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    Meniere’s disease

    Meniere’s disease is a disease of the inner ear that causes episodes of vertigo, noises in the ear (tinnitus), a feeling of fullness or pressure in the ear and fluctuating hearing loss. It is named after a french physician who first described it in 1861.

    A typical attack is preceded by fullness in one or both ears, hearing fluctuation or tinnitus (ringing sounds in the ears). The attack involves severe vertigo (spinning sensation), nausea, vomiting, sweating in severe cases. An attack usually lasts from minutes to a few hours. The episodes may occur as several attacks in a short time or in other cases, months or even years may pass between episodes. Between the acute attacks, most people are free of symptoms or experience only mild imbalance and tinnitus. In 75 percent of cases, the disease is confined to one ear, in the rest, both ears may be involved. In most cases a progressive hearing loss occurs in the affected ear. Though acute attacks are incapacitating, the disease itself is not fatal.

    Mechanism of symptoms of Meniere’s disease

    The inner ear serves the body’s functions of hearing and balance. It is a system of hollow coiled tubes containing fluid (endolymph) and suspended in fluid (perilymph). The hearing and balance are in continuityanatomically and ohysiologically. In a normal ear, the endolymph is maintained at a constant volume. An acute attack of Meniere’s disease is believed to result from from fluctuating pressure of the endolymph fluid within the inner ear. The underlying cause of Meniere’s disease is unknown

    Diagnosis of Meniere’s disease

    The diagnosis is based on history, findings at clinical examination and results of hearing tests like Audiometry and Impedance Bridge studies and vestibular (balance) tests like Electronystagmography (E.N.G.), the gold standard by which the function of the balance organ is measured.. Rarely an M.R.I. brain scan may be required to exclude a rare tumour of the nerve of balance. (Ac neuroma) which presents with symptoms of Meniere’s disease. See vertigo testing Click

    Management of an acute attack

    During an acute attack, one must lie down on a firm surface. Do not move till the severity of vertigo subsides, then get up slowly. The eyes must be kept open and fixed on a stationary object. Do not drink water. It may cause vomiting.. If the vomiting and vertigo persist, send for the family physician . If relief is still not obtained, an E.N.T. specialist has to be consulted.

    How does one cope up with the symptoms?

    Avoid maneuvers involving neck twisting, Be extra careful during crossing roads, avoid sitting on two wheelers, avoid dangerous heights, etc. From now on, you will have to rely more on the two other modalities for maintenance of balance – namely – vision and proprioception (sensations from the peripheral sensory inputs of skin, muscle and joint sense. It is advisable to tell colleagues at work what to do if an acute attack occurs.

    What can be done to reduce the symptoms?

    Between attacks, different medications and different types of Vestibular rehabilitation exercises may be prescribed to help to encourage coordination between ears, eyes, cervical spine and stance and gait.

    Salt restriction during the acute attack helps prevent water logging within the internal ear and helps early recovery. A permanent tinnitus (ringing in the ears) or a progressive hearing loss may be the consequence of a long term Meniere’s disease. In severe cases not responding to medication, surgery may be advised to block the transmission of information from the affected ear to the brain. The surgical methods available can be discussed with doctor when the need arises.

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    Vestibular neuritis

    For Anatomy and Physiology of the Ear, Click here

    Vestibular neuronitis / neuritis Vestibular neuritis is The secondmost common cause of vertigo arising from a disorder of thelabyrinth is caused by inflammation of the vestibular nerve, thenerve that connects the balance portion of the inner ear to the brain.It is manifested by a sudden attack of rotatory vertigo often associated with nausea, vomiting, and sweating.

    What are the causes? (Aetiology and pathology)

    Vestibular Neuritis is thought to be caused by a viral infection of the balance nerve that runs from the inner ear to the brain. Various theories have been proposed to account for the cause of vestibular neuritis including inflammation of the vestibular nerve and ischemia of the labyrinth. Many of the histological features of vestibular neuritis when evalu¬ated in postmortem studies are similar to those observed in other sensory epithelia in known viral disorders. Herpes simplex virus type 1 (HSV -1) DNA has been detected on autopsy with the use of polymerase chain reaction in 66% of human vestibular ganglia. Reactivation of a latent infection with HSV -1 is presumed to account for the occurrence of vestibular neuritis.

    The condition chiefly affects adults between the ages of 30 and 50 years without preference for sex.

    Vestibular neuritis affects the superior division of the vestibular nerve more commonly than the inferior division. The superior division has a longer course through bone than does the inferior division and is therefore more liable to affection from ischemia, injury and entrapment.

    Because of the association of the disorder with reactivation of HSV-l, the condition is also referred to as vestibular neuronitis.

    Some patients will report having an upper respiratory infection (common cold) or a flu prior to the onset of the symptoms of vestibular neuritis, others will have no viral symptoms prior to the vertigo attack.

    What are the symptoms?

    The main symptom of vestibular neuronitis is vertigo, which appears suddenly, often with nausea and vomiting. Vertigo usually lasts for several days or weeks. It can come as a single attack or as a series of attacks of vertigo or a constant sense of balance carrying on for two to four weeks before diminishing. It may follow an upper respiratory tract infection. The cochlea (hearing portion) of the inner ear is unaffected and therefore the patient’s hearing function is normal.

    Clinical features

    Onset:- (The Acute phase) Vertigo is the leading symptom. The onset is sudden with, in some cases, transient paroxysms of vertigo accompanied by black-outs or drop-attacks, in others a feeling of imbalance, especially when walking or standing, aggravated by movements of the head indicating a sudden and partial or complete loss of vestibular function on one side,. Vertigo may be accompanied by nausea or vomiting but never by tinnitus or deafness. The presence of hearing loss in the affected ear may indicate labyrinthitis, an acute Meniere disease attack or infarct of the brainstem or cerebellum (often in the territory of the ante¬rior inferior cerebellar artery).

    The patient should be made to walk, however difficult it may be, as severe gait ataxia strongly points to a central cerebrovascular event such as cerebellar infarction – especialli in the territory of the poste¬rior inferior cerebellar artery (PICA). Magnetic resonance imaging (MRI) with diffusion weighted images should be performed when indicated based upon clinical suspicion of an infarct.

    Later:- (The Subacute phase) The intense vertigo of acute vestibular neuri¬tis can last from hours to days and rarely weeks. This phase is characterized by imbalance and disequilibrium that noticeably improves over this time. Patients will have sensitivity to motion and may avoid head turns and rapid movements.

    They may develop brief attacks of vertigo that are not as intense as the initial attack. Vestibu1ar rehabilitation during this phase may speed recovery.

    At the end of the subacute phase the patient will be near their baseline balance function but may notice small disturbances of equilibrium with rapid motions or in challenging environ¬ments. If evaluated for dizziness at this late stage, a diagnosis of vestibular neuritis is based largely on a suspicious history of severe vertigo within the prior months to year. Additional test¬ing, as described below, may also demonstrate a unilateral weakness confirming an insult to the inner ear. Commonly in this stage anxiety plays a major role in the patients perception of their debility. A significant portion of patients with acute vertigo will develop anxiety regarding their balance and potential for having recurring ver¬tigo. They will often limit activities such as driving, withdraw socially and become intensely fixated on any abnormal sensation of equilibrium. A psychological consultation in any vestibular neuritis patient with a dependent or insecure personality type is advisable.

    In rare cases it can take months to go away entirely. Vestibular neuronitis does not lead to loss of hearing. One may notice that vision is disturbed or jumpy on looking to a particular side.

    How is the diagnosis confirmed?

    Pure tone Audiometry, Impedance bridge studies and vestibular (balance) tests – Electronystagmography is the gold standard by which the function of the balance organ is measured. A C.T.Scan or M.R.I.Scan of the brain is not required immediately and usually turns out to be normal.

    Evaluation and Diagnostic Testing

    Physical Examination. Findings on physi¬cal examination will generally depend upon the stage of vestibular neuritis. In the acute phase, the examiner will note spontaneous nystagmus the eyes move in the plane of the affected semicircular canal(s).

    The nystagmus will increase in amplitude with gaze toward the horizontal fast phase component, which is usu¬ally toward the nonaffected ear. The nystagmus should suppress with visual fixation but may be of such intensity as to be reduced in amplitude but remain noticeable. Direction changing nys¬tagmus and lack of visual suppression should raise the suspicion of a central event and prompt imaging for stroke evaluation. The presence of ataxia is also suggestive of central vestibular dys¬function or, rarely, a drug reaction.

    Hearing should be checked during the acute phase A hearing loss is inconsis¬tent with vestibular neuritis, and the practitioner should consider labyrinthitis, Meniere disease, perilymphatic fistula, or acute otitis media among otologic causes of acute cochleovestibular symptoms.

    The spontaneous nystagmus has usually resolved in the subacute phase although nys¬tagmus may be observed with gaze toward the unaffected ear

    Electronystagmography Objective testing can be used to identify the unilateral vestibular hypofunction characteristic of vestibular neuritis. Caloric test¬ing showing an asymmetry is consistent with a history of unilateral vestibular insult. This test is more sensitive than either head thrust or head shake for identifying such an asymmetry. The ENG battery of tests can also be used to assess for the presence of.BPPV which occurs often after vestibular neuritis. In the acute and subacute phases, ENG can identify and document spontaneous and gaze evoked nys¬tagmus as well as determine their direction thus helping to identify the affected side. The ENG is important to distinguish a PICA thrombosis (in which ENG is normal) from Vestibular neuronitis in which it is always abnormal.

    Imaging. The acute phase of vestibular neu¬ritis is of such severity and duration that clini¬cal examination alone may not be sufficient to rule-out central vascular events. Thus, computed tomography (CT) scan is the initial imaging test of choice to look for an acute hemorrhage involving the brainstem or cerebellum. MRI of the internal auditory canals during an acute phase of vestibu¬lar neuritis may show subtle enhancement of the superior vestibular nerve at the region of Scarpa ganglion. Beyond the acute phase, MRI with gadolinium enhancement is most useful for eval¬uating for other intracranial lesions that could account for an attack of vertigo or prolonged vestibular dysfunction. Tl-weighted images with contrast can demonstrate the presence of vestib¬ular schwannoma. Sudden vertigo is the initial presenting sign for vestibular schwannoma in approximately 15% of cases. It is rare in isolation and usually accompanies hearing loss. The presence of Chiari I malfor¬mation, cerebellar tumor, cerebellopontine angle arachnoid cyst, old brainstem infarct, or vascular loop can also be identified with MRI.

    Management. Supportive treatment should also be given during the acute phase of vestibular neuritis.

    Acute phase – Combination treatment of Methylprednisolone in a dosage of 48 mg. daily for the first 3 days tapered by 16 mg every 3 days for a total treatment time of 20 days and

    Va1cyclovir admiistered as 1,000 mg three times per day for 1 week.

    Patients should be hydrated if they are having significant vomiting and provided antiemetics.

    Vestibular suppressants can also be prescribed to attenuate the severity of the attack. The treatment of vestibular neuronitis is medical, and depends entirely upon the severity of symptoms. Some patients’ will be so disabled as to require a period of rest in bed, others will be able to continue to get about, but all will probably require labyrinthine sedation to tide over the period of activity of the disease. As in Meniere’s disease promethazine theoclate (Avomine) or dimenhydrinate (Dramamine) tablets are useful drugs for suppressing the symptoms of vertigo and nausea.

    Low dose valium is an effective vestibular suppressant, and mini¬mally sedating dosages of 2 mg every 6 hours as needed can be provided. Attempts should be made to wean the patient off of vestibular suppressants as soon as possible to allow central compensation of the unilateral hypofunction.

    Once the patient has entered the subacuate phase of their attack, vestibular rehabilitation exercises should be recommended VOR exercises can speed central compensation for the unilateral weakness Patients experiencing chronic daily disequililibrium should be evaluated for psychogenic dizziness trigered by the initial neurotologic disorder. Additionally, an attack of vestibular neuritis may exacerbate underlying psychiatric or anxiety disorders.

    The condition pursues a benign although sometimes protracted course and symptomatic recovery is the rule. Reassurance that recovery is confidently to be anticipated. Even when vertigo has been initially severe and immobilizing the recovery period does not often exceed 3 weeks.

    Caloric responses generally remain permanently abnormal.

    D.D. In Meniere’s disease deafness is always present, a feature which should immediately eliminate a diagnosis of vestibular neuronitis

    Other forms of labyrinthitis, toxic, vascular or infective, may at times be difficult to differentiate, but if it is remembered that the diagnosis of vestibular neuronitis requires the stringent double verification of abnormal caloric reactions and normal cochlear audiograms.

    Treatment

    How is an acute attack managed?

    During an acute attack, lie down on a firm surface. Stay as motionless as possible and keep your eyes open and fixed on a stationery object in front of you. Do not try to sip or drink water as this may cause vomiting. Stay like this till the severity of vertigo subsides. Avoid the position causing the vertigo.

    How is it treated?

    Medical treatment based on results of investigations by a vertigo specialist usually involves a combination of medication and vestibular rehabilation therapy and course of exercises is advised. Also special exercises help to come back to normal early.

    Appropriate Vestibular Rehabilitation Excersies help to recover quickly.

    Acoustic Neuroma (Tumour of the 8th cranial nerve)

    Anatomy and Physiology of the Ear Click here

    The 8th cranial nerve is the nerve that serves the hearing and balance functions of the body. A tumour of the balance portion of this nerve (Acoustic neuroma) is a cause of a balance disorder.

    Causes of a Tumour of the nerve of balance

    An acoustic neuroma arises from the fibrous sheath of the nerve of balance (vestibular nerve) within the internal auditory canal.

    Symptoms

    The initial symptom of an acoustic neuroma is tinnitus (noise in the ear). Deafness appears later and so does vertigo. Occasionally the presentation is by a sudden deafness. The vertigo is usually a constant sense of imbalance. As the tumour grows in size, it presses on adjoining areas – cerebellum and brain stem. Pressure on the Cerebellar causes increasing imbalance, increasing tinnitus and increasing heraing loss. Pressure on the Brainstem causes various neurological problems.

    Confirmation of the diagnosis

    Pure tone Audiometry, Impedance bridge studies and vestibular (balance) tests. Electronystagmography is the gold standard by which the function of the balance organ is measured. An M.R.I.Scan of the brain will show a suspicious shadow occupying the internal audiitory canal and cerebello pontine angle.

    How is it treated?

    Early diagnosis is extremely important as the treatment is surgical removal of the tumour. Every case of noise in th ear should be properly investigated by Pure tone Audiometry, Impedance bridge studies and vestibular (balance) tests. Electronystagmography. The sooner this is done, the better, since this the tumour grows in a closed space, next to vital brain stem structures responsible for cardiac function and respiration and the larger it is, the more difficult it is to remove. There is no place for medical treatment.

    Vestibular Rehabil Exercises Click here

    Precautions during vertgo attacks Click here

    Results of Audio – Vestibular investigations of a patient with Right Acoustic Neuroma

    Pure Tone Audiogram showing a moderately severe to severe sensori neural hearing loss in the Right ear

    Electro Nystagmography recordings of a patient with a Right Acoustic Neuroma

    Recordings of the Caloric test

    Right ear warm stimulus

    Right ear cold stimulus

    Left ear warm stimulus

    Left ear cold stimulus

    Recordings of right and left ear caloric responses for frequency calulations

    Cerebello Pontine Angle/Internal Auditory Canal Mass Lesions

    Cerebello Pontine Angle / Internal Auditory Canal Mass Lesions

    Solid lesions

    Acoustic Schwanomma – The most common CPA-IAC mass

    Meningioma of CPA        –  2nd most common CPA-IAC mass

    -   2nd most common primary intracranial tumour (15 –25 %)

    Meningioma                        -  intracanalicular may mimic AS

    Neurosarcoidosis

    Facial Nerve Schwannoma confined to CPA / IAC may mimic AS

    Metastasis & Lymphoma

    Idiopathic Hypertrophic Pachymeningitis (rare)

    Cystic lesions

    Epidermoid cyst 3rd common

    Arachnoid cyst

    Benign cystic neoplasm – cystic meningioma, cystic ependymoma and cystic schwannoma

    Malignant cystic neoplasm – Ependymoma pedunculating from brainstem

    - Astrocytoma pedunculating from 4th ventricle

    Aneurysmal lesions

    Aneurysm of PICA, VA, AICA

    Vertebrobasilar Dolichoectasia

    Venous Varix

    Labyrinthine conditions

    Labyrinthine Ossificans following meningitis

    Inner Ear Schwannoma – Intra Vestibular, Cochlear, Vestibulo-Cochlear, Translabyrinthine

    Facial Nerve Schwannoma with Secondary Erosion Into Inner Ear

    Endolymphatic Sac Tumour

    Cerebellopontine Angle Lesions:

    1. Acoustic schwannoma

    * most common mass in the CPA, up to 75% of cases

    * usually arises from the superior vestibular nerve

    * usually a solid space-occupying mass with a tail in the internal acoustic meatus/ canal that uniformally enhances    with contrast; can cause compression of the pons and cerebellar peduncles

    * surgical approaches- A. Suboccipital retrosigmoid (Figure 1)

    Figure 1: T1 -weighted coronal view (with contrast) of a left cerebellopontine angle lesion showing enhancement. The lesion is predominately in the posterior fossa with a tail in the internal acoutic canal. This lesion was excised through a suboccipital/ retrosigmoid approach.

    B. Trans-labyrinthine presigmoid (Figure 2)

    Figure 2: A: T1-weighted coronal view (with contrast) of a right cerebellopontine angle lesion showing uniform enhancement. This lesion is mostly in the internal acoustic canal and was excised through a translabyrinthine approach. The patient had no useful hearing preoperatively and had preservation of the facial nerve postoperatively.

    B: Intraoperative of the tumor resection. The tumor is carefully dissected away from the cranial nerves in the porus acousticus.

    C: Note the preservation of the cranial nerves after complete resection of the tumor.

    C. Middle Fossa (Figure 3)

    Figure 3: T1-weighted axial view (with contrast) of a small intracanalicular left acoustic tumor (arrow). The patient had useful hearing preoperatively and thus this lesion was resected through a middle fossa approach. The patient had preserved hearing and facial function postoperatively.

    2. Meningioma

    * second most common lesion, up to 10% of cases

    * uniformally enhancing mass; dural tail

    3. Ectodermal inclusion tumors: Epidermoid (Figure 4)- also known as ‘congenital cholesteatoma”; 5-7% of cases in the CPA; cystic space-occupying, non-enhancing lesion

    Figure 4: T2-weighted axial view showing a hyperintense lesion in the left cerebellopontine angle. This is a typical appearance for an epidermoid lesion.

    Dermoid- rare

    4. Metastases

    5. Paraganglioma- “glomus jugulare tumor” arising in the jugular foramen and extending into the CPA; incidence: 2-10%

    6. Other schwannomas: 2-5% incidence; trigeminal and facial nerves are probably the most common sites of nonacoustic schwannomas. Other cranial nerves involved are: VI, IX, X, XI and rarely XII.

    7. Vascular lesions (2-5% incidence)

    * dolichobasilar ectasia: 3-5%

    * aneurysm: 1-2%

    * vascular malformation: 1%

    8. Choroid plexus papilloma: 1%; primary in the CPA or extension via the lateral foramina of Luschka

    9. Ependymoma: 1%; extension from the 4th ventricle

    10. Rare lesions: incidence <1%

    * arachnoid cyst

    * lipoma (CPA is the 2nd most common site in brain)

    * exophytic brain stem or cerebellar astrocytoma

    * chordoma

    * osteocartilaginous tumors

    * cysticercosis

    Cranial Nerves at the Internal Acoustic Meatus (Figure 5):

    Figure 5: A diagrammatic view of the cranial nerves at the internal acoustic meatus. Taken from Surg Neurology 8:388,1977.

    * there are five nerves in the meatus: nervus intermedius (sensory component of the VIIth nerve), facial motor root, cochlear nerve, inferior and superior vestibular nerves.

    * position of the 5 nerves is most constant in the lateral portion of the meatus, which is divided into a superior and an inferior portion by a horizontal ridge (transverse or falciform crest): facial and superior vestbular nerves (SVN) are superior to the crest; facial nerve is anterior to the SVN and is separated from it at the lateral end of the meatus by a vertical ridge of bone (Bill’s bar); nervus intermedius (NI) is between the facial motor root and the SVN (it may be adherent to the SVN); cochlear nerve and the inferior vestibular nerve (IVN) run below the transverse crest with the cochlear nerve located anteriorly.

    FACIAL NERVE: Anterior-superior

    SVN: Posterior-superior

    COCHLEAR NERVE: Anterior-inferior

    IVN: Posterior-inferior

    *because acoustic neurinomas most frequently arise in posteriorly placed vestibular nerves, they usually displace the VIIth nerve anteriorly (facial nerve is stretched around the anterior half of the tumor capsule).

    *because the facial nerve enters the facial canal at the anterior-superior quadrant of the lateral margin of the meatus, it is usually easiest to locate it here after the posterior lip of the meatus has been removed, rather than at a more medial location where the degree of displacement of the nerve is more variable, depending on the site of origin and growth characteristics of the tumor.

    *while the posterior meatal lip is removed, mastoid air cells that extend into the lip may be opened, and must then be sealed carefully to prevent CSF leak or meningitis.

    *during removal of the posterior meatal wall, care is taken to avoid the posterior semicircular canal, which is lateral to the posterior wall of the meatus- to avoid this semicircular canal, bone lateral to the tranverse crest should not be removed.

    *labyrinthine arteries and their branches typically lie below the nerves- are the sole supply to the membranous labyrinth.

    The LSUHSC Skull Base Team (Neurosurgery, Otolaryngiology, Plastic Surgery, Neuroradiology, Neurophysiology departments) routinely deals with CPA lesions, especially acoustic tumors. In 1999, 10 acoustic tumors were removed at LSU: 4 suboccipital; 3 translab; 3 middle fossa

    Benign Paroxysmal Positional Vertigo (BPPV)

    For Anatomy and Physiology of the Ear    Click here

    What is BPPV? (Benign Paroxysmal Positional Vertigo)

    BPPV is a disease of the balance organ in the inner ear (vestibule) which results from the altered function of the utricle and posterior semi  circular canal.. Small crystals of calcium carbonate (“otoconia”) normally present in the utricle, drop into the posterior semi  circular canal during head movement. The crystals can lodge in the posterior semi circular canal (Commonest) (Canalithiasis) or in the Cupula of the posterior canal (Cupulolithiasis) The vertigo occurs in sudden brief episodes and is short lived (paroxysmal); it is positional because the symptoms are precipitated by head movement. Some people feel it when the head is taken back to look up, while others feel it if they lie down suddenly or get up suddenly.

    BPPV is a common cause of dizziness. About 20% of all dizziness is due to BPPV. In the elderly,  about 50% of  dizziness is due to BPPV

    What causes it?

    BPPV can be due to simple infections like common colds, and degeneration of the inner ear as in ageing. However, BPPV may rarely occur for no known reason.

    The most common cause of BPPV in people under age 50 is head injury with damage to the utricle. There is also an association with migraine. In older people, the most common cause is degeneration of the vestibular system of the inner ear. BPPV becomes much more common with advancing age. In half of all cases, BPPV is called “idiopathic,” which means it occurs for no known reason. Viruses affecting the ear such as those causing vastibular neuritis, minor strokes such as those involving anterior inferior cerebellar artery (AICA Syndrome, and Meniere’s disease are unusual causes. Occasionally BPPV follows surgery. The cause b in such cases could be a combination of a prolonged period of supine positioning, or ear trauma when the surgery is to the inner ear.

    How is the diagnosis confirmed?

    Positional testing by the Hallpike maneuvers help identify the specific positions provoking the vertigo.

    Pure tone Audiometry, Impedance bridge studies and vestibular (balance) tests – Electronystagmography is the gold standard by which the function of the balance organ is measured.  A C.T.Scan or M.R.I.Scan of the brain is not required immediately and usually turns out to be normal. Low blood pressure can give rise to positional vertigo. However in these cases the giddiness is only on sitting up (postural hypotension) and never on lying down.

    How is an acute attack managed?

    During an acute attack, lie down on a firm surface. Stay as motionless as possible and keep your eyes open and fixed on a stationery object in front of you. Do not try to sip or drink water as this may cause vomiting. Stay like this till the severity of vertigo subsides. Avoid the position causing the vertigo.

    How is it treated?

    The specific positions provoking the vertigo are identified by the vertigo specialist and avoided and a combination of medication and vestibular rehabilation therapy and course of exercises is advised. Also special exercises help to come back to normal early. The Eppley-Semont manoeuvres are effective in helping the symptoms subside.

    Certain modifications in your daily activities may be necessary to cope with your dizziness. Use two or more pillows at night. Avoid sleeping on the “bad” side. In the morning, get up slowly and sit on the edge of the bed for a minute. Avoid bending down to pick up things, and extending the head, such as to get something out of a cabinet. Be careful when at the dentist’s office, the beauty parlor when lying back having ones hair washed, when participating in sports activities and when you are lying flat on your back.

    The specific positions provoking the vertigo are identified by the E.N.T Surgeon and avoided and a combination of medication and vestibular therapy is advised. Labyrinthine sedatives, vasodilators. Also special exercises help to come back to normal early. The Eppley-Semont manoeuvre performed by an E.N.T Surgeon are effective in helping the symptoms subside.

    Balance is maintained by 3 sources of input to the brain – Inner, ear, the main balance organ, eyes – vision to information received from your feet, ankle and legs assist you in keeping your balance and moving around.

    Modifications in the daily activities will help you cope with your dizziness.

    The exercises aim at helping one Dependance on vision.- on the information received from the eyes.

    Because of this you should take special precautions in situations where clear, normal vision is not available to you to avoid injury in case you fall. At home, when walking through dark rooms, keep lights or night lights on all the time. Eliminate slippery floor surfaces, maintain clear a path to your bathroom and move away objects that could injure you, should you have a fall. Do not drive your car at night, during stormy weather or when visibility is poor. Do not carry large objects which obstruct the view in front.

    Dependance on inputs from awareness of contact with the floor through the skin, joint position awareness, muscle tone awareness

    Take great care when walking on soft rugs, carpeted floors, sand or loose gravel and other uneven surfaces. Make sure, the floors at home are free from obstructions. Maintain a clear path to your bathroom and move away all objects along the floor that could entangle your feet or injure you, should you have a fall. Most important, do not place yourself in a situation where you might lose your balance and be at risk of falling and serious injury; stay off chairs, stools, ladders, roofs. Exercise special care in the kitchen, near an open flame. Take extra care crossing roads, avoid sitting on two wheelers and avoid heights.

    CERVICAL VERTIGO – PATHOPHYSIOLOGY AND DIAGNOSIS

    Cervical vertigo is a vertigo or dizziness that is provoked by a particular neck posture For example, dizziness provoked by turning the head about the vertical axis, while sitting upright no matter what the orientation of the head is to gravity. A pathological nystagmus, occurring during turning of the trunk in relation to the head, which is held stationary in space, clearly points towards a cervical origin of vestibular vertigo. Such a cervical nystagmus may have a vascular origin by the compression of the vertebral arteries, or a proprioreceptive origin via the upper neck joints, or it may possibly be due to functional disturbances of the upper cervical spine

    The usual symptoms are dizziness associated with neck movement.

    Persistent unsteadiness

    Hearing is not affected. Tinnitus may be present.

    Ear pain from referred from the cervical spine may be present.

    Visual disturbances on shaking his head forcefully, a spot in the vision, sudden lost vision in one half of the visual field attributed to poor circulation to the back of the brain (diagnosis suggestive

    of vertebral basilar compression).

    Positional vertigo elicited by turning the head to the sides, accompanied by ear fullness, and at one point

    Symptoms can be triggered off by standing up, rapid head movements, walking in a dark room, not eating, exercise, and coughing or sneezing can trigger symptoms.

    The causes of cervical vertigo may be:

    1. Cervical cord compression – In this case, the ascending or descending tracts in the spinal cord that connect with the cerebellum, vestibular nucleus or vestibulospinal tracts are compressed by disk prolapse, spondylitis, spondylolisthesis, atlanto axial joint dislocation, spinal canal stenosis, neck surgery and chiropractic manipulation are all potential precipitants of neurological symptoms including stroke. This may be painless. This is the most common mechanism of cervical vertigo. (Hain).

    2. Vascular compression – There are two distinct mechanisms here – compression and dissection.

    The vertebral arteries in the neck can be compressed by the vertebrae (which they traverse), or other structures, the causes being similar to the above. . Arthritis, neck surgery, Dissection can occur at the points where they are anchored in the upper cervical spine, by a stretching force. Hence it is dangerous to volunteer for chiropractic treatment of vertigo that includes “snapping” or forceful manipulation of the vertebrae in persons with unstable necks.

    Whiplash (flexion-extension injuries to the neck, usually associated with an auto accident involving a rear end collision) and patients who sustain closed-head injuries may experience late onset symptoms of dizziness, vertigo and disequilibrium possibly due to stretching of the upper portions of the vertebral arteries.

    Neck injuries have increased in most parts of the world with auto accidents, presumably due to interaction between use of seat-belts and chest restraints. While chest restraints reduce the risk of death, mechanically by restraining the trunk, they can be associated with greater relative movement of the unrestrained head on neck due to simple biomechanics involving momentum transfer.

    3. Abnormal sensory input from neck proprioceptors. (Cervico- vestibular-ocular reflex) Sensory information from the neck is combined with vestibular and visual information to determine the position of the head on the neck and space. It is possible that some individuals are more sensitive than others, and also that neck inputs interact with other causes of vertigo. If sensory information from the neck is unreliable or absent.

    Before assuming a cervical origin of a vestibular vertigo, an examination for cervical nystagmus should be carried out by the Head-turning upright test. Such a cervical nystagmus is the only definite pointer towards a relation between an upper cervical spine syndrome and vertigo

    Cervical nystagmus caused by proprioceptors of the neck (Reker U).

    Examination shows that nystagmus occurs during the turning of the head in relation to the body. In the extreme positions, the proprioreceptive nystagmus does not persist.

    Contrary to this, a cervical nystagmus due to vascular causes shows a latency period of 20 to 30 seconds after torsion of the neck, increases and persists if the head remains in the extreme position.

    4. Cerebrospinal Fluid (CSF) leak due to tear of cervical root sleeve with dizziness and headache For example, a whiplash injury may tear a cervical root sleeve causing low CSF pressure and hearing symptoms. CSF leaks can cause low-tone sensorineural hearing loss, resembling bilateral

    Meniere’s disease.

    DIAGNOSIS OF CERVICAL VERTIGO:

    Criteria used to diagnose Cervical Vertigo

    • Lack of reasonable alternatives.

    • Positional testing with ENG in the sitting up position on head turning to the left, right, up and down with eyes closed

    • Abnormal cervical MRI with disk abutting cervical cord, or readily apparent high-cervical disease.

    A combination of criteria must be used to diagnose cervical vertigo (Hain).

    First, one excludes other causes of vertigo such as vestibular neuritis, BPPV, Meniere’s syndrome, central vertigo, post traumatic vertigo (whenever a history of head injury is present), psychogenic vertigo (often including malingering when there are legal issues), and medical causes of vertigo. There should be a sufficient cause of neck injury (whiplash injury or severe arthritis). Symptoms elicited by massage of the neck or vibration to the neck add to the clinical suspicion.

    Audiogram and Impedance testing are usually normal. Referred ear pain (otalgia), as part of the ear is supplied by sensory afferents from the high cervical nerve roots, may be complained of..

    On physical examination, there should be no spontaneous nystagmus, but there may be positional nystagmus. Many patients who have vertigo in the context of neck disease have a BPPV type nystagmus on positional testing. This suggests that the neck afferents may interact strongly with vestibular inputs derived from the posterior canal.

    Often it is helpful to compare nystagmus elicited with the head prone to with the head supine, as if the nystagmus does not reverse, cervic al vertigo seems fairly certain.

    Head-turning upright test. (The vertebral artery test)Another useful maneuver is to turn the head to one side to the limit of range, while the examinee is upright and simply wait for 30 seconds. The figure below shows a weak positive and the movie below in the case section shows a strong positive. Clinically, nystagmus that changes direction according to the direction of the head on neck, rather than with gravity, makes cervical vertigo likely. Persons who are positive on this test often have a disk abutting their cervical cord, generally at C5-6.

    Examination shows that nystagmus occurs during turning of the body in relation to the head (“phasic neck reflex”). On the other hand, when remaining in the extreme positions, the proprioreceptive nystagmus does not persist. Contrary to this, a cervical nystagmus due to vascular causes shows a latency period after torsion of the neck and increases if the head remains in the extreme position.

    Before assuming a cervical origin of a vestibular vertigo, an examination for cervical nystagmus should be carried out. Such a cervical nystagmus is the only definite pointer towards a relation between an upper cervical spine syndrome and vertigo, which is sometimes assumed rather uncritically.

    Spontaneous nystagmus recording (Head centre) (Upright position) (Patient M.M)

    Cervical nystagmus recorded with head turned left (Upright position) (Patient M.M)

    Laboratory studies: If cervical vertigo still seems likely after excluding reasonable alternatives, one next needs to look for positive confirmation. Routine studies in working up cervical vertigo

    • Computerized ElectroNystagmography (CENG)

    • Audiogram and Impedance studies

    • MRI-neck (see above) and MRI-brain

    • Flexion/extension x-rays of neck

    • CT-angiography (if MRI-neck is negative or there is strong suspicion of vascular etiology, given that renal function is adequate for use of large amounts of iodine contrast)

    Angiography: CT-angiography has been rapidly improving in recent years and it is excellent for detection of vertebral hypoplasia — which is as much as you may be able to determine anyway. Three-dimensional reconstructions can be very helpful.

    The “gold standard test” for the cervical vertigo due to compression of the vertebral arteries is selective vertebral angiography with the head turned to either side. This, however, is a risky procedure by itself, often it is decided not to proceed to this step. There is also another problem — tiny risk of a stroke during a radiographic procedure, radiologists may simply choose not to turn the head. They will refuse to turn the head to end rotation to diagnose it.. Thus, in some settings, it may be simply impossible to diagnose vertebral artery occlusion because of radiologist risk aversion.

    Our position is that one should not attempt vertebral angiography, but simply do CT-angiography as long as kidney function is adequate.

    Other tests:

    Ordinary MRA and vertebral doppler procedures are rarely abnormal, and sometimes are used as a screening procedure to decide whether vertebral angiography is necessary. We are unenthusiastic about this as it seems unreasonable to us to use methods that are unreliable as screening procedures.

    An MRI scan of the neck and flexion-extension X-ray films of the neck are suggested in all.

    Fluoroscopy of the neck may be used in persons with abnormal flexion-extension views.

    CENG testing is mandatory, largely to exclude alternative causes.

    Vertebral artery doppler may be helpful in some.

    CERVICAL VERTIGO – Cervical spine Anatomy & Vertebro basilar syStem

    The vertebral arteries are branches of the subclavian arteries. Together with the basilar artery constitute the vertebrobasilar system which supplies blood to the posterior part of Circle of Willis and anastomose with blood supplied to the anterior part of the circle of Willis from the carotid arteries.

    Cranial portion of the Vertebral arteries

    Inside the skull, the two vertebral arteries join up to form the basilar artery at the base of the medulla oblongata. The basilar artery is the main blood supply to the brain stem and connects to the Circle of Willis to potentially supply the rest of the brain if there is compromise to one of the carotids.

    Cervical portion of the Vertebral arteries – Can be divided into 4 parts for the purpose of description

    Chronic Suppurative Otitis Media (Safe Type)

    Conductive deafness due to Chronic Ear infection


    Anatomy and Physiology of the Ear Click here

    Chronic Suppurative Otitis Media   (SAFE TYPE)
    Chronic Otitis Media is chronic infection of the middle ear cleft, can be of types:
    (>3 months duration)
    1. Perforation of Tubo-tympanic or Attico – antral type.
    2. Chronic non-suppurative otitis media ego     Serous otitis media.
    3. Chronic specific otitis media e.g. following  tuberculosis.

    Types:

    I. TUBOTYMPANIC DISEASE (SAFE TYPE)
    Etiology:
    i.  Residue of an acute otitis media infection during childhood.
    ii. Repeated infections from the eustachian tube.
    Perforation – Usually in the form of a central perforation situated exclusively in the pars tensa.
    The ossicular chain often remains intact and middle ear mucosa is pink and edematous.

    Clinical features:
    1. Discharge – is mucoid, copious and non foul smelling. It becomes profuse during an upper respiratory infection.
    2. Deafness – is conductive in type. Degree varies with the position and size of perforation.

    Treatment:
    1. Aural toilet – Is performed meticulously under direct vision, preferably suction and irrigation done under the operating  Microscope.
    2. Bora-spirit – Ear drops are advised only during active discharge.
    3. Focus of infection – Are treated medically     or surgically e.g. tonsillitis, sinustitis etG.
    4. Removal of polypi or granulation tissue – if present in the middle ear.
    5. Chemical cautery – Using 50% Trichloro acetic acid for smaller perforations ( &lt; 65% area if tympanic membrane).
    6. A Myringoplasty operation – May be required for a persisting perforation.

    Chronic otitis media  (Safe type)

    Anatomy and Physiology of the Ear     Click here
    Perforation of the Ear Drum (Tympanic membrane)

    A perforated eardrum is a hole or rupture in the ear
    drum, the thin membrane that separates the ear canal
    and the middle ear.

    The Ear drum can perforate from infection or trauma.

    An Infective perforation of the eardrum
    Starts with infection from the nose after a head cold travelling up the Eustachian tube to reach the middle ear to promote an infection in the middle ear. Pus builds up in the middle ear behind the ear drum with pressure causing severe throbbing pain and breaks through a weak point in the ear drum leaving a perforation with a discharge of pus or blood.

    A Traumatic perforation of the eardrum may occur:

    - By a slap on the ear
    - As part of a skull fracture
    - After a sudden explosion from a bomb blast or fire cracker blast
    - Insertion of a pin, cotton bud or stick if pushed too far into the ear canal.
    A traumatic perforation usually has irregular shape and size and irregular edges.

    A Traumatic perforation Photograph of the left ear drum of a patient  K. E., after a Bomb blast in Mumbai

    Symptoms and Signs of a Ear drum perforation: A perforated eardrum is usually accompanied by decreased hearing, occasional discharge, tinnitus and sometimes vertigo. Pain is usually not present.

    Diminished hearing

    Due to loss of drum surface area, less sound vibrations reach the middle ear and internal ear with resulting deafness. It is difficult to determine the location of the source of sound – that is directional (stereophonic) hearing is difficult. Appreciation of stereophonic music is affected.
    When old age deafness sets in due to age related changes of the organ and nerves of hearing, the additional hearing impairment in the affected ear would be more pronounced than in the better hearing ear and becomes a definite handicap in communication.

    Usually, the larger the perforation, the greater the loss of hearing. If disruption of the chain of bones in the middle ear occurs less sound is transmitted to the inner ear, the loss of hearing is more severe. The type of of deafness is of the Conductive type.

    If the perforated eardrum is due to a sudden severe trauma (e.g. skull fracture) traumatic or explosive event like a cracker or bomb blast, because of shake up of the ultra microscopic hair cells in the inner ear, the hearing loss may be very pronounced – a mixed hearing loss from a summation of the conductive component – ear drum perforation and dislocation of the small bones in the middle ear and a sensori neural component due to inner ear damage. from damage to the inner ear structures,
    Rarely, a long standing perforation may be the precursor of a cholesteatoma

    Recurrent Eardischarge

    A perforation of the ear drum creates a system of a tube open at both ends. Water, oil or even ear drops instilled into the ear can flow freely from the external ear into the middle ear and into the back of the nose and throat by the eustachian tube. Conversely, nasal discharge can flow freely from the back of the nose via the eustachian tube into the middle ear and come out through the perforation into the external ear.
    As long as the perforation remains, there is therefore, a chance of getting recurrent ear discharge. This can happen every time after catching a cold since blowing the nose forces nasal discharge into the middle ear. It also happens if water accidentally enters the ear as during a bath or during swimming when the infected water comes into contact with the delicate lining of the middle ear and excites an inflammation (otitis media) with resulting ear discharge.

    Tinnitus (Noise in th Ear)

    A continuous or intermittent noise in the ear can be present. This usually disappears after closure of the perforation by surgery.

    Vertigo

    Continuous or intermittent episodes of vertigo may occur, since the organ of hearing and balance are one anatomically connected organ.

    Natural course of a Ear drum perforation

    Eardrum perforations of small size may heal spontaneously in a few weeks.
    Medium sized perforations may or may not heal on their own.
    Large perforations cannot heal on their own and require surgery.

    Investigations advisable
    Pure tone audiometry
    Acoustic Impedance Bridge
    X-Ray mastoid bone for central perforation &amp; C.T. Scan temporal bone for chronic mastoiditis

    Treatment of a Perforated Eardrum

    The benefits of closing a perforation include prevention of recurrent middle ear infection by preventing water entering the middle ear while showering, bathing, or swimming (which could cause ear infection), improved hearing, and diminished tinnitus. It also may prevent the development of cholesteatoma (skin cyst in the middle ear), which can cause chronic infection and destruction of ear structures.

    A small perforation can be kept under observation to see if it could close spontaneously. or try to cauterize the edges of the perforation under the operating microscope, with a chemical to stimulate growth of epithelium from the surrounding area to grow over the perforation. If healing is not achieved, surgery has to be considered.

    A large or moderate sized perforation requires a surgical operation (Tympanoplasty or Myringoplasty) to close it. There are a number of surgical techniques, all of which aim at placing a piece of fascia covering the Temporalis muscle across the perforation. Surgery is typically quite successful in closing the perforation permanently, and improving hearing.

    By a small incision within the ear canal, the ear drum perforation edges are freshened. The ear drum has 3 layers. These layers are gently separated under an operating microscope. A tissue graft (temporalis fascia) is obtained by a small separate incision above the ear (requiring one stitch). This is placed carefully in between the ear drum layers. The operation is performed under local anaesthesia with sedation.  Hospitalization is for a few hours.

    Precautions to prevent recurrent ear discharge in patients with chronic ear infection

    • Water or oil should not enter the ear at all. Before a bath, the ear canal is sealed with a cotton ball smeared with vaseline or any other hair dressing. Wash hair with head  hanging down under a running tap. Dry well with a towel before standing up again.
    • Swimming is NOT advisable at all, till the perforation has been closed by surgery. If you  have to swim, do so without dipping the head under water.  No diving at all.
    • Do NOT allow your ear to be syringed by your doctor at all.
    • Do NOT use towel corners, match sticks, hair grips to clear the ear. They provoke infection
    • Do not blow the nose when you have a head ‘cold’. This will drive the nasal discharge into the middle ear via the Eustachian tube and start a ear discharge. To clear nasal discharge, sniff in and throw out the discharge through the mouth. If you sneeze, do so with mouth open.
    • If there is any itching in the ears  or you feel the need to clean the ear, do so with cotton buds only after smearing an antibiotic-antifungal cream like Surfaz SN cream
    • Every time you catch a ‘cold’, there is a likelihood of recurrence of ear discharge. Hence avoid iced water, ice creams, cold drinks etc.  Avoid undue exposure to cold.
    • On catching a cold, immediate treatment from the family physician is started.

    Chronic Suppurative Otitis Media (Unsafe Type)

    Conductive deafness due to Chronic Ear infection

    Chronic Otitis Media is a chronic infection (ear infection lingering on for over 3 months’ duration) of the middle ear cleft. It This includes disease of the middle due to infections by bacteria, virus etc. It may be Suppurative (with pus formation) or Non suppurative (without the formation of pus).

    Anatomy and Physiology of the Ear Click here

    Chronic Suppurative Otitis Media

    1. Perforation of Tubo-tympanic type (Safe type).

    2. Perforation of the Attico­ antral type (Unsafe type).

    3 Perforation of the Marginal posterior marginal type (Unsafe type).

    Chronic Non-Suppurative Otitis MediaAlso known as Serous or Secretory Otitis Media or Otitis media with effusion (OME)

    Chronic Suppurative Otitis Media of the Unsafe type

    ATTICO – ANTRAL or MARGINAL TYPE (UNSAFE TYPE)

    It is associated with formation of cholesteatoma and therefore regarded as unsafe. The term cholesteatoma is not an accurate description as it is not a tumour and always does not contain cholesterol chrystals. A cholesteatoma, truly speaking  is ‘skin in the wrong place’ (Gray). This usually affects the postero-superior quadrant of ear drum (pars tensa) or the attic or epitympanum (Pars flaccida).

    A cholesteatoma starts life as a dimple due to localised retraction of a portion of the tympanic membrane in the attic or postero superior quadrant of the pars tensa. It is in reality a retraction pocket and not a “perforation”. Epithelial squames (flat cells of skin) acumulate inside the dimple which soon shuts off and presents as an expanding bag. As more and more epethilium accumulates within the bag, the cholesteatoma forms an expanding erosive bag. This has the potential of eroding bone. Erosion of the small bones of the middle ear – ossicles  result in conductive deafness. If it erodes the labyrinth, a sensori neural deafness ensues. Erosion of the facial nerve canal can lead to facial muscle paralysis. Erosion of the labyrinth can cause vertigo. When it grows superiorly, it can erode the tegmen tympani and cause intra cranial complications like meningitis and brain abscess.

    Classification:

    1. Congential: - originates as embryonic rest cells, which eats away the bone until it breaks through the outer attic wall. The ear drum is normal in the initial stages. Derlaki and Clemis defined congenital cholesteatoma or Primary choleasteatoma as an embryonic rest of epithelial tissue in an ear without tympanic membrane perforation, in a patient without history of ear infection.

    2. Acquired:

    i. Primary - Type occurs following an eustachian tube malfunction resulting into retraction pockets into the attic (pars flaccida). Negative middle pressure causing retraction pocket

    ii. Secondary:

    a) Immigration - Of tympanic epithelium on deep meatal skin in the posterior superior quadrant of the tympanic membrane occurs. This is possible following destruction of the annulus after a previous middle ear discharge.

    b) Metaplasia - Is provoked by chronic infection in the ciliated mucous membrane of the middle ear. Here squamous metaplasia occurs as well as there can be a marginal migration of squamous epithelium from the meatus.

    Over time, untreated cholesteatoma can lead to bone erosion and spread of the ear infection to localized areas such as the inner ear and brain causing deafness, facial muscle paralysis, brain abscess, meningitis, and even death can occur.

    Formation of a Cholesteatoma (Pathogenesis)

    A cholesteatoma usually occurs because of poor eustachian tube function as well as infection in the middle ear. The eustachian tube normally conveys air from the back of the nose into the middle ear to equalize ear pressure. When the eustachian tubes works poorly perhaps due to allergy, a cold or sinusitis, the air in the middle ear is absorbed by the body, and a partial vacuum results in the ear. The vacuum pressure sucks in a pouch or sac by stretching the eardrum inwards, especially the superior part of the pars tensa or pars flaccida of the ear drum or areas weakened by previous infections.

    Cholesteatomas It usually takes the form of a cyst or pouch that containing scales of accumulated skin arranged in onion – like layers.

    Symptoms of a Cholesteatoma

    Initially, the ear may discharge off and on. The discharge may have a characteristic foul odour. As the cholesteatoma pouch or sac enlarges, it can cause a full feeling or pressure in the ear, along with hearing loss. Dizziness due to involvement of the balance organ and facial muscle weakness on the same side as the cholesteatoma can occur. Ideally, urgent evaluation is required as soon as the diagnosis of cholesteatoma is made.

    Dangers of ignoring a Cholesteatoma

    Ear cholesteatomas can be dangerous because of their ability to erode bone.They occur in an area crowded with important structures. There is only a thin plate of bone separating a cholesteatoma from the brain and meninges and lie close to the small bones (ossicles) of the middle ear, the organ of hearing and balance in the internal ear, facial nerve. should never be ignored. Bone erosion can cause the infection to spread into the surrounding areas, including the inner ear and brain. If untreated, deafness, brain abscess, meningitis, and rarely death can occur.

    These are indicated by headache, giddiness, increasing deafness and noises in the ear and weakness of the facial muscles.  Over time, the cholesteatoma sac  increases in size, the mouth of the sac being blocked by skin flakes. With expansion, it starts eroding surrounding structures of the middle ear

    Progression of Cholesteatoma & Chronic mastoiditis and Complications

    Treatment of Chronic Mastoiditis and Cholesteatoma

    Hearing and balance tests, CT scans of the mastoid bone may be necessary to determine the hearing level and the extent of destruction the cholesteatoma has caused.

    A cholesteatoma usually requires surgical treatment to prevent serious complications. Surgery (called Tympano- Mastoidectomy involving extensive bone drilling of the mastoid bone and removal of disease from the middle ear is required. It may be performed under general or local anesthesia. The primary purpose of surgery is to remove the cholesteatoma and infection and achieve an infection-free, self-cleansing dry ear. Hearing preservation or restoration is a secondary goal of surgery. If the disease has been satisfactorily removed. The small bones of the middle ear are repositioned to restore the hearing. Various inert material prosthesis of teflon, stainless steel, silicone and hydroxyapetite as well as homo or auto graft of bone and cartilage may also be used. In cases of severe ear destruction, restoration of normal hearing  may not be possible. Reconstruction of the middle ear to its normal anatomy is usually not possible in one operation; and therefore, a second operation (if deemed necessary) may be performed later. Facial nerve repair or procedures to control dizziness are rarely required.

    Follow-up office visits after surgical treatment are necessary and important, because cholesteatoma sometimes recurs. In cases where an open mastoidectomy cavity has been created, office visits every few months are needed in order to clean out the mastoid cavity and prevent new infections. In some patients, there must be lifelong periodic ear examinations.

    Complications of Chronic mastoiditis and Cholesteatoma