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STROKE STROKE ANDI BASUKI P. B. , dr, SpS Sub-bagian Cerebrovascular Disease Sub-bagian Neurotraumatologi Bagian Ilmu Penyakit Saraf FK - UNPAD / RSUP dr. Hasan Sadikin Bandung
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Stroke & Vertigo

Oct 25, 2015

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Page 1: Stroke & Vertigo

STROKESTROKE

ANDI BASUKI P. B. , dr, SpS

Sub-bagian Cerebrovascular DiseaseSub-bagian Neurotraumatologi

Bagian Ilmu Penyakit SarafFK - UNPAD / RSUP dr. Hasan Sadikin

Bandung

Page 2: Stroke & Vertigo

CEREBROVASCULAR DISEASE :

1. Asymptomatic

2. Focal brain dysfunction

TIA ( Transient ischemic attack )

STROKE

3. Vascular dementia

4. Hypertensive encephalopathy

Page 3: Stroke & Vertigo

I. PATHOPHYSIOLOGY I. PATHOPHYSIOLOGY OF STROKEOF STROKE

Page 4: Stroke & Vertigo

Focal / Global Neurological Deficits

Sudden - very rapid development of symptoms

> 24 H or Death

No other Cause than primary CVD

DEFINITION of STROKE

Primary CVD = present of risk factorsGlobal brain dysfunction = unconsciousnessTIA : Complete recovery < 24 H

Page 5: Stroke & Vertigo

RISK FACTORSRISK FACTORSModifiableModifiable UnModifiableUnModifiable

HipertensionHipertension

Cardiac DiseaseCardiac Disease

Diabetes MellitusDiabetes Mellitus

HyperCholesterolHyperCholesterol

ObesityObesity

SmokingSmoking

Drugs + AlcoholDrugs + Alcohol

AgeAge

SexSex

HeredityHeredity

Race / ethnicRace / ethnic

Page 6: Stroke & Vertigo

Different Types of Stroke, 2000Different Types of Stroke, 2000

American Heart Association (AHA). Heart Disease and Stroke Statistics — 2003 Update. 2003. Available at: http://www.americanheart.org/downloadable/heart/10590179711482003HDSStatsBookREV7-03.pdf. Accessed October 13, 2003.

Ischemic Stroke

85% Cerebral Thrombosis

61%

TIA 3%

Cerebral Embolus

24%

Intracerebral Hemorrhage

9%

Subarachnoid Hemorrhage

3%

HemorrhagicStroke

12%

Page 7: Stroke & Vertigo

Ischemic Stroke ( ATHEROTROMBOTIK )Ischemic Stroke ( ATHEROTROMBOTIK )

Page 8: Stroke & Vertigo

INFARCTION STROKE CLINICAL CATEGORIES ( cont’ )

1. Atherothrombotic infarction

Superimposed trombus to the atherosclerotic plaque

Atherosclerotic plaque extracranial or intracranial arteries

Two mechanisms :

a. Atherosclerotic plaque stenotic / occlusion

b. Embolism or plaque fragments occlusion

( artery – to – artery embolus )

Page 9: Stroke & Vertigo

Embolic Source ( Cardio emboli )Embolic Source ( Cardio emboli )

Page 10: Stroke & Vertigo

INFARCTION STROKE CLINICAL CATEGORIES ( cont’ )

2. Cardioembolic Maximal / complete deficit at onset

Usually at activity

Source of embolus :

Cardiac :

AF, AMI, CHF, mitral or aortic valve disease

Transcardiac ( paradoxical embolus ) :

Right to left cardiac shunt

The source of clot : peripheral venous thrombus

Page 11: Stroke & Vertigo

INFARCTION STROKE CLINICAL CATEGORIES ( cont’ )

3. Lacunar infarction

Clinical diagnosis usually rests on :

Brain imaging

Small lesions, 1.5 cm in greatest diameter

Clinical syndrome ( anatomic location )

Pure motor hemiparesis

Pure sensory stroke

Ataxic hemiparesis

Dysarthria clumsy hand syndrome

Prognosis is generally good

Large lesions ( giant lacunes ) are due to multiple penetrating arteries

Page 12: Stroke & Vertigo

BRAIN INFARCTION

Normal metabolism and blood flow

Brain : A very metabolically active organ( Glucose & oxygen consumption )ATP as energy for maintain neuronal integrity keep Ca++ outside and K+ within the cells

Brain requirement O2 500 mLGlucose 75-100 mg

Each minute !!

Page 13: Stroke & Vertigo

BRAIN INFARCTION

Normal metabolism and blood flow

Cerebral Blood Flow (CBF) 53 ml/100 gm brain/minute (range 50-60)

Cerebral Metabolism Rate for Oxygen (CMRO2) Cerebral O2 Consumption

3.5 ml/mg/minute Maximum compensation to maintain CMRO2

at CBF 20-25 ml/100 gm/min

Page 14: Stroke & Vertigo

BRAIN INFARCTION If CBF decreases to 15-18 ml electrical failure

< 15 ml change in somato-sensory evoked potential

< 10 ml ionic failureExtra cellular K+ , Intracellular Ca++ Free fatty acid releases, ATP breakdown, intracellular acidosis neuronal death

between electrical and ionic failure) Neuron not functioning, but still viable = PENUMBRA

It is a target of intervention !!.

Page 15: Stroke & Vertigo

BRAIN INFARCTION

Factors that determine CBF

Regional Cerebral Blood Flow (rCBF) Auto-regulation Microcirculation change Metabolic and neuro-chemical control

Page 16: Stroke & Vertigo

BRAIN INFARCTION

Regional CBFHagen Poisseuille Law

V =

V = velocity of blood flow to the brainp = intravascular pressurer4 = radius of the arteryn = blood viscosityl = arterial length

p . r4 .

n . l . 8

Page 17: Stroke & Vertigo

Auto-regulation

Capacity of brain circulation to maintain constant CBF

CBF relatively constant in MABP 50-150 mmHg

Chronic hypertension : shift of Upper and lower levels ofauto-regulation

If BP increases vessels will constrict if BP decreases dilate.

Page 18: Stroke & Vertigo

BRAIN INFARCTION

Auto-regulation

25

50

75

50 100 150 200

CBF

MABP

Page 19: Stroke & Vertigo

BRAIN INFARCTION

Micro-circulation change

Vessel occlusion result in Low shear stress

blood aggregation blood viscosity and resistency

Vasoconstriction caused by extracellular K

Page 20: Stroke & Vertigo

BRAIN INFARCTION

Metabolic and neuro-chemical changes

K+ moves across the cell membrane into the extracellular space potentiate and enhance cell deathProduction of O2 free radicals peroxidation fatty acid in cell organelles and plasma membrane damage cell functionAnerobic glycolysis accumulation of lactic acid and lowering pH acidosis impaire cell metabolic function

Page 21: Stroke & Vertigo

BRAIN INFARCTION

Metabolic and neuro-chemical changes

Production of excitatory neurotransmitter (glutamate, aspartate, kainic acid) Na+ and Ca++ influx into cells Water and Cl- follow Na+

cytotoxic edema

Page 22: Stroke & Vertigo

Intracerebral Hemorrhage

Rupture of cerebral vessels Bleeding into the brain

in aging or chronic HT microaneurysms at penetrating arteries + 1mm

Charcot-Bouchard aneurysm

Brain hemorrhage : Compressive effect Extend to ventricle or Subarachnoid

Most common : Basal Ganglia.

Page 23: Stroke & Vertigo

Subarachnoid Bleeding

The causes :Ruptured aneurysmRuptured AVMRuptured angiomaBlood dyscrasia

Aneurysm : found commonly in Willis circle and its branches

Aneurysm ruptures blood fills in subarachnoidspace and brain parenchym close to it.

Page 24: Stroke & Vertigo

Subarachnoid Space

Complications

Vasospasm : Narrowing of arteries at the brain day 2 - 12 after onset. Hydrocephalus

Rebleeding : occurs in a few weeks after the onset

Hyponatremia

Seizures

Page 25: Stroke & Vertigo

II. CLINICAL MANIFESTATION II. CLINICAL MANIFESTATION OF STROKEOF STROKE

Page 26: Stroke & Vertigo

Vascular location

Carotid system

Vertebro - Basilar ( VB ) system

Clinical manifestation Depend on :

Large of lesion

Site of Vascular lesion (Vascular system)

Page 27: Stroke & Vertigo

Circle of WillisCircle of Willis& &

Brain VascularizationBrain Vascularization

Page 28: Stroke & Vertigo

CLASSIFICATION

Clinical appearance and Temporal profile

( CVD III )

• TIA

• RIND • Improving stroke

( Reversible ischemic neurological deficit )

• S.I.E. • Worsening stroke

( Stroke – in – evolution / Progressing stroke )

• Completed stroke • Stable stroke

Page 29: Stroke & Vertigo

Improving stroke

Complete recovery : 24 Hours to 3 weeks

Worsening stroke Progresivity of symptom ( qualitative- quantitative)

in anamnestic or follow up

50 % cases in several minutes and hours

Sub type : - Smooth worsening - Steplike worsening - Fluctuating worsening

Page 30: Stroke & Vertigo

CLINICAL MANIFESTATION

A. Carotid system Motor dysfunction

Contralateral hemiparesis

Ipsilateral paresis : CN and extremities

dysarthria

Sensory dysfunction

Contralateral hemihypesthesia

ipsilateral hypesthesia : CN and extremities

Page 31: Stroke & Vertigo

CLINICAL MANIFESTATION ( cont’ )

A. Carotid system Visual disturbances

Contralateral homonymous hemianopsia

Amaurosis fugax ( TIA )

Higher cortical dysfunction

Aphasia

Agnosia

Page 32: Stroke & Vertigo

CLINICAL MANIFESTATION ( cont’ )

B. VB system Motor dysfunction

Alternating hemiparesis

( CN Paresis is contralateral to extrimities paresis )

Dysarthria

Sensory dysfunction

Alternating hemihypesthesia

(CN Hypesthesia is contralateral to extrimities hypesthesia)

Page 33: Stroke & Vertigo

CLINICAL MANIFESTATION ( cont’ )

B. VB system

Visual disturbances

Homonymous hemianopsia

Cortical blindness ( TIA : blackout )

Others

Loss of balance

Vertigo

Diplopia

Page 34: Stroke & Vertigo

CLINICAL MANIFESTATION ( cont’ )

Brain hemorrhage

The onset is acute, severe headache, unconsciousness

The blood pressure usually is elevated at onset

The most common locations of hypertensive bleeding are basal ganglia, thalamus, lobe of a hemisphere, cerebellum, pons

Page 35: Stroke & Vertigo

CLINICAL MANIFESTATION ( cont’ )

Brain hemorrhage

Lobar hemorrhage : in elderly usually an amyloid angiopathy

Thalamic hemorrhage

oculomotor disturbance (downgaze or upgaze palsy), unreactive miotic pupils, convergence paralysis

Page 36: Stroke & Vertigo

CLINICAL MANIFESTATION ( cont’ )

Brain hemorrhage

Cerebellar hemorrhage :

Disequilibrium, limb ataxia, nausea, vomiting, headache and dizziness

peripheral facial palsy, nystagmus, miosis, decreased corneal reflex, abducens palsy

Page 37: Stroke & Vertigo

CLINICAL MANIFESTATION ( cont’ )

Brain hemorrhage

Primary hemorrhage into the brain stem :

Usually Fatal

The common site is pons

Clinical diagnosis CT – Scan to differentiate small hemorrhage and infarction

Page 38: Stroke & Vertigo

CLINICAL MANIFESTATION ( cont’ )

Subarachnoid hemorrhage ( SAH )

Bleeding into the subarachnoid space

Clinical finding :

Sudden Onset

Severe headache (dramatic, in seconds to minutes )

Decreased level of consciousness

( recovery in a few minutes )

Vomiting

Younger and less to have hypertension

Page 39: Stroke & Vertigo

CLINICAL MANIFESTATION ( cont’ )

Subarachnoid hemorrhage ( SAH )

Usually no focal findings on examination,

Meningeal irritation ( stiffneck )

Kernig’s or Brudzinski’s sign

Sub-hyaloid hemorrhage

Brain imaging Blood in the subarachnoid space

Page 40: Stroke & Vertigo

CLINICAL MANIFESTATION ( cont’ )

Subarachnoid hemorrhage ( SAH )

LP Bloody or xanthochromic CSF

Causes :

- Rupture of aneurysm (saccular aneurysm) or AVM CT - MRI – arteriogram - angiogram.

- Neoplasm

- Unknown : 10 – 15 % cases

Vasospasme may occur after 48 H onset

Page 41: Stroke & Vertigo

COMPLICATIONS

A.Neurologic complications

Brain edema

Hemorrhage infarction

Vasospasm

Hydrocephalus

Hygroma

Page 42: Stroke & Vertigo

B. Non – neurologic

1. Intracranial process

Increase BP, Hyperglicaemia

Pulmonary edema, Cardiac disorders

2. Immobilitation Bronchopneumonia, Thrombophlebitis

Bladder infection, Decubitus, Contracture

3. Psychosocial : Depression, Loss of Occupation

Page 43: Stroke & Vertigo

III. MANAGEMENT III. MANAGEMENT OF STROKEOF STROKE

Page 44: Stroke & Vertigo

1. Laboratory Examination Blood : Blood : - Ht, Hb, Leuco, - Ht, Hb, Leuco, - Erythr.( Polycytemia Vera, anemia) - Erythr.( Polycytemia Vera, anemia)

- Ur, creat , uric acid. (Renal Function impairment) - Ur, creat , uric acid. (Renal Function impairment) - Chol : T, HDL, LDL, & TG (Dislipidemia) - Chol : T, HDL, LDL, & TG (Dislipidemia)

- Glucose : fasting & post prandial ( DM )- Glucose : fasting & post prandial ( DM ) - SGOT, SGPT. (Liver Function)- SGOT, SGPT. (Liver Function) - Electrolytes (Ca, K, Na, Cl)- Electrolytes (Ca, K, Na, Cl)

Page 45: Stroke & Vertigo

Chest X-Ray ( LVH, Pulmonary edema)Chest X-Ray ( LVH, Pulmonary edema)

ECG ( LVH, MI, AF)ECG ( LVH, MI, AF)

Carotid USG ( stenosis of carotid artery )Carotid USG ( stenosis of carotid artery )

Angiography ( Carotid - Vertebrobasilar system. Angiography ( Carotid - Vertebrobasilar system.

Page 46: Stroke & Vertigo

CT ( Computerized Tomography )Scanning : CT ( Computerized Tomography )Scanning :

Infarction : Hypo densityInfarction : Hypo density

Hemorrhage : Hyper densityHemorrhage : Hyper density

MRI ( Magnetic Resonance Imaging )MRI ( Magnetic Resonance Imaging )

Brainstem Lesion ( More sensitive)Brainstem Lesion ( More sensitive)

LP ( Lumbar Puncture )LP ( Lumbar Puncture )

If CT Scan or MRI unavailableIf CT Scan or MRI unavailable

Page 47: Stroke & Vertigo

ISCHEMIC / INFARCTION ISCHEMIC / INFARCTION STROKESTROKE

Page 48: Stroke & Vertigo

Hemorrhagic STROKEHemorrhagic STROKE

Page 49: Stroke & Vertigo

SAHSAH

n engl j med 355;9

Page 50: Stroke & Vertigo

2. MANAGEMENT Airway Airway }} important for important for Breathing Breathing } } oxygenationoxygenation

Cardiovascular system : maintenance CBFCardiovascular system : maintenance CBF

Don’t treat BP if :Don’t treat BP if :

- Infarction < 220 / 120 mmHg - Infarction < 220 / 120 mmHg

- Hemorrhagic < 180 / 105 mmHg- Hemorrhagic < 180 / 105 mmHg

( reactive Hypertension in acute phase) ( reactive Hypertension in acute phase)

Page 51: Stroke & Vertigo

Water and electrolyte balance : Water and electrolyte balance :

- Infus : isotonic water haemodilution, - Infus : isotonic water haemodilution,

- Maintenance input, food and drink, Diet - Maintenance input, food and drink, Diet

basal metabolism 1500 cal.basal metabolism 1500 cal.

( 23 cal/kg/weight ) : orally or NGT.( 23 cal/kg/weight ) : orally or NGT.

- Output Control- Output Control

Brain edema ( impending/ herniation ) Brain edema ( impending/ herniation )

Give antiedema (mannitol 20 %), Give antiedema (mannitol 20 %),

Max for 5 days ( rebound phenomen prohibition)Max for 5 days ( rebound phenomen prohibition)

Page 52: Stroke & Vertigo

Sign of impending herniation : Sign of impending herniation :

- Decrease of consciousness- Decrease of consciousness

- - Pupil miosis and reactivePupil miosis and reactive

- Cheyne’s stokes respiration - Cheyne’s stokes respiration

- Bilateral Babinski (Pathologic Reflex)- Bilateral Babinski (Pathologic Reflex)

Sign of Herniation : Sign of Herniation :

- Decrease of consciousness - Decrease of consciousness

- - Pupil anisocorPupil anisocor

- Central Neurogenic Respiration - Central Neurogenic Respiration

- Bilateral Babinski - Bilateral Babinski

Page 53: Stroke & Vertigo

Manitol Contraindication : Manitol Contraindication :

-- Hipotension Hipotension

-- Renal Impairment Renal Impairment

- Dehydration - Dehydration

- Decompensatio Cordis - Decompensatio Cordis

Head elevation 30Head elevation 300 0

Hyperglycemia : if > 250 mg% give antidiabeticHyperglycemia : if > 250 mg% give antidiabetic

Control Complication and Underlying diseaseControl Complication and Underlying disease

Page 54: Stroke & Vertigo

Control Vegetative function.Control Vegetative function.

Passive PhysiotherapyPassive Physiotherapy

as soon as possibleas soon as possible

for preventing contracture, thrombophlebitis for preventing contracture, thrombophlebitis ( DVT )( DVT )

Active Physiotherapy Active Physiotherapy

If No complication - ContraindicationIf No complication - Contraindication

Page 55: Stroke & Vertigo

secondary prevention : Antiplatelet agent secondary prevention : Antiplatelet agent

a. Asetilosalysilic acid ( ASA )a. Asetilosalysilic acid ( ASA )

(cyclooxygenation enzyme inhibitor) (cyclooxygenation enzyme inhibitor)

decrease tromboxan A2, decrease tromboxan A2,

Inhibit platelet agregation Inhibit platelet agregation

dose ( Varied ) : 250 mg/daysdose ( Varied ) : 250 mg/days

b. Clopidogrelb. Clopidogrel : : 1 x 75 mg1 x 75 mg

Page 56: Stroke & Vertigo

Cardio-embolic Infarction PreventionCardio-embolic Infarction Prevention

- Anticoagulant :- Anticoagulant :

first : heparin iv,first : heparin iv,

continue with : oral anticoagulant continue with : oral anticoagulant

(Coumarin)(Coumarin)

Page 57: Stroke & Vertigo

Recanalization thrombosis : Recanalization thrombosis :

-- rTPa, Streptokinase. rTPa, Streptokinase. Complication : bleeding Complication : bleeding

Inhibition Vasospasme : Inhibition Vasospasme :

(SAH Complication) (SAH Complication)

2 - 3 days after onset 2 - 3 days after onset

Clinically worsening, Clinically worsening,

decrease level of consciousness decrease level of consciousness

neurological deficitneurological deficit

Page 58: Stroke & Vertigo

Vasospasme Vasospasme

Mechanism : Mechanism :

Prostaglandin + cathecolamin accumulation. Prostaglandin + cathecolamin accumulation.

Therapy : Ca antagonist ( Nimodipin ) Therapy : Ca antagonist ( Nimodipin )

Within 3 days of onsetWithin 3 days of onset

Page 59: Stroke & Vertigo

VERTIGOVERTIGO

Page 60: Stroke & Vertigo

DefinitionsDefinitions

Latin : vertere, to spin

The illusory / subjective sensation of movement May feel either that patients involving in space

or that objects in the environment are moving around him.

Etiology : central, peripheral

Page 61: Stroke & Vertigo

SymptomsSymptoms PallorPallor

SweatingSweating

Nausea/VomitingNausea/Vomiting

Auditory Symptoms :Hearing loss, Tinnitus,Auditory Symptoms :Hearing loss, Tinnitus,

Neurologic Symptoms: numbness, weakness, Neurologic Symptoms: numbness, weakness, difficulty with swallowing or speechdifficulty with swallowing or speech

Page 62: Stroke & Vertigo

AnatomyAnatomyReceptorReceptor Transduction : mechanic Transduction : mechanic bio-elektro-kimia. bio-elektro-kimia. Receptor : vestibulum, retina, proprioseptif (skin, muscle, Receptor : vestibulum, retina, proprioseptif (skin, muscle,

joint)joint)

Saraf Aferen. Saraf Aferen. Transmision : impuls – equilibrium centerTransmision : impuls – equilibrium center through N.VIII, N. II, spino-vestibulo-serebelaris.through N.VIII, N. II, spino-vestibulo-serebelaris.

Brain equilibrium center. Brain equilibrium center. Modulation, comparation, coordination, perception. Modulation, comparation, coordination, perception. Nucl.N.VIII, cerebellum, cortex cerebri (Limbik & Prefrontal), Nucl.N.VIII, cerebellum, cortex cerebri (Limbik & Prefrontal),

Hypothalamus, Brain stem otonomic center (Vomit center, Hypothalamus, Brain stem otonomic center (Vomit center, Nucl. okulomotorius, Formatio reticularis )Nucl. okulomotorius, Formatio reticularis )

Page 63: Stroke & Vertigo

FISIOLOGIFISIOLOGI

GERAKAN GERAKAN Reseptor :

Vestibularis ( 50 %)Visual (30%)

Proprioseptif (20)

Gerakan endolimfeMenekuk cilia

Stimulus listrik kiri - kananeksitator : Glu, Asp, Ach, His, Subst Pinhibitor : GABA, GLY, NA, Dop, Ser

INTI VESTIBULARISPUSAT KESEIMBANGAN

Page 64: Stroke & Vertigo

PatofosiologiPatofosiologi11. Sensory conflict Theory . Sensory conflict Theory Right – Left sensory input imbalance.Right – Left sensory input imbalance.

2. Neural mismatch Theory 2. Neural mismatch Theory New Type of Movement (Motoric Memory)New Type of Movement (Motoric Memory)

3. Autonomic imbalance Theory 3. Autonomic imbalance Theory Sympatic – parasympatic imbalance.Sympatic – parasympatic imbalance.

4. Neurohumoral Theory 4. Neurohumoral Theory Physic/Psychic Stress Physic/Psychic Stress Kortikotropin releasing factor from Kortikotropin releasing factor from

Hypothalamus. Hypothalamus. Sympatic dominacy : palour, cold skin, moist skin, panic, vertigo. Sympatic dominacy : palour, cold skin, moist skin, panic, vertigo. Parasympatic dominacy : nausea, hipersalivation, vomitus.Parasympatic dominacy : nausea, hipersalivation, vomitus.

Page 65: Stroke & Vertigo

ClassificationClassificationPerifer :

- Vestibulum – nucl. vestibuler - Severe vertigo synd, severe illness, panic. - Nistagmus : fast freq, high amplitudo, latency, fatique. - Usually Ears disease

Vestibuler

Sentral : - Nucl.Vestibuler – Brain Cortex- Sindroma vertigo ringan, sakit sedang- Nistagmus : slow freq, low amplitudo, latency (-), fatique (-) - Other Neurolocal deficit.

Non Vestibuler Eyes or somatosensorik.Dizzines, uncomfortable walking, light headedness, nauseaNo nistagmus.

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EtiologiEtiologi

PERIPHERALOuter ear : cerumen, corp. alienMiddle ear : Timpanic membrane, otitis media, labirintitis, cholesteatoma, traumaInner ear : trauma, vasculer, alergy, hidrops labirinN.VIII : infection, trauma, thrombosis, tumorNucl. vestibularis : infection, trauma, thrombosis, tumor, multiple sclerosis.

CENTRALCNS dis. : vasculer, infection, trauma, tumor, migraine, epilepsy.Endocrine : hypothyroid, hypoglicemia, adrenal tumorPsikiatri : depresion, neurosa, anxiety

NON VESTIBULERMata : refraktion, ocular muscleProprioseptif : polineuropaty

Page 67: Stroke & Vertigo

Determine : a peripheral or a central Determine : a peripheral or a central problemproblem

peripheral peripheral (99:100) refers to the inner ear or (99:100) refers to the inner ear or vestibular nerve up to the root entry zone in vestibular nerve up to the root entry zone in the brain stemthe brain stem

centralcentral (1:100) refers to the brain, usually (1:100) refers to the brain, usually associated with focal neurologic findings, associated with focal neurologic findings, may be from cerebellar infarctmay be from cerebellar infarct

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Peripheral vs Central Peripheral vs Central VertigoVertigo

FeaturesFeatures Peripheral VertigoPeripheral Vertigo Central VertigoCentral Vertigo

ConsciousConscious ConsciousConscious UnconsciousUnconscious

NystagmusNystagmus Horizontal/rotaryHorizontal/rotary

always beats in one always beats in one direction; inhibited with direction; inhibited with fixation; usually fixation; usually disappears within a few disappears within a few daysdays

VerticalVertical

typically changes typically changes direction toward the direction toward the direction of gaze; not direction of gaze; not inhibited with fixation; inhibited with fixation; last > 1-2 dayslast > 1-2 days

Related to Related to position position

changingchanging

YesYes NoNo

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Peripheral vs Central Peripheral vs Central VertigoVertigo

FeaturesFeatures Peripheral VertigoPeripheral Vertigo Central VertigoCentral Vertigo

History & History & physicalphysical

Ear / Auditory Ear / Auditory symptoms (aural symptoms (aural fullness,tinnitus ,hefullness,tinnitus ,hearing loss, pain)aring loss, pain)

Neurologic symptoms Neurologic symptoms (disequilibrium,gait)(disequilibrium,gait)

vascular risk fact. : age vascular risk fact. : age >60, HTN, smoking, >60, HTN, smoking, atherosclerotic cardiac, atherosclerotic cardiac, peripheral vascular diseaseperipheral vascular disease

Degree of Degree of imbalancimbalancee

Pts Pts prefer to lie prefer to lie downdown, , can get upcan get up and and walk if asked but walk if asked but tend tend to veer to one sideto veer to one side

Pts with cerebellar lesions Pts with cerebellar lesions have severe imbalance that have severe imbalance that they they cannot stand up cannot stand up

Page 70: Stroke & Vertigo

Double visionDouble visionusually suggests central brainstem usually suggests central brainstem involvement, but may occur in peripheral involvement, but may occur in peripheral inner-ear or vestibular nerve damageinner-ear or vestibular nerve damage

peripheral lesionsperipheral lesions siemicircular canal siemicircular canal nystagmus nystagmus otolith organs otolith organs slight static eye slight static eye

displacement, use cover-uncover testdisplacement, use cover-uncover test

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Central vertigoCentral vertigo Brainstem LesionsBrainstem Lesions Intravascular: Vertebrobasilar Intravascular: Vertebrobasilar

insufficiencyinsufficiency TumorsTumors Intracranial infectionIntracranial infection Demyelinating diseases: Multiple Demyelinating diseases: Multiple

Sclerosis, SyringobulbiaSclerosis, Syringobulbia

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Peripheral VertigoPeripheral Vertigo 1. 1. BPPVBPPV (most common in adults)(most common in adults) 2. Acute Labyrinthitis2. Acute Labyrinthitis 3 Toxic Labyrinthitis. 3 Toxic Labyrinthitis. 4. Chronic Labyrinthitis (Meniere’s 4. Chronic Labyrinthitis (Meniere’s

Syndrome) Syndrome) 4. Vestibular Neuronitis (viral labyrinthitis)4. Vestibular Neuronitis (viral labyrinthitis) 5. Otitis Media5. Otitis Media 6. Vestibular migraine6. Vestibular migraine 7. ‘Senile’ vestibulopathy7. ‘Senile’ vestibulopathy 8. Vestibular Neuronitis8. Vestibular Neuronitis 9. Acoustic Nerve Lesions9. Acoustic Nerve Lesions 10. Labyrinthine Ischemia10. Labyrinthine Ischemia

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Benign Positional Benign Positional VertigoVertigo

vertigo produced by vertigo produced by change in positionchange in position the the most common cause of vertigomost common cause of vertigo results from the free movement of results from the free movement of

dislodged utricle particulate debris - dislodged utricle particulate debris - calcium carbonate crystals - in the calcium carbonate crystals - in the semicircular canalssemicircular canals

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BPVBPVdiagnostic testingdiagnostic testing

Dix-Hallpike testDix-Hallpike test positional testing using the head-hanging positional testing using the head-hanging

technique technique patients with benign positional vertigo will patients with benign positional vertigo will

show a burst of nystagmus after a delay of 5 show a burst of nystagmus after a delay of 5 to 10 seconds, the nystagmus lasts about 30 to 10 seconds, the nystagmus lasts about 30 secondsseconds

the test is never subtly positivethe test is never subtly positive

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Dix-Hallpike ManeuverDix-Hallpike Maneuver

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Vertigo of Central Vertigo of Central OriginOrigin

Diagnotic cluesDiagnotic clues risk factors, focal neurologic findingsrisk factors, focal neurologic findings

Diagnostic testsDiagnostic tests MRIMRI MR angiographyMR angiography

TreatmentTreatment Due to etiologyDue to etiology

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Neurologic examsNeurologic exams

NystagmusNystagmus

Romberg’s Romberg’s

GaitGait

Dix-Hallpike ManeuverDix-Hallpike Maneuver

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TREATMENTTREATMENT

CAUSALCAUSAL

SYMPTOMATICSYMPTOMATIC

REHABILITATIONREHABILITATION

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SymptomaticSymptomatic Ca entry blockerCa entry blocker

Antihistamin Antihistamin

Antikolinergik Antikolinergik

Monoaminergik Monoaminergik

AntidopaminergikAntidopaminergik

BensodiasepinBensodiasepin

Histaminik : Histaminik :

AntiepilepticAntiepileptic

Page 80: Stroke & Vertigo

Drug treatment of Drug treatment of dizzinessdizziness

Glutamate, Glutamate, GABA and ACh GABA and ACh (Hist, 5HT, (Hist, 5HT, peptides, DA, peptides, DA, NA)NA)

ProchlorperazineProchlorperazine Betahistine Betahistine (Serc)(Serc)

CinnarazineCinnarazine CyclizineCyclizine HyoscineHyoscine promethazine promethazine

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REHABILITATIONREHABILITATION

Brandt Daroff Brandt Daroff MethodsMethods

Epley maneuvreEpley maneuvre : BPPV treatment. : BPPV treatment.

Visual vestibuler exerciseVisual vestibuler exercise

Walking / gait exerciseWalking / gait exercise

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Brandt DaroffBrandt Daroff

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Epley Particle Repositioning Epley Particle Repositioning ManoeuvreManoeuvre

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