approach to a patient with vertigo and common vertigo causes and their clinical features

1. Topic presentation
Vertigo
Dr. Sadia Reza Baishakhi
Indoor Medical Officer
Dept. of Medicine
EMCH

2. CONTENTS
• Definition of vertigo
• Causes of vertigo
• How to know its central or peripheral
• Approach to a patient with vertigo

3. Definition
• Vertigo is defined as an abnormal perception
of movement of the environment or self, and
occurs because of conflicting visual,
proprioceptive and vestibular information
about a person’s position in space

4. Causes of vertigo
• Peripheral causes
o Benign paroxysmal positional vertigo
o Vestibular neuritis
o Labyrinthitis
o Meniere’s disease
o Ethanol intoxication
o Inner ear barotraumas
o Semicircular canal dehiscence

5. • Central causes
o Seizure
o Multiple sclerosis
o Wernicke’s encephalopathy
o Chiari malformations
o Cerebellar ataxia syndromes

6. • Mixed central and peripheral causes
– Migraine
– Stroke and vascular insufficiency
• Posterior inferior cerebellar artery
• Anterior inferior cerebellar artery
• Vertebral artery insufficiency
• Vasculitides
– Cerebellopontine angle tumors
• Vestibular schwannoma
• Meningioma
– Infections
• Lyme disease
• Syphilis
– Vascular compression
– Hyperviscosity syndromes

7. Peripheral Vs Central
Peripehral vertigo Central vertigo
Onset Sudden Usually slow onset
Severity of vertigo Intense Usually mild
Pattern Paroxysmal Constant
Exacerbate by movement Yes Variable
Autonomic Frequent Variable
Laterality Unilateral Uni or bilateral
Nystagmus Horizontal Any
Fatigable/fixation Yes No
Auditory symptoms Yes No
Tympanic membrane May be abnormal Normal
CNS symptoms Absent Present

8. Approach to a patient with vertigo

9. • History:
– Duration and frequency of episodes
– Aggravating and provoking factors (position, head
movement)
– Associated ‘fullness in the ear’ during the episode
(meniere’s disease)
– Associated focal neurological sign (cerebrovascular
event)
– Fluctuating hearing loss or tinnitus
– Associated headaches, nausea or aura (migrane)
– Previous significant head injury; previous URTI

10. Ask the Patient:
• Do you feel that environment is moving or you
moving around environment
• Onset- is it sudden or gradual
• Is it episodic or persistent
• If recurrent what is the frequency and
duration
• Does it relate to head posture
• How severe is it

11. Cont…
• Is it associated with tinnitus or hearing loss
• Is it associated with double vision,focal
weakness
• Did you suffer any head trauma
• Also take any drug

12. • Physical examination:
–Ear examination:
• Otoscopic examination to visualize the
tympanic membranes for any vesicles
(herpes zoster infection) or retraction
pockets as seen in cholesteatoma
• vertigo triggered by pushing on the tragus
or with the valsalva manoeuvre is seen in a
perilymphatic fistula

13. – Eye movements (the range of eye
movements and whether they are equal
in each eye should be observed)
• peripheral eye movement disorders are usually
disconjugate (different in the two eyes)
• central pathology are usually associated with poor
pursuit (the ability to follow a smoothly moving
target) or inaccurate (dysmetric) saccades (the
ability to look back and forth accurately between
two targets)
• alignment of the two eyes can be checked by a
cover test

14. –Cardiovascular examination:
• pulse, blood pressure postural hypotension should be
checked
• carotid examination to identify bruits
– Vestibular function test
• Spontaneous nystagmus
• Head impulse test
• Fistula test
• Romberg test
• GAIT
• Hall –pike manoeuvre
• Test of cerebellar function

15. Spontaneous nystagmus
– Nystagmus of peripheral origin can be suppressed by optic
fixation by looking at a fixed point and are typically causes
unidirectional horizontal nystagmus
– Nystagmus of central origin can not be suppressed by optic
fixation, they include
• Torsional nystagmus (lesions of branistem)
• Vertical downbeat nystagmus (lesions of cranio cervical
region)
• Vertical upbeat nystagmus (lesions at the junctions of
pons and medulla or pons and mid brain)
• Pendular nystagmus (congenital or acquired)

17. • Head impulse test
– The vestibuloocular reflex (VOR) is assessed with
small-amplitude rapid head rotations while the
patient fixates on a target

19. • Romberg test
– The patient is asked to stand with feet together
and arms by the side with eyes first open and then
closed
– In peripheral vestibular lesions, the patient sways
to the side of the lesion
– In central vestibular lesion disorder, patient shows
instability

21. • Gait
– The patient is asked to walk along a straight line to
a fixed point, first with eyes open and then closed
– In peripheral vestibular lesions, the patient
deviated to the affected side with eyes closed

22. • Hallpike manoeuvre
– Patients are asked to sit upright close to the edge
of the couch. Turn their head 45 degree to one
side and then rapidly lower them so that their
head is now 30 degree below the horizontal. Ask
them to keep their eyes open and to report any
vertigo they experience.watch their eyes carfully
for nystagmus.
– Repeat the test,turning the pt’s head to the other
side

24. • Test of cerebellar dysfunction
– Finger-nose test
– Dysdiadochokinesis
– Rebound phenomenon

25. • Laboratory tests
– Caloric test
– Electronystagmography
– Optokinetic test
– Rotation test
– Posturography
– MRI of the brain
– Carotid doppler

26. Most commonly encountered vestibular
disorders

27. Benign paroxysmal positional vertigo
• Pathophysiology: BPPV occurs due to the presence of
otolithic debris from the saccule or utricle affecting the
free flow of endolymph in the semicircular canals
(cupulolithiasis).
• It may follow minor head injury but typically
spontaneous
• Clinical feature:
– Recurrent spells of vertigo
– Episodes are brief (<1min and typically 15-20s)
– Always provoked by changes in head position relative to
gravity, such as lying down, rolling over in bed, rising from
a supine position and extending the head to look upward

28. • Diagnosis can be confirmed by Hallpike
manoeuvre
• Treatment:
– Explanation and reassurance
– reposition maneuvers (the Epley maneuver or
Brandt-Daroff exercises)
– Re-educate the brain to cope with the
inappropriate signals (Cawthrone-cooksey
exercises)

29. Epley Maneuver

30. Brandt- Daroff exercises
– Start in an upright, seated position.
– Move into the lying position on one side with your
nose pointed up at about a 45-degree angle.
– Remain in this position for about 30 seconds (or
until the vertigo subsides, whichever is longer)
– Repeat on the other side.

32. Cawthrone-cooksey exercises

34. Labyrinthitis
• Clinical feature:
– Acute onset of continuous, usually severe vertigo
lasting several days to a week
– Accompanied by hearing loss and tinnnitus
• During recovery hearing may return to normal or
remain permanently impaired in the involved ear
• Treatment:
– Antibiotics (if the patient is febrile or has symptoms of
bacterial infection)
– Vestibular suppressants (during acute phase of attack)
(diazepam, meclizine)

35. Vestibular Neuronitis
• Clinical feature:
– A paroxysmal, usually single attack of vertigo occurs
without accompanying impairment of auditory
function and will persist for several days to a week
before gradually abating
– On examination reveals nystagmus and absent
responses to caloric stimulation on one or both sides
• Treatment:
– For acute stage: Diazepam (2-5mg every 6-12 hours)
or Meclizine (25-100mg divided 2-3 times daily)
– Vestibular therapy

36. Vestibular migraine
• Episodic vertigo lasting for minutes to hours or
maybe for days to weeks
• Associated with or without headache
• Motion sensitivity and sensitivity to visual motion
are common
• Migraine features maybe present (such as
photophobia, phonophobia, or a visual aura)
• Treatment: treated with medications that are
used for prophylaxis of migrane headaches (such
as beta blocker, amitryptyline, flunarizine)

37. Meniere’s disease
• Clincial feature:
– Episodic vertigo accompanied by tinnitus and fullness
in the ear, each attack typically lasting a few hours.
– Gradually patient may develop progressive deafness
(typically low-tone on audiometry)
• Management:
– Low salt diet
– Vestibular sedatives (cinnarizine or prochlorperazine)
– Surgery to increase endolymphatic drainage from the
vestibular system

38. Superior Semicircular Canal
Dehiscence
• Clinical feature:
– Deficiency in the bony covering of the superior
semicircular canal maybe asscoaited with vertigo
triggered by loud noise exposure, straining and an
apparent conductive hearing loss
– Autophony is also a common feature
• Diagnosis is with coronal high resolution CT scan
and vestibular evoked myogenic potential (VEMP)
• Treatment:
– Surgically resurfacing or plugging the dehiscent canal

39. Psychosomatic and functional dizziness
• Dizziness maybe somatic manifestation of some
psychiatric condition
• Major depression
• Anxiety
• Panic disorder
• Or, patient may develop anxiety and autonomic
symptoms as a consequence or co morbidity of
an independent vestibular disorder.
• This is now termed as persistent postural-
perceptual dizziness (PPPD)

40. Persistent postural-perceptual
dizziness (PPPD)
• Clinical feature:
– Chronic feeling (3 months or longer) of fluctuating dizziness and
disequilibrium that is present at rest and worst while standing
– There is an increased sensitivity to self-motion and visual
motion (e,g, watching movies)
– Intensification of symptoms occurs when moving through
complex visual environments such as super-markets
– The neurootologic and vestibular function testing are normal
• Treatment:
– Selective serotonin reuptake inhibitors
– Cognitive- behavioral psychotherapy
– Vestibular rehabilitation

41. Drugs causing vertigo
• Antibiotics-
aminoglycisides,macrolides,nitrofurantoin
• Anticonvulsants-
levetiracetam,phenytoin,pregabalin
• Antiinflammatory-