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ERROR: type should be string, got "https://profreg.medscape.com/px/getpracticeprofile.do?method=getProfessionalProfile&urlCache=aHR0cHM6Ly9lbWVkaWNpbmUubWVkc2NhcGUuY29tL2FydGljbGUvMjg5ODQ4LW92ZXJ2aWV3\nDrugs & Diseases > Psychiatry\nAlcohol-Related Psychosis\nAuthor: Zhongshu Yang, MD, PhD; Chief Editor: Ana Hategan, MD, FRCPC more...\nSections Alcohol-Related Psychosis\nImaging Studies\nAntialcoholic agents\nNarcotic antagonists\nInpatient & Outpatient Medications\nAlcohol-related psychosis is a secondary psychosis that manifests as prominent hallucinations and delusions occurring in a variety of alcohol-related conditions. For patients with alcohol use disorder, previously known as alcohol abuse and alcohol dependence, psychosis can occur during phases of acute intoxication or withdrawal, with or without delirium tremens. In addition, alcohol hallucinosis and alcoholic paranoia are 2 uncommon alcohol-induced psychotic disorders, which are seen only in chronic alcoholics who have years of severe and heavy drinking. [1] Lastly, psychosis can also occur during alcohol intoxication, also known as pathologic intoxication, an uncommon condition the diagnosis of which is considered controversial. [2, 3]\nIn chronic alcoholic patients, lack of thiamine is a common condition. Thiamine deficiency is known to lead to Wernicke-Korsakoff syndrome, which is characterized by neurological findings on examination and a confusional-apathetic state. Korsakoff psychosis (or Korsakoff amnesic- or amnesic-confabulatory state) refers to a state that memory and learning are affected out of proportion to other cognitive functions in an otherwise alert and responsive patient. [4]\nAlcohol is a neurotoxin that damages the brain in a complex manner through prolonged exposure and repeated withdrawal, resulting in significant morbidity and mortality. Alcohol-related psychosis is often an indication of chronic alcoholism; thus, it is associated with medical, neurological, and psychosocial complications.\nAlcohol-related psychosis spontaneously clears with discontinuation of alcohol use and may resume during repeated alcohol exposure. Distinguishing alcohol-related psychosis from schizophrenia or other primary psychotic disorders through clinical presentation often is difficult. It is generally accepted that alcohol-related psychosis remits with abstinence, unlike schizophrenia. If persistent psychosis develops, diagnostic confusion can result. Comorbid psychotic disorders (eg, schizophrenia spectrum and other psychotic disorders) and severe mood disorder with psychosis may exist, resulting in the psychosis being attributed to the wrong etiology.\nSome characteristics that may help differentiate alcohol-induced psychosis from schizophrenia are that alcohol-induced psychosis shows later onset of psychosis, higher levels of depressive and anxiety symptoms, fewer negative and disorganized symptoms, better insight and judgment towards psychotic symptoms, and less functional impairment. [5]\nAlcohol idiosyncratic intoxication is an unusual condition that occurs when a small amount of alcohol produces intoxication that results in aggression, impaired consciousness, prolonged sleep, transient hallucinations, illusions, and delusions. These episodes occur rapidly, can last from only a few minutes to hours, and are followed by amnesia. Alcohol idiosyncratic intoxication often occurs in elderly persons and those with impaired impulse control.\nUnlike alcoholism, alcohol-related psychosis lacks the in-depth research needed to understand its pathophysiology, demographics, characteristics, and treatment. This article attempts to provide as much possible information for adequate knowledge of alcohol-related psychosis and the most up-to-date treatment.\nCase 1: A 37-year-old white male infantryman stationed in Iraq arrived at a field hospital complaining that his superior officer placed poisonous ants in his helmet. His face is covered with excoriations from persistent scratching. On further examination, he is stuporous and has mildly slurred speech, tremor, and mint odor to his breath. Later his troop leader mentioned that his Humvee was littered with empty bottles of mouthwash and that the man has been reprimanded for falling asleep at his post. After a night of rest, he discussed his excessive use of mouthwash in place of alcohol, which is the only available form of alcohol in Iraq.\nCase 2: At 5 pm you are asked to consult on a 44-year-old white female who is 2 days postsurgical hysterectomy. She is complaining of rabbits running across the room and demands the nurses stop intruding \"every minute of every hour.\" She is tremulous, disoriented to time and place, and irritable. A review of her laboratory data shows an elevated gamma-glutamyl transferase (GGT) and slightly elevated liver function test values. White blood cell count is normal. Urinalysis is normal and blood alcohol level is 0.01. Her medications, which were held prior to the surgery, included acamprosate 666 mg three times daily and clonazepam 1 mg 4 times a day. Her sister later informs the nursing staff that this woman is usually on her fourth Manhattan cocktail by this hour of the day.\nEthanol is a small molecule that readily distributes to the brain and reaches peak levels in blood approximately 30 minutes after ingestion of an alcoholic drink. Ethanol affects proteins that are associated with a wide variety of neurotransmitters and pathways. These include the dopamine pathway, serotonin pathway, proteins associated with GABAA receptor, glutamate receptors (ie, N -methyl-D-aspartate [NMDA]/α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid [AMPA]/Kainate), mGlu receptors, nicotinic receptors, cannabinoid CB1 receptors, voltage-gated calcium ion channels, and calcium-activated potassium channels. [6]\nLike other psychotic disorders, the exact etiology of alcohol-related psychosis remains unclear, but most likely it is related to dopamine in the limbic and possibly other systems, such as the glutamatergic neurotransmitter system. The dopamine hypothesis often is applied to psychosis involving excessive activity of the dopaminergic system. Animal studies have shown dopaminergic activity to increase with increased release of dopamine when alcohol is administered.\nOn the other hand, alcohol withdrawal generates a decrease in the firing of dopaminergic neurons in the ventral tegmental area and a decrease in the release of dopamine from the neuron. Ethanol acutely disrupts glutamatergic neurotransmission by inhibiting the response of the NMDA receptor. Prolonged inhibition of the NMDA receptor by ethanol leads to supersensitivity. During the phase of withdrawal, acute removal of ethanol causes marked augmentation of activity of postsynaptic neurons, such as those in the noradrenergic system, and, in the extreme, glutamate-induced excitotoxicity. [6, 7]\nThe pathophysiologies of intoxication, withdrawal, and alcohol idiosyncratic intoxication are all are different, and their exact relationships to psychosis are unclear, but one can certainly postulate the underlying mechanisms are complex, considering alcohol’s broad impact on a variety of neurotransmitter pathways. To some degree, they all involve the neurotoxicity of alcohol and its damage at the genetic, biochemical, and cellular levels leading to physiological and neurological pathology.\nDepending on the individual and amount consumed, alcohol intoxication can result in disinhibition, sedation, and anesthesia or even coma by acute depression of the cerebral cortex and reticular activating system. The pathophysiology of alcoholism involves alterations in short-term membrane regulation and long-term effects on gene expression at the cellular level.\nIn patients who are dependent on alcohol, alcohol withdrawal results in adrenergic hypersensitivity of the limbic system and brainstem. Thiamine deficiency also is a contributing factor and is known to be associated with more severe episodes of withdrawal psychosis, which may present as a delirious state known as Wernicke-Korsakoff syndrome. The psychosis often is self-limited and recurs with subsequent withdrawals.\nRoughly 3% of persons with alcoholism experience psychosis during acute intoxication or withdrawal. Approximately 10% of patients who are dependent on alcohol and are in withdrawal experience severe withdrawal symptomatology, including psychosis. Twins studies have shown concordance rates for alcohol-related psychosis to be 17.3% in monozygotic twins and 4.8% in dizygotictwins. [8]\nThose with first-episode psychosis are twice more likely than the general population to present with comorbid substance abuse and are more commonly males than females. The most commonly reported substance is cannabis (51%) followed by alcohol (43%). [9]\nIn as much as 50% of Japanese, Chinese, and Korean populations, the likelihood of alcohol-related disorders occurring is less because of the absence of aldehyde dehydrogenase. This causes an Antabuse-like reaction involving facial flushing and palpitations.\nStudies of the Soviet Slavic Republic of Belarus from 1970-2005 suggest a correlation between cultural and social context of alcohol consumption and alcohol-related suicides and alcohol-induced psychosis. [10] Furthermore, there appears to be a close correlation between alcohol psychosis and higher mortality rates compared with alcohol consumption and no psychosis. Studies on alcohol consumption and psychosis are easier to study in Belarus as they are among highest consumers of alcohol in the world, with an annual consumption of 14 liters per capita per year. [11]\nMortality/Morbidity\nThe appearance of alcohol-related psychosis usually occurs with long-term alcohol use disorder; therefore, it is associated with the same morbidity and mortality of long-term alcoholism. The presence of alcohol-related psychosis is a serious indicator of medical, neurological, and psychosocial complications that can hinder appropriate treatment and lead to negative outcomes. The prognosis for alcohol-related psychosis with treatment is considered good, with only 10-20% of psychosis cases becoming chronic. Alcohol-related psychosis itself does not have specific morbidity or mortality; instead, it correlates with a cluster of risk factors that indicate higher morbidity and mortality in patients with alcoholism. [12]\nPsychiatric complications of alcohol-related psychosis include higher rates of depression, anxiety, and suicide. The potential for violence also exists.\nAlcohol-related psychosis that does not remit with abstinence may indicate undiagnosed schizophrenia or other psychotic disorders. Contrary to amphetamine-induced psychosis, alcohol-induced psychosis tends to be short-lived and is much less likely to be chronic. The use of alcohol may potentiate or initiate psychosis through kindling, a process where repetitive neurologic insult results in greater expression of the disease.\nSubstance abuse is a major contributing factor to the outcome and course of treatment in mentally ill patients with psychosis. The prevalence is up to 87% in those with schizophrenia and 77% in those who are bipolar, with cannabis and alcohol being the most commonly abused. [13]\nSome of the medical complications observed with alcohol-related psychosis and chronic alcoholism include liver disease, pulmonary tuberculosis, diabetes mellitus, musculoskeletal injury, hypertension, and cerebrovascular disease.\nWith intoxication, mortality is associated with the alcohol level in the blood. A blood alcohol level (BAL) greater than 400 mg/dL in nontolerant individuals can result in lethal respiratory arrest. [14]\nIn withdrawal, auditory hallucinations can be indicative of early-stage withdrawal (6-24 h), the stage associated with withdrawal seizures. Symptoms of visual, auditory, and tactile hallucinations are indicative of late-stage withdrawal (36-72 h), the stage associated with delirium tremens and a mortality rate of 5-15%.\nNeurologic abnormalities may clear in 20% of patients with Wernicke-Korsakoff syndrome who receive treatment with thiamine and who abstain from consuming alcohol. [15]\nCultural influences on alcohol-related psychosis stem from cultural norms about alcohol. Irish males who traditionally drink to the point of intoxication are at higher risk, while Jewish males who traditionally shun intoxication have lower risks. Considering the relationship of thiamine to Wernicke-Korsakoff syndrome, cultures that have a low intake of thiamine and high rates of alcohol abuse also are at higher risk for the complication of Wernicke-Korsakoff syndrome.\nAlcohol abuse and dependency has a male-to-female ratio of 5:1. Females develop alcohol-related disorders later in life because they start heavy use later than males.\nAlcohol-related psychosis occurs after extended periods of alcohol abuse that result in an alteration of neuronal membranes, genetic expression, and thiamine deficiency. Early-onset alcoholism results in a greater chance of complications earlier in life and an outcome that is influenced by psychosocial function. Late-onset alcoholism only delays the onset of complications. As a general rule, alcohol-related psychosis occurs more frequently in older populations. Most alcohol-related disorders have an onset in persons aged 35-40 years.\nPuri BK. Medication- and substance-induced disorders. Textbook of Clinical Neuropsychiatry and Behavioral Neuroscience. London, United Kingdom: Hodder Arnold; 2012. 70(6): 786-804.\nReed T, Page WF, Viken RJ, Christian JC. Genetic predisposition to organ-specific endpoints of alcoholism. Alcohol Clin Exp Res. 1996 Dec. 20(9):1528-33. [Medline].\nPerr IN. Pathological intoxication and alcohol idiosyncratic intoxication--Part I: Diagnostic and clinical aspects. J Forensic Sci. 1986 Jul. 31(3):806-11. [Medline].\nVictor M, Collins GH. The Wernicke-Korsakoff Syndrome and Related Neurologic Disorders Due to Alcoholism and Malnutrition. 2nd ed. Philadelphia, Pa: FA Davis; 1989.\nJordaan GP, Nel DG, Hewlett RH, Emsley R. Alcohol-induced psychotic disorder: a comparative study on the clinical characteristics of patients with alcohol dependence and schizophrenia. J Stud Alcohol Drugs. 2009 Nov. 70(6):870-6. [Medline].\nGalanter M, Kleber HD. Textbook of Substance Abuse Treatment. 4th ed. Washington, DC: American Psychiatric Publishing; 2008.\nTsai G, Gastfriend DR, Coyle JT. The glutamatergic basis of human alcoholism. Am J Psychiatry. 1995 Mar. 152(3):332-40. [Medline].\nBarnett JH, Werners U, Secher SM, et al. Substance use in a population-based clinic sample of people with first-episode psychosis. Br J Psychiatry. 2007 Jun. 190:515-20. [Medline].\nRazvodovsky YE. Suicide and alcohol psychoses in Belarus 1970-2005. Crisis. 2007. 28(2):61-6. [Medline].\nRazvodovsky YE. Alcohol psychoses and all-cause mortality in Belarus. Adicciones. 2008. 20(4):395-405. [Medline].\nSoyka M. [Alcohol-induced hallucinosis. Clinical aspects, pathophysiology and therapy]. Nervenarzt. 1996 Nov. 67(11):891-5. [Medline].\nSaddichha S, Sur S, Sinha BN, Khess CR. How is substance use linked to psychosis? A study of the course and patterns of substance dependence in psychosis. Subst Abus. 2010 Jan. 31(1):58-67. [Medline].\nAlkhour I, Ravindranath D, Brower K. Substance-Related Psychiatric Emergencies. Riba MD, ed. Clinical Manual of Emergency Psychiatry. Washington, DC: American Psychiatric Publishing; 2010. 187-206.\nPreuss UW, Soyka M. [Wernicke-Korsakow syndrome: clinical aspects, pathophysiology and therapeutic approaches]. Fortschr Neurol Psychiatr. 1997 Sep. 65(9):413-20. [Medline].\nAmerican Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 5th ed. Washington, DC: American Psychiatric Association; 2013.\nSadock B.J.S.VA. Kaplan & Sadock's Synopsis of Psychiatry. Lippincott Williams & Wilkins; 2007.\nMcLay R, McBrien C, Kleyensteuber B, Reeves J. Intoxication with mouthwash presenting as psychosis and delirium in a combat theater. Mil Med. 2009 Aug. 174(8):828-31. [Medline].\nMaldonado JR. Novel Algorithms for the Prophylaxis and Management of Alcohol Withdrawal Syndromes-Beyond Benzodiazepines. Crit Care Clin. 2017 Jul. 33 (3):559-599. [Medline].\nBaker AL, Hiles SA, Thornton LK, Hides L, Lubman DI. A systematic review of psychological interventions for excessive alcohol consumption among people with psychotic disorders. Acta Psychiatr Scand. 2012 Oct. 126(4):243-55. [Medline].\nJohnson BA, Ait-Daoud N, Bowden CL, DiClemente CC, Roache JD, Lawson K, et al. Oral topiramate for treatment of alcohol dependence: a randomised controlled trial. Lancet. 2003 May 17. 361 (9370):1677-85. [Medline].\nJohnson BA, Rosenthal N, Capece JA, Wiegand F, Mao L, Beyers K, et al. Topiramate for treating alcohol dependence: a randomized controlled trial. JAMA. 2007 Oct 10. 298 (14):1641-51. [Medline].\nLev-Ran S, Balchand K, Lefebvre L, Araki KF, Le Foll B. Pharmacotherapy of alcohol use disorders and concurrent psychiatric disorders: a review. Can J Psychiatry. 2012 Jun. 57(6):342-9. [Medline].\nZhongshu Yang, MD, PhD Associate Physician, Department of Adult Psychiatry, San Jose Medical Center, The Permanente Medical Group, Inc\nZhongshu Yang, MD, PhD is a member of the following medical societies: American Psychiatric Association\nGlen L Xiong, MD Associate Clinical Professor, Department of Psychiatry and Behavioral Sciences, Department of Internal Medicine, University of California, Davis, School of Medicine; Medical Director, Sacramento County Mental Health Treatment Center\nGlen L Xiong, MD is a member of the following medical societies: AMDA - The Society for Post-Acute and Long-Term Care Medicine, American College of Physicians, American Psychiatric Association, Central California Psychiatric Society\nAna Hategan, MD, FRCPC Associate Clinical Professor, Department of Psychiatry and Behavioral Neurosciences, Division of Geriatric Psychiatry, McMaster University School of Medicine; Geriatric Psychiatrist, St Joseph's Health Care Hamilton, Canada\nAna Hategan, MD, FRCPC is a member of the following medical societies: Canadian Academy of Geriatric Psychiatry, Canadian Coalition for Seniors' Mental Health, Canadian Psychiatric Association, International Psychogeriatric Association, Ontario Medical Association, Royal College of Physicians and Surgeons of Canada\nDisclosure: Book royalties and/or honoraria for articles from American Psychiatric Publishing, Springer, and Current Psychiatry.\nJennifer S Morse, MD Associate Medical Director, Optum Health\nJennifer S Morse, MD is a member of the following medical societies: Academy of Psychosomatic Medicine, Aerospace Medical Association, American Psychiatric Association\nMichael F Larson, DO Clinical Instructor, Department of Child and Adolescent Psychiatry, Harvard Medical School; Psychiatrist, Harvard Vanguard Medical Associates and Private Practice\nMichael F Larson, DO is a member of the following medical societies: American Academy of Addiction Psychiatry, American Academy of Child and Adolescent Psychiatry, and American Society of Addiction Medicine\nencoded search term (Alcohol-Related Psychosis) and Alcohol-Related Psychosis\nAlcohol and Substance Abuse Evaluation\nFast Five Quiz: How Much Do You Know About Alcoholism?\nAlcoholic Ketoacidosis\nAlcoholic Cardiomyopathy\nPerinatal Drug Abuse and Neonatal Drug Withdrawal\nPhysician Lifestyle Report 2015\nChildhood Smoking and Depression Contribute to Young Adult Opioid Use\nNaltrexone and Bupropion Promising Combo for Meth Addiction\nAlcohol Abuse: Complications and Consequences\nAccording to Psychiatrists\nRepurposed Antidepressant Shows Early Promise in COVID-19\nFrom Cradle to Grave, Alcohol Is Bad for the Brain\nPsilocybin Delivers 'Remarkable' Relief in Severe Depression\nThe Secret Behind Cocoa's Brain-Boosting Ability\nSimple Language Test May Predict Alzheimer's Years Before Symptoms\nAlcohol Use Up During Pandemic, Especially in Binge Drinkers\nAlcohol Use and Types of Cancer: A National Health Survey 0.25 CME / CE / ABIM MOC Credits Clinical Review\nAlcohol Use and Types of Cancer: A National Health Survey\nDiseases & Conditions Alcohol and Substance Abuse Evaluation"