speaking or performing in public. From the Diagnostic and Statistical Manual of Mental Disorders, 5th ed. pp 202 203. Copyright 2013. American Psychiatric Association. Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. Chapter 38 u Anxiety Disorders, Obsessive Compulsive Disorder, and Post traumatic Stress Disorder 249 ASSESSMENT There is no recommendation for routine screening of children and adolescents for anxiety disorders. Freely available general screening instruments such as the Pediatric Symptom Checklist and Strengths and Difficulties Questionnaire can be used to identify anxiety concerns in primary care and school settings. Rating scales can be used to sup port diagnosis and to follow response to treatment, but they are not diagnostic on their own. Commonly used anxiety rating scales include the Screen for Child Anxiety Related Emotional Disorders (SCARED), the Spence Childrens Anxiety Scale (SCAS), the Preschool Anxiety Scale, the Generalized Anxiety Disorder 7 (GAD 7), and the Patient Reported Outcomes Measurement Information System (PROMIS) Pediatric Short Form Anxiety 8a. Symptoms of anxiety are typically identified through the clinical interview by asking questions about worries, fears, and stress or by the patient and familys spontaneous report. The interview must be developmentally sensitive, and further discussions with the family may reveal environmental reinforcements, including the caregivers parent ing style and enabling of avoidance behaviors. Because some degree of anxiety is considered normal, it is impor tant to clarify when the symptom severity reaches the point of being pathologic and to differentiate between the subtypes (Table 38.9). The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM 5) has specific criteria for each type of anxiety with require ments for frequency, duration, and extent of functional impairment. DIFFERENTIAL DIAGNOSIS AND COMORBIDITIES In addition to determining whether diagnostic criteria are met for a specific anxiety disorder, it is also crucial to rule out alternative explanations. The differential diagnosis includes numerous medical conditions and medication induced anxiety (Table 38.10). Anxiety dis
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orders also frequently occur with not just other anxiety subtypes but also other psychiatric comorbidities, notably depression and substance use disorders (Table 38.11; see Table 38.1). TREATMENT OF ANXIETY Cognitive Behavioral Therapy (CBT) Cognitive behavioral therapy (CBT) is a therapy that targets the cog nitions, behaviors, and physiologic symptoms of anxiety, with a par ticular focus on the interconnections between the three. Its framework typically involves homework assignments for practicing the skills in real life environments. The goal is to achieve functional improvement within approximately 18 sessions. Because it is a skills based treatment, CBT is thought to be a durable treatment, an important consideration when treating children and adolescents. It is specifically recommended to patients 6 18 years old with social anxiety, generalized anxiety, sepa ration anxiety, specific phobia, and panic disorder. Specialized training and experience are paramount to the effective delivery of this treatment modality, and it is worth taking the time to ensure that patients identify therapists with the training and experience to provide rigorous CBT. CBT typically should incorporate graduated exposure, in which stepwise mastery of a hierarchy of fearful stimuli results in desensitization. Table 38.6 DSM 5 Diagnostic Criteria for Panic Disorder A. Recurrent unexpected panic attacks. A panic attack is an abrupt surge of intense fear or intense discomfort that reaches a peak within minutes, and during which time four (or more) of the following symptoms occur: Note: The abrupt surge can occur from a calm state or an anxious state. 1. Palpitations, pounding heart, or accelerated heart rate. 2. Sweating. 3. Trembling or shaking. 4. Sensations of shortness of breath or smothering. 5. Feelings of choking. 6. Chest pain or discomfort. 7. Nausea or abdominal distress. 8. Feeling dizzy, unsteady, light headed, or faint. 9. Chills or heart sensations. 10. Paresthesias (numbness or tingling sensations). 11. Derealizations (feeling or unreality) or depersonalization (being detached from oneself). 12. Fear of losing control or going crazy. 13. Fear of dying. Note: Culture specific symptoms (e.g., tinnitus, neck soreness, headache, uncontrollable screaming or crying) may be seen. Such symptoms should not count as one of the four required symptoms. B. At least one of the attacks has been followed by 1 mo (or more) of one or both of the following: 1. Persistent concern or worry about additional panic attacks or their consequences (e.g., losing control, having a heart attack, going crazy). 2. A significant maladaptive change in behavior related to the attacks (e.g., behaviors designed to avoid having panic attacks, such as avoidance of exercise or unfamiliar situations). C. The disturbance is not attributable to the physiologic effects of a substance (e.g., a drug of abuse, a medication) or another medical condition (e.g., hyperthyroidism, cardiopulmonary disorders). D. The disturbance is not better explained by another mental disorder (e.g., the panic attacks do not occur only in response to feared social situations, as in social anxiety disorder; in response to circumscribed phobic objects or situations, as in specific phobia; in response to obsessions, as in obsessive
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compulsive disorder; or in response to reminders of traumatic events, as in posttraumatic stress disorder; or in response to separation from attachment figures, as in separation anxiety disorder). From the Diagnostic and Statistical Manual of Mental Disorders, 5th ed. pp 208 209. Copyright 2013. American Psychiatric Association.. Table 38.5 DSM 5 Diagnostic Criteria for Generalized Anxiety Disorder A. Excessive anxiety and worry (apprehensive expectation), occurring more days than not for at least 6 mo, about a number of events or activities (such as work or school performance). B. The individual finds it difficult to control the worry. C. The anxiety and worry are associated with three (or more) of the following six symptoms (with at least some symptoms having been present for more days than not for the past 6 mo): Note: Only one item is required in children. 1. Restlessness or feeling keyed up or on edge. 2. Being easily fatigued. 3. Difficulty concentrating or mind going blank. 4. Irritability. 5. Muscle tension. 6. Sleep disturbance (difficulty falling or staying asleep, or restless, unsatisfying sleep). D. The anxiety, worry, or physical symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning. E. The disturbance is not attributable to the physiologic effects of a substance (e.g., a drug of abuse, a medication) or other medical condition (e.g., hyperthyroidism). F. The disturbance is not better explained by another mental disorder (e.g., anxiety or worry about having panic attacks in panic disorder, negative evaluation in social anxiety disorder social phobia, contamination or other obsessions in obsessive compulsive disorder, separation from attachment figures in separation anxiety disorder, remainders of traumatic events in posttraumatic stress disorder, gaining weight in anorexia nervosa, physical complaints in somatic symptom disorder, perceived appearance flaws in body dysmorphic disorder, having a serious illness in illness anxiety disorder, or the content of delusional beliefs in schizophrenia or delusional disorder). From the Diagnostic and Statistical Manual of Mental Disorders, 5th ed. p 222. Copyright 2013. American Psychiatric Association. Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. 250 Part III u Behavioral and Psychiatric Disorders Table 38.7 DSM 5 Diagnostic Criteria for Agoraphobia A. Marked fear or anxiety about two (or more) of the following five situations: 1. Using public transportation (e.g., automobiles, buses, trains, ships, planes). 2. Being in open spaces (e.g., parking lots, marketplaces, bridges). 3. Being in enclosed places (e.g., shops, theaters, cinemas). 4. Standing in line or being in a crowd. 5. Being outside of the home alone. B. The individual fears or avoids these situations because of thoughts that escape might be difficult or help might not be available in the event of a developing panic like symptoms or other incapacitating or embarrassing symptoms (e.g., fear or falling in the elderly, fear of incontinence). C. The agoraphobic situations almost always provoke fear or anxiety. D.
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The agoraphobic situations are actively avoided, require the presence of a companion, or are endured with intense fear or anxiety. E. The fear or anxiety is out of proportion to the actual danger posed by the agoraphobic situations and to the sociocultural context. F. The fear, anxiety, or avoidance is persistent, typically lasting for 6 mo or more. G. The fear, anxiety, or avoidance causes clinically significant distress or impairment in social, occupational, or other important area of functioning. H. If another medical condition (e.g., inflammatory bowel disease, Parkinson disease) is present, the fear, anxiety, or avoidance is clearly excessive. I. The fear, anxiety, or avoidance is not better explained by the symptoms or another mental disorderfor example, the symptoms are not confined to specific phobia or situational type; do not involve only social situations (as in social anxiety disorder); and are not related exclusively to obsessions (as in obsessive compulsive disorder), reminders or traumatic events (as in posttraumatic stress disorder), or fear of separation (as in separation anxiety disorder). Note: Agoraphobia is diagnosed irrespective of the presence of panic disorder. If an individuals presentation meets criteria for panic disorder and agoraphobia, both diagnoses should be assigned. From the Diagnostic and Statistical Manual of Mental Disorders, 5th ed. pp 217 218. Copyright 2013. American Psychiatric Association. Table 38.8 DSM 5 Diagnostic Criteria for Posttraumatic Stress Disorder POSTTRAUMATIC STRESS DISORDER Note: The following criteria apply to adults, adolescents, and children older than 6 yr. For children 6 yr and younger, see corresponding criteria below. A. Exposure to actual or threatened death, serious injury, or sexual violence in one (or more) of the following ways: 1. Directly experiencing the traumatic event(s). 2. Witnessing, in person, the event(s) as it occurred to others. 3. Learning that the traumatic event(s) occurred to a close family member or close friend. In cases of actual or threatened death of a family member or friend, the event(s) must have been violent or accidental. 4. Experiencing repeated or extreme exposure to aversive details of the traumatic event(s) (e.g., first responders collecting human remains; police officers repeatedly exposed to details of child abuse). Note: Criterion A4 does not apply to exposure through electronic media, television, movies, or pictures, unless this exposure is work related. B. Presence of one (or more) of the following intrusion symptoms associated with the traumatic event(s), beginning after the traumatic event(s) occurred: 1. Recurrent, involuntary, and intrusive distressing memories of the traumatic event(s). Note: In children older than 6 yr, repetitive play may occur in which themes or aspects of the traumatic event(s) are expressed. 2. Recurrent distressing dreams in which the content andor effect of the dream are related to the traumatic event(s). Note: In children, there may be frightening dreams without recognizable content. 3. Dissociative reactions (e.g., flashbacks) in which the individual feels or acts as if the traumatic event(s) were recurring. (Such reactions may occur on a continuum, with the more extreme expression being a complete loss or awareness of present surroundings.)
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Note: In children, trauma specific reenactment may occur in play. 4. Intense or prolonged psychologic distress at exposure to internal or external cues that symbolize or resemble an aspect of the traumatic event(s). 5. Marked physiologic reactions to internal or external cues that symbolize or resemble an aspect of the traumatic event(s). C. Persistent avoidance of stimuli associated with the traumatic event(s), beginning after the traumatic event(s) occurred, as evidenced by one or both of the following: 1. Avoidance of or efforts to avoid distressing memories, thoughts, or feelings about or closely associated with the traumatic event(s). 2. Avoidance of or efforts to avoid external reminders (people, places, conversations, activities, objects, situations) that arouse distressing memories, thoughts, or feelings about or closely associated with the traumatic event(s). D. Negative alterations in cognitions and mood associated with the traumatic event(s), beginning or worsening after the traumatic event(s) occurred, as evidenced by two (or more) of the following: 1. Inability to remember an important aspect of the traumatic event(s) (typically due to dissociative amnesia and not to other factors such as head injury, alcohol, or drugs). 2. Persistent and exaggerated negative beliefs or expectations about oneself, others, or the world (e.g., I am bad, No one can be trusted, The world is completely dangerous, My whole nervous system is permanently ruined). 3. Persistent, distorted cognitions about the cause or consequences of the traumatic event(s) that lead the individual to blame himselfherself or others. 4. Persistent negative emotional state (e.g., fear, horror, anger, guilt, or shame). 5. Markedly diminished interest or participation in significant activities. Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. Chapter 38 u Anxiety Disorders, Obsessive Compulsive Disorder, and Post traumatic Stress Disorder 251 Family therapy is often needed as an adjunct to CBT. Its focus is to improve relationships, strengthen problem solving and communication skills, address parental anxiety, and foster adaptive coping within the family unit. School directed interventions can also be an important Table 38.8 DSM 5 Diagnostic Criteria for Posttraumatic Stress Disordercontd 6. Feelings of detachment or estrangement from others. 7. Persistent inability to experience positive emotions (e.g., inability to experience happiness, satisfaction, or loving feelings). E. Marked alterations in arousal and reactivity associated with the traumatic event(s), beginning or worsening after the traumatic event(s) occurred, as evidenced by two (or more) of the following: 1. Irritable behavior and angry outbursts (with little or no provocation) typically expressed by verbal or physical aggression toward people or objects. 2. Reckless or self destructive behavior. 3. Hypervigilance. 4. Exaggerated startle response. 5. Problems with concentration. 6. Sleep disturbance (e.g., difficulty falling or staying asleep or restless sleep). F. Duration of the disturbance (Criteria B, C, D, and E) is more than 1 mo. G. The disturbance causes clinically significant distress or impairment in social, occupational, or other important areas of functioning. H. The
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disturbance is not attributable to the physiologic effects of a substance (e.g., medication, alcohol) or another medical condition. Specify whether: With dissociative symptoms: The individuals symptoms meet the criteria for posttraumatic stress disorder, and in addition, in response to the stressor, the individual experiences persistent or recurrent symptoms of either of the following: 1. Depersonalization: Persistent or recurrent experiences of feeling detached from, and as if one were an outside observer of, ones mental processes or body (e.g., feeling as though one were in a dream; feeling a sense of unreality of self or body or of time moving slowly). 2. Derealization: Persistent or recurrent experiences of unreality of surroundings (e.g., the world around the individual is experienced as unreal, dreamlike, distant, or distorted). Note: To use this subtype, the dissociative symptoms must not be attributable to the physiologic effects of a substance (e.g., blackouts, behavior during alcohol intoxication) or another medical condition (e.g., complex partial seizures). Specify if: With delayed expression: If the full diagnostic criteria are not met until at least 6 mo after the event (although the onset and expression of some symptoms may be immediate). POSTTRAUMATIC STRESS DISORDER FOR CHILDREN 6 YEARS AND YOUNGER A. In children 6 yr and younger, exposure to actual or threatened death, serious injury, or sexual violence in one (or more) of the following ways: 1. Directly experiencing the traumatic event(s). 2. Witnessing, in person, the event(s) as it occurred to others, especially primary caregivers. Note: Witnessing does not include events that are only in electronic media, television, movies, or pictures. 3. Learning that the traumatic event(s) occurred to a parent or caregiving figure. B. Presence of one (or more) of the following intrusion symptoms associated with the traumatic event(s), beginning after the traumatic event(s) occurred: 1. Recurrent, involuntary, and intrusive distressing memories of the traumatic event(s). Note: Spontaneous and intrusive memories may not necessarily appear distressing and may be expressed as play reenactment. 2. Recurrent distressing dreams in which the content andor effect of the dream is related to the traumatic event(s). Note: It may not be possible to ascertain that the frightening content is related to the traumatic event. 3. Dissociative reactions (e.g., flashbacks) in which the child feels or acts as if the traumatic event(s) were recurring. (Such reactions may occur on a continuum, with the most extreme expression being a complete loss of awareness of present surroundings.) Such trauma specific reenactment may occur in play. 4. Intense or prolonged psychologic distress at exposure to internal or external cues that symbolize or resemble an aspect of the traumatic event(s). C. One (or more) of the following symptoms, representing either persistent avoidance of stimuli associated with the traumatic event(s) or negative alterations in cognitions and mood associated with the traumatic event(s), must be present, beginning after the event(s) or worsening after the event(s): PERSISTENT AVOIDANCE OF STIMULI 1. Avoidance of or efforts to avoid activities, places, or physical reminders that arouse recollections or the traumatic event(s). 2. Avoidance of
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or efforts to avoid people, conversations, or interpersonal situations around recollections of the traumatic event(s). NEGATIVE ALTERATIONS IN COGNITIONS 3. Substantially increased frequency of negative emotional states (e.g., fear, guilt, sadness, shame, confusion). 4. Markedly diminished interest or participation in significant activities, including constriction of play. 5. Socially withdrawn behavior. 6. Persistent reduction in expression of positive emotions. D. Alterations in arousal and reactivity associated with the traumatic event(s), beginning or worsening after the traumatic event(s) occurred, as evidenced by two (or more) of the following: 1. Irritable behavior and angry outbursts (with little or no provocation), typically expressed as verbal and physical aggression toward people or objects (including extreme temper tantrums). 2. Hypervigilance. 3. Exaggerated startle response. 4. Problems with concentration. 5. Sleep disturbance (e.g., difficulty falling asleep or staying asleep or restless sleep). E. The duration of the disturbance is more than 1 mo. F. The disturbance causes clinically significant distress or impairment in relationships with parents, siblings, peers, or other caregivers or with school behavior. G. The disturbance is not attributable to the physiologic effects of a substance (e.g., medication or alcohol) or another medical condition. Continued Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. 252 Part III u Behavioral and Psychiatric Disorders Table 38.8 DSM 5 Diagnostic Criteria for Posttraumatic Stress Disordercontd Specify whether: With dissociative symptoms: The individuals symptoms meet the criteria for posttraumatic stress disorder, and the individual experiences persistent or recurrent symptoms of either of the following: 1. Depersonalization: Persistent or recurrent experiences of feeling detached from, and as if one were an outside observer of, ones mental processes or body (e.g., feeling as though one were in a dream; feeling a sense of unreality of self or body or of time moving slowly). 2. Derealization: Persistent or recurrent experiences of unreality of surroundings (e.g., the world around the individual is experienced as unreal, dreamlike, distant, or distorted). Note: To use this subtype, the dissociative symptoms must not be attributable to the physiologic effects of a substance (e.g., blackouts, behavior during alcohol intoxication) or another medical condition (e.g., complex partial seizures). Specify if: With delayed expression: If the full diagnostic criteria are not met until at least 6 mo after the event (although the onset and expression of some symptoms may be immediate). From the Diagnostic and Statistical Manual of Mental Disorders, 5th ed. pp 271 274. Copyright 2013. American Psychiatric Association. Table 38.9 Core Diagnostic Features and Characteristics for Anxiety Disorders SELECTIVE MUTISM SEPARATION ANXIETY SPECIFIC PHOBIA SOCIAL ANXIETY DISORDER AGORAPHOBIA PANIC DISORDER GENERALIZED ANXIETY DISORDER Core emotions or cognitions Consistent failure to speak in situations for which there is an expectation to speak, despite language competence Unrealistic, persistent fear or anxiety about separation from, or loss of, attachment figure, or adverse events occurring to them Marked, excessive, and unreasonable fear or anxiety of circumscribed objects
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or situations (e.g., animals, natural forces, blood injection, or places) Marked, excessive, and unreasonable fear or anxiety of scrutiny or negative judgement by other people Marked, excessive, and concerning fear of leaving home, entering closed or open public places, crowds, or transportation Recurrent, unexpected panic attacks with sustained mental (e.g., fear, fear of losing control, or feeling of alienation) manifestations Marked, uncontrollable, and anxious worry and fears about everyday events and problems Physical symptoms No physical symptoms Nightmares and symptoms of distress No physical symptoms Blushing, fear of vomiting, urgency or fear of micturition or defecation No physical symptoms Multiple symptoms (e.g., palpitations, dyspnea, diaphoresis, chest pain, dizziness, paresthesia, or nausea) Restlessness, fatigue, irritability, difficulty concentrating, muscle tension, sleep disturbance, or autonomic arousal Behavior Disturbance interferes with (educational) achievement or social communication Reluctance to leave attachment figure; disturbance impairs social, school, or other functioning Avoidance of circumscribed objects or situations; disturbance impairs social, school, work, or other functioning Avoidance of social interactions and situations; disturbance impairs social, school, work, or other functioning Avoidance of fear inducing situations; disturbance impairs social, school, work, or other functioning Changed behavior in maladaptive ways related to the attacks; disturbance impairs social, school, work or other functioning Disturbance impairs social, school, work, or other functioning Required symptom duration 1 month (beyond first school month) 1 mo (childhood; 4 18 yr); 6 months (adulthood; 18 yr or older) 6 mo 6 mo 6 mo 1 mo 6 mo Median age of onset Childhood (5 yr) Childhood (around 6 yr) Childhood (around 8 yr) Early adolescence (around 13 yr) Late adolescence (around 20 yr) Adulthood (around 25 yr) Adulthood (around 30 yr) For OCD see Table 38.3; for PTSD see Table 38.8. Characteristics and features for anxiety disorders were based on criteria from the Diagnostic and Statistical Manual of Mental Disorders (Fifth Edition) and International Classification of Diseases (11th Edition). From Penninx BWJH, Pine DS, Holmes EA, Reif A. Anxiety disorders. Lancet. 2021;397:914926. Table 1, p. 915. Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. Chapter 38 u Anxiety Disorders, Obsessive Compulsive Disorder, and Post traumatic Stress Disorder 253 component of treatment, and specific plans for anxiety management can be included in a childs 504 plan or individualized education plan (IEP). The therapy with the most evidence for PTSD is a subtype of CBT called trauma focused CBT (TF CBT). Given that standard anxiety medications are less effective in PTSD, it is particularly crucial that clinicians refer these patients to trauma focused therapy. In TF CBT, the therapist amplifies stress management techniques in preparation for exposure based interventions with the goal of achieving mastery over trauma triggers. In small adult trials, ketamine or 3,4 methyl enedioxymethamphetamine (MDMA) assisted therapy have shown benefit. There is insufficient evidence to currently recommend either therapy. Selective Serotonin Reuptake Inhibitors Selective serotonin reuptake inhibitors (SSRIs) as
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a class are effective in treating anxiety. The available options include citalopram, escitalopram, fluoxetine, fluvoxamine, paroxetine, sertraline, and vilazodone. Despite randomized clinical trials (RCTs) providing support for the safety and effectiveness of this medication class, no specific SSRIs are U.S. Food and Drug Administration (FDA)approved for anxiety in children. SSRIs are generally well tolerated, with the most common side effects involving xerostomia, gastrointestinal upset, headache, somnolence or insomnia, dizziness, fatigue, and changes in appetite (see Chapter 33). RCTs in children and adolescents with PTSD found no significant dif ference between SSRI and placebo. SSRIs may be considered in pediatric patients with PTSD who have comorbid conditions responsive to SSRIs, including depression, affective numbing, and anxiety (see Table 33.5). All of the SSRIs carry a black box warning for suicidal thinking and behavior through age 24 years, and this specific risk must be discussed with the patient and caregiver and documented before initiation. Other potential adverse effects include behavioral activation, hypomanic or manic symptoms, and serotonin syndrome (see Chapter 33). Combination Treatment The combination of CBT and an SSRI is generally thought to be better than either treatment alone for moderate to severe anxiety. It is impor tant to continue recommending CBT even after the decision has been made to start pharmacologic treatment. Serotonin Norepinephrine Reuptake Inhibitors Duloxetine is a serotonin norepinephrine reuptake inhibitor (SNRI) and has an FDA indication for the treatment of generalized anxiety dis order in children ages 7 17. However, it is still considered a second line treatment as SSRIs tend to be more effective. The other SNRI options are venlafaxine and desvenlafaxine. Potential side effects of dulox etine include xerostomia, diaphoresis, abdominal discomfort, gastro intestinal distress, headache, tremor, sedation or insomnia, decreased appetite, and weight loss. Of note, it is less likely to cause behavioral activation than the SSRIs. Agonists Clonidine and guanfacine are agonists and may be helpful for PTSD by targeting sleep disturbances like nightmares, persistent physiologic arousal, and exaggerated startle response. OBSESSIVE COMPULSIVE DISORDER AND PEDIATRIC ACUTE ONSET NEUROPSYCHIATRIC SYNDROME Obsessive compulsive symptoms can be effectively treated with SSRIs (sertraline, fluoxetine). If the patients symptoms prove to be treatment refractory to the standard options, then one might consider fluvoxamine andor clomipramine, which is a heterocyclic antidepres sant. These are indicated when a patient has failed two or more SSRI trials. Habit reversal training is an important nonpharmacologic treat ment modality for OCD as well. A proportion of abrupt onset OCD cases are attributed to an immune response that targets the brain (pediatric acute onset neuropsychiatric syndrome PANS). The immune response may be brought about by Table 38.10 Differential Diagnosis of Anxiety Disorders GENERAL PSYCHIATRIC MEDICAL Shyness Substance use (including caffeine) Substance use withdrawal Body dysmorphic disorder ADHD (distractibility, restlessness) ASD (social withdrawal, social skills deficits, distractibility) MDD (distractibility, insomnia, somatic symptoms) Bipolar disorder Delusional disorder Learning disorders (worry about school performance) ODD (refusal to do activity) Antihistamines Bronchodilators Nasal decongestants Steroids Dietary supplements Stimulants Hyperthyroidism Allergic reactions Asthma Cardiac conditions Autoimmune encephalitis Chronic
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pain Headaches CNS disease Diabetes Dysmenorrhea Lead intoxication Hypoglycemia Hypoxia Pheochromocytoma Mast cell disorders Carcinoid syndrome Hereditary angioedema Systemic lupus erythematosus Table 38.11 Psychiatry and Medical Comorbidities of Anxiety PSYCHIATRIC MEDICAL Depression ADHD Bipolar disorder Eating disorder Learning disorder Language disorder Substance related disorders Somatic symptoms Headaches GI disorders Asthma Allergies Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. 254 Part III u Behavioral and Psychiatric Disorders infections (commonly, but not exclusively, streptococcal infections) or other mechanisms that activate the immune system. There are no DSM 5 diagnostic criteria for PANS. One suggested approach to PANS diagnostic criteria is noted in Table 38.12. Of note is the abrupt sudden onset of OCD, the presence of additional psychi atric disorders (e.g., anxiety, depression, emotional lability), and the requirement to rule out other disorders like Sydenham chorea. If PANS is suspected, a comprehensive evaluation is warranted primarily to rule out neurologic and medical conditions (see Table 38.12). Children with an abrupt onset of psychiatric and neuro logic findings should be evaluated with MRI, electroencephalo gram (EEG), and blood plus cerebrospinal fluid (CSF) autoimmune encephalitis antibody testing. Children with a sudden onset of only psychiatric symptoms (OCD, tics, anxiety) do not require exten sive testing except for testing for a group A streptococcus, unless they have severe and disabling psychiatric features, The latter group should be evaluated to rule out the disorders noted in Table 38.12. Once diagnosed, clinicians should prioritize the target symptoms of the individual patient and select treatments accordingly. The three realms of PANS treatment are psychotherapeutic, antimicrobial, and immunomodulatory. Because behavioral interventions take time to work, psychiatric interventions should begin expeditiously for symptomatic relief. Antibiotics may eliminate the underlying source of neuroinflammation, and immunomodulatory options can help treat immune system disturbances. SPECIFIC PHOBIAS Specific phobias may not typically require treatment with an SSRI and may be better targeted with exposure response prevention thera pies and with premedicating with a blocker before an anticipated exposure. The exception to this is needle phobia; premedication with a blocker is not indicated in this instance because of the risk of exacerbating the vasovagal response. Physical maneuvers, such as crossing the legs and tensing the muscles, may be effective in needle phobia. Visit Elsevier eBooks at eBooks.Health.Elsevier.com for Bibliography. Table 38.12 Diagnostic Criteria for Pediatric Acute Onset Neuropsychiatric Syndrome CRITERION 1 Abrupt, dramatic onset of obsessive compulsive disorder or severely restricted food intake. CRITERION 2 Concurrent presence of additional neuropsychiatric symptoms with similarly severe and acute onset from at least two of the following seven categories: 1. Anxiety. 2. Emotional lability or depression. 3. Irritability, aggression, or severely oppositional behaviors. 4. Behavioral (developmental) regression. 5. Deterioration in school performance. 6. Sensory or motor abnormalities. 7. Somatic signs and symptoms, including sleep disturbances, enuresis, or urinary frequency. CRITERION 3 Symptoms are not better explained by a known neurologic or
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medical disorder, such as Sydenham chorea, systemic lupus erythematosus, Tourette disorder, autoimmune encephalitis, or others. The diagnostic workup of patients with suspected PANS must be comprehensive enough to rule out these and other relevant disorders. The nature of the co occurring symptoms will dictate the necessary assessments, which may include MRI scans, lumbar puncture, electroencephalograms, or other diagnostic tests. PANS, Pediatric acute onset neuropsychiatric syndrome. Modified from Johnson M, Fernell E, Preda I, et al. Paediatric acute onset neuropsychiatric syndrome in children and adolescents: an observational cohort study. Lancet Child Adolesc Health. 2019;3(3):175180. Mood disorders encompass several different entities on the spectrum between depression and mania. Mood disorders are interrelated sets of psychiatric symptoms characterized by a core deficit in emotional self regulation. Classically, the mood disorders have been divided into depressive and bipolar disorders, representing the two emotional polarities, dysphoric (low) and euphoric (high) mood. Mood disor ders in children and adolescents are highly prevalent and are the most common psychiatric illnesses seen after attention deficithyperactivity disorder (ADHD) and anxiety. Primary care is often their first point of contact when seeking treatment. 39.1 Depressive Disorders Colleen K. Manak and Rosa K. Kim Depressive disorders include major depressive, persistent depressive, disruptive mood dysregulation, other specifiedunspecified depressive, premenstrual dysphoric, and substancemedication induced disor ders, as well as depressive disorder caused by another medical condi tion (Fig. 39.1). DESCRIPTION Major depressive disorder (MDD) is characterized by a distinct period of at least 2 weeks (an episode) in which there is a depressed or irritable mood andor loss of interest or pleasure in almost all activi ties that is present for most of the day, nearly every day (Table 39.1 and Fig. 39.2). Major depression is associated with characteristic veg etative and cognitive symptoms, including disturbances in appetite, sleep, energy, and activity level; impaired concentration; thoughts of worthlessness or guilt; and suicidal thoughts or actions. Major depression is considered mild if few or no symptoms in excess of those required to make the diagnosis are present, and the symptoms are mildly distressing, manageable, and result in minor functional impairment. Major depression is considered severe if symptoms sub stantially in excess of those required to make the diagnosis are pres ent, and the symptoms are highly distressing, unmanageable, and markedly impair function. Moderate major depression is intermedi ate in severity (Fig. 39.3). Persistent depressive disorder is characterized by depressed or irri table mood for more days than not, for at least 1 year (in children and adolescents). This chronic form of depression is associated with char acteristic vegetative and cognitive symptoms; however, the cognitive symptoms of persistent depression are less severe (e.g., low self esteem rather than worthlessness, hopelessness rather than suicidality). Persis tent depressive disorder is characterized as mild, moderate, or severe (Table 39.2). Overall, the clinical presentation of major and persistent depres sive disorders in children and adolescents is similar to that in adults. The prominence of the symptoms can change with age: irritability and somatic complaints may be more common in
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children, and energy, activity level, appetite, and sleep disturbances may be more common in adolescents. Because of the cognitive and linguistic immaturity of young children, symptoms of depression in that age group may be more likely to be observed than self reported. The core feature of disruptive mood dysregulation disorder (DMDD) is severe, persistent irritability evident most of the day, nearly every day, for at least 12 months in multiple settings (at home, at school, with peers). The irritable mood is interspersed Chapter 39 Mood Disorders Colleen K. Manak and Rosa K. Kim Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. Chapter 39 u Mood Disorders 255 Are there symptoms of mania or hypomania (abnormally elevated mood)? Yes No No Is there substance use? SubstanceInduced Mood Disorder Are there significant disruptive behaviors? Disruptive Mood Dysregulation Disorder (DMDD) Was there a recent death? Bereavement Was there a precipitating event? Adjustment Disorder Major Depressive Disorder Bipolar I Disorder Bipolar II Disorder SubstanceInduced Mood Disorder Cyclothymia No Yes Yes Are criteria for major depressive disorder met? (At least 2 weeks of depressed mood or irritability or loss of interest causing significant impairment with at least five of the following: change in appetite, change in sleep, fatigue or loss of energy, feelings of worthlessness or guilt, poor concentration, psychomotor symptoms, thoughts of suicide) Are criteria for mania met? (Abnormally elevated mood of greater than 1 week in duration, associated with grandiosity, impulsivity, excessive goaldirected activity, and decreased need for sleep) Fig. 39.1 Evaluation of mood disorders. (From Kliegman RM, Lye, PS, Bordini BJ, et al., eds. Nelson Pediatric Symptom Based Diagnosis. Elsevier, 2018; Fig, 27.2, p. 426.) Table 39.1 DSM 5 Diagnostic Criteria for Major Depressive Episode A. Five (or more) of the following symptoms have been present during the same 2wk period and represent a change from previous functioning; at least one of the symptoms is either (1) depressed mood or (2) loss of interest or pleasure. 1. Depressed most of the day, nearly every day, as indicated by either subjective report (e.g., feels sad, empty, hopeless) or observation made by others (e.g., appears tearful). Note: In children and adolescents, can be irritable mood. 1. Markedly diminished interest or pleasure in all, or almost all, activities most of the day, nearly every day (as indicated by either subjective account or observation). 2. Significant weight loss when not dieting or weight gain (e.g., a change of more than 5 of body weight in a month), or decrease or increase in appetite nearly every day. Note: In children, consider failure to make expected weight gain. 1. Insomnia or hypersomnia nearly every day. 2. Psychomotor agitation or retardation nearly every day (observable by others, not merely subjective feelings of restlessness or being slowed down). 3. Fatigue or loss of energy nearly every day. 4. Feelings of worthlessness or excessive or
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inappropriate guilt (which may be delusional) nearly every day (not merely self reproach or guilt about being sick). 5. Diminished ability to think or concentrate, or indecisiveness, nearly every day (either by subjective account or as observed by others). 6. Recurrent thoughts of death (not just fear of dying), recurrent suicidal ideation without a specific plan, or a suicide attempt or a specific plan for committing suicide. B. The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning. C. The episode is not attributable to the physiologic effects of a substance or to another medical condition. Note: Criteria A C represent a major depressive episode. D. The occurrence of the major depressive episode is not better explained by schizoaffective disorder, schizophrenia, schizophreniform disorder, delusional disorder, or other specified and unspecified schizophrenia spectrum and other psychotic disorders. E. There has never been a manic episode or a hypomanic episode. From the Diagnostic and Statistical Manual of Mental Disorders, 5th ed. pp. 125126. Copyright 2013. American Psychiatric Association. with frequent (3 timesweek) and severe temper outbursts (verbal rages, physical aggression; Table 39.3). This diagnosis is intended to characterize more accurately the extreme irritability, which some investigators had considered a developmental presentation of bipo lar disorder, and to distinguish extreme irritability from the milder presentations characteristic of oppositional defiant disorder (ODD) and intermittent explosive disorder. Table 39.4 highlights some of the similarities and differences between the various mood disorders and also factors that distinguish mood disorders from grief experi enced in response to loss. Other specifiedunspecified depressive disorder (subsyndromal depressive disorder) applies to presentations in which symptoms characteristic of a depressive disorder are present and cause clini cally significant distress or functional impairment but do not meet the full criteria for any of the disorders in this diagnostic class. EPIDEMIOLOGY The current prevalence of depressive disorder in the United States among 3 17 year olds is approximately 3.2; the lifetime prevalence rates increase to 4.9 for ages 6 17 and to 12.8 for 12 17 year olds. The male:female ratio (excluding DMDD) is approximately 1:1 during childhood and beginning in early adolescence rises to 1:1.5 3.0 by adulthood. Based on rates of chronic and severe persistent irritability, which is the core feature of DMDD, the overall 6 month to 1 year prevalence has been estimated in the 25 range. In three community samples, the 3month prevalence rate of DMDD ranged from 0.83.3, with the highest rates occurring in preschoolers (although Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition DSM 5 does not permit this diagnosis until age 6 years). Approximately 510 of chil dren and adolescents are estimated to have subsyndromal (unspeci fied) depression. Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. 256 Part III u Behavioral and Psychiatric Disorders ETIOLOGY AND RISK FACTORS Models of vulnerability to depressive
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disorders are grounded in genetic and environmental pathways. Genetic studies have demonstrated the heritability of depressive disorders, with monozygotic twin studies find ing concordance rates of 4065. In families, both bottom up (children to parents) and top down (parents to children) studies have shown a two to fourfold bidirectional increase in depression among first degree relatives. Cerebral variations in structure and function (particu larly serotonergic), the function of the hypothalamic pituitary adrenal axis, difficult temperamentpersonality (i.e., negative affectivity), and Symptoms of depression (2 weeks) Cumulative functional impairment Fundamental symptoms Emotional symptoms Neurovegetative symptoms Neurocognitive symptoms or Depressed mood Fatigue or loss of energy Ability to think or concentrate, or indecisiveness Psychomotor retardation or agitation Anhedonia Feelings of worthlessness or guilt Suicidal ideation, plan, or attempt Sleep Weight or appetite or Fig. 39.2 Defining major depressive disorder. Key symptoms of Diag nostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM) 5 for major depressive disorder. For a diagnosis of major depressive disorder, the individual needs to present with five or more of any of the symptoms nearly every day during the same 2 week period, pro vided at least one of these symptoms is a fundamental one. The clinical symptoms of major depressive disorder are usually accompanied by functional impairment. The greater the number and severity of symp toms (as opposed to particular symptoms), the greater the probability of the functional impairment they are likely to confer. The symptoms of depression can be grouped into emotional, neurovegetative, and neurocognitive domains. Importantly sleep, weight, and appetite are usually diminished in depression but can also be increased, and sui cidal ideation, plans, or an attempt should be documented whenever depression is suspected. (From Malhi GS, Mann JJ. Depression. Lancet. 2018;39210161:22992312:Fig. 1, p. 2300.) ruminative, self devaluating cognitive style have been implicated as components of biologic vulnerability. The great majority of depressive disorders arise in youth with long standing psychosocial difficulties, among the most predictive of which are physicalsexual abuse, neglect, chronic illness, school difficulties (bullying, academic failure), social isolation, family or marital disharmony, divorceseparation, parental psychopathology, and domestic violence. Longitudinal studies demon strate the greater importance of environmental influences in children who become depressed than in adults who become depressed. Factors shown to be protective against the development of depression include better family function, a prosocial peer group, higher IQ, greater edu cational aspirations, a positive relationship with a caregiver, and closer caregiver supervision, monitoring, and involvement. SCREENING AND DIAGNOSIS Screening Adolescents presenting in the primary care setting should be queried, along with their caregiver(s), about depressed mood as part of the rou tine clinical interview. A typical screening question would be, Every one feels sad or angry some of the time; how about you (or your teen)? The caregivers of younger children can be queried about overt signs of depression, such as tearfulness, irritability, boredom, or social isola tion. A number of standardized screening instruments widely used in the primary care setting (e.g., Pediatric Symptom Checklist, Strengths and Difficulties Questionnaire, Vanderbilt
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ADHD Diagnostic Rating Scales) have items specific to sad mood and as such can be used to focus the interview. Additionally, screening tools specific to depression, such as the Patient Health Questionnaire 9 (PHQ 9) and Beck Depression Inventory, can be utilized as part of routine screening (Table 39.5). The role of universal depression screening using standardized depression specific instruments is unclear. A Cochrane review found that the use of depression screening in primary care has little or no impact on the recognition, management, or outcome of depression. Nonetheless, the U.S. Preventive Services Task Force (USPSTF) recom mends the universal use of depression screening instruments, but only among adolescents and only when systems are in place to ensure ade quate follow up. Targeted screening of known high risk groups (e.g., youth who are homeless, refugees, attracted to the same sex, involved with child welfare or juvenile justice), or youth experiencing known psychosocial adversities or self reporting a dysphoric mood, may be a higher yield case finding strategy than universal screening. Assessment Youth (andor their caregivers) presenting in the primary care setting who self report, or respond affirmatively to queries about a distressing life experience or a depressed or irritable mood should be offered the opportunity to talk about the situation with the pediatric practitioner (separately with the older youth). By engaging in active listening (e.g., Illness pattern Single episode Recurrent episode Rapid cycling Seasonal Remission status Onset Severity Clinical features Anxious distress Mixed features Atypical Melancholic Catatonic Psychotic Early Late Postpartum Mild Moderate Severe Mild Moderate Severe Mood congruent Mood incongruent Partial Full Major depressive disorder specifiers Fig. 39.3 Major depressive disorder specifiers. Episodes of major depression can be described in greater depth by specifiers (outlined in Diagnos tic and Statistical Manual of Mental Disorders, Fifth Edition DSM 5) that provide additional information regarding the pattern of the illness and its clinical features. Specifiers can also indicate the severity of the episode, when it first emerged (onset), and whether it has remitted (status). For exam ple, in clinical practice, a typical episode of depression can be described as suffering from a recurrence of depression that is moderately severe with melancholic features and has partly remitted in response to initial treatment. (From Malhi GS, Mann JJ. Depression. Lancet. 2018;39210161:2299 2312:Fig. 2, p. 2301.) Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. Chapter 39 u Mood Disorders 257 Table 39.2 DSM 5 Diagnostic Criteria for Persistent Depressive Disorder A. Depressed mood for most of the day, for more days than not, as indicated either by subjective account or observation by others, for at least 2 yr. Note: In children and adolescents, mood can be irritable and duration must be at least 1 yr. B. Presence, while depressed, of two (or more) of the following: 1. Poor appetite or overeating. 2. Insomnia or hypersomnia. 3. Low energy
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or fatigue. 4. Low self esteem. 5. Poor concentration or difficulty making decisions. 6. Feelings of hopelessness. C. During the 2 yr period (1 yr for children or adolescents) of the disturbance, the individual has never been without the symptoms in Criteria A and B for more than 2 mo at a time. D. Criteria for a major depressive disorder may be continuously present for 2 yr. E. There has never been a manic episode or a hypomanic episode, and criteria have never been met for cyclothymic disorder. F. The disturbance is not better explained by a persistent schizoaffective disorder, schizophrenia, delusional disorder, or other specified or unspecified schizophrenia spectrum and other psychotic disorder. G. The symptoms are not attributable to the physiologic effects of a substance (e.g., a drug of abuse, a medication) or another medical condition (e.g., hypothyroidism). H. The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning. Note: Because the criteria for a major depressive episode include four symptoms that are absent from the symptom list for persistent depressive disorder (dysthymia), a very limited number of individuals will have depressive symptoms that have persisted longer than 2 yr but will not meet criteria for persistent depressive disorder. If full criteria for a major depressive episode have been met at some point during the current episode of illness, they should be given a diagnosis of major depressive disorder. Otherwise, a diagnosis of other specified depressive disorder or unspecified depressive disorder is warranted. From the Diagnostic and Statistical Manual of Mental Disorders, 5th ed. pp. 168169. Copyright 2013. American Psychiatric Association. Table 39.3 DSM 5 Diagnostic Criteria for Disruptive Mood Dysregulation Disorder A. Severe recurrent temper outbursts manifested verbally (e.g., verbal rages) andor behaviorally (e.g., physical aggression toward people or property) that are grossly out of proportion in intensity or duration to the situation or provocation. B. The temper outbursts are inconsistent with developmental level. C. The temper outbursts occur, on average, three or more times per week. D. The mood between temper outbursts is persistently irritable or angry most of the day, nearly every day, and is observable by others (e.g., parents, teachers, peers). E. Criteria A D have been present for 12 or more months. Throughout that time, the individual has not had a period lasting 3 or more consecutive months without all of the symptoms in Criteria A D. F. Criteria A and D are present in at least two of three settings (i.e., at home, at school, with peers) and are severe in at least one of these. G. The diagnosis should not be made for the first time before age 6 yr or after age 18 yr. H. By history or observation, the age at onset of Criteria A E is before 10 yr. I. There has never been a distinct period lasting more than 1 day during which the full symptom criteria, except duration, for a manic or hypomanic episode have been met. Note: Developmentally
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appropriate mood elevation, such as occurs in the context of a highly positive event or its anticipation, should not be considered as a symptom of mania or hypomania. J. The behaviors do not occur exclusively during an episode of major depressive disorder and are not better explained by another mental disorder (e.g., autism spectrum disorder, posttraumatic stress disorder, separation anxiety disorder, persistent depressive disorder dysthymia). Note: The diagnosis cannot coexist with oppositional defiant disorder, intermittent explosive disorder, or bipolar disorder, though it can coexist with others, including major depressive disorder, attention deficithyperactivity disorder, conduct disorder, and substance use disorders. Individuals whose symptoms meet criteria for both disruptive mood dysregulation disorder and oppositional defiant disorder should only be given the diagnosis of disruptive mood dysregulation disorder. If an individual has ever experienced a manic or hypomanic episode, the diagnosis of disruptive mood dysregulation disorder should not be assigned. K. The symptoms are not attributable to the physiologic effects of a substance or to another medical or neurologic condition. From the Diagnostic and Statistical Manual of Mental Disorders, 5th ed. p. 156. Copyright 2013. American Psychiatric Association. I hear how upset you have been feeling; tell me more about what hap pened to make you feel that way), the clinician can begin to assess the onset, duration, context, and severity of the symptoms and associated dangerousness, distress, and functional impairment. In the absence of acute dangerousness (e.g., suicidality, psychosis, substance abuse) and significant distress or functional impairment, the pediatric practitioner can schedule a follow up appointment within 1 2 weeks to conduct a depression assessment. At this follow up visit, to assist with decision making about appropriate level of care, a depression specific screening or standardized rating scale can be administered to assess symptom severity (see Table 39.5), and additional risk factors can be explored. DIFFERENTIAL DIAGNOSIS A number of psychiatric disorders, general medical conditions, and medications can generate symptoms of depression or irritability and must be distinguished from the depressive disorders. The psychiatric disorders include autism spectrum disorder (ASD), ADHD, and bipo lar, anxiety, trauma and stressor related, disruptiveimpulse control conduct, and substance related disorders. Medical conditions include neurologic disorders (including autoimmune encephalitis), endocrine disorders (including hypothyroidism and Addison disease), infectious diseases, tumors, anemia, uremia, failure to thrive, chronic fatigue dis order, and pain disorder. Medications include narcotics, chemotherapy agents, blockers, corticosteroids, and contraceptives. The diagnosis of a depressive disorder should be made after these and other potential explanations for the observed symptoms have been ruled out. COMORBIDITY Major and persistent depressive disorders often co occur with other psychiatric disorders. Depending on the setting and source of refer ral, 4090 of youths with a depressive disorder have other psychiatric disorders, and up to 50 have two or more comorbid diagnoses. The most common comorbid diagnosis is an anxiety disorder and as such may reflect a common diathesis; other common comorbidities include ADHD and disruptive behavior, eating, and substance use disorders. The development of depressive disorders can both lead to and follow
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the development of comorbid disorders. DMDD may occur with other psychiatric disorders, including other depressive disorders, ADHD, conduct disorder, and substance use dis orders. Because the symptoms of DMDD overlap in part with symp toms of bipolar disorder, ODD, and intermittent explosive disorder, by DSM 5 convention, hierarchical diagnostic rules apply. Thus bipolar disorder takes precedence over DMDD if a manichypomanic episode Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. 258 Part III u Behavioral and Psychiatric Disorders has ever occurred, and DMDD takes precedence over ODD and inter mittent explosive disorder if full criteria for DMDD are met. TREATMENT Treatment decisions should be guided by the understanding that depression in youth is highly responsive to placebo (5060) or brief nonspecific intervention (1530). The goal of treatment is remission, defined as a period of at least 2 weeks with no or very few depressive symptoms, and ultimately recovery, defined as a period of at least 2 months with no or very few depressive symptoms. Assessment of remission and recovery can be aided using the depression specific standardized rating scales, in which remission is defined as scores below the scale specific clinical cut point. For mild symptoms (manageable and not functionally impairing) and in the absence of major risk factors (e.g., suicidality; psychosis; substance use; history of depression, mania, or traumatic exposures; parental psychopathology, particularly depression; severe family dysfunction), guided self help (anticipatory guidance) with watch ful waiting and scheduled follow up may suffice. Guided self help can include provision of educational materials (e.g., pamphlets, books, workbooks, apps, internet sites) that provide information to the youth about coping adaptively with stressful situations, as well as advice to caregivers about strengthening the caregiver child relationship and modifying triggering exposures (e.g., taking action against bullying, increasing opportunities for social interac tion and support, protecting child from exposure to marital dis cord). Additional self help activities that have shown promise in improving mild depressive symptoms include behavioral activation (e.g., physical exercise, social engagement, participation in a hobby), mindfulness (e.g., yoga, meditation), and a regular sleep schedule. For youths who continue to have mild depression after a few weeks of guided self help, supportive therapy by a mental health profes sional may be an appropriate subsequent step. For youths who have not responded to approximately 48 weeks of supportive psychother apy, or who from the outset exhibit moderate to severe, comorbid, or recurrent depression or suicidality, or who have a history of mania, traumatic exposures, or severe family dysfunction or psychopathology, Table 39.4 A Comparison of Features of Depression, Persistent Depressive Disorder, Disruptive Mood Dysregulation Disorder, and Grief in Children with Developmental Considerations MAJOR DEPRESSIVE DISORDER PERSISTENT DEPRESSIVE DISORDER DISRUPTIVE MOOD DYSREGULATION DISORDER GRIEF Core feature(s) Sadness, irritability, anhedonia Sadness, irritability, anhedonia Irritability and anger with behavioral outbursts (verbal, physical) Sadness in response to the lossdeath of a loved
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one Duration 2 weeks with symptoms nearly every day 1 year with symptoms more days than not 1 year with outbursts at least three timesweek Ongoing, can continue recur indefinitely (e.g., around anniversaries, birthdays, holidays) Associated symptoms Changes in appetite, sleep, energy and activity level; impaired concentration; hopelessness, worthlessness and guilt; suicidal ideations actions Changes in appetite, sleep, energy and activity level; impaired concentration; hopelessness, worthlessness and guilt; suicidal ideationsactions Persistent irritability between episodes Anger; guilt; regret; anxiety; intrusive images; overwhelmed; lonely Age considerations Younger children may be irritable and complain of somatic symptoms Cannot be diagnosed before age 6 or after age 18 Developmental level and understanding of death can influence grief symptoms Table 39.5 Depression Specific Rating Scales NAME OF INSTRUMENT INFORMANT(S) AGE RANGE (YR) ITEMS (NO.) Beck Depression Inventory Youth 13 21 Beck Depression Inventory for Youth Youth 7 14 20 Center for Epidemiologic Studies Depression Children Youth 6 18 20 Childrens Depression Rating Scale Revised Youth, Parent, Clinician 6 18 47 Childrens Depression Inventory, Second Edition Youth, Parent, Teacher 7 17 281712 Depression Self Rating Scale Youth 7 13 18 Mood and Feelings Questionnaire Youth, Parent 7 18 33 34 Patient Health Questionnaire 9 Youth 1213 9 Preschool Feelings Checklist Parent 3 5.6 20 PROMIS Emotional Distress Depressive Symptoms Youth, Parent 817 (youth report) or 517 (parent report) 86 Reynolds Child Depression Scale Youth 8 13 30 Reynolds Adolescent Depression Scale, Second Edition Youth 11 20 30 Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. Chapter 39 u Mood Disorders 259 assessment and treatment by a child trained mental health clinician should be obtained. For moderate to severe depression, specific manualized psychothera pies, antidepressant medication, or a combination of both should be considered. There is insufficient evidence on which to base definitive conclusions about the relative effectiveness of these treatments. Psychotherapies Clinical trials of acute treatments have generated support for the effi cacy of cognitive behavioral therapy (CBT)behavioral activation therapy and interpersonal therapy as monotherapies in depressed youth, but overall effect sizes are modest. CBT focuses on identifying and correcting cognitive distortions that may lead to depressed mood and teaches problem solving, behavior activation, social communica tion, and emotional regulation skills to combat depression. Interper sonal therapy focuses on enhancing interpersonal problem solving and social communication to decrease interpersonal conflicts. Each of these therapies typically involves 8 12 weekly visits. Limited evidence suggests that family therapy may be more effective than no treatment in decreasing depression and improving family functioning. Manual ized CBT treatment as well as alternative therapy modalities such as play therapy are also available for younger children. Pharmacologic Treatment Two selective serotonin reuptake inhibitors (SSRIs), fluoxetine and escitalopram, are the only antidepressants approved by the U.S. Food and Drug Administration (FDA) for the treatment of depression in youth; fluoxetine alone is approved for preadolescents. Other SSRIs, with
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the exception of paroxetine, which has been shown to be ineffec tive in children, are frequently used off label and may be considered for use in depressed children and teens despite the lack of FDA approval. There are several considerations to keep in mind when starting an SSRI, including family history of response to SSRIs, comorbid medical conditions, and other concurrent medications. Fluoxetine should be given in the morning, given its propensity to be activating for some patients; escitalopram is preferentially dosed in the evening as it can be sedating. Sertraline has the advantage of a very wide dosing range, which can be helpful when small dosing changes are preferred. All SSRIs carry a black box warning for increased suicidal thinking in patients under age 25 that must be discussed with all patients and caregivers before starting an SSRI. The risk for this side effect is high est when initiating treatment and when making dose adjustments. All SSRIs can cause akathisia, an uncomfortable feeling of internal restless ness; this side effect is more common in children than it is in adults. Gastrointestinal upset and headaches are among the most common side effects; they typically self resolve after a few weeks. However, they may recur when dose increases are made. Education around the expected course and resolution of these side effects can be helpful when provid ing informed consent and may lead to improved adherence in the early phase of treatment. Sexual side effects of SSRIs, including decreased libido and difficulty reaching orgasm, are also important considerations and should be addressed with patients before treatment initiation. If the first trial of an SSRI is unsuccessful, a trial of a second SSRI should be considered. An adequate trial of an SSRI requires that a suffi cient dose be achieved and that it be continued for a reasonable amount of time. Given the length of time it takes for SSRIs to take full effect, an adequate trial would be at least 6 8 weeks at a target dose. Trials may end early if patients experience intolerable side effects. For patients who do not respond to two adequate trials of an SSRI, it is appropriate to consider referral to a psychiatrist for further management. Clinical severity, comorbidity, family conflict, low drug concentra tion, nonadherence, anhedonia, sleep difficulties, subsyndromal manic symptoms, and child maltreatment have all been related to treatment resistance. Approximately 50 of depressed youth failing to respond to the first SSRI respond after switching to a second antidepressant plus CBT, vs approximately 40 who respond to a second medication alone. For youth with psychotic depression, augmenting the antidepressant with an atypical antipsychotic medication should be considered, while monitoring closely for side effects. Because of the high rate of recurrence, successful treatment should continue for 6 12 months. The findings from one trial suggested that the addition of relapse prevention CBT to ongoing medication man agement reduces the risk of relapse more than medication management alone, even after the end of treatment. When treatment
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concludes, all antidepressants (except possibly fluoxetine because of its long half life) should be discontinued gradually to avoid withdrawal symptoms (gas trointestinal upset, disequilibrium, sleep disruption, flulike symptoms, sensory disturbances). Patients with recurrent (two or more episodes), chronic, or severe major depression may require treatment beyond 12 months. Ketamine or esketamine, glutamatergic N methyl d aspartate (NMDA) receptor antagonists have demonstrated efficacy in treating treatment resistant depression in adults. There are no rigorous studies evaluating the effectiveness of phar macologic or psychosocial treatment approaches to persistent depres sive disorder or DMDD. The aforementioned treatments for MDD may prove helpful in persistent depressive disorder. In suspected cases of DMDD, child and adolescent psychiatry consultation may be helpful to clarify diagnosis and suggest treatment approaches. LEVEL OF CARE Most children and adolescents with mild to moderate depressive disor ders can be safely and effectively treated as outpatients, provided that a clinically appropriate schedule of visits can be maintained through the phases of treatment. Inpatient treatment should be considered for youth who present with a substantial risk of suicide, serious self harm, or self neglect, or when the family is not able to provide an appropri ate level of supervision or follow up with outpatient treatment recom mendations, or when comprehensive assessment for diagnostic clarity is needed. When considering inpatient admission for a young person with depression, the benefits of inpatient treatment need to be bal anced against potential detrimental effects, such as separation from family and community support. CLINICAL COURSE Major depression may first appear at any age, but the likelihood of onset greatly increases with puberty. Incidence appears to peak in the 20s. The median duration of a major depressive episode is about 5 8 months for clinically referred youth and 3 6 months for community samples. The course is quite variable in that some individuals rarely or never experience remission, whereas others experience many years with few or no symptoms between episodes. Persistent depressive disorder often has an early and insidious onset and, by definition, a chronic course (average untreated duration in both clinical and com munity samples: 3.5 years). Depressed children appear to be more likely to develop nondepres sive psychiatric disorders in adulthood than depressive disorders. However, depression in adolescents has a probability of recurrence reaching 5070 after 5 years. The persistence of even mild depres sive symptoms during remission is a powerful predictor of recurrence; other negative prognostic factors include more severe symptoms, lon ger time to remission, history of maltreatment, and comorbid psychi atric disorders. Up to 20 of depressed adolescents develop a bipolar disorder; the risk is higher among adolescents who have a high genetic risk for bipolar disorder, who have psychotic depression, or who have had pharmacologically induced mania. SEQUELAE Approximately 60 of youths with MDD report thinking about suicide; 30 attempt suicide. Youths with depressive disorders are also at high risk of substance abuse, impaired family and peer relationships, early pregnancy, legal problems, educational and occupational underachieve ment, and poor adjustment to life
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