STROKESTROKE
ANDI BASUKI P. B. , dr, SpS
Sub-bagian Cerebrovascular DiseaseSub-bagian Neurotraumatologi
Bagian Ilmu Penyakit SarafFK - UNPAD / RSUP dr. Hasan Sadikin
Bandung
CEREBROVASCULAR DISEASE :
1. Asymptomatic
2. Focal brain dysfunction
TIA ( Transient ischemic attack )
STROKE
3. Vascular dementia
4. Hypertensive encephalopathy
I. PATHOPHYSIOLOGY I. PATHOPHYSIOLOGY OF STROKEOF STROKE
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
RISK FACTORSRISK FACTORSModifiableModifiable UnModifiableUnModifiable
HipertensionHipertension
Cardiac DiseaseCardiac Disease
Diabetes MellitusDiabetes Mellitus
HyperCholesterolHyperCholesterol
ObesityObesity
SmokingSmoking
Drugs + AlcoholDrugs + Alcohol
AgeAge
SexSex
HeredityHeredity
Race / ethnicRace / ethnic
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%
Ischemic Stroke ( ATHEROTROMBOTIK )Ischemic Stroke ( ATHEROTROMBOTIK )
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 )
Embolic Source ( Cardio emboli )Embolic Source ( Cardio emboli )
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
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
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 !!
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
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 !!.
BRAIN INFARCTION
Factors that determine CBF
Regional Cerebral Blood Flow (rCBF) Auto-regulation Microcirculation change Metabolic and neuro-chemical control
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
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.
BRAIN INFARCTION
Auto-regulation
25
50
75
50 100 150 200
CBF
MABP
BRAIN INFARCTION
Micro-circulation change
Vessel occlusion result in Low shear stress
blood aggregation blood viscosity and resistency
Vasoconstriction caused by extracellular K
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
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
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.
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.
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
II. CLINICAL MANIFESTATION II. CLINICAL MANIFESTATION OF STROKEOF STROKE
Vascular location
Carotid system
Vertebro - Basilar ( VB ) system
Clinical manifestation Depend on :
Large of lesion
Site of Vascular lesion (Vascular system)
Circle of WillisCircle of Willis& &
Brain VascularizationBrain Vascularization
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
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
CLINICAL MANIFESTATION
A. Carotid system Motor dysfunction
Contralateral hemiparesis
Ipsilateral paresis : CN and extremities
dysarthria
Sensory dysfunction
Contralateral hemihypesthesia
ipsilateral hypesthesia : CN and extremities
CLINICAL MANIFESTATION ( cont’ )
A. Carotid system Visual disturbances
Contralateral homonymous hemianopsia
Amaurosis fugax ( TIA )
Higher cortical dysfunction
Aphasia
Agnosia
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)
CLINICAL MANIFESTATION ( cont’ )
B. VB system
Visual disturbances
Homonymous hemianopsia
Cortical blindness ( TIA : blackout )
Others
Loss of balance
Vertigo
Diplopia
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
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
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
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
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
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
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
COMPLICATIONS
A.Neurologic complications
Brain edema
Hemorrhage infarction
Vasospasm
Hydrocephalus
Hygroma
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
III. MANAGEMENT III. MANAGEMENT OF STROKEOF STROKE
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)
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.
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
ISCHEMIC / INFARCTION ISCHEMIC / INFARCTION STROKESTROKE
Hemorrhagic STROKEHemorrhagic STROKE
SAHSAH
n engl j med 355;9
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)
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)
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
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
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
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
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)
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
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
VERTIGOVERTIGO
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
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
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 )
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
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.
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.
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
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
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
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
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
Central vertigoCentral vertigo Brainstem LesionsBrainstem Lesions Intravascular: Vertebrobasilar Intravascular: Vertebrobasilar
insufficiencyinsufficiency TumorsTumors Intracranial infectionIntracranial infection Demyelinating diseases: Multiple Demyelinating diseases: Multiple
Sclerosis, SyringobulbiaSclerosis, Syringobulbia
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
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
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
Dix-Hallpike ManeuverDix-Hallpike Maneuver
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
Neurologic examsNeurologic exams
NystagmusNystagmus
Romberg’s Romberg’s
GaitGait
Dix-Hallpike ManeuverDix-Hallpike Maneuver
TREATMENTTREATMENT
CAUSALCAUSAL
SYMPTOMATICSYMPTOMATIC
REHABILITATIONREHABILITATION
SymptomaticSymptomatic Ca entry blockerCa entry blocker
Antihistamin Antihistamin
Antikolinergik Antikolinergik
Monoaminergik Monoaminergik
AntidopaminergikAntidopaminergik
BensodiasepinBensodiasepin
Histaminik : Histaminik :
AntiepilepticAntiepileptic
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
REHABILITATIONREHABILITATION
Brandt Daroff Brandt Daroff MethodsMethods
Epley maneuvreEpley maneuvre : BPPV treatment. : BPPV treatment.
Visual vestibuler exerciseVisual vestibuler exercise
Walking / gait exerciseWalking / gait exercise
Brandt DaroffBrandt Daroff
Epley Particle Repositioning Epley Particle Repositioning ManoeuvreManoeuvre