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    Otosclerosis – A common cause of middle ear deafness

    What is Otosclerosis?

    Otosclerosis is a disease of the hearing mechanism in the middle (and internal) ear in which the third bone of the chain of 3 bones in the middle ear gradually gets fixed due to new bone formation and decreasing the vibrations of sound entering the inner ear.  (see diagram). The cause of the disease is unknown. It usually manifests after the age of 15 years and is commoner in females. In 80 % of cases, the disease affects both ears to a greater or lesser extent.

    The patient or relatives notice increasing difficulty in hearing, mainly in one ear. One’s own voice may sound loud and hence the patient tends to speak softly as compared with patients with a weakness of the hearing nerve (sensori neural hearing loss) who tend to speak loudly. In some patients the first complaint is an intermittent or  continuous spontaneous noise in the ear (tinnitus).

    For some reason, in females, every pregnancy increases the deafness.

    As the disease process advances, the otosclerosis can involve the opposite ear (in80% patients). When the inner ear is also affected by the process (cochlear Otosclerosis) a “mixed” deafness (conductive and sensori-neural) develops.

    Whites are the most affected race, with the prevalence in the Black and Asian populations being much lower. Females are twice as likely as males to be affected. Usually noticeable hearing loss begins at middle-age, but can start much sooner. The hearing loss often grows worse during pregnancy.

    The disease is inherited as an autosomal dominant fashion.

    Special tests for hearing

    Pure Tone Audiometry shows the exact levels of hearing and confirm a conductive deafness where hearing by bone conduction is better than hearing by air conduction. Acoustic Impedance Bridge studies confirm a fixation of the 3rd bone (Stapes) and also confirm normal middle ear pressure but diminished ear drum movement.

    What is the treatment?

    The main treatment is surgical. The ear drum is lifted up and the middle ear is entered. Under an operating microscope, the joint between the 2nd bone (Incus) and third bone (Stapes) is separated. The upper part of the Stapes bone (super structure) is removed. A very small microscopic hole of 0.6 to 0.8 mm diameter is made in footplate of the stapes bone (Stapedotomy). One end of a teflon piston is inserted through this hole, either directly or through a vein graft. The other end of the piston is hooked around the 2nd bone (Incus). The ear drum is then replaced back in the original position.

    Sound vibrations now travel from the ear drum via the  teflon piston.

    Hearing is restored to normal on the operating table in 97 to 98% of cases.

    A Hearing aid will also give satisfaction, as in any case of conductive deafness. However, it can  never give the satisfaction of normal natural hearing as a successful operation does.

    Otosclerosis is a slowly progressive disease. As years go by, deafness increases and the opposite ear too shows signs of involvement. In females, every pregnancy increases the deafness. Gradually, after the age of 45 or 50 years, when old age deafness sets in due to age related changes of the nerves of hearing, the hearing impairment becomes more pronounced and a definite handicap in communication.

    Treatment of otosclerosis relies on two primary options: hearing aids (more recently including bone-conduction hearing aids) and a surgery called a stapedectomy. Hearing aids are usually very effective early in the course of the disease, but eventually a stapedectomy may be required fordefinitive treatment. Early attempts at hearing restoration via the simple freeing the stapes from its sclerotic attachments to the oval window were met with temporary improvement in hearing, but the conductive hearing loss would almost always recur. A stapedectomy consists of removing a portion of the sclerotic stapes footplate and replacing it with an implant that is secured to the incus. This procedure restores continuity of ossicular movement and allows transmission of sound waves from the eardrum to the inner ear.

    A modern variant of this surgery called a stapedotomy, is performed by drilling a small hole in the stapes footplate with a micro-drill or a laser, and the insertion of a piston-like prothesis. The success rate of either a stapedotomy or a stapedectomy depends greatly on the skill and the familiarity with the procedure of the surgeon.

    Other less successful treatment includes fluoride administration, which theoretically becomes incorporated into bone and inhibits otosclerotic progression. This treatment cannot reverse conductive hearing loss, but may slow the progression of both the conductive and sensorineural components of the disease process. Recently, some success has been reported with bisphosphonate medications, which stimulate bone-deposition without stimulating bony destruction.

    Sequence of a Stapedectomy operation

     

    Barotrauma

    Mechanism of middle ear pressure changes during air travel

     

     

     

     

     

    Need for Second opinion in E.N.T

    The Complexity of Radiology & Imaging Today

    Today, radiology and imaging includes a large number of modalities and covers virtually all organs in the body. It is virtually impossible for any one individual to keep abreast of all developments and to be as good in all of them.

    We, at Jankharia Imaging, have subspeciality training in specific organ systems and modalities and each one of us is an expert in our area of expertise

    Today, radiology and imaging includes a large number of modalities and covers virtually all organs in the body. It is virtually impossible for any one individual to keep abreast of all developments and to be as good in all of them.


    There are many situations in which, after you have had a radiology examination performed (e.g., x-ray, mammogram, bone densitometry, CT scan or MRI), you may feel the need for another opinion. The reasons may include one or more of those listed below:

    • When assurance is need about the report’s conclusions from another expert radiologist
    • When a subspeciality opinion is required as against that of a generalist
    • When the case is complex, and a diagnosis has not yet been reached

    Radiology Opinions

    Using our expertise, we will read your examinations, sent to us on CT, films or via the Internet, as the case may be and will get back to you within two working days at the most. We are happy to receive examinations from

    · Patients

    · Referring Doctors

    · Radiologists

    Drop attacks and frequent falls

    A drop attack is a sudden fall, with or without unconsciousness, due either to collapse of muscle tone or abnormal muscle contraction in the legs. Many neurological diseases, cardiac diseases, ear diseases, muscle dysfunction conditions like myoclonic syndromes and startle responses can cause drop attacks. In about 30% of drop attacks the cause is unknown.

    Weakness of muscles of the legs

    Weakness of the hip and knee extensor muscles (important for maintaining an erect posture)
    Some causes include muscular dystrophy, neurogenic atrophy, polymyositis, myasthenia gravis and spinal cord ischemic attacks. Duchenne’s muscular dystrophy is the most common cause of muscle dystrophy.

    Isolated quadriceps weakness – secondary to diseases like polymyositis, inclusion body myositis and neurogenic atrophy, and the legs may suddenly give way without warning to cause falls

    Intermittent spinal ischemia can produce sudden attacks of transient paraparesis or falls, and causes include syphilitic arteritis, arteriosclerosis of the distal aorta, adhesive arcachnoiditis, spinal compression due to spinal stenosis or disc herniation; the attacks are often precipitated by exercise and relieved by rest

    Neurodegenerative diseases

    Patients with Parkinson’s disease often fall due to defective postural reflexes, sudden freezing, and uncoordinated turning; their stooped flexed posture predisposes them to falling forward because their centre of gravity is displaced forward when standing or walking.
    Other neurodegenerative diseases associated with frequent falls include progressive supranuclear palsy, corticobasal degeneration, Huntington’s chorea, multiple system atrophy and Alzheimer’s disease

    Transient ischemic attacks
    A patient with vertebro-basilar artery ischemia can present with a sudden loss of tone in their legs, causing their knees to buckle. The patient falls powerlessly without protective arm movements; There may be no precipitating head or neck movements or loss of consciousness, The patient can get up and walk immediately or within one minute. Usually other symptoms of brainstem ischemia are present (vertigo, diplopia, blurred vision, sensory changes, motor weakness, which suggest the diagnosis.

    Epilepsy
    Drop attacks can be due to sudden muscle contractions associated with generalized convulsive epilepsy, or a sudden loss of postural tone due to atonic epilepsy or epileptic negative myoclonus.
    Atonic epileptic attacks in children can occur when standing or sitting or lying, and there is no aura or state of confusion; sudden drop attacks can cause the patient to collapse with triple flexion of the legs and no involvement of the arms. The patient can usually get up immediately after an attack.

    Various myoclonic syndromes
    Mycoclonus is a sudden brief, shock-like muscle movement caused by a brief muscle contraction (positive myoclonus) or inhibition of a muscle contraction (negative myoclonus)
    It can mimic idiopathic drop attacks, and the patient can fall suddenly with buckling of the legs

    Startle reactions
    Pathological startle reactions (hypereflexia) are characterized by an exaggerated motor response to unexpected auditory stimuli, and less frequently to visual or somasthetic stimuli.
    They consist of both brief myoclonic jerks and longer tonic spasms
    Hypereflexia may have a variety of causes eg. idiopathic, hereditary, or secondary to acquired brainstem diseases – post-anoxic encephalopathy, viral or paraneoplastic brainstem encephalitis, multiple sclerosis, sarcoidosis or brainstem strokes. Myoclonic jerks occur frequently during the day, but also at night when the patient is asleep, and mainly affect the legs
    Sterotyped tonic spasms consist of facial grimacing, flexion of the neck and trunk, flexion or extension of the hips and knees, and characteristic abduction of the shoulders with flexion of the elbows. The patient falls forwards rigidly like a log, but sometimes falls backwards; protective reflexes are impossible and injuries common; consciousness is maintained during the fall and recovery is fast

    Cataplexy and paroxysmal choreoathetosis
    Cataplexy can cause sudden falls without LOC, but the patient cannot speak during the fall
    Characteristic precipitating factors include laughter or a sudden emotional stimulus. Minor symptoms of cataplexy may consist of a brief drop of the jaw and sagging of the head, but severe attacks can cause loss of tone in all the antigravity muscles and the patient falls powerlessly and loosely and remains immobile for many seconds (longer than in hypereflexia)

    Paroxysmal choreoathetosis – attacks are usually precipitated by sudden leg movements during standing or running or social embarrassment => the patient may suddenly lose control due to tonic spasms or an involuntary choreoathetotic muscle movement and fall like a log

    Posterior cranial fossa pathology
    Mass lesions around the foramen magnum can cause drop attacks
    Odontoid process fractures
    Arnold-Chiari type I malformations
    Drop attacks can be precipitated by neck movements, coughing or sneezing, or vertical head compression;
    the drop attack patient presents with a stiff neck, spastic paraplegia and limb paresthesias
    Posterior fossa arachnoid cysts, midline metastatic cerebellar tumors, vermis hemangioblastomas, and obstructive hydrocephalus due to third ventricle cysts

    Meniere’s drop attacks (Tumarkin’s otolithic crisis)
    Seen in the early or late stages of Meniere’s disease when there is a sudden change in endolymphatic pressure which causes end-organ stimulation with a reflex-like vestibulospinal loss of postural tone. The patient suddenly loses control of balance and falls and he sometimes with a distinct feeling of being pushed or thrown to the ground. The patient does not lose consciousness.
    (* a patient with Wallenberg’s syndrome, due to a lateral medullary stroke, may have a similar transient sensation of being pulled or pushed to the side, and the patient suddenly falls to the side without realizing that it is his active shift of the centre of gravity – lateropulsion – that causes the momentary imbalance)

    Idiopathic drop attacks (no specific cause found)
    A fall without warning, not associated with loss of consciousness, not apparently due to any malfunction of the legs, not induced by changes of posture or movement of the head, and not accompanied by vertigo or other cephalic sensation, and not associated with myoclonic jerks
    It usually appears between the ages 40 – 60 years. Patients only fall when standing or walking, and they usually buckle at the knees and fall forwards.
    The attacks occur very suddenly and the patient cannot remember if he lost consciousness, or not; the patient can get up immediately unless accidental injury occurs (minor upper limb fractures and/or dislocations are common in the elderly)
    Serial attacks are rare, and spontaneous remission is common (25 – 80%)

    Scope of ENT speciality

    Superior canal dehiscence syndrome (SCDS)

    Superior canal dehiscence syndrome (SCDS)

    Superior canal dehiscence syndrome (SCDS) is a rare condition of the inner ear, first described in 1998 by Dr.Lloyd Minor of Johns Hopkins University, Baltimore, USA, leading to hearing and balance disorders in those affected. The symptoms are caused by a thinning or complete absence of the part of the temporal bone overlying the superior semi circular canal. This may result from slow erosion of the bone or physical trauma to the skull and there is evidence that the defect or susceptibility is congenital.
    Symptoms

    Autophony – Patients with SCDS-related autophony report hearing their own voice as a disturbingly loud and distorted sound deep inside the head as if relayed through “a cracked loudspeaker.” Additionally they may hear the creaking and cracking of joints, the sound of their footsteps when walking or running, their heartbeat and the sound of chewing and other digestive noises. A distinctive feature of this condition almost exclusively associated with SCDS is hearing the sound of the eyeballs moving in their sockets (e.g. when reading in a quiet room) “like sandpaper on wood”.
    Tullio phenomenon, another of the more identifiable symptoms leading to a positive SCD diagnosis is sound-induced loss of balance. Patients showing this symptom may experience vertigo, a feeling of motion sickness or even actual nausea, triggered by normal everyday sounds. Although this is often associated with loud noises, volume is not necessarily a factor. Patients describe a wide range of sounds that affect balance: a telephone ringing; a knock at the door; music; the sound of children playing and even the patient’s own voice are typical examples of sounds that can cause a loss of balance when this condition is present, although there are countless others. For such persons, a visit to the concert hall or to a noisy playground may seem like being at the epicenter of an earthquake. A change of pressure within the middle ear (for example when flying or nose-blowing) may equally set off a bout of disequilibrium or nystagmus.
    Low-frequency conductive hearing loss is present in many patients with SCDS and is explained by the dehiscence acting as a “third window.” Vibrations entering the ear canal and middle ear are then abnormally diverted through the superior semi circular canal and up into the intracranial space instead of being registered as sound in the hearing center, the cochlea. This hearing loss being greater in the lower frequencies and may initially be mistaken for otosclerosis.

    Pulsatile tinnitus is yet another of the typical symptoms of SCDS and is caused by the gap in the dehiscent bone allowing the normal pulse-related pressure changes within the cranial cavity to enter the inner ear abnormally. This pressure change thus becomes audible and an existing tinnitus will be perceived as containing a pulse-synchronized “wave” or “blip” which patients describe as a “swooshing” sound.
    Brain fog and fatigue are both common SCDS symptoms and are caused by the brain having to spend an unusual amount of its energy on the simple act of keeping the body in a state of equilibrium when it is constantly receiving confusing signals from the dysfunctional semicircular canal.
    Headache and migraine are also often mentioned by patients showing other symptoms of SCDS. A direct causal link has yet to be proven.
    Causes
    In approximately 2.5% of the general population the bones of the head develop to only 60-70% of their normal thickness in the months following birth. In SCDS the section of temporal bone separating the superior semicircular canal from thecranial cavity, normally 0.8 mm thick, shows a thickness of only 0.5 mm, making it more fragile and susceptible to damage through physical head trauma or from slow erosion.

    Diagnosis
    The presence of dehiscence can be detected by a high definition (0.6 mm or less) coronal CT Scan of the temporal bone, currently the most reliable way to distinguish between superior canal dehiscence syndrome (SCDS) and other conditions of the inner ear involving similar symptoms such as Meniere’s disease and Perilymph fistula. Other diagnostic tools include the VMPtest, CENG (Computerized ElectroNystagmography) or VNG, electrocochleography (ECOG) and the rotational chair test. An accurate diagnosis is of great significance as unnecessary exploratory middle ear surgery may thus be avoided. Several of the symptoms typical to SCDS (e.g. vertigo and Tullio) may also be present singly or as part of Ménière’s disease, sometimes causing the one illness to be confused with the other. There are reported cases of patients being affected by both Ménière’s disease and SCDS concurrently.

    Treatment
    Once diagnosed, the gap in the temporal bone can be repaired by surgical resurfacing of the affected bone or plugging of the superior semicircular canal. These techniques are performed by accessing the site of the dehiscence either via a middle fossa craniotomy or via a canal drilled through the transmastoid bone behind the affected ear.

    Dr. A. K. Chaudri – Consultant ENT Surgeon

    Degrees/Fellowships

    • MBBS (University of Mumbai, India)
    • DORL (Diplomate of the College of Physicians & Surgeons, Mumbai)
    • FCPS (Fellow of College of Physicians & Surgeons, Mumbai, by examination)
    • MS (Master of Surgery [ENT], University of Mumbai, India
    • DLO (Diplomate by examination in 2 parts of the Royal College of Surgeons (London)
    • FRCS (Edinburgh) – Fellowship by examination in 2 parts of the Royal College of Surgeons

    Credentials

    Dr. A. K. Chaudri graduated from the University of Mumbai, India

    He had advanced post graduate training in the ENT speciality and in Plastic surgery at the K.E.M.Hospital, and the L.T.M.G. Hospital,Mumbai . He then proceeded for super specialization to the U.K. where he had extensive training in the more advanced aspects of the speciality for 5 years.

    He passed the Diploma in E.N.T. Examinations – both parts at first appearance DLO of the Royal College of Surgeons (London)

    He became a fellow of the Royal College of Surgeons of Edinburgh ie FRCS ( Edinburgh) after successfully passing the primary and final parts of the FRCS at first appearance in both examinations.

    He has done an advanced course in hearing and vertigo testing at the Institute of Sound and Vibration Research, University of Southampton, England. He has undergone special training in ear surgery with Dr. IanThorburn, well known Ear Surgeon, for 1 year at Blackpool, England.

    He has attended several courses at Gray’s Inn Road E.N.T Hospital, King’s Cross, London, the well recognised Centre of E.N.T. learning

    Back in India he has participated in several camps in ear surgery at Nashik and Dhule, in Maharashtra and in Dahanu with the Rotary Club of Mumbai South of which he was the Medical Chairman. He has worked with well known Ear surgeons Dr. Gadre, Dr. Tepan, Dr. Karnik and Dr. Anklesaria. He has performed free examination of school children in hundreds.

    After his initial training abroad, in the U.K., he has been travelling extensively to learn personally from world renowned ENT surgeons in their fields of expertise. He has visited the authorities in the European subcontinent – Professor Tauno Palva at the Korrva Klinika in Helsinki, Finland, Professor Plester at the University of Tubingen, West Germny, Prof. Jean Marquet in Belgium, Prof Claus Jannsen in West Germany, Professor Claus Claussen, Professor of NeuroOtology a world renown authority on vertigo at Bad Kisengen in West Germany.

    Commitment to Excellence
    Dr. Chaudri has a special interest in ear pathologies, ear surgery, hearing assessment and fitting of hearing aids, treatment for ear drum perforations andcholesteatoma, sino-nasal pathology and allergy management.

    As ear problems are extremely common in the Indian sub continent, he has vast experience in the surgical treatment of these conditions.

    Commitment to Community
    Dr. Chaudri is actively serving the medical profession at various levels.His special ability and interest lies in explanatory talks on medicaltopcs to laymen, students and doctors alike. He has been an invitee at various Rotary clubs, Giants clubs etc.

    He is on Advisory Panel of some magazines and is often sought for his views and opinions about ENT conditions by both English and local newspapers. He has appeared on TV and he gives talks on medical related topics

    He participates in community events such as deafness screening of senior citizens and free examination of hundreds of school children.

    Commitment to Positive Thinking and Healthy Living
    Being a firm believer of lifelong learning, he is a regular reader of medical books and magazines, devoted to research activities, regularly recording endoscopic clips of E.N.T. disease and presenting them as interesting case studies for laymen and the medical profession.

    BTM (Basilar Type Migraine)

    Basilar-Type Migraine

    This form of migraine was previously known as Basilar Artery Migraine (BAM). Under the International Headache Society’s International Classification of Headache Disorders, 2nd Edition, the new designation for this form of Migraine is Basilar-Type Migraine (BTM). It has also been called Bickerstaff syndrome, brainstem Migraine, and vertebrobasilar Migraine.

    The term Basilar-Type Migraine is actually a bit misleading as it implies that the Migraine attack is vascular in origin due to spasm of the basilar artery and the subsequent ischemia.

    Since the time when the term Basilar came into use, however, it has been shown that Migraine is a genetic neurological disease, and BTM, as other types of Migraine are neural in origin.

    As with all Migraine, there is a vascular component once the Migraine begins, but the origin is  neurological. Early literature (Bickerstaff 1962) suggested that BTM was most  common in adolescent females. However, presently it is seen to affect all age groups and both male and female.

    BTM does exhibit the same female predominance seen overall in Migraine; three times as many female sufferers as male. A Basilar-Type Migraine is a Migraine that has aura symptoms originating from the brainstem and/or affecting both hemispheres of the brain at the same time, but with no motor weakness.
    The aura of BTM usually lasts less than 60 minutes, but in some cases can be more extended. Many Migraineurs  who have BTM also report Migraine with typical aura. The aura of BTM can include temporary blindness, which is one reason they can be quite terrifying. However,

    BTM is actually essentially Migraine with aura with the aura localized to the brainstem. Still, because of that localization, Migraine-specific medications such as the triptans and ergotamines are contraindicated for BTM. Of the preventive medications, it’s recommended that beta blockers be avoided in cases of BTM.

    Because of the medication contraindications, I highly recommend that Migraineurs who experience BTM  wear some kind of medical identification at all times. Diagnosis of BTM requires at least two attacks meeting the following criteria:

    Aura consisting of at least two of the following fully reversible symptoms, but no motor weakness:
    Dysarthria (impairments or clumsiness in the speaking of words due to diseases that affect the oral,
    lingual, or pharyngeal muscles)
    vertigo
    tinnitus
    hypacusia (impaired hearing)
    diplopia (double vision)
    visual symptoms simultaneously in both temporal and nasal fields of both eyes
    ataxia
    decreased level of consciousness
    simultaneously bilateral paresthesias (abnormal or unpleasant sensation often described as numbness
    or as a prickly, stinging, or burning feeling)

    At least one of the following:
    at least one aura symptom develops gradually over five or more minutes and/or different aura
    symptoms occur in succession over five or more minutes
    each aura symptom lasts five or more and 60 minutes or less headache meeting criteria Migraine
    without aura begins during the aura or follows aura within 60 minutes

    Migraine experts caution that when there is motor weakness, great care be taken to arrive at the proper
    diagnosis as there are times when it can be  difficult to differentiate between Basilar-Type Migraine and
    Hemiplegic Migraine. The IHS criteria also note that if motor weakness is present, the disorder should
    be coded as Familial Hemiplegic or Sporadic Hemiplegic Migraine.
    Another reason great care must be taken in diagnosis is that many of the symptoms of BTM are also
    stroke symptoms.
    Basilar-Type Migraine presents symptoms that can mimic other, far more serious conditions. It is
    essential that the diagnosis be definitive and correct. An imaging study such as a CT scan or MRI
    should be performed to rule out other causes for the symptoms, and an EEG is often performed to
    rule out seizure disorders. If the doctor making the diagnosis is hesitant about it, definitely seek a second
    opinion from another doctor. Since BTM is not common, seeing a Migraine specialist is advisable when
    possible. It is also important to continue medical treatment as advised by your doctor and not skip follow-
    up appointments.

    Some other conditions that should be ruled out in diagnosing BTM are:
    seizure disorders
    space-occupying lesions of the brain
    brainstem Arteriovenous Malformation (AVM): a congenital defect consisting of a tangle of abnormal
    arteries and veins with no capillaries in between. The blood pressure in the veins is higher than
    normal and may result in a rupture of the vein and bleeding into the brain.
    vertebrobasilar disease
    stroke

    As with other forms of Migraine, BTM can be disabling. Because of the neurological symptoms that can
    occur during Basilar-Type Migraine aura, it can present a larger hurdle than Migraine with aura because
    the aura itself is debilitating and can last longer. This can mean special problems for people in the
    traditional work force or trying to care for young children. If they are in an environment where others are
    not educated about Migraine disease, it is particularly important that efforts be made  to educate those
    around them.
    Basilar-Type Migraine is one of the most frightening of head pain disorders, but the symptoms are
    usually more frightening than harmful.
    However, as with other forms of Migraine, if the pain is extreme, it is best to seek emergency care. BTM
    does increase the risk of stroke slightly more than Migraine with aura and Migraine without aura, so
    additional care should be taken. Once diagnosed with BTM, it is important (as with any form of
    Migraine) to consult your doctor if your symptoms or Migraine pattern change. Without consulting a
    doctor, it’s impossible to be sure that new symptoms or changes in pattern are attributable to BTM, and
    that no other condition is present. While BTM isn’t cause to panic, it is more than reason to be sensible
    and take good care of yourself.

    In basilar migraine and in other migraine equivalent vertigos the otological aspect is subsidiary to the
    main disease. Investigation fails to reveal a primary labyrinthine disorder and treatment is the province of medical or neurological specialties.

    1. Endoscopic examination of Ear, Nose, Throat, Vocal cords

    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.

    For Vestibular rehabilitation exercises Click