دهيثم

Lecture ( 2 ) ENT Dr. Haitham Alnori

30 /3/ 2017
Vertigo
Vertigo is defined as illusion of movement (verter = spin in Latin). It includes sensation of rotation, linear motion and tendency to stagger to one side. Cortical representation of balance in the brain is very small leading to difficulty of the patient to describe his complaint.

Physiology of vestibular system

Normal balance is maintained by visual, vestibular and proprioceptive stimuli. These are integrated and modulated in the brain stem, cerebellum and higher cortical centers.

Peripheral vestibular lesions affect labyrinth or vestibular division of vestibulo-cochlear nerve. They tend to produce severe vertigo and nystagmus, with nausea, vomiting and sweating. Nystagmus is horizontal or rotatory, e.g. BPPV and Meniere's disease.

Central vestibular lesions affect brainstem nuclei or their connections. They tend to produce severe postural imbalance with minimal vertigo and nystagmus. Nausea and vomiting are infrequent. Nystagmus is vertical or horizontal or sometimes absent, e.g. brain tumor and vertebra-basillar ischemia.

Dizziness is light headedness NOT associated with sensation of movement of environment. It is not a vestibular symptom. Vertigo is the symptom of vestibular system impairment whereas the sign is nystagmus.

Benign Paroxysmal Positional Vertigo BPPV

Recurrent short lived attacks of vertigo provoked by certain critical positions of the head. There are NO other aural or neurological findings.

Aetiology

Idiopathic.
Head injury.
Viral infection.
Degenerative ( aging).

Patho-physiologyogy

The disease is thought to be due to displacement of otoliths (calcium carbonate particles) from the utricle and saccule to the copula of the posterior semicircular canal ( copulo-lithiasis).

Clinical picture

Brief attacks of severe vertigo with any head movement but especially when rolling in bed and putting the affected ear down. After vertigo subsides patients may complain of dizziness and/ or disequilibrium for hours or even days. Hearing is normal and there is no tinnitus.
Typically vertigo recurs for few days and then subsides spontaneously or with treatment for months or years.

Examination

Diagnosis is clinical and supported by normal otoscopy and audiometry.
Positional test is diagnostic and called Dix-Hallpike test. The classical features are horizontal or rotator nystagmus which has latency for few seconds and duration of less than one minute. Fast component of nystagmus is beating toward the undermost ear. It is fatigable when repeating the test.

Treatment

Reassurance and avoidance of the provocating position.
Epley's maneuver: it is particle repositioning maneuver, it has high success rate.
Cinnarzine (stugeron)and betahistine (betaserc) are of limited benefit.
Posterior semicircular canal denervation for resistant cases.


Prognosis
Usually the attack is self-limiting within few days. There is tendency for recurrence , which may be delayed for several months.
It is very vital to differentiate BPPV from central positional vertigo.
Central positional vertigo
Disequilibrium and nystagmus provoked by certain head movement, with less severe vertigo. It may be due to cerebellar hemorrhage or posterior fossa tumor. It is distinguished from BPPV by Dix-Hallpike test. Here nystagmus has no latent period and persists for minutes. This nystagmus is not fatigable when repeating the test. Frequently, there are other associated CNS signs.

Vestibular neuronitis
It is also called epidemic vertigo, it is characterized by sudden unilateral vestibular failure resulting in imbalance of the vestibular input to the brain. It is frequently preceded by a virus infection.
Aetiology
The condition is thought to be due to viral infection of the vestibular nerve.

Clinical picture

It is characterized by severe vertigo for several days without deafness or tinnitus and no signs of neurological involvement. There are marked neuro-vegetative symptoms (nausea, vomiting and sweating) and the patient is confined to bed.

Diagnosis

The patient has horizontal nystagmus and caloric test reveals canal paresis on the affected side.

Treatment

I.V. fluid if there is severe vomiting. Prochlorperazine (stemetil) is antiemetic and sedative, cinnarzine (stugeron) is labyrinthine suppressant, and betahistine (betaserc) is H3 antagonist and vasodilator. These patients should not be left in bed for long time: early mobilization allows good central compensation. Cinnarzin is given for only few days in old people: it prevents adequate compensation leading to life-long unsteadiness!
There is gradual recovery with improvement resulting from central compensation. Young people recover quickly but an old person may be unsteady for months following an attack.


Meniere's Disease
The disease is characterized by paroxysmal attacks of vertigo associated with deafness and tinnitus. Meniere's disease gets its name from the French physician Prosper Meniere, who first described the illness in 1861.
Pathology
Endolymphatic hydrops (dilatation of the endolymphatic compartment of both cochlea and vestibule).

Aetiology

Unknown, different theories have been postulated to explain the condition: hereditary factor, defective absorption of endolymph and local ischemia .

Clinical picture( Vertigo, Deafness, Tinnitus)

Menier's disease may occur at any age and female are affected more than male? The disorder is usually unilateral, but the other labyrinth is eventually affected. Recurrence of attacks is typical and the next attack may come after few weeks or several years.
Vertigo: sudden onset of severe vertigo lasting for few hours, and associated with vomiting, nystagmus, sweating and bradycardia. The patient may fall and injure himself but he is fully conscious. Some patients get warning before attack by fullness sensation in the ear (aura).
Deafness: SNHL starts during the attack and returns to normal after the attack. As the disease progresses, hearing deteriorates and finally severe deafness results in the affected ear.
Tinnitus in the affected ear, later on becomes permanent.
Aural fullness: Due to increase pressure in the endolymph.

Diagnosis

Between the attacks, clinical examination may be completely normal. During the attack, the patient is unsteady with nystagmus.
Otoscopy: normal.
Audiogram: low frequency perceptive HL.
Caloric test: canal paresis in the affected ear.


Treatment
I. Medical
Bed rest, anxiolytic: I.V.diazepam, fluid and salt restriction with diuretics.
Prochlorperazine (stemetil),cinnarzine (stugeron) and betahistine (betaserc), the latter is often prescribed for few months.
II. Surgical
Endolymphatic sac decompression and shunt.
Vestibular nerve section.
Perilymph fistula
A perilymph leak into the middle ear arising from a defect of the oval and/or round window. It should not be confused with labyrinthine fistula, which is a fistula in the cortical labyrinthine bone secondary to cholesteatoma.

Aetiology

Head injyry.
Barotrauma.
Iatrogenic; mostly stapedectomy surgery.

Clinical features

Intermittent vertigo, fluctuating SNHL and tinnitus( DDx Meniere).