1. Sequelae1.1. TympanosclerosisTympanosclerosis is thought to be a complication of otitis media in which hyalin and calcium deposits accumulate within the tympanic membrane and the submucosa middle ear. It often occurs as a result of inflammation or trauma and is therefore commonly seen after recurrent episodes of AOM and OME and after ventilation tube insertion. In most patients, these plaques are clinically insignificant and cause little or no hearing impairment.Tympanosclerotic plaques within the tympanic membrane appear as a semicircular crescent or horseshoe-shaped white plaque within the tympanic membrane.If the process is limited to the tympanic membrane (ie, myringosclerosis), then hearing is usually unaffected. However, if the middle ear is involved, then the ossicular chain can become immobilized, resulting in a conductive hearing loss. Attempts at surgical correction by Tympanoplasty and ossicular reconstruction can be performed in ears with tympanosclerosis1.2. AtelectasisAtelectasis is thought to result mainly from long-standing eustachian tube dysfunction. One of the main functions of the eustachian tube is ventilation. Opening of the eustachian tube allows exchanging of gases and equalization between the environment and middle ear. If the atelectasis develops, the tympanic membrane becomes retracted. Tympanic membrane comprises two parts, thepars tensa, which is the main part of the eardrum, and thepars flaccida, which is a smaller part of the eardrum located above the pars tensa. Either or both of these parts may become retracted. The retracted segment of eardrum is often known as a retraction pocket. In atelectatic ears, the middle ear space is partially or completely obliterated, but the Retraction of the tympanic membrane may lead to erosion of the long process of the incus and the stapes structure.The management of atelectasis is controversial. If eustachian tube function is still considered to be present, the insertion of ventilation tubes could potentially reverse the changes in the tympanic membrane by normalizing the pressure in the middle ear space. If no improvement is observed and the location of the retraction raises the concern of subsequent cholesteatoma formation, then excision and grafting of the affected portion of the tympanic membrane are recommended. The recurrence of tympanic membrane retraction after this procedure is not uncommon; therefore, prolonged observation is advised.

2. Intratemporal complications2.1. MastoiditisMastoiditis is an inflammation or infection of the mastoid bone, which is a portion of the temporal bone. Inflammation in the mastoid itself is quite rare. It is almost always a result of inflammation or infection in the middle ear space. Since there is a direct communication between the mastoid and the middle ear space, any inflammatory process occurring in the middle ear space is directly transmitted into the mastoid. Infection can spread into the lateral sinus, causing an infected clot to form within it (lateral sinus thrombosis). The infection can also extend directly inferiorly, presenting as an abscess deep to a muscle that is attached to the mastoid (sternocleidomastoid muscle). These abscesses are termed Bezolds abscesses. Acute mastoiditis was also associated with high incidence of meningitis, which is an extension of the bacterial infection from the mastoid into the lining surrounding the brain. Untreated meningitis has a very high mortality rate; and those individuals who do survive are often left with significant neurologic dysfunction. Lastly, acute mastoid infections can also create a cerebellar abscess. Since the cerebellum is involved in fine motor coordination and control of the central part of the body, especially during walking, these individuals often would lose coordination or have significant difficulties walking.Mastoid infections can assume two different patterns. Chronic mastoiditis is a disease process that is occurring more than three months and acute mastoiditis is occurring less than three weeks.a. Acute mastoiditisAcute mastoiditisis almost always a consequence of an acute ear infection that is not treated or is incompletely treated. In acute mastoiditis there is a direct bacterial infection in the mastoid. Often the skin overlying the mastoid directly behind the outer ear becomes inflamed and as a consequence is red and swollen. If the infection continues for more than 10 to 14 days, the small, bony walls that form the air-filled honeycomb begin to be destroyed. This bone destruction is termed coalescent mastoiditis. If the infection continues, then there can be direct pus accumulation under the skin behind the ear, with a resultant abscess. b. Chronic mastoiditisChronic mastoiditis occurs whenever there is a chronic inflammatory process that affects the mastoid. This is usually termed chronic otitis media, where there is a perforation in the eardrum, with intermittent infected material draining through the hole in the eardrum. In chronic mastoiditis there is no bone destruction as is seen in coalescent mastoiditis. Instead the lining inside the mastoid often becomes thickened and inflamed.

2.2. PetrositisThis rare complication of OM occurs in both acute and chronic forms. In the acute form, there is extension of acute mastoiditis into a pneumatized petrous apex. The chronic form of petrositis usually occurs as a result of mucosal or cholesteatomatous CSOM; pneumatization of the petrous apex is not a prerequisite as the infection spreads by thrombophlebitis, hematogenous dissemination, or direct extension. Because of the close relationship of the ophthalmic division of the trigeminal nerve and the abducens nerve to the petrous apex, the classic features of petrositis are otorrhea associated with retroorbital pain and lateral rectus palsy (Gradenigo syndrome). Because of the high incidence of an intracranial extension of infection from petrositis, a combination of antibiotics and surgical drainage of the petrous apex is the management of choice.

2.3. Facial Nerve ParalysisFacial nerve palsy can occur as a result of either acute or chronic OM. There are two mechanisms by which OM can result in facial nerve paralysis: 1. as a result of the locally produced bacterial toxins2. from direct pressure applied to the nerve by cholesteatoma or granulation tissue. An episode of AOM can lead to inflammatory edema of the nerve and a subsequent paresis. This situation should be managed by myringotomy with aspiration of pus from the middle ear along with antibiotic therapy, which will mostly result in the rapid resolution of paralysis. Further surgical exploration of the facial nerve is not indicated unless the paralysis fails to resolve. If facial nerve paralysis occurs as a result CSOM, urgent surgical exploration, with decompression of the facial nerve, is indicated.Facial paralysis associated with chronic otitis media suggests a high probability of cholesteatoma, and surgical intervention is appropriate. The mechanism of facial paralysis associated with cholesteatoma could be compression or inflammation. Djeric studied autopsy specimens from patients who had chronic otitis media but no antemortem evidence of facial paralysis. Two of 20 facial nerves had focal areas of demyelination, suggesting that adjacent inflammation may be more important than pressure.2.4. LabyrinthitisLabyrinthinitis is an uncommon complication of acute otitis media and mastoiditis. there are serous labyrinthitis, suppurative labyrinthitis, and labyrinthine fistula.Suppurative labyrinthitis results from bacterial invasion of the inner ear from contiguous areas of the temporal bone or meninges. Serous labyrinthitisis an irritation of the labyrinth caused by otitic or meningitic infection without bacterial invasion of the inner ear. Fistulization of the labyrinth occurs most commonly as a result of erosion of the bony covering of the lateral semicircular canal by cholesteatomaa. Serous labyrinthitisSerous (or toxic) labyrinthitis results from irritation of the labyrinth by the by-products of infection and inflammation. Toxins are thought toenter the inner ear via the oval and round windows or through a fistula in the bony labyrinth. Serous labyrinthitis may be a complication of acute orchronic otitis media; meningitis, in which case the condition may be masked by the more severe meningeal symptoms.The patient presents with vertigo, which may be transient and recurrent over months or years; sensorineural hearing loss may fluctuate and is less severe than that seen in purulent labyrinthitis. It may not be distinguishable from purulent labyrinthitis, except for retention of some audiovestibular function. The signs and symptoms are less dramatic than those of purulent labyrinthitis, and the pathologic consequences in the inner ear are less destructive. Management is directed toward the infectious source. If the labyrinthitis results from acute otitis media, myringotomy and antibiotic therapy are sufficient. If coalescent mastoiditis or chronic otitis media with possible cholesteatoma is present, labyrinthine fistula should be suspected and mastoidectomy should be performed.b. Suppurative labyrinthitisSuppurative labyrinthitis can develop as a complication of acute and chronic otitis media from migration of the bacteria through the preformed pathways of the oval window, round window, and preexisting fractures of the temporal bone and from direct invasion by erosion of the labyrinthine bone by cholesteatoma. Bacteria may traverse the cochlear aqueduct in bacterial meningitis. Bacterial invasion of the inner ear produces irreversible damage to the neuroepithelium, atrophy of the stria vascularis, collapse of Reissners membrane, and endolymphatic hydrops. If the patient survives without surgery, healing occurs with fibrosis and obliterative osteitis of the labyrinth and cochlea. No audiovestibular function isretained.The symptoms are most severe during the acute bacterial invasion of the labyrinth. The vertigo and nystagmus result from sudden loss of the healthytonic neural impulses from the involved labyrinth, without any change in the input from the healthy side. Recovery from a unilateral peripheralvestibular lesion is attributed to the brains ability to compensate for the sensory mismatch by adapting to the asymmetric sensory input. This occursgradually as the cerebellum and brainstem integrate the conflicting information and adapt over time to a stable lesion. The severity of the symptomsgradually lessens over the next few days, but central compensation occurs over several weeks with complete resolution of nystagmus and vertigo.c. Labyrinthine fistulaFistulization of the labyrinth occurs most commonly as a result of erosion of the bony covering of the lateral semicircular canal by cholesteatoma. The patient will have active or inactive chronic otitis media for many years. The mainstay of the diagnosis, the fistula test, is performed by application of positive and negative pressure to the middle ear with a pneumatic otoscope. A positive fistula test produces nystagmus with the fast component toward the tested ear with application of positive pressure, and away from the tested ear with application of negative pressure. The nystagmus results from motion of the soft tissue over the fistula; positive pressure causes ampullofugal movement of endolymph (away from the ampulla), and negative pressure causes ampullopetal movement of the endolymph (toward the ampulla. Management is mastoidectomy with eradication of cholesteatoma

3. Intracranial ComplicationsThe most common early symptoms of intracranial extension of infection are persistent headache and fever. Other features include lethargy, irritability, and neck stiffness. A decreasing level of consciousness and seizures are late signs associated with a poor prognosis. The incidence of intracranial complications has been considerably reduced since the introduction of antibiotics. Despite this fact, once an intracranial complication develops, it carries a significant risk to life. Therefore, early recognition and treatment are vital to improve the prognosis. It is not uncommon for more than one intracranial complication to occur simultaneously. 3.1. MeningitisAcute otitis media is the most common cause of bacterial meningitis. It can occur as a result of hematogenous spread, of direct extension from the middle ear through a bony dehiscence, or through the cochlear aqueduct via the inner ear. The most common organisms responsible for otic meningitis are S pneumoniae and H influenzae type B. The classic presentation is with headaches,photophobia, neck stiffness, and fluctuating levels of consciousness. The evaluation should include an MRI of the brain to rule out other intracranial complications as well as a lumbar puncture. If meningitis is secondary to AOM, then a myringotomy should be performed once antibiotic therapy has been initiated. In the case of CSOM resulting in meningitis, the patient should be fully stabilized before considering surgical management of the chronic ear disease.

3.2. Intracranial Abscess Brain, subdural, and extradural abscesses can all arise as a complication of middle ear infections (commonly associated with chronic disease). Intracranial abscesses are usually caused by multiple aerobic and anaerobic bacteria. Commonly cultured organisms include streptococci, S aureus, S pneumoniae, H influenzae, P aeruginosa, Bacteroides fragilis, and Proteus species.a. Brain abscessMost otogenic brain abscesses develop within the temporal lobe or cerebellum. The progression of symptoms from a brain abscess can be gradual, occurring over days or even weeks. In addition to the generalized symptoms, focal neurologic signs can develop depending on the anatomic location of the abscess within the brain. As the abscess enlarges, features typical of raised intracranial pressure develop. Once a brain abscess has been diagnosed, urgent neurosurgical intervention is indicated to drain the abscess. Surgery for the associated ear disease is less urgent and should be planned when the patients condition is more stable.b. Subdural abscessA subdural abscess forms between the dura mater and the arachnoid mater. Symptoms and signs tend to progress much more rapidly than those seen with a brain abscess. Drainage of the abscess is the mainstay of treatment.c. Extradural abscessExtradural abscesses are typically formed in the middle fossa between the dura mater and the thin bony plate of the tegmen. They can also occur in the posterior fossa, where they are commonly associated with lateral sinus thrombosis. The clinical features are often nonspecific and may fluctuate if a dehiscence in the tegmen is present, allowing the abscess to partially drain into the mastoid cavity. As with other intracranial complications, headache and fever are the most common features. Because of its location, an extradural abscess can usually be drained through a mastoidectomy approach while treating the underlying middle ear disease.

3.3. Lateral Sinus ThrombosisBecause of its close proximity to the mastoid air cells, the lateral, or sigmoid, sinus is prone to involvement in middle ear infections, which may lead to thrombosis. Once an infected thrombus has formed in the lateral sinus, it may propagate both distally and proximally and may give rise to infected emboli. Typically, there are intermittent episodes of high pyrexia associated with rigors. If the thrombus propagates into the neck, there will be neck tenderness along the internal jugular vein and neck stiffness or torticollis. Proximal extension of the thrombus to the sagittal sinus can result in symptoms and signs of raised intracranial pressure. MRI most reliably makes the diagnosis of lateral sinus thrombosis. The management of lateral sinus thrombosis requires broad-spectrum antibiotics and surgery. A complete mastoidectomy should be performed, with exposure of the lateral sinus. Once the diagnosis has been confirmed by needle aspiration, the sinus is opened and the infected thrombus evacuated. If symptoms persist after this procedure, consideration should be given to ligation of the ipsilateral internal jugular vein, once the possibility of other intracranial complications has been excluded.

3.4. Otic HydrocephalusOtic hydrocephalus is a rare complication in which raised intracranial pressure develops as a result of a middle ear infection, but its pathophysiology is poorly understood. The usual features are headache, vomiting, disturbed mental state, visual disturbance, and papilledema associated with a middle ear infection. Imaging of the brain reveals the ventricular size to be normal, but lumbar puncture confirms raised cerebrospinal fluid pressure. Management is aimed at resolving the middle ear infection while normalizing intracranial pressure with the use of steroids, diuretics (eg, mannitol), and, if required, intermittent drainage of cerebrospinal fluid.

Facial Nerve

Motor Component of Facial NerveThe nucleus of the motor component of the facial nerve is located in the ventrolateral portion of the pontine tegmentum. The neurons of this motor nucleus are analogous to the anterior horn cells of the spinal cord, but are embryologically derived from the second branchial arch. The root fibers of this nucleus take a complicated course.Within the brainstem, they wind around the abducens nucleus (forming the so-called internal genu of the facial nerve), thereby creating a small bump on the floor of the fourth ventricle (facial colliculus). They then form a compact bundle, which travels ventrolaterally to the caudal end of the pons and then exits the brainstem, crosses the subarachnoid space in the cerebellopontine angle, and enters the internal acoustic meatus together with the nervus intermedius and the eighth cranial nerve (the vestibulocochlear nerve).Within the meatus, the facial nerve and nervus intermedius separate from the eighth nerve and travel laterally in the facial canal toward the geniculate ganglion. At the level of the ganglion, th e facial canal takes a sharp downward turn (external genu of the facial nerve). At the lower end of the canal, the facial nerve exits the skull through the stylomastoid foramen. Its individual motor fibers are then distributed to all regions of the face (some of them first traveling through the parotid gland). They innervate all of the muscles of facial expression that are derived fromthe second branchial arch, i.e., the orbicularis oris and oculi, buccinator, occipitalis, and frontalis muscles and the smaller muscles in these areas, as well as the stapedius, platysma, stylohyoid muscle, and posterior belly of the digastric muscle.

Motor lesions involving the distribution of the facial nerve.The muscles of the forehead derive their supranuclear innervation from both cerebral hemispheres, but the remaining muscles of facial expression are innervated only unilaterally, i.e., by the contralateral precentral cortex. If the descending supranuclear pathways are interrupted on one side only, e. g., by a cerebral infarct, the resulting facial palsy spares the forehead muscles: the patient can still raise his or her eyebrows and close the eyes forcefully. This type of facial palsy is called central facial palsy.In a nuclear or peripheral lesion, however, all of the muscles of facial expression on the side of the lesion are weak. One can thus distinguish central from nuclear or peripheral facial palsy by their different clinical appearances. The motor nuclei of the facial nerve are innervated not only by the facial cortex but also by the diencephalon, which plays a major role in emotion-related facial expressions. Further input is derived from the basal ganglia; in basal ganglia disorders (e. g., Parkinson disease), hypomimia or amimia can be seen. There are also various dyskinetic syndromes affecting the muscles of facial expression with different types of abnormal movement: hemifacial spasm, facial dyskinesias, and blepharospasm, among others. The site of the causative lesion in these syndromes remains unknown.

Differetial Diagnosis of Facial Paralysis

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