vertigo

THE EAR

Dr. Mohamad S. Aziz

Otolaryngologist
CABMS (ORL-HNS)
ENT Dept, College of Medicine, University of Mosul

Undergraduate, The EAR, 2015/2016

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VESTIBULAR SYSTEM PHYSIOLOGY
consists of the three SCC, the saccule and the utricle. They are fluid filled and have cells with cilia which bend as the fluid moves relative to them. This excites or depresses the nerve cells .
The semicircular canals detect changes in angular acceleration.
The utricle and saccule detect linear acceleration.
The nerve impulses from the labyrinth go to the vestibular nuclei in the brain stem. Here they are integrated with vision and proprioception. The brain stem computerizes these three inputs and with the help of the cerebellum maintains the balance and co-ordination of the head and body
Vertigo is defined as illusion of movement of oneself or the environment (rotating)


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Assessment of Vestibular Function

A. Clinical Tests

1. Spontaneous Nystagmus

Nystagmus is defined as involuntary, rhythmical, oscillatory movement of eyes.
It may be horizontal, vertical or rotatory.
Vestibular nystagmus has a slow and a fast component, and by convention, the direction of nystagmus is indicated by the direction of the fast component.
The examiner keeps his finger about 30 cm from the patient's eye in the central position and moves it to the right or left, up or down.
Presence of spontaneous nystagmus always indicates an organic lesion


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2. Fistula Test
induce nystagmus by producing pressure changes in the external canal which are then transmitted to the labyrinth. Stimulation of labyrinth results in nystagmus and vertigo.
performed by applying intermittent pressure on the tragus or by using Siegle's speculum.
It is positive when there is erosion of horizontal semicircular canal as in cholesteatoma, abnormal opening in the oval window or the round window .
A positive fistula also implies that the labyrinth is still functioning; it is absent when labyrinth is dead



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3. Romberg Test
The patient is asked to stand with feet together, and arms by the side with eyes first open and then closed. With the eyes open, patient can still compensate the imbalance but with eyes closed, vestibular system is at more disadvantage.
4. Gait
The patient is asked to walk along a straight line to a fixed point, first with eyes open and then closed.

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5. Dix-Hallpike Manoeuvre (Positional Test)
This test is particularly useful when patient complains of vertigo in certain head positions. It also helps to differentiate a peripheral from a central lesion.




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Test of Cerebellar Dysfunction

All cases of giddiness should be tested for cerebellar disorders.

Disease of the cerebellar hemisphere causes:

(i) Asynergia (abnormal finger-nose test)

(ii) Dysmetria (inability to control range of motion)

(iii) Adiadochokinesia (inability to perform rapid alternating movements)

(iv) Rebound phenomenon (inability to control movement of extremity when opposing forceful restraint is suddenly released)

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B. Laboratory Tests of Vestibular Function
1. Caloric Test
induce nystagmus by thermal stimulation of the vestibular system. Advantage is that each labyrinth can be tested separately.


(a) Modified Kobrak test
quick office procedure. Ear is irrigated with ice water for 60 seconds. Normally, nystagmus will be seen with 5 ml of ice water. No response to 40 ml water indicates dead labyrinth.

(b) Fitzgerald-Hallpike test (bithermal caloric test)

Ears are irrigated for 40 seconds alternately with water at 30°C and at 44°C and eyes observed for appearance of nystagmus till its end point. Time taken from the start of irrigation to the end point of nystagmus is recorded and charted on a calorigram . Cold water induces nystagmus to opposite side and warm water to the same side (remember mnemonic COWS: Cold-Opposite, Warm-Same).

(c) Cold-air caloric test

done when there is perforation of tympanic membrane. The test employs Dundas Grant tube .

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2. Electronystagmography
It is a method of detecting and recording of nystagmus . The test depends on the presence of corneoretinal potentials . The test is also useful to detect nystagmus which is not seen with the naked eye

3. Optokinetic Test Patient is asked to follow a series of vertical stripes on a moving drum. Thus this test is useful to diagnose a central lesion.

4. Rotation Test

5. Galvanic Test

6. Posturography

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Disorders of vestibular system
A. Peripheral
involve vestibular end organs and their first order neurons (i.e. the vestibular nerve). The cause lies in the internal ear or the VIIIth nerve. They are responsible for 85% of all cases of vertigo.

B. Central

involve central nervous system after the entrance of vestibular nerve in the brainstem and involve vestibulo-ocular, vestibulo-spinal and other central nervous system pathways.


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Benign paroxysmal positional vertigo (BPPV)


characterised by vertigo for seconds when the head is placed in a certain critical position(e.g : rolling in bed). no hearing loss or other neurologic symptoms.
Positional testing by Hallpike manoeuvre establishes the diagnosis and helps to differentiate it from positional vertigo of central origin .
Disease is caused by a disorder of posterior semicircular canal though many patients have history of head trauma and ear infection.
The vertigo is fatiguable on assuming the same position repeatedly.
treated by performing Epley's manoeuvre.





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Vestibular neuronitis

characterised by severe vertigo of sudden onset with no cochlear symptoms. Attacks may last from a few days to 2 or 3 weeks.
It is thought to occur due to a virus that attacks vestibular ganglion. Management of acute attack is similar to that in Meniere's disease. The disease is usually self-limiting.

Vestibulotoxic drugs

Aminoglycoside antibiotics particularly streptomycin, gentamicin & kanamycin affect hair cells of the crista ampullaris and maculae.
other drugs which cause dizziness or unsteadiness are antihypertensives, labyrinthine sedatives, oestrogen preparations, diuretics, antimicrobials (nalidixic acid, metronidazole) and antimalarials.


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Labyrinthitis
There are three types of labyrinthitis:
A-Circumscribed Labyrinthitis (Fistula of Labyrinth)or (Paralabyrinthitis)
B-Diffuse Serous Labyrinthitis
C-Diffuse Suppurative Labyrinthitis

A-Circumscribed Labyrinthitis (Fistula of Labyrinth)

thinning or erosion of bony capsule of the horizontal semicircular canal.
Aetiology
•CSOM with cholesteatoma •Neoplasms of middle ear
•Surgical or accidental trauma to labyrinth.
Clinical features
Patient complains of transient vertigo often induced by pressure on tragus, cleaning the ear or performing Valsalva manoeuvre.
It is diagnosed by "fistula test" which can be performed in two ways.
• Pressure on tragus. Sudden inward pressure is applied on the tragus. Nystagmus may also be induced.
(b) Siegle's speculum.
Treatment
In CSOM or cholesteatoma, mastoid exploration .
Systemic antibiotic therapy should be instituted before and after operation .


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B-Diffuse Serous Labyrinthitis
diffuse intralabyrinthine inflammation without pus formation and is reversible if treated early.
Aetiology
• pre-existing circumscribed labyrinthitis .
•In acute infections of middle ear inflammation spreads through annular ligament or the round window.
• It can follow stapedectomy or fenestration operation.
Clinical features
in severe cases, vertigo is worse with marked nausea, vomiting and even spontaneous nystagmus.
Cochlea is also affected with some degree of SNHL &/or tinnitus.
Serous labyrinthitis may pass onto suppurative labyrinthitis with total loss of vestibular and cochlear function.
Treatment
Medical.
(a) Patient is put to bed. (b) Antibacterial therapy.
(c)Labyrinthine sedative as prochlorperazine (Stemetil).
(d) Myringotomy is if drum is bulging.
Surgical.
Cortical mastoidectomy (in acute mastoiditis) or modified radical mastoidectomy (in chronic middle ear infection or cholesteatoma).

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C-Diffuse Suppurative Labyrinthitis
This is diffuse pyogenic infection of the labyrinth with permanent loss of vestibular and cochlear functions.


Aetiology
It usually follows serous labyrinthitis, pyogenic organisms entering through a pathological or surgical fistula.

Clinical features

There is severe vertigo with nausea and vomiting . Spontaneous nystagmus. Patient is markedly toxic. There is total loss of hearing. Relief from vertigo is seen after 3-6 weeks due to adaptation.

Treatment

It is same as for serous labyrinthitis.
Rarely, drainage of the labyrinth is required, if intralabyrinthine suppuration is a source of intracranial complications, e.g. meningitis or brain abscess.

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Head trauma
Head injury may cause concussion of labyrinth, completely disrupt the bony labyrinth or VIIIth nerve, or cause a perilymph fistula.

Severe acoustic trauma, such as that caused by an explosion can also disturb the vestibular end organ (otoliths) and result in vertigo.

Perilymph fistula

perilymph leaks into the middle ear through the oval or round window.

It can be a complication of stapedectomy, sudden pressure changes in the middle ear (e.g. barotrauma, diving, forceful Valsalva) or raised intracranial pressure (weightlifting or vigorous coughing).

A perilymph fistula causes intermittent vertigo and fluctuating SNHL, sometimes with tinnitus and sense of fullness in the ear (compare Meniere's disease).


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Vertebrobasilar insufficiency
common cause of central vertigo in patients over the age of 50 years. There is transient decrease in cerebral blood flow.

Common cause is atherosclerosis. Ischaemia in these patients may also be precipitated by hypotension or neck movements when cervical osteophytes press on the vertebral arteries during rotation and extension of head.

Vertigo is abrupt in onset, lasts several minutes and is associated with nausea and vomiting , with other neurological symptoms.

Posterior inferior cerebellar artery syndrome (Wallenberg's syndrome)

Thrombosis of the posterior inferior cerebellar artery cuts off blood supply to lateral medullary area. There is violent vertigo along with other neurological signs.

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Basilar migraine

Basilar artery migraine produces occipital headache, visual disturbances, diplopia and severe vertigo which is abrupt and may last for 5-60 minutes.
common in adolescent girls with strong menstrual relationship and positive family history.

Cerebellar disease

Cerebellum may be affected by haemorrhage (hypertension), infarction (occlusion of arterial supply), infection (otogenic cerebellar abscess) or tumours (glioma, teratoma or haemangioma).


Multiple sclerosis

It is a demyelinating disease affecting young adults.
Vertigo and dizziness are common complaints.
There are other multiple neurological signs and symptoms, e.g. blurring or loss of vision, diplopia, dysarthria, paraesthesia and ataxia. Spontaneous nystagmus may be seen.

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Tumours of brainstem and floor of IVth ventricle
Gliomas, astrocytomas ; medulloblastoma, ependymomas, epidermoid cysts or teratomas . other neurological signs and symptoms in addition to vertigo and dizziness. Positional vertigo and nystagmus may also be the presenting features. CT scan and MRI are useful in their diagnosis.

Epilepsy

Vertigo may occur as an aura in temporal lobe epilepsy.
The history of seizure and/or unconsciousness following the aura may help in the diagnosis. Sometimes, vertigo is the only symptom of epilepsy .
E.E.G. may show abnormalities during the attack.

Cervical vertigo

Vertigo may follow injuries of neck 7-10 days after the accident.
It is usually provoked with movements of neck to the side of injury. Examination shows tenderness of neck, spasms of cervical muscles and limitation of neck movements.
X-rays show loss of cervical lordosis
Exact mechanism is not known.


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Ocular vertigo
Normally, balance is maintained by integrated information received from the eyes, labyrinths and somatosensory system.
A mismatch of information from any of these organs causes vertigo and in this case from the eyes.
Ocular vertigo may occur in case of acute extraocular muscle paresis or high errors of refraction.

Psychogenic vertigo

suspected in patients suffering from emotional tension and anxiety. Often other symptoms of neurosis, e.g. palpitation, breathlessness, fatigue, insomnia, profuse sweating and tremors are also present.
Symptom of vertigo is often vague in the form of floating or swimming sensation or light-headedness. There is no nystagmus or hearing loss.

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Meniere's Disease

Meniere's Disease, also called endolymphatic hydrops, is a disorder of the inner ear where the endolymphatic system is distended with endolymph.
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. Cochlear duct may completely fill the scala vestibuli; there is marked bulging of Reissner's membrane . 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. The distended saccule may come to lie against the stapes footplate.








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Aetiology
either increased production of endolymph or its faulty absorption or both. Normally, endolymph is secreted by stria vascularis and is absorbed through the endolymphatic sac .

The exact cause of Meniere's disease is not yet known.

1. Defective absorption by endolymphatic sac
Experimental obstruction of endolymphatic sac and its duct also produces hydrops .

2. Vasomotor disturbance

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, increased permeability, with increased production of endolymph.

3. Allergy: Nearly 50% of patients with Meniere's disease have concomitant inhalant and/or food allergy.

4. Sodium and water retention

5. Hypothyroidism: About 3% of cases are due to hypothyroidism.

6. Autoimmune and viral aetiologies (measles)

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Clinical Features
age group of 35-60 years. Males are affected more. Usually unilateral.
Cardinal symptoms are:
1. Vertigo
It comes in sudden attacks, with periods of spontaneous remission lasting for weeks, months or years. Usually accompanied by nausea and vomiting with ataxia and nystagmus. may be accompanied by other symptoms of vagal disturbances such as abdominal cramps, diarrhoea, cold sweats, pallor and bradycardia.

2. Hearing loss

It usually accompanies vertigo or may precede it. Hearing improves after the attack . This fluctuating nature of hearing loss is quite characteristic of the disease.
Distortion. A tone of a particular frequency may appear normal in one ear and of higher pitch in the other leading to diplacusis.
Intolerance to loud sounds due to recruitment phenomenon. They are poor candidates for hearing aids.

3. Tinnitus

low-pitched roaring type, and is aggravated during acute attacks.

4. Sense of fullness or pressure

It also fluctuates. It may accompany or precede an attack of vertigo.


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Examination
Otoscopy Normal
Nystagmus is seen only during acute attack.
TF tests indicate SNHL. Rinne test is positive, ABC is reduced in the affected ear and Weber is lateralised to the better ear.
Investigations
1. Pure tone audiometry
There is SNHL. 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




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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
indicate the cochlear nature of disease and help to differentiate from retrocochlear lesions, e.g. acoustic neuroma .
(a) Recruitment test is positive.
(b) SISI (short increment sensitivity index) test.
(c) Tone decay test.
4. Electrocochleography
Normally, ratio of summating potential (SP) to action potential (AP) is 30%. In Meniere's disease, SP/AP ratio is greater than 30% .








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5. Caloric test
shows reduced response on the affected side in 75% of cases( canal paresis)

6. Glycerol test

Glycerol is a dehydrating agent. When given orally, it reduces endolymph pressure and thus causes an improvement in hearing.
Audiogram and speech discrimination scores are recorded before and 1-2 hours after ingestion of glycerol. An improvement of 10 dB 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

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Treatment
A. General Measures
1. Reassurance

2. Cessation of smoking

3. Low salt diet

4. Avoid excessive intake of water

5. Avoid over-indulgence in coffee, tea and alcohol

6. Avoid stress and bring a change in life-style Mental relaxation exercises and yoga are helpful to decrease stress

7. Avoid activities requiring good body balance

professions such as flying, under-water diving or working at great heights should be avoided.

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B. Management of Acute Attack

1. Reassurance and psychological support to allay worry and anxiety.

2. Bed rest with head supported on pillows to prevent excessive movements.

3. Vestibular sedatives should be administered intramuscularly or intravenously if vomiting precludes oral administration. Drugs useful in acute attack are dimenhydrinate (Dramamine), promethazine (Avomine) or prochlorperazine (Stemetil).
Diazepam (Valium ) 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.


4. Vasodilators
• Inhalation of carbogen (5% CO2 with 95% O2).
• Histamine drip.

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C. Management of Chronic Phase
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

Nicotinic acid, Betahistine (Betaserc) 8-16 mg, thrice a day, given orally, also increases labyrinthine blood flow by releasing histamine in the body.

3. Diuretics

Furosemide, 40 mg tablet, taken on alternate days with potassium supplement if not controlled by vasodilators or vestibular sedatives.

4. Propantheline bromide: (Probanthine), 15 mg, thrice a day, can be given alone or in combination with vasodilator and is quite effective.

5. Elimination of allergen: Sometimes a food or inhalant allergen is responsible for attacks. It should be found and eliminated or desensitisation done.

6. Hormones: Investigations to find any endocrinal disorder such as hypothyroidism, and appropriate replacement therapy given. Control of stress by change in life-style is important. About 80% of the patients can be effectively managed by medical therapy alone.


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D. Surgical Treatment
It is used only when medical treatment fails.
1. Conservative procedures
when hearing is still useful and needs to be preserved. They are:
• Decompression of endolymphatic sac
• Endolymphatic shunt operation.
(iii) Sacculotomy (Fick's operation) Or Cochleosacculotomy
(iv) Section of vestibular nerve.
(v) Ultrasonic destruction of vestibular labyrinth. Cochlear function is preserved.
(vi) Transtympanic corticosteroid infusion of middle ear.
• Intratympanic gentamicin therapy (chemical labyrinthectomy). Gentamicin is mainly vestibulotoxic. daily or biweekly injections into the middle ear absorbed through the round window and causes destruction of the vestibular labyrinth. Total control of vertigo in 60-80% of patients . Hearing in 4-30% of patients.
• Intermittent low pressure pulse therapy [Meniett device therapy]: A prerequisite for such a therapy is to perform a myringotomy and insert a ventilation tube

2. Destructive procedures

used only when cochlear function is not serviceable.
Labyrinthectomy.
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