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CENTRAL VESTIBULAR
    DISORDERS




         Dr. ANITA BHANDARI
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.
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
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
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
CEREBELLAR TUMORS
      Primary in children, sec. in
                adults
     S/S depend on tumor location
                 size

             Growth rate


          Positional vertigo


              Headaches


          Gait disturbances


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



               MRI enhanced




         Neurosurgical intervention
BRAINSTEM LESIONS

Caused by neoplastic, traumatic or
vascular lesions



Vertigo may be mild or severe




Positional vertigo but no nystagmus
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
GENESIS OF THE MIGRAINE SYNDROME

 OLDER HYPOTHESIS : VASCULAR REACTIVITY

      Reduced regional blood flow through cortex

              AURA

  Dilatation of scalp arteries

           HEADACHE
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
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)
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
Neuropeptide
                   release causes
                   excitation of
Dizziness occurs   baseline firing
with release of    rate of sensory
neuropeptides      epithelium of
                   inner ear & vest.
                   nuclei in pons
Asymmetric peptide
                          release causes vertigo




 Symmetrical peptide
   release leads to
increase sensitivity to
    motion due to
 increased vestibular
      firing rate
MRV


 Vasospasm of internal auditory artery


         Ischemia of labyrinth


Peripheral cochleovestibular dysfunction
Classification by
                                          IHS




                                                                      Benign
Migraine without   Migraine with    Migraine with       Migraine    paroxysmal
      aura             aura        prolonged aura      infarction    vertigo of
                                                                     childhood
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%
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
During headache at least one of the
        following prevails:
      Nausea and/or vomiting



      Photo and phonophobia
2. Migraine with aura


Formerly called CLASSIC Migraine


15%
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
BASILAR MIGRAINE

• VARIANT OF CLASSICAL MIGRAINE




• FEATURES OF BASILAR ART. INV.
  • VERTIGO
  • TINNITUS
  • DYSARTHRIA
  • ATAXIA
  • VISUAL SYMPTOMS
  • TINGLING , NUMBNESS, WEAKNESS OF LIMBS
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
5. Benign paroxysmal vertigo of
           childhood
    Brief episodes of disequilibrium, anxiety,
    nystagmus or vomiting


    Normal neurological findings



    Normal EEG
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
MALE : FEMALE
• FEMALE PREPONDERANCE




                           FEMALE
                           MALE
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.
Prior to
                 headache


Vertigo may
              During headache
   occur

              In headache free
                interval (most
                  common)
True Episode
                               Vertigo




   Light                                               Positional
headedness                                              Vertigo


                          Manifestations




           Movement
                                            Constant
           associated
                                           Imbalance
         disequilibrium
Duration

Seconds              7%
Min- 2hrs            31%
 2-6hrs              5%
 >24 hrs             49%
Photophobia & phonophobia were
      common symptoms.
AUDIOLOGICAL PRESENTATION

Most had normal hearing

Any SNHL was not related to MV
MOTION SICKNESS
• Has been reported to occur
  commonly in MV due to a
  optokinetic stimulation
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
MANAGEMENT


 History

No diagnostic test

Neurotological Exam Normal

Therapeutic trial If history unclear
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.
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
Treatments for Migraine

  Abortive agents
  • Triptans, Ergots
  • Symptom agents
  • Analgesics
  • Antiemetics
  • Prevention
  • Interrupt the feedback loop
Central vestibular disorders
Central vestibular disorders
Central vestibular disorders
Central vestibular disorders
Central vestibular disorders
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.
Central vestibular disorders
Central vestibular disorders
Central vestibular disorders
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
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.
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
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
NEUROTOLOGICAL MANIFESTATIONS
       Depends on:
        1.Location of stasis or stenosis


        2.Size of embolus or thrombus

        3.Presence or absence of collateral
        circulation
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
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
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
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 .
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
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
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
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
VBI : INVESTIGATIONS

Vascular imaging
1.Non-invasive
A]Doppler USG
B]MR Angiography
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.
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.
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
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.
MULTIPLE SCLEROSIS

Characteristics:

Age of onset : 20-40 yrs

More in females

Positive family history in 10-20%
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
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
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
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
MULTIPLE SCLEROSIS:
OPHTHALMOLOGICAL FEATURES


     INTERNUCLEAR
     OPHTHALMOPLEGIA
     • Weakness on lateral gaze
     • Normal adduction
     • Dissociated nystagmus

     OPTIC NEURITIS
MULTIPLE SCLEROSIS: TREATMENT

 • ? Etiology – no curative or preventive T/T
 • Symptomatic T/T
   Steroids
   ACTH IM
   Interferon
   Cyclophosphamide
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
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
CLINICAL EXAMINATION


• No spontaneous nystagmus

• Gaze evoked down beating nystagmus

• Tandem walking – unsteady,

• Unterburger test– ataxic

• Caloric testing – hyperactive response
Differential Diagnosis


• Migraine related vertigo
• Cerebellar disorder
• Multiple sclerosis
• Drug intoxication
• Vitamin B12 deficiency
McRae’s Line
 Herniation of
 tonsil
Central vestibular disorders
Treatment Plan

• Neurosurgical consultation and decision
  for neurosurgery [ Chiari surgery]
POST-TRAUMATIC
• Peripheral lesions
• BPPV
• Perilymph fistula
• Labyrinthine concussion



• Central lesions
• Cerebral concussion
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]
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
VESTIBULAR EPILEPSY

   • D/D
   • Other epilepsies
   • Multiple sclerosis
   • Migraine, BPV of childhood
   • Drop attacks




   • Treatment
   • 1st line - carbamezepine , pheytoin
   • 2nd line – gabapentine, Na valproate
Central vestibular disorders

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Central vestibular disorders

  • 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
  • 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