Vertigo Dr. Saad Y. Sulaiman

There are 4 types of Dizziness: Vertigo Lightheadedness Presyncope Disequilibrium Disorders of vestibular system cause vertigo.

Disorder of vestibular system cause vertigo. Vertigo accounts for 54% of all dizziness Vertere = Spin (Latin) Vertigo is an illusion of movement of the patient’s body or patient’s environment. It should be restricted to sensation of rotation and linear motion(staggering to one side)

Aetiology Peripheral which involve the vestibular end organs and their 1st order neuron (i.e. the vestibular nerve) 85% of all cases of vertigo. Central ( non-otological) which involve the CNS after the entrance of the vestibular nerve in the brainstem e.g. intracranial tumors, multiple sclerosis, vestibulobasillar ischaemia, Temporal lobe epilepsy and migraine.

Nystagmus Involuntary, Rhythmic oscillation of the eyes Types Physiological; rotational & caloric test Pathological Occular Vestibular Central lesions

Occular nystagmus Pendular/The two phases of oscillation are of the same speed Vestibular Nystagmus Horizontal Named according to the direction of rapid component Fatigable Nystagmus associated with central lesions Vertical ( 80%) Non-fatigable.

Peripheral vestibular disorders

Meniere's disease ( Endolymphatic hydrops) It is a disorder of the inner ear where the endolymphatic system is distended by endolymph. It is characterized by (1) Vertigo (2) SNHL (3) Tinnitus.

The Inner Ear The inner ear, or labyrinth, consists of: Bony capsule (otic capsule) Membranous labyrinth

Bony capsule (otic capsule) Membranous labyrinth

There are two types of fluid in the inner ear; Very similar to the ECF and CSF (has low k+ and high Na+ concentration). Similar to the ICF (has high K+ and low Na+ concentration)

The Membranous Labyrinth Membranous cochlear duct (scala media) Saccule and utricle Membranous semicircular ducts 2 1 3

Pathology of Meniere’s disease Dilatation of the endolymphatic compartment due to abnormality of endolymph formation or absorption or both.

Aetiology: The exact cause of Meniere's disease is not yet known. Various theories have been postulated: Defective absorption due to ischemia of sac. Vasomotor disturbance. Allergy. Sodium and water retention. Hypothyroidism. Autoimmune and viral aetiology.

Clinical features Age: 35-60 years. Sex: no gender bias Usually the disease starts unilateral but the other ear may be affected after a few years.

Cardinal symptoms of Meniere's disease are: Episodic vertigo Fluctuating hearing loss Tinnitus sense of fullness or pressure in the involved ear. Remission is typical The suddenness of the attack (characterestic) Aura ( change in tinnitus or fullness sensation)

1- Vertigo: Sudden. Last for few hours. Associated with vomiting, nystagmus and bradycardia. The patient may fall and injure himself, BUT he has normal level of consciousness.

2- Hearing loss: SNHL during or just after the attack. In the early stages of the disease the hearing return to normal as the attacks become more frequent complete loss of hearing results in the affected ear.

3- Tinnitus: Referred to the affected ear. Precedes or accompany the vertigo.

Examination Between the attacks, clinical examination may be completely normal. During the attacks, the patient is : disoriented, unable to stand and usually lie down with: (1) Nystagmus (2) Normal Otoscopy (3) Tuning fork examination  SNHL.

Investigation: Audiological (PTA): SNHL. Vestibular (Caloric test): canal paresis in the affected ear

Caloric test The ears are irrigated in turn with water at 30 C then at 44 C (7 C above and below body temperature). This situation causes nystagmus with its quick component away from the ear on the cold testing and towards the ear on hot caloric testing (COWS). This nystagmus commonly lasted for about 2 minutes from the beginning of stimulation.

Canal paresis is present if the duration of nystagmus is reduced equally for both hot and cold tests. Canal paresis is suggestive of a lesion in the peripheral vestibular apparatus e.g. vestibule or vestibular nerve.

Treatment Medical During the acute attack Complete bed rest. Antihistamine& labyrinthine sedatives: prochlorperazine (stemetil) and cinnarzine (stugeron). Anxiolytics: IV diazepam. Surgical: Endolymphatic sac decompression or shunt. Vestibular nerve section.

Benign Paroxysmal Positional Vertigo ( BPPV) Recurrent Paroxysmal short lived attacks of vertigo initiated by certain critical positions of the head. There are no other aural symptoms

Aetiology Idiopathic. Head injury. Viral infection. Aging process. Pathology The disease is thought to be due to displacement of otoliths (calcium carbonate particles) from the utricle and saccule to the capula of the semicircular canal.

Cupula

Clinical picture Brief attacks of vertigo when the patient put his head in the critical position. Absence of aural symptoms: hearing is normal and there is no tinnitus.

Examination 1- Positional nystagmus which is elicited by performing Hallpike maneuvers .The classical features of BPPV are: A latent period of 5-10 sec. followed by rotatory nystagmus lasting up to 30 seconds. The fast component of the nystagmus is directed towards the undermost ear. The nystagmus fatigue rapidly. 2- Normal Otoscopy and audiometry. Investigation: Caloric test: Normal.

Treatment of BPPV Medical: Reassurance and avoidance of the provocating position. Antivertigo drugs: prochlorperazine (stemetil), Cinnarzine (stugeron) and Betahistine (Serc). Surgical: Posterior semicircular canal denervation

Prognosis There is normal tendency for spontaneous cure, which may be delayed for several months.

Vestibular Neuronitis This condition is characterized by a SEVERE vertigo of Sudden onset Without deafness or tinnitus and with NO sign of neurological involvement. Causes: Viral ( URTI)

Clinical picture Examination Hx. of URTI (1 w.- 10 days). Vertigo which can last several days before a gradual recovery begins. Nausea and vomiting. Absence of aural symptoms: Hearing is normal and there is no tinnitus. Examination Spontaneous nystagmus of the vestibular type. Investigations: Caloric test: canal paresis on the affected side.

Other causes of vestibular disorder ( vertigo) Labyrinthitis Vestibulotoxic drugs: e.g. Aminoglycosides Head trauma Perilymph fistula: Causes: complication of ear surgery (stapedectomy), barotrauma, raised intracranial pressure.

Vestibular Schwannoma (Acoustic neuroma) Nerve sheath tumors which arise from Schwann cells covering the superior and inferior vestibular nerve . Rarely they originate from the cochlear nerve. 8% of all intracranial tumors 80% of cerebellopontine angle tumors. Slowly growing tumors &do not infiltrate local tissues or metastasize BUT compress the adjacent tissues.

Aetiology The cause is unknown although neurofibromatosis type 1 (NF1) and NF2 are associated with Vestibular schwannoma. Bilateral Vestibular schwannoma are common in NF2.

Clinical picture Sex: M=F Age: 30-60yr I.Otological symptoms Progressive unilateral SNHL+ Unilateral tinnitus ± Vertigo II. Facial and trigeminal nerve dysfunction III. Further expansion leads to brainstem and cerebellar compression and increase intracranial pressure.

Investigation Audiological: PTA: asymmetrical SNHL, Imaging: MRI with gadolinium contrast is the gold standard for the diagnosis. CT scan may detect large tumors Caloric test: canal paresis in the affected side.

Treatment Observation if the life expectancy of the patient is shorter than the growth time required for the vestibular schwannoma to cause neurological symptoms Surgical removal. Stereotatic radiation using cobalt-60 gamma knife system.

How to differentiate between central and peripheral type of vertigo?

4- History of medications, toxins, DM, hypertension. 1- Timing and duration The longer the symptoms last  central Sudden onset  peripheral Early morning vertigo peripheral 2- Provoking Factors: Positional changes Recent viral illness Trauma, excessive straining (perilymphatic fistula) 3- Associated symptoms 4- History of medications, toxins, DM, hypertension. 5-Family history: Migraine, CVA risk.

Examination 1- Otological: 2- Cardiovascular TM: Vesicles Cholesteatoma (CSOM). Hennebert’s sign &Valsalva maneuver 2- Cardiovascular Orthostatic changes (drop of BP by 20 mmHg) arrhythmias, carotid bruits or other signs of atherosclerosis.

3- Neurological: Cranial nerves palsies & SNHL Nystagmus Vertical– 80% sensitive for vestibular nuclear or cerebellar lesions Horizontal– suggests peripheral cause Gait and balance If peripheral, pt will be able to walk Central –pt usually will be severely impaired in walking Hallpike maneuvers