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SECTION I — Diseases of Ear
Figure 14.11. Longitudinal fracture of the temporal bone right side. (A) CT scan showing the fracture line. (B) Fracture line as seen during the
operation (arrow).
TABLE 14.2 DIFFERENCES IN LONGITUDINAL AND TRANSVERSE FRACTURES OF TEMPORAL BONE
Longitudinal Transverse
Frequency More common (80%) Less common (20%)
Type of injury Parietal blow Occipital blow
Fracture line Runs parallel to long axis of petrous pyramid.
Starts at squamous part of temporal bone to
end at foramen lacerum
Bleeding from ear Common, due to injury to tegmen and
tympanic membrane
Cerebrospinal fluid otorrhoea Present, often mixed with blood Absent or unmanifested
Structures injured Tegmen, ossicles and tympanic membrane Labyrinth or CN VIII
Hearing loss Conductive Sensorineural
Vertigo Less often; due to concussion Severe, due to injury to labyrinth or CN VIII
Facial paralysis Less (20%), delayed onset. Nerve is injured
in tympanic segment, distal to geniculate
ganglion
2. Ear or Mastoid Surgery
Facial nerve is injured during stapedectomy, tympanoplasty
or mastoid surgery. Paralysis may be immediate or delayed
and treatment is the same as in temporal bone trauma.
Sometimes, nerve is paralyzed due to pressure of packing
on the exposed nerve and this should be relieved first.
Operative injuries to facial nerve can be avoided if at-
tention is paid to the following:
(a) Anatomical knowledge of the course of facial nerve,
possible variations and anomalies and its surgical
landmarks. Cadaver dissections should be an important part of the training in ear surgery.
(b) Always working along the course of nerve and never
across it.
(c) Constant irrigation when drilling to avoid thermal in-
jury. Use diamond burr when working near the nerve.
Runs across the petrous. Starts at foramen magnum
or jugular foramen towards the foramen
spinosum
Absent because tympanic membrane is intact.
Haemotympanum may be seen
Most common (50%). Immediate onset. Injury to
nerve in meatal or labyrinthine segment proximal
to geniculate ganglion.
(d) Gentle handling of the nerve when it is exposed,
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avoiding any pressure of instruments on the nerve.
(e) Not to remove any granulations that penetrate the nerve.
(f) Using magnification; never to work on facial nerve
without an operating microscope.
3. Parotid Surgery and Trauma to Face
Facial nerve may be injured in surgery of parotid tumours
or deliberately excised in malignant tumours. Accidental
injuries in the parotid region can also cause facial paralysis. Application of obstetrical forceps may also result in
facial paralysis in the neonate due to pressure on the extratemporal part of nerve.
D. NEOPLASMS
1. Intratemporal Neoplasms
Carcinoma of external or middle ear, glomus tumour,
rhabdomyosarcoma and metastatic tumours of temporal
bone, all result in facial paralysis. Facial nerve neuroma
occurs anywhere along the course of nerve and produces
paralysis of gradual or sudden onset. It is treated by excision and nerve grafting. High-resolution CT scan and
gadolinium-enhanced MRI is very useful for facial nerve
tumour.
2. Tumours of Parotid
Facial paralysis with tumour of the parotid almost always
implies malignancy (see Tumours of salivary glands).
Chapter 14 — Facial Nerve and Its Disorders
Figure 14.12. Topographical localization of the VIIth nerve lesions.
(A) Suprageniculate or transgeniculate lesion. Secretomotor fibres to
the lacrimal gland leave at the geniculate ganglion and are interrupted
in lesions situated at/or proximal to the geniculate ganglion. (B) Suprastapedial lesions cause loss of stapedial reflex and taste but preserve
lacrimation. (C) Infrastapedial lesions cause loss of taste but preserve
stapedial reflex and lacrimation. (D) Infrachordal lesions cause loss of
facial motor function alone.
Scan to play Anatomy and Functions of Facial Nerve.
107
E. SYSTEMIC DISEASES AND FACIAL
PARALYSIS
Peripheral facial paralysis is mostly of idiopathic variety but
always needs exclusion of diabetes, hypothyroidism, leukaemia, sarcoidosis, periarteritis nodosa, Wegener’s granulomatosis, leprosy, syphilis and demyelinating disease.
LOCALIZATION OF FACIAL LESION
A. CENTRAL FACIAL PARALYSIS
It is caused by cerebrovascular accidents (haemorrhage,
thrombosis or embolism), tumour or an abscess. It causes
paralysis of only the lower half of face on the contralateral side. Forehead movements are retained due to bilateral innervation of frontalis muscle. Involuntary emotional movements and the tone of facial muscles are also
retained.
B. PERIPHERAL FACIAL PARALYSIS
All the muscles of the face on the involved side are paralyzed. Patient is unable to frown, close the eye, purse the
lips or whistle.
A lesion at the level of nucleus is identified by associated
paralysis of VIth nerve.
A lesion at cerebellopontine angle is identified by the presence of vestibular and auditory defects and involvement
of other cranial nerves such as Vth, IXth, Xth and XIth.
A lesion in the bony canal, from internal acoustic meatus
to stylomastoid foramen, can be localized by topodiagnostic tests.
A lesion outside the temporal bone, in the parotid area,
affects only the motor functions of nerve. It may sometimes be incomplete as some branches of the nerve may
not be involved in tumour or trauma.
TOPODIAGNOSTIC TESTS FOR LESIONS IN
INTRATEMPORAL PART (FIGURE 14.12 )
The following tests are useful in finding the site of lesion
in paralysis of lower motor neuron.
1. schirmer Test. It compares lacrimation of the two
sides. A strip of filter paper is hooked in the lower fornix
of each eye and the amount of wetting of strip measured.
Decreased lacrimation indicates lesion proximal to the
geniculate ganglion as the secretomotor fibres to lacrimal
gland leave at the geniculate ganglion via greater superficial petrosal nerve.
2. stapedial ReFlex. Stapedial reflex is lost in lesions
above the nerve to stapedius. It is tested by tympanometry.
3. taste Test. It can be measured by a drop of salt
or sugar solution placed on one side of the protruded
tongue, or by electrogustometry. Impairment of taste indicates lesion above the chorda tympani.
4. submandibular SaliVary Flow Test. It also measures function of chorda tympani. Polythene tubes are
passed into both Wharton ducts and drops of saliva
counted during one minute period. Decreased salivation
shows injury above the chorda.
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SECTION I — Diseases of Ear
COMPLICATIONS FOLLOWING FACIAL
PARALYSIS
Peripheral facial paralysis due to any cause may result in
any of the following complications:
1. incomplete RecoVery. Facial asymmetry persists.
Eye cannot be closed resulting in epiphora. A weak oral
sphincter causes drooling and difficulty in taking food.
2. exposure Keratitis. Eye cannot be closed, tear film
from the cornea evaporates causing dryness, exposure
keratitis and corneal ulcer. This is worse when tear production is also affected. It can be prevented by use of artificial tears (methylcellulose drops) every 1–2 h, eye ointment and proper cover for the eye at night.
Temporary tarsorrhaphy may also be indicated. Eye
closure can also be improved by using gold-weight implant sutured to the tarsal plate deep to levator palpebrae
muscle.
3. synkinesis (Mass MoVement). When the patient
wishes to close the eye, corner of mouth also twitches or
vice versa. It is due to cross innervation of fibres; there is
no treatment.
4. tics and Spasms. They are the result of faulty regeneration of fibres. Involuntary movements are seen on the
affected side of the face.
5. contractures. They result from fibrosis of atrophied
muscles or fixed contraction of a group of muscles. They
affect movements of face but facial symmetry at rest is
good.
6. crocodile Tears (Gustatory Lacrimation). There
is unilateral lacrimation with mastication. This is due to
faulty regeneration of parasympathetic fibres which now
supply lacrimal gland instead of the salivary glands. It
can be treated by section of greater superficial petrosal
nerve or tympanic neurectomy.
7. Frey’s Syndrome (Gustatory Sweating). There is
sweating and flushing of skin over the parotid area during
mastication. It results from parotid surgery.
8. psychological and Social Problems. Drooling
during eating and drinking and impairment of speech
cause social problems.
Figure 14.13. Hemifacial spasm. Note all the facial muscles and
platysma in the spasm. Picture taken during paroxysm of clonic contractions.
is acoustic neuroma, congenital cholesteatoma or glomus
tumour. Many cases of hemifacial spasm are due to irritation of the nerve because of a vascular loop at the cerebellopontine angle. Microvascular decompression through
posterior fossa craniotomy has met with high success rate
in these cases. Idiopathic type has been treated by selective section of the branches of facial nerve in the parotid
or by puncturing the facial nerve with a needle in its tympanic segment.
Botulinum toxin has been used in the affected muscle.
It blocks the neuromuscular junction by preventing release of acetylcholine.
2. blepharospasm. Twitchings and spasms are limited
to orbiculars oculi muscles on both sides. The eyes are
closed due to muscle spasms causing functional blindness. The cause is uncertain, but probably lies in the basal
ganglia. It is treated by selective section of nerves supplying muscles around the eye on both sides.
Botulinum-A toxin injected into the periorbital muscles gives relief for 3–6 months. Injection can be repeated,
if necessary.
SURGERY OF FACIAL NERVE
HYPERKINETIC DISORDERS
OF FACIAL NERVE
They are characterized by involuntary twitching of facial
muscles on one or both sides.
1. hemiFacial Spasm. It is characterized by repeated,
uncontrollable twitchings of facial muscles on one side
(Figure 14.13). It is of two types (i) essential or idiopathic,
where cause is not known and (ii) secondary, where cause
1. decompression. The nerve may be compressed by
oedema, haematoma or a fractured bone in its intratemporal part. The bony canal is exposed and uncapped. The
sheath of nerve is also slit to relieve pressure due to oedema or intraneural haematoma.
2. end-to-End Anastomosis. This is done when the
gap between severed ends of the nerves is only a few millimetres. It is a suitable procedure for extratemporal part
of the nerve. There should not be any tension in the approximated ends.
Chapter 14 — Facial Nerve and Its Disorders
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3. nerVe GraFt (Cable GraFt). When the gap between
severed ends cannot be closed by end-to-end anastomosis, a nerve graft is more suitable than extensive rerouting or mobilization of nerve. Nerve graft is taken from
greater auricular, lateral cutaneous nerve of thigh or the
sural nerve. In the bony canal, the graft may not require
any suturing.
4. hypoglossal-Facial Anastomosis. Hypoglossal
nerve is anastomosed to the severed peripheral end of the
facial nerve. It improves the muscle tone and permits some
movements of facial muscles, but at the expense of atrophy of tongue on that side. However, disability of tongue
due to atrophy is not so severe and patient adjusts to the
difficulty in chewing and articulation after a few weeks.
5. plastic Procedures. They are used to improve cosmetic appearance when nerve grafting is not feasible or
has failed. The procedures include facial slings, face lift
operation or slings of masseter and temporalis muscle.
The latter also gives some movement to face in addition
to symmetry.
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Chapter 15
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Ménière’s Disease
Ménière’s disease, also called endolymphatic hydrops, is a
disorder of the inner ear where the endolymphatic system is distended with endolymph. It is characterized by
(i) vertigo, (ii) sensorineural hearing loss, (iii) tinnitus and
(iv) aural fullness.
PATHOLOGY
The main pathology is distension of endolymphatic system, mainly affecting the cochlear duct (scala media)
and the saccule, and to a lesser extent the utricle and
semicircular canals. The dilatation of cochlear duct is
such that it may completely fill the scala vestibuli; there
is marked bulging of Reissner’s membrane, which may
even herniate through the helicotrema into the apical
part of scala tympani (Figure 15.1). The distended saccule may come to lie against the stapes footplate. The
utricle and saccule may show outpouchings into the
semicircular canals.
AETIOLOGY
The main pathology in Ménière’s disease is distension of
endolymphatic system due to increased volume of endolymph. This can result either from increased production
of endolymph or its faulty absorption or both. Normally,
endolymph is secreted by stria vascularis, fills the membranous labyrinth and is absorbed through the endolymphatic sac (see p. 11 for inner ear fluids).
The exact cause of Ménière’s disease is not yet known.
Various theories have been postulated (Figure 15.2).
1. deFectiVe Absorption by Endolymphatic Sac.
Normally, endolymph is carried by the endolymphatic
duct to the sac where it is absorbed. Defective absorption by the sac may be responsible for raised endolymph
pressure. Experimental obstruction of endolymphatic sac
and its duct also produces hydrops. Ischaemia of sac has
been observed in cases of Ménière’s disease undergoing
sac surgery, indicating poor vascularity and thus poor absorption by the sac. Distension of membranous labyrinth
leads to rupture of Reissner’s membrane and thus mixing
of perilymph with endolymph, which is thought to bring
about an attack of vertigo.
2. Vasomotor Disturbance. There is sympathetic over-
activity resulting in spasm of internal auditory artery and/
or its branches, thus interfering with the function of cochlear or vestibular sensory neuroepithelium. This is responsible for deafness and vertigo. Anoxia of capillaries of stria
vascularis also causes increased permeability, with transudation of fluid and increased production of endolymph.
3. allergy. The offending allergen may be a foodstuff
or an inhalant. In these cases, inner ear acts as the “shock
organ” producing excess of endolymph. Nearly 50% of
patients with Ménière’s disease have concomitant inhalant and/or food allergy.
It is possible that Ménière’s disease is multifactorial,
resulting in the common end point of endolymphatic hydrops with classical presentation.
4. sodium and Water Retention. Excessive amounts
of fluid are retained leading to endolymphatic hydrops.
5. hypothyroidism. About 3% of cases of Ménière’s
disease are due to hypothyroidism. Such cases benefit
from thyroid replacement therapy.
6. autoimmune and Viral Aetiologies have also been
suggested on the basis of experimental, laboratory and
clinical observations.
CLINICAL FEATURES
Age and sex. Disease is commonly seen in the age group of
35–60 years. Males are affected more than females. Usually, disease is unilateral but the other ear may be affected
after a few years.
Cardinal symptoms of Ménière’s disease are (i) episodic
vertigo, (ii) fluctuating hearing loss, (iii) tinnitus and (iv)
sense of fullness or pressure in the involved ear.
1. Vertigo. It comes in attacks. The onset is sudden. Patient gets a feeling of rotation of himself or his environment. Sometimes, there is feeling of “to and fro” or “up
and down” movement. Attacks come in clusters, with periods of spontaneous remission lasting for weeks, months
or years. Usually, an attack is accompanied by nausea and
vomiting with ataxia and nystagmus. Severe attacks may
be accompanied by other symptoms of vagal disturbances
such as abdominal cramps, diarrhoea, cold sweats, pallor
and bradycardia. Usually, there is no warning symptom of
an oncoming attack of vertigo but sometimes the patient
may feel a sense of fullness in the ear, change in character
of tinnitus or discomfort in the ear which herald an attack.
Some cases of Ménière’s disease show Tullio phenomenon.
It is a condition where loud sounds or noise produce vertigo and is due to the distended saccule lying against the
stapes footplate. This phenomenon is also seen when there
are three functioning windows in the ear, e.g. a fenestration of horizontal canal in the presence of a mobile stapes.
2. hearing Loss. It usually accompanies vertigo or may
precede it. Hearing improves after the attack and may be
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Figure 15.1. (A) Normal cochlear duct. (B) Cochlear duct is distended with endolymph pushing the Reissner’s membrane into scala vestibuli.
SECTION I — Diseases of Ear
EXAMINATION
1. otoscopy. No abnormality is seen in the tympanic
membrane.
2. nystagmus. It is seen only during acute attack. The
quick component of nystagmus is towards the unaffected
ear.
Figure 15.2. Aetiologic factors and symptomatology of Ménière’s
disease (endolymphatic hydrops).
normal during the periods of remission. This fluctuating
nature of hearing loss is quite characteristic of the disease.
With recurrent attacks, improvement in hearing during
remission may not be complete; some hearing loss being
added in every attack leading to slow and progressive deterioration of hearing which is permanent.
• Distortion of sound. Some patients complain of distort-
ed hearing. A tone of a particular frequency may appear normal in one ear and of higher pitch in the other
leading to diplacusis. Music appears discordant.
• Intolerance to loud sounds. Patients of Ménière’s disease
cannot tolerate amplification of sound due to recruitment
phenomenon. They are poor candidates for hearing aids.
3. tinnitus. It is low-pitched roaring type and is aggravated during acute attacks. Sometimes, it has a hissing character. It may persist during periods of remission.
Change in intensity and pitch of tinnitus may be the
warning symptom of attack.
3. tuning Fork Tests. They indicate sensorineural hear-
ing loss. Rinne test is positive, absolute bone conduction is
reduced in the affected ear and Weber is lateralized to the
better ear.
INVESTIGATIONS
1. pure Tone Audiometry. There is sensorineural hear-
ing loss. In early stages, lower frequencies are affected and
the curve is of rising type. When higher frequencies are
involved curve becomes flat or a falling type (Figure 15.3).
4. sense oF Fullness or Pressure. Like other symptoms, it also fluctuates. It may accompany or precede an
attack of vertigo.
5. other Features. Patients of Ménière’s disease often
show signs of emotional upset due to apprehension of
the repetition of attacks. Earlier, the emotional stress was
considered to be the cause of Ménière’s disease.
Figure 15.3. (A) Audiogram in early Ménière’s disease. Note: Hearing loss is sensorineural and more in lower frequencies—the rising
curve. As the disease progresses, middle and higher frequencies get
involved and audiogram becomes flat or falling type (B & C).
Chapter 15 — Ménière’s Disease
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TABLE 15.1 RESULTS OF VARIOUS TESTS TO DIFFERENTIATE A COCHLEAR FROM A RETROCOCHLEAR LESION
Normal Cochlear lesion Retrocochlear lesion
Pure tone audiogram Normal Sensorineural hearing loss Sensorineural hearing loss
Speech discrimination score 90–100% Below 90% Very poor
Roll over phenomenon Absent Absent Present
Recruitment Absent Present Absent
SISI score 0–15% Over 70% 0–20%
Threshold tone decay test 0–15 dB Less than 25 dB Above 25 dB
Stapedial reflex Present Present Absent
Stapedial reflex decay (page 107) Normal Normal Abnormal
BERA Normal interval between wave I & V Normal interval between wave I & V Wave V delayed or absent
BERA, brainstem evoked response audiometry.
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2. speech Audiometry. Discrimination score is usually
55–85% between the attacks but discrimination ability is
much impaired during and immediately following an attack.
3. special Audiometry Tests. They indicate the
cochlear nature of disease and thus help to differentiate from retrocochlear lesions, e.g. acoustic neuroma
(Table 15.1).
(a) Recruitment test is positive.
(b) SISI (short increment sensitivity index) test. SISI score is
better than 70% in two-thirds of the patients (normal
15%).
(c) Tone decay test. Normally, there is decay of less than
20 dB.
4. electrocochleography. It shows changes diagnostic of Ménière’s disease. Normally, ratio of summating potential (SP) to action potential (AP) is 30%. In Ménière’s
disease, SP/AP ratio is greater than 30% (Figure 15.4).
5. caloric Test. It shows reduced response on the affected side in 75% of cases. Often, it reveals a canal paresis on the affected side (most common) but sometimes
there is directional preponderance to healthy side or a
combination of both canal paresis on the affected side
and directional preponderance on the opposite side.
6. glycerol Test. Glycerol is a dehydrating agent.
When given orally, it reduces endolymph pressure and
thus causes an improvement in hearing.
Patient is given glycerol (1.5 mL/kg) with an equal
amount of water and a little flavouring agent or lemon
juice. Audiogram and speech discrimination scores are
recorded before and 1–2 h after ingestion of glycerol. An
improvement of 10 dB in two or more adjacent octaves
or gain of 10% in discrimination score makes the test
positive. There is also improvement in tinnitus and in the
sense of fullness in the ear. The test has a diagnostic and
prognostic value. These days, glycerol test is combined
with electrocochleography.
VARIANTS OF MÉNIÈRE’S DISEASE
1. cochlear Hydrops. Here, only the cochlear symptoms and signs of Ménière’s disease are present. Vertigo is
absent. It is only after several years that vertigo will make
its appearance. It is believed that in these cases, there is
block at the level of ductus reuniens, thereby confining
the increased endolymph pressure to the cochlea only
(Figure 15.5).
Figure 15.4. Electrocochleography. (A) Normal ear. (B) Ear with Ménière’s disease. Voltage of summating potential (SP) is compared with
that of action potential (AP). Normally SP is 30% of AP. This ratio is
enhanced in Ménière’s disease.
2. Vestibular Hydrops. Patient gets typical attacks of
episodic vertigo while cochlear functions remain normal.
It is only with time that a typical picture of Ménière’s
Figure 15.5. Left membranous labyrinth.
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SECTION I — Diseases of Ear
disease will develop. Many of the cases of vestibular Ménière’s disease are labelled “recurrent vestibulopathy” as
endolymphatic hydrops could not be demonstrated in
the study of temporal bones in such cases.
3. drop Attacks (tumarkin’s Otolithic Crisis). In
this, there is a sudden drop attack without loss of consciousness. There is no vertigo or fluctuations in hearing
loss. Patient gets a feeling of having been pushed to the
ground or poleaxed. It is an uncommon manifestation
of Ménière’s disease and occurs either in the early or late
course of disease. Possible mechanism is deformation of
the otolithic membrane of the utricle or saccule due to
changes in the endolymphatic pressure.
4. lermoyeZ Syndrome. Here symptoms of Ménière’s
disease are seen in reverse order. First there is progressive
deterioration of hearing, followed by an attack of vertigo,
at which time the hearing recovers.
MÉNIÈRE’S DISEASE VS MÉNIÈRE’S
SYNDROME
Ménière’s disease is an idiopathic condition while Ménière’s syndrome, though resembling Ménière’s disease
clinically (episodic vertigo, fluctuating hearing loss, tinnitus and ear fullness), results from a variety of conditions such as trauma (head injury or ear surgery), viral
infections (following measles or mumps), syphilis (congenital or late acquired), Cogan’s syndrome, otosclerosis
or autoimmune disorders. It is also called secondary Ménière’s disease.
DIAGNOSIS OF MÉNIÈRE’S DISEASE
Committee on Hearing and Equilibrium of the American
Academy of Otolaryngology—Head and Neck Surgery
(AAOHNS) classified the diagnosis of Ménière’s disease as
follows:
1. Certain. Definite Ménière’s disease confirmed by
histopathology.
2. Definite. Two or more definitive spontaneous episodes
of vertigo lasting 20 min or longer.
(a) Audiometrically documented hearing loss on at
least one occasion.
(b) Tinnitus or aural fullness in the affected ear.
(c) All other causes excluded.
3. Probable
(a) One definitive episode of vertigo.
(b) Audiometrically documented hearing loss on at
least one occasion.
(c) Tinnitus or aural fullness in the treated ear.
(d) Other causes excluded.
4. Possible
(a) Episodic vertigo of Ménière’s type without docu-
mented hearing loss (vestibular variant) or
(b) Sensorineural hearing loss, fluctuating or fixed,
with disequilibrium but without definitive episodes (cochlear variant).
(c) Other causes excluded.
TABLE 15.2 STAGING OF MÉNIÈRE’S DISEASE
Stage Pure tone average in dB in previous 6 months
1
2 26–40
3 41–70
4
≤25
>70
STAGING OF MÉNIÈRE’S DISEASE
This can be done in certain and definite cases of Ménière’s
disease. It is based on the average of pure tone thresholds
at 0.5, 1, 2 and 3 kHz (rounded to the nearest whole) of
the worst audiogram during a period of 6 months before
treatment (see Table 15.2).
TREATMENT
A. GENERAL MEASURES
1. Reassurance. Patient anxiety can be relieved by reassurance and by explaining the true nature of disease. This
is particularly important in acute attack.
2. Cessation of smoking. Nicotine causes vasospasm.
Smoking should be completely stopped. For some patients, this may be the only treatment necessary.
3. Low salt diet. Patient should take salt-free diet as far
as possible. No extra salt should be permitted. Salt intake
should not exceed 1.5–2.0 g/day.
4. Avoid excessive intake of water.
5. Avoid over-indulgence in coffee, tea and alcohol.
6. Avoid stress and bring a change in lifestyle. Mental
relaxation exercises and yoga are helpful to decrease stress.
7. Avoid activities requiring good body balance. As the
attack of Ménière’s disease is abrupt, sometimes with no
warning symptom, professions such as flying, underwater
diving or working at great heights should be avoided.
B. MANAGEMENT OF ACUTE ATTACK
During the acute attack, there is severe vertigo with nausea
and vomiting. Patient is apprehensive. Head movements
provoke giddiness. Therefore, treatment would consist of:
1. Reassurance and psychological support to allay worry
and anxiety.
2. Bed rest with head supported on pillows to prevent
excessive movements.
3. Intravenous fluids and electrolyte administration
to combat their loss due to vomiting.
4. Vestibular sedatives to relieve vertigo. They should be
administered intramuscularly or intravenously, if vomiting precludes oral administration. Drugs useful in acute
attack are dimenhydrinate (Dramamine), promethazine
theoclate (Avomine) or prochlorperazine (Stemetil).
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Diazepam (Valium or Calmpose) 5–10 mg may be given intravenously. It has a tranquillizing effect and also
suppresses the activity of medial vestibular nucleus.
In some patients, acute attack can be stopped by atropine, 0.4 mg, given subcutaneously.
5. Vasodilators: Carbogen (5% CO2 with 95% O2) is a
good cerebral vasodilator and its inhalation improves
labyrinthine circulation.
C. MANAGEMENT OF CHRONIC PHASE
When patient presents after the acute attack, the treatment consists of:
1. Vestibular sedatives. Prochlorperazine (Stemetil)
10 mg, thrice a day, orally for two months and then
reduced to 5 mg thrice a day for another month.
2. Vasodilators. Betahistine (Vertin) 8–16 mg, thrice
a day, given orally, also increases labyrinthine blood
flow by releasing histamine in the body.
3. Diuretics. Sometimes, diuretic furosemide, 40 mg
tablet, taken on alternate days with potassium supple-
ment helps to control recurrent attacks, if not con-
trolled by vasodilators or vestibular sedatives. Thi-
azide diuretics (hydrochlorothiazide), 12.5 mg daily
can also be used.
4. Propantheline bromide (Probanthine), 15 mg, thrice
a day, can be given alone or in combination with vas-
odilator and is quite effective. However, they are not
preferred by many due to side effects.
5. Elimination of allergen. Sometimes, a food or inhal-
ant allergen is responsible for such attacks. It should be
found and eliminated or desensitization done.
6. Hormones. Investigations should be directed to find
any endocrinal disorder such as hypothyroidism, and
appropriate replacement therapy given. Control of
stress by change in lifestyle is important to prevent re-
current attacks.
About 80% of the patients can be effectively managed
by medical therapy alone.
Intratympanic gentamicin therapy
(chemical labyrinthectomy)
Gentamicin is mainly vestibulotoxic. It has been used in
daily or biweekly injections into the middle ear. Drug is
absorbed through the round window and causes destruction of the vestibular labyrinth. Total control of vertigo
spells has been reported in 60–80% of patients with some
relief from symptoms in others. Hearing loss, sometimes
severe and profound, has been reported in 4–30% of patients treated with this mode of therapy.
Microwick
It is a small wick made of polyvinyl acetate and measures 1 mm × 9 mm. It is meant to deliver drugs from
external canal to the inner ear and thus avoid repeated intratympanic injections. It requires a tympanostomy tube
(grommet) to be inserted into the tympanic membrane
and the wick is passed through it. When soaked with a
drug, the wick delivers the drug to the round window to
be absorbed into the inner ear. It has been used to deliver
steroids in sudden deafness and gentamicin to destroy
vestibular labyrinth in Ménière’s disease.
D. SURGICAL TREATMENT
It is used only when medical treatment fails.
1. conserVatiVe Procedures. They are used in cases
where vertigo is disabling but hearing is still useful and
needs to be preserved. They are:
(a) Decompression of endolymphatic sac.
(b) Endolymphatic shunt operation. A tube is put, connect-
ing endolymphatic sac with subarachnoid space, to
drain excess endolymph.
(c) Sacculotomy (Fick’s operation). It is puncturing the
saccule with a needle through stapes footplate. A distended saccule lies close to stapes footplate and can
be easily penetrated. Cody’s tack procedure consists
of placing a stainless steel tack through the stapes
footplate. The tack would cause periodic decompression of the saccule when it gets distended. Both these
operations were claimed to have shown good results
but they could not be reproduced by others and thus
abandoned. Cochleosacculotomy is another similar
procedure in which, instead of saccule, cochlear duct
is punctured and drained into the perilymph (oticperiotic shunt). The procedure is performed with a
curved needle passed through the round window to
puncture cochlear duct.
(d) Section of vestibular nerve. The nerve is exposed by ret-
rosigmoid or middle cranial fossa approach and selectively sectioned. It controls vertigo but preserves
hearing.
(e) Ultrasonic destruction of vestibular labyrinth. Cochlear
function is preserved.
2. destructiVe Procedures. They totally destroy
cochlear and vestibular function and are thus used only
when cochlear function is not serviceable.
• Labyrinthectomy. Membranous labyrinth is completely
destroyed either by opening through the lateral semicircular canal by transmastoid route or through the
oval window by a transcanal approach. This gives relief
from the attacks of vertigo.
3. intermittent Low-Pressure Pulse Therapy
[meniett DeVice Therapy (Figure 15.6)]. It is ob-
served that intermittent positive pressure delivered to
inner ear fluids brings relief from the symptoms of Ménière’s disease. Not only there is improvement in vertigo,
tinnitus and ear fullness, but hearing may also improve.
Intermittent positive pressure waves can be delivered
through an instrument called Meniett device which has
been approved by FDA. A prerequisite for such a therapy
is to perform a myringotomy and insert a ventilation
tube so that the device when coupled to the external ear
canal can deliver pressure waves to the round window
membrane via the ventilation tube. Pressure waves pass
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