Depending on the orthotic, they can be expensive.  3D printing  can be a cost-effective alternative. 3D printing is an additive manufacturing process where filament is layered on top of itself to create a three-dimensional object. This differs from more traditional subtractive manufacturing processes, like drilling, where the material is taken away to form a whole. Free online versions of different orthotics are available to print if a more general model is suitable; they can also be adapted to fit the owner and pet's needs. Libraries may be a source of complimentary or donation-based printing for the public. Custom orthotics can also be designed in  3D modeling  software. [ 10 ]


Otology  is a branch of  medicine  which studies normal,  pathological   anatomy  and  physiology  of the  ear  ( hearing ). Otology also studies  vestibular   sensory systems , related structures and functions, as well as their  diseases ,  diagnosis  and treatment. [ 1 ] [ 2 ]  Otologic surgery generally refers to surgery of the  middle ear  and  mastoid  related to chronic  otitis media , such as  tympanoplasty  (ear drum surgery), ossiculoplasty (surgery of the hearing bones) and  mastoidectomy .  Otology also includes surgical treatment of conductive hearing loss, such as  stapedectomy  surgery for  otosclerosis .


Neurotology  (a related field of medicine and subspecialty of  otolaryngology ) is the study of diseases of the inner ear, which can lead to hearing and balance disorders.  Neurotologic surgery generally refers to surgery of the inner ear, or surgery that involves entering the inner ear with risk to the hearing and balance organs, including  labyrinthectomy , cochlear implant surgery, and surgery for tumors of the temporal bone, such as intracanalicular  acoustic neuromas .  Neurotology is expanded to include surgery of the lateral skull base to treat intracranial tumors related to the ear and surrounding nerve and vascular structures, such as large cerebellar pontine angle  acoustic neuromas ,  glomus jugulare  tumors and facial nerve tumors.


Some of the concerns of otology include:


Related concerns of neurotology include:


Otorhinolaryngology  ( / oʊ t oʊ ˌ r aɪ n oʊ ˌ l ær ɪ n ˈ ɡ ɒ l ə dʒ i /   oh-toh- RY -noh- LARR -in- GOL -ə-jee , abbreviated  ORL  and also known as  otolaryngology ,  otolaryngology   –   head and neck surgery  ( ORL–H&N  or  OHNS ), or  ear, nose, and throat  ( ENT ) ) is a surgical subspecialty within medicine that deals with the surgical and medical management of conditions of the head and neck. Doctors who specialize in this area are called otorhinolaryngologists, otolaryngologists, head and neck surgeons, or ENT surgeons or physicians.


Patients seek treatment from an otorhinolaryngologist for diseases of the  ear ,  nose ,  throat ,  base of the skull , head, and neck. These commonly include functional diseases that affect the senses and activities of eating, drinking, speaking, breathing, swallowing, and hearing. In addition, ENT surgery encompasses the surgical management of  cancers  and  benign tumors  and reconstruction of the head and neck as well as  plastic surgery  of the face, scalp, and neck.


The term is a combination of  Neo-Latin   combining forms  ( oto-  +  rhino-  +  laryngo-  +  -logy ) derived from four  Ancient Greek  words: [ 1 ]  ( cf.  Greek  ωτορινολαρυγγολόγος   ' otorhinolaryngologist ' ).


Otorhinolaryngologists are  physicians  ( MD ,  DO ,  MBBS ,  MBChB , etc.) who complete both medical school and an average of five–seven years of post-graduate surgical training in ORL-H&N. In the United States, trainees complete at least five years of surgical residency training. [ 2 ]  This comprises three to six months of  general surgical  training and four and a half years in ORL-H&N specialist surgery. In Canada and the United States, practitioners complete a five-year residency training after medical school.


Following residency training, some otolaryngologist-head & neck surgeons complete an advanced sub-specialty fellowship, where training can be one to two years in duration. Fellowships include head and neck surgical oncology, facial plastic surgery,  rhinology  and sinus surgery,  neuro-otology , pediatric otolaryngology, and laryngology. In the United States and Canada, otorhinolaryngology is one of the most competitive specialties in medicine in which to obtain a residency position following medical school. [ 3 ] [ 4 ]


In the United Kingdom, entrance to higher surgical training is competitive and involves a rigorous national selection process. [ 5 ]  The training programme consists of 6 years of higher surgical training after which trainees frequently undertake fellowships in a sub-speciality prior to becoming a consultant.


The typical total length of education, training and post-secondary school is 12–14 years. Otolaryngology is among the more highly compensated surgical specialties in the United States. In 2022, the average annual income was $469,000. [ 6 ]


reconstruction


(*Currently recognized by  American Board of Medical Subspecialties )


Study of diseases of the outer ear, middle ear and mastoid, and inner ear, and surrounding structures (such as the facial nerve and lateral skull base)


Rhinology includes nasal dysfunction and sinus diseases.


Facial plastic and reconstructive surgery is a one-year fellowship open to otorhinolaryngologists who wish to begin learning the aesthetic and reconstructive surgical principles of the head, face, and neck pioneered by the specialty of Plastic and Reconstructive Surgery.


Sleep surgery encompasses any surgery that helps alleviate obstructive sleep apnea and can anatomically include any part of the upper airway.


Microvascular reconstruction repair is a common operation that is done on patients who see an otorhinolaryngologist. It is a surgical procedure that involves moving a composite piece of tissue from the patient's body and to the head and/or neck. Microvascular head-and-neck reconstruction is used to treat head-and-neck cancers, including those of the larynx and pharynx, oral cavity, salivary glands, jaws, calvarium, sinuses, tongue and skin. The tissue that is most commonly moved during this procedure is from the arms, legs, and back, and can come from the skin, bone, fat, and/or muscle. [ 8 ]


When performing this procedure, the decision on which is moved is determined on the reconstructive needs. Transfer of the tissue to the head and neck allows surgeons to rebuild the patient's jaw, optimize tongue function, and reconstruct the throat. When the pieces of tissue are moved, they require their own blood supply for a chance of survival in their new location. After the surgery is completed, the blood vessels that feed the tissue transplant are reconnected to new blood vessels in the neck. These blood vessels are typically no more than 1 to 3 millimeters in diameter, which means that these connections need to be made with a microscope, which is why the procedure is called "microvascular surgery". [ citation needed ]


Instruments used specially in  Otolaryngology  ( Otorhinolaryngology, head and neck surgery ) i.e. ENT are as follows: [ 1 ] [ 2 ]


The  abducens nerve  or  abducent nerve , also known as the  sixth cranial nerve ,  cranial nerve VI , or simply  CN VI , is a  cranial nerve  in humans and various other animals that controls the movement of the  lateral rectus muscle , one of the  extraocular muscles  responsible for outward  gaze . It is a  somatic   efferent nerve .


The  abducens nucleus  is located in the pons, on the floor of the  fourth ventricle , at the level of the  facial colliculus . Axons from the facial nerve loop around the abducens nucleus, creating a slight bulge (the facial colliculus) that is visible on the dorsal surface of the floor of the fourth ventricle.  The abducens nucleus is close to the midline, like the other motor nuclei that control eye movements (the  oculomotor  and  trochlear nuclei ). [ citation needed ]


Motor axons leaving the abducens nucleus run ventrally and caudally through the pons. They pass lateral to the  corticospinal tract  (which runs longitudinally through the pons at this level) before exiting the brainstem at the pontomedullary junction. [ citation needed ]


The abducens nerve emerges from the  brainstem  at the junction of the  pons  and the  medulla , [ 1 ]  superior to the  medullary pyramid , [ 2 ]  and medial to the  facial nerve . It runs upwards and forwards from this position to reach the eye.


The nerve enters the  subarachnoid space  (more precisely, the  pontine cistern [ 2 ] ) when it emerges from the brainstem. It runs upward between the pons and the  clivus , and then pierces the  dura mater  to run between the dura and the skull through  Dorello's canal . [ 3 ] [ 4 ]  At the apex of the  petrous part of the temporal bone , it makes a sharp turn forward to enter the  cavernous sinus . [ 1 ]  In the cavernous sinus, it runs anterior-ward alongside (inferolateral to) the  internal carotid artery . It enters the orbit through (medial end of) the  superior orbital fissure , passing through the  common tendinous ring  to reach and innervate the  lateral rectus muscle  of the eye. [ 2 ]


The human abducens nerve is derived from the  basal plate  of the  embryonic   pons .


The abducens nerve supplies the  lateral rectus muscle  of the  human eye . This muscle is responsible for outward gaze. [ 1 ]  The abducens nerve carries axons of type GSE,  general somatic efferent .


Damage to the peripheral part of the abducens nerve will cause double vision ( diplopia ), due to the unopposed muscle tone of the  medial rectus muscle . The affected eye is pulled to look towards the midline. In order to see without double vision, patients will rotate their heads so that both eyes are toward the temple. [ citation needed ]  Partial damage to the abducens nerve causes weak or incomplete abduction of the affected eye. The diplopia is worse on attempts at looking laterally.


The long course of the abducens nerve between the brainstem and the eye makes it vulnerable to injury at many levels.  For example, fractures of the petrous temporal bone can selectively damage the nerve, as can  aneurysms  of the intracavernous carotid artery.  Mass lesions that push the brainstem downward can damage the nerve by stretching it between the point where it emerges from the pons and the point where it hooks over the petrous temporal bone.


The central anatomy of the sixth nerve predicts (correctly) that infarcts affecting the dorsal pons at the level of the abducens nucleus can also affect the facial nerve,  producing an ipsilateral facial palsy together with a lateral rectus palsy.  The anatomy also predicts (correctly) that infarcts involving the ventral pons can affect the sixth nerve and the corticospinal tract simultaneously, producing a lateral rectus palsy associated with a contralateral hemiparesis. These rare syndromes are of interest primarily as useful summaries of the anatomy of the brainstem.


Complete interruption of the peripheral sixth nerve causes  diplopia  (double vision), due to the unopposed action of the  medial rectus muscle . The affected eye is pulled medially. In order to see without double vision, patients will turn their heads sideways so that both eyes are looking sideways. On formal testing, the affected eye cannot abduct past the midline – it cannot look sideways, toward the temple. Partial damage to the sixth nerve causes weak or incomplete abduction of the affected eye.  The diplopia is worse on attempted lateral gaze, as would be expected (since the lateral gaze muscle is impaired).


Peripheral sixth nerve damage can be caused by tumors, aneurysms, or fractures – anything that  directly compresses or stretches the nerve.  Other processes that can damage the sixth nerve include strokes (infarctions), demyelination, infections (e.g.  meningitis ), cavernous sinus diseases and various neuropathies. Perhaps the most common overall cause of sixth nerve impairment is  diabetic neuropathy .  Iatrogenic injury is also known to occur, with the abducens nerve being the most commonly injured cranial nerve in halo orthosis placement. [ 5 ]  The resultant palsy is identified through loss of lateral gaze after application of the orthosis.


Rare causes of isolated sixth nerve damage include  Wernicke–Korsakoff syndrome  and  Tolosa–Hunt syndrome . Wernicke–Korsakoff syndrome is caused by thiamine deficiency, classically due to alcoholism.  The characteristic ocular abnormalities are nystagmus and lateral rectus weakness.  Tolosa-Hunt syndrome is an idiopathic granulomatous disease that causes painful oculomotor (especially sixth nerve) palsies.


Indirect damage to the sixth nerve can be caused by any process ( brain tumor ,  hydrocephalus ,  pseudotumor cerebri , hemorrhage, edema) that exerts downward pressure on the brainstem, causing the nerve to stretch along the clivus. This type of traction injury can affect either side first. A right-sided brain tumor can produce either a right-sided or a left-sided sixth nerve palsy as an initial sign.  Thus a right-sided sixth nerve palsy does not necessarily imply a right-sided cause.  Sixth nerve palsies are infamous as "false localizing signs." Neurological signs are described as "false localizing" if they reflect dysfunction distant or remote from the expected anatomical location of pathology. Isolated sixth nerve palsies in children are assumed to be due to brain tumors until proven otherwise.


Damage to the abducens nucleus does not produce an isolated  sixth nerve palsy , but rather a horizontal  gaze palsy  that affects both eyes simultaneously.  The abducens nucleus contains two types of cells: motor neurons that control the lateral rectus muscle on the same side, and interneurons that cross the midline and connect to the contralateral oculomotor nucleus (which controls the medial rectus muscle of the opposite eye).  In normal vision, lateral movement of one eye (lateral rectus muscle) is precisely coupled to medial movement of the other eye (medial rectus muscle), so that both eyes remain fixed on the same object.


The control of  conjugate gaze  is mediated in the brainstem by the  medial longitudinal fasciculus  (MLF), a nerve tract that connects the three extraocular motor nuclei (abducens, trochlear and oculomotor) into a single functional unit.  Lesions of the abducens nucleus and the MLF produce observable sixth nerve problems, most notably  internuclear ophthalmoplegia  (INO).


The sixth nerve is one of the final common pathways for numerous cortical systems that control eye movement in general.  Cortical control of eye movement ( saccades , smooth pursuit,  accommodation ) involves  conjugate gaze , not unilateral eye movement.


15–40% of people with tuberculosis have some resulting cranial nerve deficit.  The sixth nerve is the most commonly affected cranial nerve in immunocompetent people with tuberculosis. [ 6 ]


The Latin name for the sixth cranial nerve is "nervus abducens".  The  Terminologia Anatomica  officially recognizes two different English translations: "abducent nerve" and "abducens nerve". [ 7 ]


"Abducens" is more common in recent literature, while "abducent" predominates in the older literature.  The  United States National Library of Medicine  uses "abducens nerve" in its Medical Subject Heading ( MeSH ) vocabulary to index the vast  MEDLINE  and  PubMed  biomedical databases.  The 39th edition of  Gray's Anatomy  (2005) also prefers "abducens nerve." [ 1 ]


The abducens nerve controls the movement of a single muscle, the  lateral rectus muscle  of the eye.  In most other  mammals  it also innervates the  musculus retractor bulbi , which can retract the eye for protection.  Homologous abducens nerves are found in all  vertebrates  except  lampreys  and  hagfishes .


The  accessory nerve , also known as the  eleventh cranial nerve ,  cranial nerve XI , or simply  CN XI , is a  cranial nerve  that supplies the  sternocleidomastoid  and  trapezius muscles . It is classified as the eleventh of twelve pairs of cranial nerves because part of it was formerly believed to originate in the brain. The sternocleidomastoid muscle tilts and rotates the head, whereas the trapezius muscle, connecting to the  scapula , acts to shrug the shoulder.


Traditional descriptions of the accessory nerve divide it into a spinal part and a cranial part. [ 1 ]  The cranial component rapidly joins the  vagus nerve , and there is ongoing debate about whether the cranial part should be considered part of the accessory nerve proper. [ 2 ] [ 1 ]  Consequently, the term "accessory nerve" usually refers only to nerve supplying the sternocleidomastoid and trapezius muscles, also called the  spinal accessory nerve . [ 3 ]


Strength testing of these muscles can be measured during a  neurological examination  to assess function of the spinal accessory nerve. Poor strength or limited movement are suggestive of damage, which can result from a variety of causes. Injury to the spinal accessory nerve is most commonly caused by medical procedures that involve the head and neck. [ 4 ]  Injury can cause wasting of the  shoulder  muscles,  winging of the scapula , and weakness of shoulder abduction and  external rotation . [ 5 ]


The accessory nerve is derived from the  basal plate  of the  embryonic  spinal segments C1–C6. [ 6 ]


The fibres of the spinal accessory nerve originate solely in  neurons  situated in the upper  spinal cord , from where the spinal cord begins at the junction with the  medulla oblongata , to the level of about C6. [ 1 ] [ 7 ]  These fibres join to form rootlets, roots, and finally the spinal accessory nerve itself. The formed nerve enters the skull through the  foramen magnum , the large opening at the skull's base. [ 1 ]  The nerve travels along the inner wall of the skull towards the  jugular foramen . [ 1 ]  Leaving the skull, the nerve travels through the jugular foramen with the  glossopharyngeal  and  vagus nerves . [ 8 ]  The spinal accessory nerve is notable for being the only cranial nerve to both enter and exit the skull. This is due to it being unique among the cranial nerves in having neurons in the spinal cord. [ 9 ]


After leaving the skull, the cranial component detaches from the spinal component. The spinal accessory nerve continues alone and heads backwards and downwards. In the neck, the accessory nerve crosses the internal jugular vein around the level of the posterior belly of digastric muscle. As it courses downwards, the nerve pierces through the  sternocleidomastoid muscle  (approximately 1 cm above  Erb's point ) while sending it  motor  branches, then continues down until it reaches the  trapezius muscle  (entering at the junction of the middle and lower third of the anterior border of the  trapezius ) to provide motor innervation to its upper part. [ 10 ]


The fibres that form the spinal accessory nerve are formed by  lower motor neurons  located in the upper segments of the  spinal cord . This  cluster of neurons , called the  spinal accessory nucleus , is located in the lateral aspect of the anterior horn of the spinal cord, and stretches from where the spinal cord begins (at the junction with the medulla) through to the level of about C6. [ 1 ]  The lateral horn of high cervical segments appears to be continuous with the  nucleus ambiguus  of the  medulla oblongata , from which the cranial component of the accessory nerve is derived. [ 9 ]


In the neck, the accessory nerve crosses the internal jugular vein around the level of the posterior belly of  digastric muscle , in front of the vein in about 80% of people, and behind it in about 20%, [ 9 ]  and in one reported case, piercing the vein. [ 11 ]


Traditionally, the accessory nerve is described as having a small cranial component that descends from the  medulla  and briefly connects with the spinal accessory component before branching off of the nerve to join the vagus nerve. [ 1 ]  A study, published in 2007, of twelve subjects suggests that in the majority of individuals, this cranial component does not make any distinct connection to the spinal component; the roots of these distinct components were separated by a fibrous sheath in all but one subject. [ 7 ]


The accessory nerve is derived from the  basal plate  of the embryonic spinal segments C1–C6. [ 12 ]


The spinal component of the accessory nerve provides motor control of the  sternocleidomastoid  and  trapezius   muscles . [ 8 ]  The trapezius muscle controls the action of shrugging the shoulders, and the sternocleidomastoid the action of turning the head. [ 8 ]  Like most muscles, control of the trapezius muscle arises from the opposite side of the brain. [ 8 ]   Contraction of the upper part of the trapezius muscle elevates the scapula. [ 13 ]  The nerve fibres supplying sternocleidomastoid, however, are thought to change sides ( Latin :  decussate ) twice. This means that the sternocleidomastoid is controlled by the brain on the same side of the body. Contraction of the stenocleidomastoid fibres turns the head to the opposite side, the net effect meaning that the head is turned to the side of the brain receiving visual information from that area. [ 8 ]  The cranial component of the accessory nerve, on the other hand, provides motor control to the muscles of the soft palate, larynx and pharynx.


Among researchers there is disagreement regarding the terminology used to describe the type of information carried by the accessory nerve. As the trapezius and sternocleidomastoid muscles are derived from the  pharyngeal arches , some researchers believe the spinal accessory nerve that innervates them must carry specific  special visceral efferent  (SVE) information. [ 14 ]  This is in line with the observation that the spinal accessory nucleus appears to be continuous with the  nucleus ambiguus  of the medulla. Others consider the spinal accessory nerve to carry  general somatic efferent  (GSE) information. [ 15 ]  Still others believe it is reasonable to conclude that the spinal accessory nerve contains both SVE and GSE components. [ 16 ]


The accessory nerve is tested by evaluating the function of the  trapezius  and  sternocleidomastoid muscles . [ 8 ]  The trapezius muscle is tested by asking the patient to shrug their shoulders with and without resistance. The sternocleidomastoid muscle is tested by asking the patient to turn their head to the left or right against resistance. [ 8 ]


One-sided weakness of the trapezius may indicate injury to the nerve on the same side of an injury to the spinal accessory nerve on the same side (Latin:  ipsilateral ) of the body being assessed. [ 8 ]  Weakness in head-turning suggests injury to the contralateral spinal accessory nerve: a weak leftward turn is indicative of a weak right sternocleidomastoid muscle (and thus right spinal accessory nerve injury), while a weak rightward turn is indicative of a weak left sternocleidomastoid muscle (and thus left spinal accessory nerve). [ 8 ]


Hence, weakness of shrug on one side and head-turning on the other side may indicate damage to the accessory nerve on the side of the shrug weakness, or damage along the nerve pathway at the other side of the brain. Causes of damage may include trauma, surgery, tumours, and compression at the jugular foramen. [ 8 ]  Weakness in both muscles may point to a more general disease process such as  amyotrophic lateral sclerosis ,  Guillain–Barré syndrome  or  poliomyelitis . [ 8 ]


Injury to the spinal accessory nerve commonly occurs during neck surgery, including  neck dissection  and  lymph node  excision. It can also occur as a result of blunt or penetrating trauma, and in some causes spontaneously. [ 17 ] [ 5 ]  Damage at any point along the nerve's course will affect the function of the nerve. [ 10 ]  The nerve is intentionally removed in "radical" neck dissections, which are attempts at exploring the neck surgically for the presence and extent of cancer. Attempts are made to spare it in other forms of less aggressive dissection. [ 5 ]


Injury to the accessory nerve can result in neck pain and weakness of the trapezius muscle. Symptoms will depend on at what point along its length the nerve was severed. [ 5 ]  Injury to the nerve can result in shoulder girdle depression, atrophy, abnormal movement, a protruding scapula, and weakened  abduction . [ 5 ]  Weakness of the shoulder girdle can lead to traction injury of the  brachial plexus . [ 10 ]  Because diagnosis is difficult,  electromyogram  or  nerve conduction studies  may be needed to confirm a suspected injury. [ 5 ]  Outcomes with surgical treatment appear to be better than conservative management, which entails physiotherapy and pain relief. [ 17 ]  Surgical management includes  neurolysis , nerve end-to-end suturing, and surgical replacement of affected trapezius muscle segments with other muscle groups, such as the  Eden-Lange procedure . [ 17 ]


Damage to the nerve can cause  torticollis . [ 18 ]


English anatomist  Thomas Willis  in 1664 first described the accessory nerve, choosing to use "accessory" (described in  Latin  as  nervus accessorius ) meaning in association with the vagus nerve. [ 19 ]


In 1848,  Jones Quain  described the nerve as the "spinal nerve accessory to the vagus", recognizing that while a minor component of the nerve joins with the larger vagus nerve, the majority of accessory nerve fibres originate in the spinal cord. [ 3 ] [ 20 ]  In 1893 it was recognised that the heretofore named nerve fibres "accessory" to the vagus originated from the same nucleus in the  medulla oblongata , and it came to pass that these fibres were increasingly viewed as part of the vagus nerve itself. [ 3 ]  Consequently, the term "accessory nerve" was and is increasingly used to denote only fibres from the spinal cord; the fact that only the spinal portion could be tested clinically lent weight to this opinion. [ 3 ]


In  anatomy , the  pharyngeal tonsil , also known as the  nasopharyngeal tonsil  or  adenoid , is the  superior -most of the  tonsils . It is a mass of  lymphoid tissue  located behind the  nasal cavity , in the roof and the posterior wall of the  nasopharynx , [ 1 ]  where the  nose  blends into the  throat . In  children , it normally forms a soft mound in the roof and back wall of the nasopharynx, just above and behind the  uvula .


The term  adenoid  is also used to represent  adenoid hypertrophy , the abnormal growth of the pharyngeal tonsils. [ 2 ]


The adenoid is a mass of  lymphoid tissue  located behind the nasal cavity, in the roof and the posterior wall of the  nasopharynx , [ 1 ]  where the nose blends into the throat. The adenoid, unlike the  palatine tonsils , has  pseudostratified epithelium . [ 3 ]   The adenoids are part of the so-called  Waldeyer ring  of lymphoid tissue which also includes the palatine tonsils, the  lingual tonsils  and the  tubal tonsils .


Adenoids develop from a subepithelial infiltration of  lymphocytes  after the 16th week of embryonic life. After birth, enlargement begins and continues until ages 5 to 7 years.


Part of the immune system, adenoids trap and recognize pathogens such as bacteria and viruses. In response, the adenoid produces  T cells  and  B cells  to combat infection, contributing to the synthesis of IgA  immunoglobulins , assisting in the body's immunologic memory. [ 4 ]


Species of bacteria such as  lactobacilli , anaerobic streptococci,  actinomycosis ,  Fusobacterium  species, and  Nocardia  are normally present by 6 months of age. Normal flora found in the adenoid consists of  alpha-hemolytic streptococci  and  enterococci ,  Corynebacterium  species,  coagulase-negative staphylococci ,  Neisseria  species,  Haemophilus  species,  Micrococcus  species, and  Stomatococcus  species. [ citation needed ]


An enlarged adenoid, or  adenoid hypertrophy , can become nearly the size of a  ping pong ball  and completely block airflow through the nasal passages. Even if the enlarged adenoid is not substantial enough to physically block the back of the nose, it can obstruct airflow enough so that breathing through the nose requires an uncomfortable amount of work, and inhalation occurs instead through an open mouth. The enlarged adenoid would also obstruct the nasal airway enough to affect the voice without actually stopping nasal airflow altogether.


Symptomatic enlargement between 18 and 24 months of age is not uncommon, meaning that snoring, nasal airway obstruction and obstructed breathing may occur during sleep. However, this may be reasonably expected to decline when children reach school age, and progressive shrinkage may be expected thereafter. [ citation needed ]


Enlargement of the adenoid, especially in children, causes an atypical appearance of the face, often referred to as  adenoid facies . [ 5 ]  Features of adenoid facies include  mouth breathing , an elongated face, prominent incisors,  hypoplastic   maxilla , short upper lip, elevated nostrils, and a high arched palate. [ 6 ]


Surgical removal of the adenoid is a procedure called  adenoidectomy . Adenoid infection may cause symptoms such as excessive  mucus  production, which can be treated by its removal. Studies have shown that adenoid regrowth occurs in as many as 19% of the cases after removal. [ 7 ]  Carried out through the mouth under a  general anaesthetic  (or less commonly a  topical ), adenoidectomy involves the adenoid being  curetted ,  cauterized ,  lasered , or otherwise  ablated . The adenoid is often removed along with the  palatine tonsils . [ 8 ]


Adenoid hypertrophy , also known as  enlarged adenoids  refers to an enlargement of the  adenoid  (pharyngeal  tonsil ) that is linked to nasopharyngeal mechanical blockage and/or chronic inflammation. [ 1 ]  Adenoid hypertrophy is a characterized by  hearing loss , recurrent  otitis media , mucopurulent  rhinorrhea , chronic  mouth breathing , nasal  airway obstruction , increased infection susceptibility, and dental malposition.


The exact cause of adenoid hypertrophy in children remains unclear, but it is likely linked to immunological responses, hormonal factors, or genetic components. Adenoid hypertrophy is an immunological abnormality characterized by altered  cytokine  production, with children experiencing higher levels of proinflammatory cytokines. Adenoid hypertrophy can also be caused by gastric juice exposure during  gastroesophageal reflux disease , passive smoking, and recurrent bacterial and viral infections. Pathogen colonization can disrupt the  immune system 's equilibrium with the adenoid's natural flora. Genetic factors, such as variations in  TLR2  and  TLR4  genes, also contribute to the condition. Adenoids naturally undergo  hypertrophy  between 6-10 and atrophy around 16 years old.


A clinical examination and  nasoendoscopy  are the gold standard for diagnosing adenoid hypertrophy. Visual examinations should be conducted to identify adenoid facies,  eczema , and similar signs in diseases like partial  choanal atresia , significant palatine tonsil hyperplasia, nasal airway blockage, endonasal foreign bodies, nasal concha hyperplasia, and allergic or viral  rhinitis .  Neoplasms , benign or malignant ones, should be ruled out. Screening for  juvenile nasopharyngeal angiofibroma  is crucial in male adolescents, while adult patients should be evaluated for  carcinoma  and  lymphoma .  Thornwaldt cysts  should also be considered in differential diagnosis.


Patients with adenoid hyperplasia alone should follow conservative therapy and off-label intranasal  corticosteroids . Patients with significant symptoms and unsatisfactory responses to conservative measures may be candidates for  adenoidectomy . An  adenoidectomy  can shrink and reduce nasal obstruction in patients. Patients usually experience improved eustachian tube function, reduced obstruction, and decreased nasal discharge. The prevalence of adenoid hypertrophy in the pediatric population is estimated to be 34%.


Enlarged adenoids can become nearly the size of a  ping pong ball  and completely block airflow through the nasal passages. Even if enlarged adenoids are not substantial enough to physically block the back of the nose, they can obstruct airflow enough so that  nasal breathing  requires an uncomfortable amount of work, and inhalation occurs instead through  mouth breathing . Adenoids can also obstruct the nasal airway enough to affect the voice without actually stopping nasal airflow altogether. [ 2 ]


Adenoid hypertrophy is characterized by a number of typical signs and symptoms, including  conductive hearing loss , recurrent  otitis media  (including  cholesteatoma ), mucopurulent  rhinorrhea , chronic  mouth breathing , nasal  airway obstruction , increased susceptibility to infection, and occasionally dental malposition. [ 1 ]


If left untreated, adenoid hypertrophy can cause  pulmonary hypertension , ear issues,  obstructive sleep apnea ,  failure to thrive , and  craniofacial abnormalities . [ 3 ] [ 4 ]


It's unclear what exactly causes adenoid hypertrophy in children. Most likely, immunological responses, hormonal factors, or genetic components have some relationship. [ 5 ]


One of the immunological abnormalities described is altered  cytokine  production. For instance, it was demonstrated that  interleukin (IL)-32  was upregulated in  adenoid  tissue. This could potentially impact the progression of adenoid hypertrophy by inducing the production of proinflammatory cytokines and inducing  pyroptosis  in human nasal  epithelial cells , which is mediated by the  NOD1 / 2 / TLR4 / NLRP3  pathway. [ 6 ]


Furthermore, it has been discovered that children with adenoid hypertrophy had higher levels of proinflammatory cytokines, including  interferon-γ  (IFN-γ), high-sensitivity  C reactive protein ,  IL-1  and  IL-10 ,  TNF-α  (tumor necrosis factor α), and  intercellular adhesion molecule-1 . [ 7 ]


Adenoid hypertrophy may also be brought on by gastric juice exposure during  gastro-oesophageal reflux disease , particularly in infants and early toddlers. [ 8 ]  An additional risk factor for adenoid hypertrophy is passive smoking. [ 9 ] [ 5 ]


Recurrent bacterial and viral infections as well as pathogen colonization might upset the normally stable equilibrium between the  immune system  and the natural flora of the adenoid. [ 10 ]  Hypertrophic processes are frequently brought on by recurrent  upper respiratory tract infections  or  allergies . [ 9 ] [ 11 ]  The bacteria  Haemophilus influenza ,  Streptococcus pneumoniae ,  Streptococcus pyogenes , and  Staphylococcus aureus  are most frequently isolated from adenoid tissue. Pathogens that are  anaerobic bacteria  are also found in chronic infections. [ 12 ]


Genetic factors include, for example, variations in the genes encoding  TLR2  and  TLR4 , SCGB1D4, and other genes. [ 13 ] [ 14 ]


The clinical and anatomic basis of hypertrophy is the enlargement of the germinal centers of  lymphoid tissue  and lymphoid follicles. The fundamental reason is thought to be a vicious cycle of  inflammation ,  hypertrophy  and/or  hyperplasia , secretory retention, and recurrent inflammation. [ 1 ]


Adenoid  is a lymphoid tissue condensation at the back of the nose or on the nasopharyngeal postrosuperior wall.  Adenoid is part of  Waldeyer's Ring . [ 15 ]  In younger children, it seems to play a significant part in the establishment of a " immunological memory ." [ 16 ]  Adenoids naturally undergo  hypertrophy  between the ages of 6 and 10 and  atrophy  around the age 16. [ 17 ]


The  tonsils  in the back of the mouth, the  adenoid , and the tonsilar tissue at the base of the tongue combine to form  Waldeyer's ring , a tissue ring that helps keep toxins,  bacteria , and  viruses  out of the body.  B lymphocytes , a kind of blood cell that produces  antibodies , make up the majority of the tissues found in the tonsils and adenoid glands. This antibody binds to toxins, germs, and viruses to render them inactive, preventing disease-causing agents from entering the body. The adenoid is situated toward the rear of the  nasal cavity  and up behind the  soft palate , in contrast to the tonsils, which are visible when one looks straight through the mouth. Similar to tonsilar tissue, the adenoid can be affected by both acute and long-term  infections . A persistent infection or inflammation may cause the adenoid to gradually get larger. Because of its location at the rear of the nasal cavity, its primary symptoms have an impact on nasal function. [ 15 ]


During the early years of life, the adenoids expand quickly due to their immunological roles. Its size and form change dramatically during childhood, with dynamic growth occurring between the ages of 3 and 6 years. This may be due to the nasopharyngeal cavity growing more slowly than expected. [ 10 ]  Under normal circumstances, the adenoid grows less after the age of six, and the nasopharyngeal cavity expands and widens the  respiratory tract . [ 5 ]  Due to the proliferation of fibrous tissue and fatty  atrophy , the lymphoid tissue experiences  involution  later in life. [ 5 ]  As a result, in the majority of people, adenoid tissue exists in a residual form but never totally vanishes. [ 18 ]


Microscopic and functional changes within are accompanied by macroscopic changes. [ 10 ]  In humans, these adenoids are most immunologically active between the ages of 4 and 10, and after puberty, they start to involute. [ 19 ]  The population of  B cells  declines and the ratio of  T cells  to  B cells  rises as a result. Inflammation of the crypts caused by infection of the adenoids causes immunologically active cells to become inactive, reducing their capacity to transfer antigens. This, in turn, causes the cells to  metaplasia  into a multilayered squamous epithelium. [ 10 ]  Such alterations result in poor cell functioning and ineffective  antigen  uptake. [ 20 ]


Currently, a thorough clinical examination combined with  nasoendoscopy  (NE), notably  nasopharyngoscopy , is the gold standard for diagnosing adenoid hypertrophy. [ 21 ]


Visual examination should be conducted primarily to determine whether adenoid facies are present. The mouth is usually open and the tip of the tongue is visible in a patient with an adenoid facies. Furthermore,  eczema  is frequently seen at the nose's opening. [ 1 ]


Similar signs and symptoms can be found in diseases such partial  choanal atresia  and significant palatine tonsil hyperplasia. Nasal airway blockage can also result from endonasal foreign bodies, nasal concha hyperplasia, and allergic or viral  rhinitis .  Neoplasms  that are benign or malignant in particular need to be ruled out. It is important to screen for  juvenile nasopharyngeal angiofibroma  in male adolescents in particular. Adult patients, on the other hand, need to be evaluated particularly for  carcinoma  and  lymphoma , which typically present with symptoms including  ulceration , bleeding, slimy coatings, size increases, and  conductive hearing loss . A spherical tumor of the nasopharynx coated in smooth mucosa called a  Thornwaldt cyst  should also be considered in the differential diagnosis. [ 1 ]


In patients with adenoid hyperplasia alone without accompanying indications or symptoms, conservative therapy, i.e., cautious waiting, is advised. [ 1 ]  Furthermore, there is data indicating that people with adenoid hyperplasia may benefit from off-label intranasal  corticosteroids . [ 22 ]


Patients exhibiting significant symptoms (such as repeated  fever  and infections, persistent ear problems) and/or unsatisfactory response to conservative measures (such as topical  cortisone , anti-allergic therapy, and watchful waiting) are candidates for  adenoidectomy . Individuals with long-term serous or mucous  otitis media  frequently have an  adenoidectomy ,  myringotomy , and/or tube insertions performed. [ 1 ]


The  adenoid  will shrink back to a smaller size and cause less nasal obstruction if it is acutely swollen and responds well to antibiotic and steroid therapy. After undergoing an  adenoidectomy , patients usually experience improvements in their eustachian tube function, a reduction in nasal obstruction, and a decrease in excessive nasal discharge. Of children who undergo  adenoidectomy  for chronic sinus disease, 25% will experience a resolution of their sinus disease. [ 15 ]


In the pediatric population, the estimated prevalence of adenoid hypertrophy is 34%. [ 23 ]


The structure that is today known as the  adenoid  was initially described by the German anatomist Conrad Victor Schneider in 1661. But it wasn't until 1868 that the Danish physician Meyer coined the term "adenoid vegetations." [ 10 ]  In an original research report, Meyer characterized these adenoid vegetations as "soft tumour masses of the nasopharynx that fill the room above the soft palate." [ 24 ]  He also realized the connection between adenoid hypertrophy, mouth breathing, snoring, nasal obstruction, and hearing loss. [ 10 ]  In addition, Meyer suggested using a specific knife that is put into the  nasopharynx  through the anterior nostrils in order to surgically treat adenoid hyperplasia. [ 25 ]


Adenoidectomy  is the  surgical  removal of the  adenoid  for reasons which include impaired breathing through the nose, chronic infections, or recurrent earaches. The effectiveness of removing the adenoids in children to improve recurrent nasal symptoms and/or nasal obstruction has not been well studied. [ 1 ]  The surgery is less commonly performed in adults in whom the adenoid is much smaller and less active than it is in children. It is most often done on an  outpatient  basis under general  anesthesia . Post-operative pain is generally minimal and reduced by icy or cold foods. The procedure is often combined with  tonsillectomy  (this combination is usually called an "adenotonsillectomy" or "T&A"), for which the recovery time is an estimated 10–14 days, sometimes longer, mostly dependent on age.


Adenoidectomy is not often performed under one year of age as adenoid function is part of the body's immune system, but its contribution to this decreases progressively beyond this age.


The indications for adenoidectomy are still controversial. [ 2 ] [ 3 ] [ 4 ]  Widest agreement surrounds the removal of the adenoid for obstructive sleep apnea, usually combined with tonsillectomy. [ 5 ]  Even then, it has been observed that a significant percentage of the study population (18%) did not respond.
There is also support for adenoidectomy in recurrent  otitis media  in children previously treated with  tympanostomy tubes . [ 6 ]
Finally, the effectiveness of adenoidectomy in children with recurrent upper respiratory tract infections, common cold, otitis media and moderate nasal obstruction has been questioned with the outcome, [ 1 ]  in some studies, being no better than watchful waiting. [ 7 ] [ 8 ]


In 1971, more than one million Americans underwent tonsillectomies and/or adenoidectomies, of which 50,000 consisted of adenoidectomy alone. [ 9 ]


By 1996, roughly a half million children underwent some surgery on their adenoid and/or tonsils in both outpatient and inpatient settings. This included approximately 60,000 tonsillectomies, 250,000 combined tonsillectomies and adenoidectomies,  and 125,000 adenoidectomies. By 2006, the total number had risen to over 700,000 but when adjusted for population changes, the tonsillectomy "rate" had dropped from 0.62 per thousand children to 0.53 per thousand. A larger decline for combined tonsillectomy and adenoidectomy was noted - from 2.20 per thousand to 1.46. There was no significant change in adenoidectomy rates for chronic infectious reasons (0.25 versus 0.21 per 1000). [ 10 ]


Adenoidectomy was first performed using a ring forceps through the  nasal cavity  by William Meyer in 1867. [ 11 ]


In the early 1900s, adenoidectomies began to be routinely combined with tonsillectomy. [ 12 ]  Initially, the procedures were performed by  otolaryngologists , general surgeons, and general practitioners but over the past 30 years have been performed almost exclusively by otolaryngologists.


Then, adenoidectomies were performed as treatment of  anorexia nervosa ,  mental retardation , and  enuresis  or to promote 'good health'. By current standards, these indications seem odd but may be explained by the  hypothesis  that children might have failed to thrive if they had chronically  sore throats  or  severe obstructive sleep apnea  (OSA). Also, children who heard poorly because of chronic  otitis media  might have had unrecognized  speech delay  mistaken for intellectual disability. Adenoidectomy might have helped to resolve ear fluid problems, speech delays, and consequent perceptions of low  intelligence .


The relationship between enuresis and obstructive apnea, and the benefit of adenoidectomy by implication, is complex and controversial. On one hand, the frequency of enuresis declines as children grow older. On the other, the size of the adenoid, and again by implication, any obstruction that they might be causing, also declines with increasing age. These two factors make it difficult to distinguish the benefits of adenoidectomy from age-related spontaneous improvement. Further, most of the studies in the medical literature which appear to show benefit from adenoidectomy have been case reports or case series. Such studies are prone to unintentional bias. Finally, a recent study of six thousand children has not shown an association between enuresis and obstructive sleep in general but an increase with advancing severity of obstructive sleep apnea, observed only in girls. [ 13 ]


A decline in the frequency of the procedure started in the 1930s as its use became controversial. Tonsillitis and adenoiditis requiring surgery became less frequent with the development of antimicrobial agents and a decline in upper respiratory infections among older school-aged children. Also, several studies had shown that adenoidectomy and tonsillectomy were ineffective for many of the indications used at that time as well as the suggestion of an increased risk of developing  poliomyelitis  after the procedure, later disproved. [ 14 ]  Prospective clinical trials, performed over the last 2 decades, have redefined the appropriate indications for tonsillectomy and adenoidectomy (T&A), tonsillectomy alone, and adenoidectomy alone. [ 9 ]


The  angular artery  is an  artery  of the  face . It is the terminal part of the  facial artery . It ascends to the medial angle of the eye's  orbit . It is accompanied by the  angular vein . It ends by anastomosing with the  dorsal nasal branch  of the  ophthalmic artery . It supplies the  lacrimal sac , the  orbicularis oculi muscle , and the outer side of the nose.


The angular artery is the terminal part of the  facial artery . [ 1 ] [ 2 ]  It ascends to the medial angle of the eye's  orbit  (the medial canthus). [ 2 ]  It is embedded in the fibers of the angular head of the  levator labii superioris muscle . [ citation needed ]  It is accompanied by the  angular vein . On the cheek, it distributes branches which anastomose with the  infraorbital artery . [ 2 ]  It ends by anastomosing with the  dorsal nasal branch  of the  ophthalmic artery .


The angular artery supplies the  lacrimal sac , [ 2 ]  most of the outer side of the  nose , [ 3 ]  part of the  lower eyelid , [ 2 ]  and the  orbicularis oculi muscle . [ citation needed ]


The angular artery is important in a nasolabial skin flap for  reconstructive surgery . [ 4 ]  It can be put at risk during acupuncture of  skin  around the inner side of the  eye . [ 5 ]


This article incorporates text in the  public domain  from  page 556  of the 20th edition of   Gray's Anatomy   (1918)


ocular group:   central retinal


The  anterior ethmoidal artery  is a branch of the  ophthalmic artery  in the orbit. [ 1 ]  It exits the orbit through the  anterior ethmoidal foramen  alongside the  anterior ethmoidal nerve . It contributes blood supply to the  ethmoid sinuses ,  frontal sinuses , the  dura mater , lateral nasal wall, and  nasal septum . It issues a meningeal branch, and nasal branches. [ 2 ]


The anterior ethmoidal artery branches from the ophthalmic artery distal to the posterior ethmoidal artery.


It travels with the  anterior ethmoidal nerve  to exit the medial wall of the orbit at the anterior ethmoidal foramen. It then travels through the anterior ethmoidal canal and gives branches which supply the  frontal sinus  and anterior and middle  ethmoid air cells . Following which, it enters the  anterior cranial fossa  where it bifurcates into a meningeal branch and nasal branch. [ citation needed ]


The nasal branch travels through  cribriform plate  to enter the  nasal cavity  and runs in a groove on the deep surface of the  nasal bone . Here it bifurcates into a medial and lateral branch. The lateral branch supplies blood to the lateral wall of the nasal cavity and the medial branch to the  nasal septum . A terminal branch of the lateral branch, called the external nasal branch passes between the nasal bone and the nasal cartilage to supply the skin of the  nose . [ citation needed ]


The  anterior ethmoidal nerve  is a nerve of the head. It is a branch of the  nasociliary nerve  (itself a branch of the  ophthalmic nerve (V 1 ) ). It arises in the orbit, and enters first the cranial cavity and then the nasal cavity. It provides sensory innervation to part of the meninges, parts of the  nasal cavity , and part of the skin of the nose.


The anterior ethmoidal nerve is a terminal branch of the  nasociliary nerve , a branch of the  ophthalmic nerve  (CN V 1 ), itself a branch of the  trigeminal nerve  (CN V). [ 1 ]  It branches near the medial wall of the  orbit .


It passes through the  anterior ethmoidal canal  alongside the  anterior ethmoidal artery [ 2 ] : 780   and vein [ 2 ] : 566   to emerge in  anterior cranial fossa  through the  anterior ethmoidal foramen [ 2 ] : 1464.e13   (at the junction of the cribiform plate of ethmoid bone and  orbital part of frontal bone [ 2 ] : 566  ).


Within the cranial cavity, it passes anterior-ward (external to the dura mater) along a groove upon the superior surface of the  cribriform plate . It descends through an aperture situated lateral to the  crista galli  to reach the  nasal cavity . [ 2 ] : 1464.e13


In the nasal cavity, it passes along a groove upon the internal aspect of the nasal bone, and issuing the medial and lateral internal nasal branches. [ 2 ] : 1464.e13


It is continued as the  external nasal nerve  beyond the inferior margin of the nasal bone. [ 2 ] : 1464.e13


Within the anterior cranial fossa, it gives sensory fibers to the  meninges  to provide sensory innervation to part of the meninges. [ 3 ]


Its medial internal nasal branch innervates the superior and anterior portions of the nasal septum. [ 2 ] : 1464.e13


Its lateral internal nasal branch innervates the anterior portion of the lateral nasal wall. [ 2 ] : 1464.e13


It gives off branches to the roof of the nasal cavity, and bifurcates into a lateral internal nasal branch and medial internal nasal branch. It sends sensory fibers to the  anterior ethmoid air cells  and the  middle ethmoidal air cells . [ citation needed ]


Its terminal branch - the  external nasal nerve  - innervates skin of the nose between the nasal bones superiorly and the tip of the nose inferiorly, except the alar portionsurrounding the external nares. [ 2 ] : 1464.e13


It is involved in the  diving reflex . [ 4 ]


This  neuroanatomy  article is a  stub . You can help Wikipedia by  expanding it .


Antral lavage  is a  largely obsolete [ citation needed ]  surgical procedure in which a  cannula   is inserted into the  maxillary sinus  via the  inferior meatus  to allow irrigation and drainage of the sinus. [ 1 ]
It is also called proof puncture, as the presence of an  infection  can be proven during the procedure. Upon presence of infection, it can be considered as therapeutic puncture. [ 2 ]  Often, multiple repeated lavages are subsequently required to allow for full washout of infection.


In contemporary practice,  endoscopic sinus surgery  has largely replaced antral lavage and as such, it is rarely performed.


It can be used as therapeutic procedure for:


It can be also used as diagnostic procedure for:


Age: Below the age of 3 years, as the size of the sinus is small due to underdeveloped  Maxillary Sinus . [ 10 ]


Bleeding disorders: May lead to  epistaxis . [ 10 ]


Fracture of  maxilla : Antral Lavage may result in escape of the fluid through fracture lines. [ 10 ]


Febrile  stage of acute maxillary sinusitis: May cause  osteomyelitis  of Maxilla. [ 10 ]


Procedure is contraindicated in diabetic and hypertensive patients.


Acute maxillary sinusitis not resolving on medical treatment. [ 1 ]


The following instruments are used in the procedure: [ 11 ]


The following difficulties may arise during antral lavage: [ 4 ]


If the returning fluid is purulent, one repeats the puncture after a week. If more than three successive puncture shows returning fluid to be persistently purulent, the patient may require  functional endoscopic sinus surgery  (FESS) and occasionally may need  Caldwell-Luc operation . [ 4 ]


As antral Washout is a much simpler procedure compared to FESS, it may be done on an  outpatient basis for Subacute Maxillary Sinusitis.  However, FESS remains gold standard in treatment of Chronic Maxillary Sinusitis. [ 16 ]


The  arcuate eminence  is a rounded [ 3 ] [ 4 ] : 567   prominence [ 3 ]  upon the superior surface of [ 3 ] [ 5 ] : 420   the  petrous part of the temporal bone [ 3 ]  forming the lateral part of the posterior wall of [ 5 ] : 509   the  middle cranial fossa . [ 4 ] : 566-567  [ 5 ] : 420, 509   The arcuate eminence indicates the position of the [ 3 ]  underlying [ 4 ] : 567  [ 5 ] : 420    superior semicircular canal (anterior semicircular canal) . [ 3 ] [ 4 ] : 567  [ 5 ] : 420, 509


The groove for the  greater petrosal nerve  is situated anteromedially to the arcuate eminence. [ 5 ] : 509


Auricular hypertrichosis  ( hypertrichosis lanuginosa acquisita ,  hypertrichosis pinnae auris ) is a genetic condition expressed as long and strong hairs growing from the  helix  of the  pinna . [ 1 ] [ page needed ]


Ear hair   generally refers to the  terminal hair  arising from  follicles  inside the  external auditory meatus  in humans. [ 2 ]  In its broader sense,  ear hair  may also include the fine  vellus hair  covering much of the ear, particularly at the prominent parts of the anterior ear, or even the abnormal hair growth as seen in  hypertrichosis  and  hirsutism . Medical research on the function of ear hair is currently very scarce.


Hair growth within the ear canal is often observed to increase in older men, [ 3 ]  together with increased growth of  nose hair . [ 4 ]  Excessive hair growth within or on the ear is known medically as  auricular  hypertrichosis . [ 5 ]  Some men, particularly in the male population of India, have coarse hair growth along the lower portion of the helix, a condition referred to as "having  hairy  pinnae " ( hypertrichosis lanuginosa acquisita ). [ 6 ]


The genetic basis of auricular hypertrichosis has not been settled. Some researchers have proposed a Y-linked pattern of inheritance and others have suggested an autosomal gene is responsible. A third hypothesis predicts the  phenotype  results from the interaction of two loci, one on the homologous part of the X and Y and one on the nonhomologous sequence of the Y. [ 7 ]  These hypotheses are not mutually exclusive, and there may be a variety of genetic mechanisms underlying this phenotype.


Lee et al. (2004), using Y-chromosomal DNA binary-marker haplotyping, suggested that a cohort of southern Indian hairy-eared males carried Y chromosomes from many  haplogroup . [ 8 ]  The hypothesis of Y- linkage would require multiple independent mutations within a single  population . No significant difference between the Y-haplogroup frequencies of hairy-eared males and those of a geographically matched control sample of unaffected males was established. The study concluded that auricular hypertrichosis is not Y-linked in southern India, though this result may not apply to all to all populations. [ 9 ]


Autoinflation  is a minimally invasive procedure to treat  serous  non-infectious  otitis media , in which a nasal balloon is inserted into the  nasopharynx , followed by the application of pressure to the  sinus cavities  by forcibly contracting the  diaphragm  against the closed nasal passageways. [ 1 ] [ 2 ]  It can also be performed by manually pinching the nasal passages and closing the back of the  pharynx , followed by forceful contraction of the diaphragm. It is not recommended in cases of bacterial, or  suppurative , otitis media, but rather serous non-infectious cases, colloquially referred to as ' glue ear '. [ 3 ]


This  medical treatment –related article is a  stub . You can help Wikipedia by  expanding it .


Balloon Eustachian tuboplasty  (BET) [ 1 ]  is a minimally invasive procedure for the causal treatment of  Eustachian tube dysfunction  (ETD), an often-chronic disorder in which the regulation of  middle ear  pressure and the removal of secretions are impaired. The dysfunction often causes significant discomfort in affected patients and can trigger additional pathologies. [ 2 ]


During dilatation of the  Eustachian tube , a purpose built dilatation catheter is inserted into the cartilaginous part of the Eustachian tube under anesthesia [ 3 ] [ 4 ]  as well as endoscopic control. Access is either contralateral or ipsilateral through the nose. If necessary, the endoscope can also be inserted through the oral cavity. An appropriate introducer is used to guide the flexible catheter safely to the tube opening. Once in position, the balloon is dilated by applying a pressure of 10 bar for 2 minutes. [ citation needed ]


The method was first used in 2009 in both Finland [ 5 ]  and Germany [ 6 ]  and has since become an established procedure worldwide. Prospective studies and numerous scientific publications now confirm the high treatment success of the procedure, both in adults [ 1 ] [ 7 ] [ 8 ] [ 9 ]  and in children. [ 10 ] [ 11 ] [ 12 ]


The  base of skull , also known as the  cranial base  or the  cranial floor , is the most  inferior  area of the  skull . It is composed of the  endocranium  and the lower parts of the  calvaria .


Structures found at the base of the skull are for example:


There are five bones that make up the base of the skull:


Bell's palsy  is a type of  facial paralysis  that results in a temporary inability to control the  facial muscles  on the affected side of the face. [ 1 ]  In most cases, the weakness is temporary and significantly improves over weeks. [ 4 ]  Symptoms can vary from mild to severe. [ 1 ]  They may include muscle twitching, weakness, or total loss of the ability to move one or, in rare cases, both sides of the face. [ 1 ]  Other symptoms include drooping of the eyebrow, [ 5 ]  a change in  taste , and pain around the ear. Typically symptoms come on over 48 hours. [ 1 ]  Bell's palsy can trigger an increased sensitivity to sound known as  hyperacusis . [ 6 ]


The cause of Bell's palsy is unknown [ 1 ]  and it can occur at any age. [ 4 ]  Risk factors include  diabetes , a recent  upper respiratory tract infection , and  pregnancy . [ 1 ] [ 7 ]  It results from a dysfunction of  cranial nerve VII  (the facial nerve). [ 1 ]  Many believe that this is due to a viral infection that results in swelling. [ 1 ]  Diagnosis is based on a person's appearance and ruling out other possible causes. [ 1 ]  Other conditions that can cause facial weakness include  brain tumor ,  stroke ,  Ramsay Hunt syndrome type 2 ,  myasthenia gravis , and  Lyme disease . [ 2 ]


The condition normally gets better by itself, with most achieving normal or near-normal function. [ 1 ]   Corticosteroids  have been found to improve outcomes, while  antiviral medications  may be of a small additional benefit. [ 8 ]  The eye should be protected from drying up with the use of  eye drops  or an  eyepatch . [ 1 ]  Surgery is generally not recommended. [ 1 ]  Often signs of improvement begin within 14 days, with complete recovery within six months. [ 1 ]  A few may not recover completely or have a recurrence of symptoms. [ 1 ]


Bell's palsy is the most common cause of one-sided facial nerve paralysis (70%). [ 2 ] [ 9 ]  It occurs in 1 to 4 per 10,000 people per year. [ 2 ]  About 1.5% of people are affected at some point in their lives. [ 10 ]  It most commonly occurs in people between ages 15 and 60. [ 1 ]  Males and females are affected equally. [ 1 ]  It is named after Scottish surgeon  Charles Bell  (1774–1842), who first described the connection of the facial nerve to the condition. [ 1 ]


Although defined as a  mononeuritis  (involving only one nerve), people diagnosed with Bell's palsy may have "myriad neurological symptoms", including "facial tingling, moderate or severe headache/neck pain, memory problems, balance problems, ipsilateral limb paresthesias, ipsilateral limb weakness, and a sense of clumsiness" that are "unexplained by facial nerve dysfunction". [ 11 ]


Bell's palsy is characterized by a one-sided facial droop that comes on within 72 hours. [ 12 ]  In rare cases (<1%), it can occur on both sides resulting in total facial paralysis. [ 13 ] [ 14 ]


The facial nerve controls many functions, such as blinking and closing the  eyes ,  smiling ,  frowning ,  lacrimation ,  salivation , flaring  nostrils  and raising  eyebrows . It also carries  taste  sensations from the anterior two thirds of the  tongue , through the  chorda tympani nerve  (a branch of the facial nerve). Because of this, people with Bell's palsy may present with  loss of taste sensation  in the anterior two thirds of the tongue on the affected side. [ 15 ]


Although the facial nerve innervates the  stapedius muscle  of the  middle ear  (through the  tympanic branch ),  sound sensitivity , causing normal sounds to be perceived as very loud ( hyperacusis ), and  dysacusis  is possible but hardly ever clinically evident. [ 15 ] [ 16 ]


The cause of Bell's palsy is unknown. [ 1 ]  Risk factors include  diabetes , a recent  upper respiratory tract infection , and  pregnancy . [ 1 ] [ 7 ]


Some viruses are thought to establish a persistent (or  latent ) infection without symptoms, e.g., the  varicella zoster virus [ 17 ]  and the  Epstein–Barr virus , both of the  herpes family . Reactivation of an existing (dormant) viral infection has been suggested as a cause of acute Bell's palsy. [ 18 ]  As the facial nerve swells and becomes inflamed in reaction to the infection, it causes pressure within the  Fallopian canal , resulting in the restriction of blood and oxygen to the nerve cells. [ 19 ]  Other viruses and bacteria that have been linked to the development of Bell's palsy include  HIV ,  sarcoidosis  and  Lyme disease . [ medical citation needed ]  This new activation could be triggered by trauma, environmental factors, and metabolic or emotional disorders. [ 20 ]


Familial inheritance has been found in 4–14% of cases. [ 21 ]  There may also be an association with  migraines . [ 22 ]


In December 2020, the U.S.  FDA  recommended that recipients of the  Pfizer  and  Moderna COVID-19 vaccines  should be monitored for symptoms of Bell's palsy after several cases were reported among clinical trial participants, though the data were not sufficient to determine a causal link. [ 23 ]


A meta-analysis of genome-wide association study (GWAS) identified the first unequivocal association with Bell's palsy. [ 24 ]


Bell's palsy is the result of a malfunction of the  facial nerve  ( cranial nerve  VII), which controls the  muscles  of the face. Facial palsy is typified by an inability to move the muscles of facial expression. The paralysis is of the infranuclear/lower motor neuron type.


It is thought that as a result of  inflammation  of the facial nerve, pressure is produced on the nerve where it exits the skull within its bony canal (the  stylomastoid foramen ), blocking the transmission of neural signals or damaging the nerve. Patients with facial palsy for which an underlying cause can be found are not considered to have Bell's palsy  per se . Possible causes of facial paralysis include  tumor ,  meningitis ,  stroke ,  diabetes mellitus ,  head trauma  and inflammatory diseases of the cranial nerves ( sarcoidosis ,  brucellosis , etc.). In these conditions, the neurologic findings are rarely restricted to the facial nerve. Babies can be born with facial palsy. [ 25 ]  In a few cases, bilateral facial palsy has been associated with  acute HIV infection .


In some research, the  herpes simplex virus  type 1 (HSV-1) has been identified in a majority of cases diagnosed as Bell's palsy through endoneurial fluid sampling. [ 26 ]  Other research, however, identified, out of a total of 176 cases diagnosed as Bell's palsy, HSV-1 in 31 cases (18%) and  herpes zoster  in 45 cases (26%). [ 18 ]


In addition, HSV-1 infection is associated with  demyelination  of nerves. This nerve damage mechanism is different from the above-mentioned—that edema, swelling, and compression of the nerve in the narrow bone canal are responsible for nerve damage. Demyelination may not even be directly caused by the virus but by an unknown  immune  response.


Bell's palsy is a  diagnosis of exclusion , meaning it is diagnosed by the elimination of other reasonable possibilities. By definition, no specific cause can be determined. There are no routine lab or imaging tests required to make the diagnosis. [ 12 ]  The degree of nerve damage can be assessed using the  House-Brackmann score .


One study found that 45% of patients are not referred to a specialist, which suggests that Bell's palsy is considered by physicians to be a straightforward diagnosis that is easy to manage. [ 11 ]


Other conditions that can cause similar symptoms include  herpes zoster ,  Lyme disease ,  sarcoidosis ,  stroke , and  brain tumors . [ 12 ]


Once the facial paralysis sets in, many people may mistake it as a symptom of a stroke; however, there are a few subtle differences. A stroke will usually cause a few additional symptoms, such as numbness or weakness in the arms and legs. And unlike Bell's palsy, a stroke will usually let patients control the upper part of their faces. A person with a stroke will usually have some wrinkling on their forehead. [ 27 ] [ 28 ]


In areas where  Lyme disease  is common, it accounts for about 25% of cases of facial palsy. [ 28 ]  In the U.S., Lyme is most common in the  New England  and  Mid-Atlantic  states and parts of  Wisconsin  and  Minnesota . [ 29 ]  The first sign of about 80% of Lyme infections, typically one or two weeks after a tick bite, is usually an  expanding rash  that may be accompanied by headaches, body aches, fatigue, or fever. [ 30 ]  In up to 10–15% of Lyme infections, facial palsy appears several weeks later, and may be the first sign of infection that is noticed as the Lyme rash typically does not itch and is not painful. [ 31 ] [ 32 ]  The likelihood that the facial palsy is caused by Lyme disease should be estimated, based on the recent history of outdoor activities in likely tick habitats during warmer months, a recent history of rash or symptoms such as headache and fever, and whether the palsy affects both sides of the face (much more common in Lyme than in Bell's palsy). If that likelihood is more than negligible, a serological test for Lyme disease should be performed, and if it exceeds 10%,  empiric therapy  with antibiotics should be initiated, without  corticosteroids , and reevaluated upon completion of laboratory tests for Lyme disease. [ 28 ]  Corticosteroids have been found to harm outcomes for facial palsy caused by Lyme disease. [ 28 ]


One disease that may be difficult to exclude in the  differential diagnosis  is the involvement of the facial nerve in infections with the  herpes zoster  virus. The major differences in this condition are the presence of small blisters, or  vesicles , on the external ear, significant pain in the jaw, ear, face, and/or neck, and hearing disturbances, but these findings may occasionally be lacking ( zoster sine herpete ). Reactivation of existing  herpes zoster  infection leading to facial paralysis in a Bell's palsy type pattern is known as  Ramsay Hunt syndrome type 2 . The prognosis for Bell's palsy patients is generally much better than for Ramsay Hunt syndrome type 2 patients. [ 33 ]


Steroids are effective at improving recovery in Bell's palsy while antivirals have not. [ 12 ]  In those who are unable to close their eyes, eye-protective measures are required. [ 12 ]  Management during pregnancy is similar to management in the non-pregnant. [ 7 ]


Corticosteroids  such as  prednisone  improve recovery at 6 months and are thus recommended. [ 3 ]  Early treatment (within 3 days after the onset) is necessary for benefit [ 34 ]  with a 14% greater probability of recovery. [ 35 ]  There is some debate regarding the optimal dosing strategy which is generally physician dependent. [ 36 ]


One review found that  antivirals  (such as  aciclovir ) are ineffective in improving recovery from Bell's palsy beyond steroids alone in mild to moderate disease. [ 37 ]  Another review found a benefit when combined with corticosteroids but stated the evidence was not very good to support this conclusion. [ 8 ]


In severe disease, it is also unclear. One 2015 review found no effect regardless of severity. [ 37 ]  Another review found a small benefit when added to steroids. [ 8 ]


They are commonly prescribed due to a theoretical link between Bell's palsy and the  herpes simplex  and  varicella zoster virus . [ 38 ]  There is still the possibility that they might result in a benefit less than 7% as this has not been ruled out. [ 35 ]


When Bell's palsy affects the blink reflex and stops the eye from closing completely, frequent use of tear-like eye drops or eye ointments is recommended during the day, and protecting the eyes with patches or taping them shut is recommended for sleep and rest periods. [ 28 ] [ 39 ]


Physiotherapy  can be beneficial to some individuals with Bell's palsy as it helps to maintain  muscle tone  of the affected  facial muscles  and stimulate the  facial nerve . [ 40 ]  It is important that muscle re-education exercises and  soft tissue techniques  be implemented before recovery to help prevent permanent  contractures  of the  paralyzed  facial muscles. [ 40 ]  To reduce  pain , heat can be applied to the affected side of the face. [ 41 ]  There is no high-quality evidence to support the role of electrical stimulation for Bell's palsy. [ 42 ]


Surgery may be able to improve outcomes in facial nerve palsy that has not recovered. [ 34 ]  A number of different techniques exist. [ 34 ]   Smile surgery  or smile reconstruction is a surgical procedure that may restore the smile for people with facial nerve paralysis. Adverse effects include hearing loss which occurs in 3–15% of people. [ 43 ]  A Cochrane review (updated in 2021), after reviewing applicable  randomized and quasi-randomized controlled trials  was unable to determine if early surgery is beneficial or harmful. [ 44 ]  As of 2007 the  American Academy of Neurology  did not recommend surgical decompression. [ 43 ]


The efficacy of  acupuncture  remains unknown because the available studies are of low quality (poor primary study design or inadequate reporting practices). [ 45 ]  There is very tentative evidence for  hyperbaric oxygen therapy  in severe disease. [ 46 ]


Most people with Bell's palsy start to regain normal facial function within three weeks—even those who do not receive treatment. [ 47 ]  In a 1982 study, when no treatment was available, of 1,011 patients, 85% showed first signs of recovery within three weeks after onset. For the other 15%, recovery occurred 3–6 months later.


After a follow-up of at least one year or until restoration, complete recovery had occurred in more than two-thirds (71%) of all patients. Recovery was judged moderate in 12% and poor in only 4% of patients. [ 48 ]  Another study found that incomplete palsies disappear entirely, nearly always in one month. The patients who regain movement within the first two weeks nearly always remit entirely. When remission does not occur until the third week or later, a significantly greater part of the patients develop  sequelae . [ 49 ]  A third study found a better prognosis for young patients, aged below 10 years old, while the patients over 61 years old presented a worse prognosis. [ 20 ]


Major possible complications of the condition are chronic loss of taste ( ageusia ), chronic facial  spasm , facial pain, and corneal infections. Another complication can occur in case of incomplete or erroneous regeneration of the damaged facial nerve. The nerve can be thought of as a bundle of smaller individual nerve connections that branch out to their proper destinations. During regrowth, nerves are generally able to track the original path to the right destination—but some nerves may sidetrack leading to a condition known as  synkinesis . For instance, the regrowth of nerves controlling muscles attached to the eye may sidetrack and also regrow connections reaching the muscles of the mouth. In this way, the movement of one also affects the other. For example, when the person closes the eye, the corner of the mouth lifts involuntarily.


Around 9% of people have some sort of ongoing problems after Bell's palsy, typically the synkinesis already discussed, or spasm, contracture,  tinnitus , or hearing loss during facial movement or crocodile-tear syndrome. [ 50 ]  This is also called gustatolacrimal reflex or  Bogorad's syndrome  and results in shedding tears while eating. This is thought to be due to  faulty regeneration  of the facial nerve, a branch of which controls the lacrimal and salivary glands. Gustatorial sweating can also occur.


The number of new cases of Bell's palsy ranges from about one to four cases per 10,000 population per year. [ 51 ]  The rate increases with age. [ 2 ] [ 51 ]  Bell's palsy affects about 40,000 people in the United States every year. It affects approximately 1 person in 65 during a lifetime.


A range of annual incidence rates have been reported in the literature: 15, [ 21 ]  24, [ 52 ]  and 25–53 [ 11 ]  (all rates per 100,000 population per year). Bell's palsy is not a  reportable disease , and there are no established registries for people with this diagnosis, [ 53 ]  which complicates precise estimation.


About 40,000 people are affected by Bell's Palsy in the United States every year. It can affect anyone of any gender and age, but its incidence seems to be highest in those in the 15- to 45-year-old age group. [ 1 ]


The Persian physician  Muhammad ibn Zakariya al-Razi  (865–925) detailed the first known description of peripheral and central facial palsy. [ 54 ] [ 55 ]


Cornelis Stalpart van der Wiel (1620–1702) in 1683 gave an account of Bell's palsy and credited the Persian physician  Ibn Sina  (980–1037) for describing this condition before him.  James Douglas  (1675–1742) and  Nicolaus Anton Friedreich  [ de ]  (1761–1836) also described it.


Scottish neurophysiologist Sir  Charles Bell  read his paper to the  Royal Society of London  on July 12, 1821, describing the role of the facial nerve. He became the first to detail the neuroanatomical basis of facial paralysis. Since then, idiopathic peripheral facial paralysis has been referred to as Bell's palsy, named after him. [ 56 ]


A notable person with Bell's palsy is former  Prime Minister of Canada   Jean Chrétien . [ 57 ]  During the  1993 Canadian federal election , Chrétien's first as leader of the  Liberal Party of Canada , the opposition  Progressive Conservative Party of Canada  ran  an attack ad  in which voice actors criticized him over images that seemed to highlight his abnormal facial expressions. The ad was interpreted as an attack on Chrétien's physical appearance and garnered widespread anger among the public, while Chrétien used the ad to make himself more sympathetic to voters. The ad had the adverse effect of increasing Chrétien's lead in the polls and the subsequent backlash clinched the election for the Liberals, which the party  won in a landslide .


On April 25, 2024,  Joel Hans Embiid  of the Philadelphia 76ers scored 50 points in Game 3 of the 76ers' first-round playoff series versus the New York Knicks while suffering from a mild case of Bell's Palsy. [ citation needed ]


A  bone-anchored hearing aid  ( BAHA ) [ 2 ]  is a type of  hearing aid  based on  bone conduction . It is primarily suited for people who have  conductive hearing losses ,  unilateral hearing loss , single-sided deafness and people with mixed hearing losses who cannot otherwise wear 'in the ear' or 'behind the ear' hearing aids. They are more expensive than conventional hearing aids, and their placement involves invasive surgery which carries a risk of complications, [ 1 ]  although when complications do occur, they are usually minor. [ 3 ]


Two of the causes of  hearing loss  are lack of function in the  inner ear  ( cochlea ) and when the sound has problems in reaching the nerve cells of the inner ear.  Examples of the first include age-related hearing loss and hearing loss due to noise exposure. A patient born without external  ear canals  is an example of the latter for which a conventional hearing aid with a mould in the ear canal opening would not be effective. Some with this condition have normal inner ear function, as the external ear canal and the inner ear are developed at different stages during pregnancy. With normal inner anatomy, sound conducted by the skull bone improves hearing.


A vibrator with a steel spring over the head or in heavy frames of eyeglasses pressed towards the bone behind the ear has been used to bring sound to the inner ear.  This has, however, several disadvantages, such as discomfort and pain due to the pressure needed. [ 4 ]  The sound quality is also impaired as much of the sound energy is lost in the soft tissue over the skull bone, [ 5 ]  particularly for the higher sound frequencies important for speech understanding in noise.


Bone-anchored hearing aids use a surgically implanted  abutment  to transmit sound by direct  conduction through bone  to the inner ear, bypassing the external auditory canal and middle ear. A titanium prosthesis is surgically embedded into the skull with a small abutment exposed outside the skin. A sound processor sits on this abutment and transmits sound vibrations to the titanium implant. The implant vibrates the skull and inner ear, which stimulate the nerve fibers of the inner ear, allowing hearing. [ 6 ]


The surgery is often performed under local anesthesia and as an outpatient procedure. An important piece of information for patients is that if they for whatever reason are not satisfied with the BAHA solution, removing the implant is easy. No other ear surgical procedure is reversible like this. [ citation needed ]


By bypassing the outer or middle ear, BAHA can increase hearing in noisy situations and help localise sounds. In addition to improved speech understanding, it results in a natural sound with less distortion and feedback compared with conventional hearing aids. [ 7 ] [ 8 ] [ 9 ] [ 10 ] [ 11 ]  The ear canal is left open for comfort, and helps to reduce any problems caused by chronic ear infections or allergies. In patients with single-sided sensorineural deafness, BAHA sends the sound by the skull bone from the deaf side to the inner ear of the hearing side. This transfer of sound gives a 360° sound awareness.


BAHAs may facilitate normal speech development. [ 12 ]


This fairly common condition is often associated with continuous or intermittent drainage from the ear canal. These patients may also have a hearing loss and need amplification. A conventional air conduction aid with a mold placed in the ear canal opening may not be appropriate due to the drainage, and may even provoke drainage. If the hearing loss is significant an air conduction aid may have difficulty overcoming the dysfunction of the eardrum and middle ear bones. Bone conduction hearing device bypassing the middle ear may be a more appropriate treatment for these patients. Good transmission of sound in the bone, with reduced attenuation and distortion may be possible.


A person with  unilateral hearing loss  may have functional difficulty hearing even when the other ear is normal, particularly in demanding situations such as noisy environments and when several people are speaking the same time. A complication in single-sided deafness is hearing impairment in the hearing ear. Conventional ear surgery involves a risk of hearing loss due to the surgical procedure. Ear surgeons may be reluctant to perform surgery on an only hearing ear. [ 13 ]  The BAHA surgery avoids this risk and may be an appropriate treatment. An extended trial of a BAHA system with a headband prior to surgery led to more realistic expectations. In the trial, 50% of the candidates wished to proceed to surgery. [ 14 ]


Irritation in the  external ear canal  due to inflammation or eczema may be a condition for which a conventional air conduction aid is not an appropriate treatment. Direct bone conduction may be an option.


Patients with malformations are not always suitable for reconstructive surgery.  Treacher Collins syndrome  patients may have significant malformations with  ossicular  defects and an abnormal route of the facial nerve. These structures, as well as the inner ear, could be in danger at surgery.


Patients with  Down syndrome  may have a narrow ear canal and middle ear malformation leading to impaired hearing. Some part of the cognitive delay seen in these children may be partly due to their poor hearing.


The surgery can only take place once the skull is at least 2.5 mm thick. [ 15 ] [ 16 ] [ needs update ]  Children with certain syndromes may have a slighter build, thinner bone, or unusual anatomy. Other children may have a thicker skull at a younger age, so it is difficult to give a specific age for surgery.


In the U.S., the  Food and Drug Administration  only approves BAHA implantation of children aged five years or older.


For infants and young children prior to surgery, the sound processor can be worn on a head band or soft band which the infant wears to hold it against the skull.


Complications of BAHA systems can be considered as either related to the bone (hard tissue) or the  soft tissue . [ 3 ]


Soft-tissue complications are much more common, and most are managed with topical treatments. Children are more likely to develop both kinds of complications than adults. Sometimes, a second surgical procedure is required. Complications are less likely with good wound hygiene. [ 3 ]  Other drawbacks of BAHA include accidental or spontaneous loss of the bone implant, and patient refusal for treatment due to stigma. [ 17 ]


The bone behind the ear is exposed through a U-shaped or straight incision or with the help of a specially designed BAHA  dermatome . A hole, 3 or 4 mm deep depending on the thickness of the bone, is drilled. The hole is widened and the implant with the mounted coupling is inserted under generous cooling to minimize surgical trauma to the bone. In a single stage procedure, the fixture and abutment are placed simultaneously. For children or patients who may damage the abutment prior to  osseointegration  of the fixture, a two stage procedure may be performed in which the fixture is placed first, and after  osseointegration  roughly 6 months later, the abutment is attached. In children, a sleeper implant may be placed to serve as a backup in case the main implant is damaged.


Some surgeons perform a reduction of the subcutaneous  soft tissue . The rationale for this is to reduce the mobility between implant and skin to avoid inflammation at the penetration site. This reduction of the soft tissue has been questioned and some surgeons do not perform any or a minimum of it. The rationale for this is that any surgery will result in some scar tissue that could be the focus of infection. The infections seen early during the development of the surgical procedure could perhaps be explained by the lack of seal between implant and abutment allowing bacteria to enter the space. A new helium tight seal may be advantageous and prevent  biofilm  formation. This will also allow the surgeon to use longer abutments should a need exist. Three to six weeks later or even earlier, the  audiologist  will fit and adjust the hearing processor according to the patient's  hearing level . The fitting will be made using a special program in a computer.


The original surgical procedure has been described in detail by Tjellström et al. 2001. [ 15 ]


An area where skin is penetrated requires care and cleaning because of the risk of inflammation around the abutment. Daily cleaning is required. [ 18 ]


Hearing is of importance for a normal speech development. [ 19 ]  The skull bone in children is often very thin and softer than in the adult. Surgery is thus often delayed until the age of four to five years. In the meantime, the child with bilateral atresia can be fitted with a band around the head with a coupling for a BAHA. This may be done at the age of one month. Infants at this age may tolerate this well. [ 16 ]  As described above, for children who may be at risk of damaging the abutment prior to  osseointegration  of the fixture, a two stage procedure may be performed in which the fixture is placed first, and after  osseointegration  roughly 6 months later, the abutment is attached. In children, a sleeper implant may be placed to serve as a backup in case the main implant is damaged.


Patients with chronic ear infection where the drum and/or the small bones in the middle ear are damaged often have hearing loss, but difficulties in using a hearing aid fitted in the ear canal. Direct bone conduction through a vibrator attached to a skin-penetrating implant addresses these disadvantages.


In 1977, the first three patients were implanted with a bone-conduction hearing solution by Anders Tjellström at the Ear, Nose, and Throat Department at  Sahlgrenska University Hospital  in Gothenburg, Sweden. A 4-mm-long titanium screw with a diameter of 3.75 mm was inserted in the bone behind the ear, and a bone conduction hearing aid was attached.


The term osseointegration was coined by Professor Brånemark. During animal studies, he found the bone tissue attached to the titanium implant without any soft tissue in between. He also showed an such an implant could take a heavy load. His definition of osseointegration was "direct contact between living bone and an implant that can take a load".


The first clinical application of titanium was in oral surgery, where implants were used for retention of dentures. Brånemark sought an acoustic way to evaluate osseointegration. A patient with implants in the jaws was fitted with a bone vibrator on one of his implants. When tested, the patient experienced very loud sound even at low stimulation levels, indicating sound could propagate very well in the bone. It has later been shown by Håkansson that the sound transmission in bone is linear, indicating low distortion of the sound.


The implant in the bone is made of titanium and will osseointegrate. The hearing instrument is impedance-matched.  Osseointegration  has been defined as the direct contact between living bone and an implant that can take a load, with no soft tissue at the interface.


There are several models of bone-anchored hearing aids available. Most common are the BAHA from Australian company  Cochlear , and the Ponto from Danish manufacturers  Oticon Medical . [ 20 ]  There are also other types of  bone conduction hearing aids , such as implants and non-surgical devices.


In the US, the cost of the Baha device is about $4,000. In the Netherlands, the cost of the device is around €3000 (in 2008). The cost of the titanium implant, surgery, and aftercare from surgeon and audiologist must also be considered.


The  buccal  branches of the  facial nerve  (infraorbital branches), are of larger size than the rest of the branches, pass horizontally forward to be distributed below the  orbit  and around the  mouth .


The  superficial branches  run beneath the  skin  and above the superficial muscles of the face, which they supply: some are distributed to the  procerus , joining at the medial angle of the orbit with the  infratrochlear  and  nasociliary  branches of the  ophthalmic .


The  deep branches  pass beneath the  zygomaticus  and the  quadratus labii superioris , supplying them and forming an  infraorbital plexus  with the infraorbital branch of the  maxillary nerve . These branches also supply the small muscles of the  nose .


The  lower deep branches  supply the  buccinator  and  orbicularis oris , and join with filaments of the  buccinator branch  of the  mandibular nerve .


The facial nerve innervates the muscles of facial expression. The buccal branch supplies these muscles


• Puff up cheeks (buccinator)


i. Tap with finger over each cheek to detect ease of air expulsion on the affected side


• Smile and show teeth (orbicularis oris)


This article incorporates text in the  public domain  from  page 905  of the 20th edition of   Gray's Anatomy   (1918)


The  buccal space  (also termed the  buccinator space ) is a  fascial space of the head and neck  (sometimes also termed  fascial  tissue spaces or tissue spaces). It is a  potential space  in the  cheek , and is paired on each side. The buccal space is superficial to the  buccinator muscle  and deep to the  platysma muscle  and the skin. The buccal space is part of the  subcutaneous  space, which is continuous from head to toe. [ 1 ]


The boundaries of each buccal space are:


In health, the space contains:


A  hematoma  may create the buccal space, e.g. due to  hemorrhage  following  wisdom teeth  surgery. Buccal space abscesses typically cause a facial swelling over the cheek that may extend from the zygomatic arch above to the inferior border of the mandible below, and from the anterior border the masseter muscle posteriorly to the angle of the mouth anteriorly. [ 1 ]  Unless another space is also involved, the tissues around the eye are not swollen. It is usually treated by surgical  incision and drainage , and the incision is located inside the mouth to avoid a scar on the face. [ 2 ]  The incision are placed below the  parotid papilla  to avoid damage to the duct, and forceps are used to divide buccinator and insert a surgical drain into the buccal space. The drain is kept in place for a variable period of time following the procedure.


Long standing buccal abscesses tend to spontaneously drain via a  cutaneous sinus  at the inferior of the space, near the inferior border of the mandible and the angle of the mouth. [ 1 ]  An untreated cutaneous sinus can cause disfiguring soft tissue  fibrosis , and the tract can become  epithelial  lined. [ 3 ]


Sometimes the buccal space is reported to be the most commonly involved fascial space by  dental abscesses , [ 2 ]  although other sources report it is the submandibular space. [ 1 ]  Infections originating in either maxillary or mandibular teeth can spread into the buccal space, usually maxillary molars (most commonly) and premolars or mandibular premolars. [ 1 ]  Odontogenic infections which erode through the buccal cortical plate of the mandible or maxilla will either spread into the buccal vestibule (sulcus) and drain intra-orally, or into the buccal space, depending upon the level of the perforation in relation to the attachment of buccinator to the maxilla above and the mandible below (see diagrams). Frequently infection spreads in both directions as the buccinator is only a partial barrier. [ 3 ]  Infections associated with mandibular teeth with apices at a level inferior to the attachment, and maxillary teeth with apices at a level superior to the attachment are more likely to drain into the buccal space.


The  canine space  (also termed the  infra-orbital space ) [ 1 ]  is a  fascial space of the head and neck  (sometimes also termed  fascial  spaces or tissue spaces). It is a thin  potential space  on the face, and is paired on either side. It is located between the  levator anguli oris muscle  inferiorly and the  levator labii superioris muscle  superiorly. [ 1 ] [ 2 ]  The term is derived from the fact that the space is in the region of the  canine fossa , and that infections originating from the  maxillary canine tooth  may spread to involve the space.  Infra-orbital  is derived from  infra-  meaning below and  orbit  which refers to the eye socket.


The boundaries of the canine space are: [ 2 ]


The canine space communicates with the buccal space posteriorly. [ 2 ]


The contents of the canine space are: [ 2 ]


Canine space infections may occur by spread of infection from the buccal space. [ 2 ]   Signs and symptoms of a canine space abscess might include swelling that obliterates the  nasolabial fold . If left untreated, infections of this space will eventually spontaneously drain via the  medial or lateral canthus  of the eye, as this is the path of least resistance. [ 2 ]  Treatment is usually by surgical  incision and drainage , and the incision is placed inside the mouth to avoid a facial scar.


Rarely, when infections of the canine space erode into the  infra-orbital vein  or the  inferior ophthalmic vein  (via the  sinuses ), there can be spread via the common ophthalmic vein through the  superior orbital fissure  and into the  cavernous sinus . This can result in septic  cavernous sinus thrombosis , which is a rare, but life-threatening condition. [ 2 ]


Odontogenic infections  may spread to involve the canine space. The most likely causative tooth is the maxillary canine or maxillary first premolar. [ 1 ]  This occurs when pus (e.g. from a  periapical abscess ), perforates the buccal cortical plate of the maxilla above the level of attachment of the levator anguli oris muscle. This is more likely if the tooth root is long (the maxillary canine has the longest root of all the teeth), and its apex lies at a level above the muscle attachment. [ 1 ]


The  carotid canal  is a passage in the  petrous part  of the  temporal bone  of the  skull  through which the  internal carotid artery  and its  internal carotid (nervous) plexus  pass from the neck into (the  middle cranial fossa  of) the  cranial cavity .


Observing the trajectory of the canal from exterior to interior, the canal is initially directed vertically before curving anteromedially to reach its internal opening. [ 1 ]


The carotid canal has two openings, namely internal and external openings. [ 2 ] [ non-primary source needed ]


It is divided in three parts, namely, ascending petrous, transverse petrous, and ascending cavernous parts. [ 2 ] [ non-primary source needed ]


The carotid canal opens into the  middle cranial fossa , at the  petrous part of the temporal bone . Anteriorly, it is limited by posterior margin of the  greater wing of sphenoid bone . Posteromedially, it is limited by  basilar part of occipital bone . [ 2 ] [ non-primary source needed ]


The external opening of carotid canal (Latin: " apertura externa canalis carotici ") is located upon the inferior aspect of the  petrous part of the temporal bone . It is situated anterior to the  jugular fossa  (the two being separated by a ridge upon which the  tympanic canaliculus  opens inferiorly), [ 3 ]  and posterolateral to the foramen lacerum. [ 2 ] [ non-primary source needed ]


The internal opening of carotid canal (Latin: " apertura interna canalis carotici ") opens into the  middle cranial fossa  at the  apex of petrous part of temporal bone . [ 4 ]  It is situated lateral to  foramen lacerum . [ 2 ] [ non-primary source needed ]


Both internal and external openings of the carotid canal lie anterior to the  jugular foramen  (which opens into the  posterior cranial fossa ). [ 2 ] [ 5 ]


The carotid canal is separated from  middle ear  and  inner ear  by a thin plate of bone. [ 6 ]


The canal transmits  internal carotid artery  together with its associated  nervous plexus  and  venous plexus . [ 1 ] [ 2 ] [ non-primary source needed ]


Any skull fractures that damage the carotid canal can put the  internal carotid artery  at risk. [ 7 ]   Angiography  can be used to ensure that there is no damage, and to aid in treatment if there is. [ 7 ]


The carotid canal starts on the inferior surface of the  temporal bone  of the  skull  at the external opening of the carotid canal (also referred to as the carotid foramen). The canal ascends at first superiorly, and then, making a bend, runs anteromedially. Its internal opening is near the  foramen lacerum , above which the internal carotid artery passes on its way anteriorly to the  cavernous sinus . [ 8 ]


The carotid canal allows the  internal carotid artery  to pass into the  cranium , [ 8 ] [ 9 ]  as well as the  carotid plexus  traveling on the artery. [ 8 ]


The carotid plexus contains  sympathetics  to the head from the  superior cervical ganglion . [ 8 ]  They have several motor functions: raise the  eyelid  ( superior tarsal muscle ), dilate  pupil  (pupillary dilator muscle), innervate  sweat glands  of face and  scalp  and constricts  blood vessels  in the head.


This article incorporates text in the  public domain  from  page 143  of the 20th edition of   Gray's Anatomy   (1918)


Catarrh  ( / k ə ˈ t ɑːr /   kə- TAR ) is an inflammation of  mucous membranes  in one of the  airways  or cavities of the body, [ 1 ] [ 2 ]  usually with reference to the  throat  and  paranasal sinuses . It can result in a thick exudate of  mucus  and  white blood cells  caused by the swelling of the  mucous membranes  in the  head  in response to an infection. It is a  symptom  usually associated with the  common cold ,  pharyngitis , and chesty  coughs , but it can also be found in patients with  adenoiditis ,  otitis media ,  sinusitis  or  tonsillitis .  The  phlegm  produced by catarrh may either discharge or cause a blockage that may become  chronic .


The word "catarrh" was widely used in  medicine  since before the era of medical science, which explains why it has various  senses  and in older texts may be synonymous with, or vaguely indistinguishable from, common cold, nasopharyngitis, pharyngitis,  rhinitis , or sinusitis. The word is no longer as widely used in American medical practice, mostly because more precise words are available for any particular disease. Indeed, to the extent that it is still used, it is no longer viewed  nosologically  as a  disease  entity but instead as a  symptom , a  sign , or a  syndrome  of both. The term "catarrh" is found in medical sources from the United Kingdom. [ 3 ]  The word has also been common in the  folk medicine  of  Appalachia , where medicinal plants have been used to treat the inflammation and drainage associated with the condition. [ 4 ]