Transcript Vertigo

Dr. Saad Y. Sulaiman
There are 4 types of Dizziness:
Vertigo
 Lightheadedness
 Presyncope
 Disequilibrium
Disorders of vestibular system
cause vertigo.

Vertigo
Disorder
of
accounts for 54% of all dizziness
vestibular
system
Vertere = Spin (Latin)
Vertigo is an illusion of movement of
cause
the patient’s body
or patient’s



vertigo.
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
1. Physiological; rotational & caloric
test
2. 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:
1. Bony capsule (otic capsule)
2. 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
1.
Membranous
cochlear duct
(scala media)
2.
Saccule and utricle
3.
Membranous
semicircular ducts
2
3
1
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
(2) Fluctuating hearing loss
(3) Tinnitus
(4) 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)
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




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?
History:
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:
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