This document discusses central vestibular disorders. It describes how central vestibular disorders can be caused by lesions in the brainstem or cerebellum that disrupt central integration of sensory information. Some specific causes mentioned include migraines, vertebrobasilar insufficiency, tumors in the posterior fossa or temporal lobe, and multiple sclerosis. Symptoms of central vestibular disorders can include spontaneous nystagmus, abnormal eye movements, and positional vertigo without nystagmus. The document also discusses evaluation and management of specific central vestibular disorders.
Learn more about the types, symptoms and causes of balance disorders. Diagnostic and treatment options such as vestibular rehabilitation and cognitive behavioral therapy will be discussed.
In-service project for clinical affiliation with Hingham PT, Inc. (Januay 2014-April 2014)
Review of vestibular system, common diagnosis and how to examine, evaluate and treat.
I also reviewed and supplied the clinic with the Four Step Square Test and Dynamic Gait Index in order to allow them to implement these outcome assessments into their clinic for individuals with balance/vestibular deficits
Learn more about the types, symptoms and causes of balance disorders. Diagnostic and treatment options such as vestibular rehabilitation and cognitive behavioral therapy will be discussed.
In-service project for clinical affiliation with Hingham PT, Inc. (Januay 2014-April 2014)
Review of vestibular system, common diagnosis and how to examine, evaluate and treat.
I also reviewed and supplied the clinic with the Four Step Square Test and Dynamic Gait Index in order to allow them to implement these outcome assessments into their clinic for individuals with balance/vestibular deficits
A detailed description of benign paroxysmal positional vertigo (BPPV): the symptoms, causes, diagnosis, and treatment methods.For more information, please visit www.everydayhearing.com
A concise presentation about BPPV and Ménière's disease and other causes of vertigo, the difference between central and peripheral vertigo, symptoms and etiology and approach to physical examination and treatment.
This ppt describes various movement disorders found commonly in elderly persons. It also describes hyper and hypokinetic disorder categorization with cause and pathophysiology of movement disorders.
A detailed description of benign paroxysmal positional vertigo (BPPV): the symptoms, causes, diagnosis, and treatment methods.For more information, please visit www.everydayhearing.com
A concise presentation about BPPV and Ménière's disease and other causes of vertigo, the difference between central and peripheral vertigo, symptoms and etiology and approach to physical examination and treatment.
This ppt describes various movement disorders found commonly in elderly persons. It also describes hyper and hypokinetic disorder categorization with cause and pathophysiology of movement disorders.
The slide contains how to take a history of seizure patient when to start and stop AEDs
general introduction of seizure and ILAE classification
anti-epileptic treatment and comorbidities
seizure and heart , lung , liver, kidney diseases
I hope this will help you in exams and also in your clinical practice.
Thank you
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Adv. biopharm. APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMSAkankshaAshtankar
MIP 201T & MPH 202T
ADVANCED BIOPHARMACEUTICS & PHARMACOKINETICS : UNIT 5
APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMS By - AKANKSHA ASHTANKAR
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
Antimicrobial stewardship to prevent antimicrobial resistanceGovindRankawat1
India is among the nations with the highest burden of bacterial infections.
India is one of the largest consumers of antibiotics worldwide.
India carries one of the largest burdens of drug‑resistant pathogens worldwide.
Highest burden of multidrug‑resistant tuberculosis,
Alarmingly high resistance among Gram‑negative and Gram‑positive bacteria even to newer antimicrobials such as carbapenems.
NDM‑1 ( New Delhi Metallo Beta lactamase 1, an enzyme which inactivates majority of Beta lactam antibiotics including carbapenems) was reported in 2008
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
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
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
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
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)
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
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
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.
46.
47.
48.
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
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
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.
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
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
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