1. CENTRAL VESTIBULAR
DISORDERS
Dr. ANITA BHANDARI

2. VERTIGO
PERIPHERAL
CENTRAL
The sensation of balance is the result of
appropriate information detected by
vestibular , ocular and proprioceptive sensory
receptors that is then properly integrated
within the cerebellum and brainstem.

3. Disruption of central integrators – brainstem and cerebellum
Sensory information mismatch – cortex
Lesion of vestibular N. or root entry – CPA lesions – affect primary
vestibular sensory info

4. 1 • Migraine
2 • Vertebrobasilar insufficiency
3 • Post. fossa CVA
4 • Cerebellar tumors
5 • Temporal lobe tumors
6
• Brainstem lesions
7 • CPA tumors
8 • Multiple sclerosis
9 • Post-traumatic

5. 1.Spontaneous nystagmus – not suppressed by fixation ,
may change direction with gaze
2.Nystagmus is purely vertical , horizontal or torsional
3.Saccade dysmetria
4.Nystagmus is paroxysmal but not fatiguable on Dix-
Hallpike test, with no latency, > 60 sec., may change
direction with diff. head positions

6. CEREBELLAR TUMORS
Primary in children, sec. in
adults
S/S depend on tumor location
size
Growth rate
Positional vertigo
Headaches
Gait disturbances
Neurosurgical intervention

7. TEMPORAL LOBE TUMORS
Recurrent attacks of vertigo ,
followed by transient
disorientation,amnesia,dysphagia
MRI enhanced
Neurosurgical intervention

8. BRAINSTEM LESIONS
Caused by neoplastic, traumatic or
vascular lesions
Vertigo may be mild or severe
Positional vertigo but no nystagmus

9. CPA TUMORS
• Vestibular schwanoma
• Meningioma
• Lipoma
• Cholesteatoma
• Metastatic
Features:
Unilateral hearing loss
Nystagmus inhibited by visual fixation
Disequilibrium rather than vertigo
unless sudden increase in tumor size

10. GENESIS OF THE MIGRAINE SYNDROME
OLDER HYPOTHESIS : VASCULAR REACTIVITY
Reduced regional blood flow through cortex
AURA
Dilatation of scalp arteries
HEADACHE

11. Migraine Pathophysiology
• Baseline sensory hyperexcitability
(thicker sensitive brains)
•Environmental events push past a threshold leading to:
•Electrical changes (cortical spreading depression -- CSD) occurs in
brain.
•Causes aura (aura is no longer a

12. Theory of cortical spreading
depression ( Cutrer and Baloh)
Spreads in all
directions from Ion fluxes
site of origin
Suppresses
central neuronal
activity
Transient
wave form
Stimulus
(chemical/
Mechanical)

13. Release of
Decreased neuropeptides sub
Cerebral blood P, neurokinin CGRP
Decreased flow in areas of (calcitonin gene
Extracellular spreading related peptide)
Calcium depression
Increased
Extracellular
Potassium
Ion fluxes

14. Neuropeptide
release causes
excitation of
Dizziness occurs baseline firing
with release of rate of sensory
neuropeptides epithelium of
inner ear & vest.
nuclei in pons

15. Asymmetric peptide
release causes vertigo
Symmetrical peptide
release leads to
increase sensitivity to
motion due to
increased vestibular
firing rate

16. MRV
Vasospasm of internal auditory artery
Ischemia of labyrinth
Peripheral cochleovestibular dysfunction

17. Classification by
IHS
Benign
Migraine without Migraine with Migraine with Migraine paroxysmal
aura aura prolonged aura infarction vertigo of
childhood

18. 1. Migraine without aura
Headache attacks : 4 to 72 hours
In children less than 15years age : 2 to 48 hours
Formerly called COMMON MIGRAINE
80%

19. Headache has at least two of the
following characteristics:
Unilateral
Pulsating
Severe intensity prevents or
inhibits daily activities
Aggravation by walking up stairs or
similar routine physical activity

20. During headache at least one of the
following prevails:
Nausea and/or vomiting
Photo and phonophobia

21. 2. Migraine with aura
Formerly called CLASSIC Migraine
15%

22. Aura with at least 2 of the following:
• Reversible aura symptoms with focal CNS
1. dysfunction
• Aura that develops over > 4 minutes
2.
• No aura symptoms which lasts for > 1 hour
3

23. BASILAR MIGRAINE
• VARIANT OF CLASSICAL MIGRAINE
• FEATURES OF BASILAR ART. INV.
• VERTIGO
• TINNITUS
• DYSARTHRIA
• ATAXIA
• VISUAL SYMPTOMS
• TINGLING , NUMBNESS, WEAKNESS OF LIMBS

24. 3. Migraine with prolonged aura
Aura for > 60 minutes but < 7 days
4. Migrainous infarction
Complicated migraine
Neurological Deficits not completely
reversed within 7 days

25. 5. Benign paroxysmal vertigo of
childhood
Brief episodes of disequilibrium, anxiety,
nystagmus or vomiting
Normal neurological findings
Normal EEG

26. CLINICAL PRESENTATION
• AGE
– ANY AGE
– OFTEN STARTS EARLY IN LIFE
– BENIGN PAROXYSMAL VERTIGO OF CHILDHOOD IS AN EARLY
MANIFESTATION OF MV
30
25
20
15
10
5
0
0-10 11-20 20-30 31-40 41-50 51-60 > 61

27. MALE : FEMALE
• FEMALE PREPONDERANCE
FEMALE
MALE

28. CLINICAL PRESENTATION
• Headache – only 50% pts. presented with H/o
headache along with or after vertigo .
• Several patients had headaches earlier in life but
now vertigo was the predominant symptom
• Duration – usually few hrs.

29. Prior to
headache
Vertigo may
During headache
occur
In headache free
interval (most
common)

30. True Episode
Vertigo
Light Positional
headedness Vertigo
Manifestations
Movement
Constant
associated
Imbalance
disequilibrium

31. Duration
Seconds 7%
Min- 2hrs 31%
2-6hrs 5%
>24 hrs 49%

32. Photophobia & phonophobia were
common symptoms.

33. AUDIOLOGICAL PRESENTATION
Most had normal hearing
Any SNHL was not related to MV

34. MOTION SICKNESS
• Has been reported to occur
commonly in MV due to a
optokinetic stimulation

35. BPPV AND MV
BPPV is a well documented sequelae to
ischemic damage of the inner ear
presumably d/t release of otoconia from
the macular membrane.
The vasospasm associated with classical
visual aura is secondary to a primary
neuronal metabolic defect

36. MANAGEMENT
History
No diagnostic test
Neurotological Exam Normal
Therapeutic trial If history unclear

37. MANAGEMENT
Lifestyle changes
• Explaining to the pt. what is going on
• Avoidance of irregular lifestyle and stress. Migrainous and
nonmigrainous brains are wired differently. Migraine pts. are
more susceptable to the effects of overexertion – mental &
physical , irregular eating and sleeping habits.

38. AVOIDANCE OF TRIGGER FACTORS
• A personal vertigo and diet diary
• Common triggers
– bright and blinking lights
– monosodium glutamate
– caffeine
– cheese
– chocolates
– alcohol
– pills
– strong smells

39. Treatments for Migraine
Abortive agents
• Triptans, Ergots
• Symptom agents
• Analgesics
• Antiemetics
• Prevention
• Interrupt the feedback loop

45. PROPHYLACTIC TREATMENT
Beta blockers
Propanolol – 40 -240 mg / day
Metoprolol – 50 -120 mg / day
Side effects –fatigue , hypotension , impotence ,
depression , nightmares , bronchial constriction
Calcium channel blockers
Flunerizine – 5-10 mg / day
Verapamil -120 -240 mg / day
Tricyclic antidepressants
Nortryptiline – 10 mg initially , upto 25 mg / day
Second line of drugs include Valproic acid and
methysergide.

49. PROPHYLAXIS TREATMENT
• Botulinum toxoid [Botox] injections into the
scalp or neck
– Mechanism – inhibition of acetylcholine in brain
– Efficacy after pericranial injection can last for 3 or
more months
– Used in case studies and trials , not yet approved

50. CEREBROVASCULAR DISEASES
The blood supply of the brainstem,
cerebellum and inner ear is obtained from
the vertebrobasilar system or posterior
circulatory system of the brain.
The blood supply of this system may be
impaired by
atherosclerosis,emboli/thrombi and
hemorrhage.

51. Subclavian art.
2 Vertebral art.
Ant. Spinal A.
Post. Spinal A. Join at pontomedullary
PICA jtn. To form
Basilar art.
Pontine art. Common
Sup. Cerebellar art.
cochlear A.
AICA Labyrinthine art.
Ant.
2 post. Cerbral A. Vestibular A.
ant. Cerebral art. ant. Communicating A.
(br. Of ICA) (br. Of ICA)
Circle of Willis
Communication of ant. & post. circulation

52. Basilar A
Bl. Of inner ear
Labryriathine A.
Ant. Common cochlear A
Vestivular A.
Supplies Main Vestibulo cochlear A.
sup. & cochlear A.
horizontal
scc &
utricle Supplies Cochlear A. Post vestibular A.
upper ¾ of
cochlea &
modiolus Supplies Supplies post. Scc
remaining ¼ & saccule
of cochlea

53. NEUROTOLOGICAL MANIFESTATIONS
Depends on:
1.Location of stasis or stenosis
2.Size of embolus or thrombus
3.Presence or absence of collateral
circulation

54. GRADING OF
VERTEBROBASILAR ISCHEMIA
1.TIA – focal neurological deficit of sudden
onset lasting <24 hrs.
2.Partial non-progressive stroke – partial
neurological deficit
3.Progressive stroke – neurological deficit
increases over time , non-reversible
4.Complete stroke – rapid non-reversible
neurological deficit

55. CVS DISEASES OF
POST. CIRCULATION
1.VBI
2.SUBCLAVIAN STEAL SYNDROME
3.LATERAL MEDULLARY/WALLENBERG’S SYND.
4.MEDIAL MEDULLARY SYND.
5.LATERAL PONTINE/FOVILLE’S SYND.
6.MEDIAL PONTINE/MILLARD-GUBLER SYND.
7.CEREBELLAR HEMORRHAGE/INFARCTION

56. VBI FEATURES
FEATURE AREA INVOLVED
1. ATAXIA INF. CEREBELLAR
PEDUNCLE
2. VERTIGO, INSTABILITY
(EXACERBATED BY HEAD
HYPEREXTENSION OR. VEST. NUCLEUS
ROTATION)
3. PERIORAL PARESTHESIA TRIGEMINAL NUCLEUS IN
PONS
4. VISUAL DISTURBANCES OCULOMOTOR NUCLEUS
5 DYSPHAGIA, NUCLEUS AMBIGUSS
HOARSENESS

57. SUBCLAVIAN STEAL SYNDROME
Exercise of arms leads to greater req.ment of bl.
which is obtained by stealing from VBS. The pt.
presents with few sec. of vertigo, ataxia ,
headache , visual disturbances.
More common in 6th-7th decade.
More on left side.
Systolic BP diff. of 20mm Hg b/w arms.
Delayed radial pulse on affected side.
Occ systolic murmur in supraclav. fossa on
exercise .

58. Etiology - bl. flow to basilar art. d/t occlusion of
subclavian art
Decreased BP distal to obstruction
Decreased BP in vertebral art.
Retrograde flow VBS into subclavian art. &
brachial art. of ipsilat. upper limb

59. LAT. MEDULLARY/WALLENBERG SYND
Cause : occlusion of PICA or vertebral
art. leading to infarction of lat.
aspect of medulla
FEATURE AREA INVOLVED
VERTIGO VEST. NUCLEUS
VOMITTING DORSAL MOTOR N. OF VAGUS
VISUAL DISTURBANCES MLF
ATAXIA INF. CEREBELLAR BODY & RESTI FORM
BODY
DYSPHAGIA, HOARSENESS NUCLEUS AMBIGUUS
HORNER’S SYND/ DESCENDING SYMP. TRAIT
LOSS OF PAIN AND & TEMP.
SENSATION
A. LIMBS LAT. SPINOTHALMIL TRACT
B. FACE SPINAL NUCLEUS OF TRIGEMINALN

60. MED.MEDULLARY SYNDROME
Cause : occlusion of ant.spinal art. Combination of lat. & med.
Medullary synd.- hemimedullary infarction d/t thrombosis of
vertebral art.
FEATURE AREA INVOLVED
PARESIS OF TONGUE XII NUCLEUS/ NERVE
LOSS OF PROPRIOCEPTION MED. LEMNISCUS
HEMIPLEGIA- CONTRALAT PYRAMIDAL TRACT
WITH SPARING OF FACE BEFORE DECUSSATION

61. CEREBELLAR HEM./INFARCTION
Each cerebellar hemisphere controls
movement of same side of body as opposed
to cerebral cortex which controls movements
of opp. side.
Cl. picture acc. to site involved

62. VBI : INVESTIGATIONS
Vascular imaging
1.Non-invasive
A]Doppler USG
B]MR Angiography

63. 2.Invasive
A]Angiography
B]CT Angiography
Cardiac profile –
lipid profile,ECG
CT angiogram showing a hypoplastic right vertebral, in a
person with symptoms of vertebrobasilar insufficiency.
Left vertebral (left lower) is large and dominant. Right
vertebral (right lower) is small and hypoplastic. This is
the same case as shown in the selective vertebral
angiogram below.

64. VBI : CLINICAL TESTS
1.George’s test – measure B/L BP , pulse,
auscultate subclavian & carotid art.
2.Maigne’s test –rotate head Rt.& Lt., then lat.ly
bend and extend head in seated position. Look for
nystagmus,nausea,vertigo,tinnitus. May indicate
vascular compromise.

65. 3.Dizziness test – to diff. dizziness d/t scc and
vertebral art. compromise. Rotate neck side to side
,then stabilize neck & rotate shoulders side to side.
If pt. experiences dizziness in both – VBI If + only
on head rotation, vestibular cause

66. MULTIPLE SCLEROSIS
Demyelinating disease of brainstem
region
More common in Caucasians, less in
Asians
Pathology – localized destruction of
myelin sheath followed by scarring.
Leads to hampered neural transmission.

67. MULTIPLE SCLEROSIS
Characteristics:
Age of onset : 20-40 yrs
More in females
Positive family history in 10-20%

68. MULTIPLE SCLEROSIS
Symptoms depend on area of involvement
Neurotological symptoms are due to
demyelination of:
1. cerebellum & its pathways
2. region of vest. nuclei
3. vestibulospinal pathway
4. vestibulo-ocular pathway
Vertigo is presenting symptom in 5% pts-
Ass. with poor prognosis
Instability is more common

69. MULTIPLE SCLEROSIS:
VESTIBULAR MANIFESTATIONS
ABNORMALITIES ON VEST. FUNCTION TESTS
1.Abnormalities on saccades , pendular
tracking, optokinetic tests
2.Gaze nystagmus - Cerebellar
lesionAtaxic nystagmus -MLF lesion
3.Hyperactive caloric response – loss of
cerebellar inhibitory effect on vest. Nuclei
4.Failure of nystagmus suppression on
visual fixation

70. 5.Dysrhythmic caloric induced nystagmus on
ENG
6.Bilateral spontaneous nystagmus – horizontal
or vertical – upbeating
7.Monocular nystagmus- when present is highly
suggestive of MS
8.Abnormal Romberg’s test
9.Abnormal Unterburger’s test

71. MULTIPLE SCLEROSIS:
AUDITORY MANIFESTATIONS
• Retrocochlear SNHL
• Unilateral HL indicates plaques in VIII N.-
between spiral ganglion & cochlear
nucleus
• Abnormal BERA – III & IV interpeak
latency
• Acoustic reflexes – present on ipsilateral
stimulation but absent on contralat. stim,
increased AR threshold

72. MULTIPLE SCLEROSIS:
OPHTHALMOLOGICAL FEATURES
INTERNUCLEAR
OPHTHALMOPLEGIA
• Weakness on lateral gaze
• Normal adduction
• Dissociated nystagmus
OPTIC NEURITIS

73. MULTIPLE SCLEROSIS: TREATMENT
• ? Etiology – no curative or preventive T/T
• Symptomatic T/T
Steroids
ACTH IM
Interferon
Cyclophosphamide

74. ARNOLD CHIARI
MALFORMATION
Protrusion of cerebellar tonsils thru the
foramen magnum
Interferes with CSF flow to & from the brain
Accumulation of CSF in empty spaces of
brain & spinal cord
Hydrocephalus

75. Vertigo- rotatory, lasting few hours,
with nausea & vomiting
Headaches- recurrent , lasting
several hours, often accompanying
vertigo ,no sensory amplification
Decreased hearing & tinnitus – 2
months , non-fluctuant
Paraesthesia – on face

76. CLINICAL EXAMINATION
• No spontaneous nystagmus
• Gaze evoked down beating nystagmus
• Tandem walking – unsteady,
• Unterburger test– ataxic
• Caloric testing – hyperactive response

77. Differential Diagnosis
• Migraine related vertigo
• Cerebellar disorder
• Multiple sclerosis
• Drug intoxication
• Vitamin B12 deficiency

78. McRae’s Line
Herniation of
tonsil

80. Treatment Plan
• Neurosurgical consultation and decision
for neurosurgery [ Chiari surgery]

81. POST-TRAUMATIC
• Peripheral lesions
• BPPV
• Perilymph fistula
• Labyrinthine concussion
• Central lesions
• Cerebral concussion

82. VESTIBULAR EPILEPSY
Pathophysiology– focal epileptic discharges in temporal lobe or parietal
association cortex
Clinical picture
rotational or linear vertigo – few sec, ”quick spin”
N/V
tinnitus
paraesthesia
Direction of nystagmus & body fall SAME [as this is a epileptic postural
response; not vestibulospinal compensation]

83. VESTIBULAR EPILEPSY
Rare variant- Volvular/Rotatory Epilepsy
paroxysmal repititive walking in small
circles without impairment of
consciousness
Investigations
EEG- focal slowing or sharp waves over
temporoparietal regions
Normal EEG does not exclude diagnosis
MRI

84. VESTIBULAR EPILEPSY
• D/D
• Other epilepsies
• Multiple sclerosis
• Migraine, BPV of childhood
• Drop attacks
• Treatment
• 1st line - carbamezepine , pheytoin
• 2nd line – gabapentine, Na valproate