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

CEREBROVASCULAR DISEASE : 1. Asymptomatic

2. Focal brain dysfunction

TIA ( Transient ischemic attack )

STROKE
3. Vascular dementia 4. Hypertensive encephalopathy

I. PATHOPHYSIOLOGY OF STROKE

DEFINITION of STROKE Focal / Global Neurological Deficits

Sudden - very rapid development of symptoms

> 24 H or Death No other Cause than primary CVD
Primary CVD = present of risk factors Global brain dysfunction = unconsciousness TIA : Complete recovery < 24 H

RISK FACTORS
Modifiable UnModifiable

Hipertension Cardiac Disease Diabetes Mellitus HyperCholesterol Obesity Smoking Drugs + Alcohol

Age Sex Heredity Race / ethnic

Different Types of Stroke, 2000

Cerebral Embolus 24%

Ischemic Stroke 85%

Cerebral Thrombosis 61%

Intracerebral Hemorrhage Hemorrhagic 9% Stroke 12% Subarachnoid Hemorrhage 3%

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 ( 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 )

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 mL Each minute !! Glucose 75-100 mg

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 failure Extra 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 CBF

Hagen Poisseuille Law V= V p r4 n l p . r4 . n.l.8 = velocity of blood flow to the brain = intravascular pressure = radius of the artery = blood viscosity = arterial length

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 of auto-regulation If BP increases vessels will constrict if BP decreases dilate.

BRAIN INFARCTION Auto-regulation

CBF
75

50

25

MABP
50 100 150 200

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 death Production of O2 free radicals peroxidation fatty acid in cell organelles and plasma membrane damage cell function Anerobic 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 aneurysm Ruptured AVM Ruptured angioma Blood dyscrasia Aneurysm : found commonly in Willis circle and its branches Aneurysm ruptures blood fills in subarachnoid space and brain parenchym close to it.

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
Subarachnoid Space

II. CLINICAL MANIFESTATION OF STROKE

Vascular location Carotid system

Vertebro - Basilar ( VB ) system

Clinical manifestation Depend on :

Large of lesion Site of Vascular lesion (Vascular system)

Circle of Willis & Brain Vascularization

CLASSIFICATION
Clinical appearance and Temporal profile ( CVD III ) TIA RIND ( Reversible ischemic neurological deficit ) S.I.E. ( Stroke in evolution / Progressing stroke ) Completed stroke Improving stroke

Worsening 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 )

Kernigs or Brudzinskis 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 OF STROKE

1. Laboratory Examination
Blood : - Ht, Hb, Leuco, - Erythr.( Polycytemia Vera, anemia) - Ur, creat , uric acid. (Renal Function impairment) - Chol : T, HDL, LDL, & TG (Dislipidemia) - Glucose : fasting & post prandial ( DM ) - SGOT, SGPT. (Liver Function) - Electrolytes (Ca, K, Na, Cl)

 Chest X-Ray ( LVH, Pulmonary edema)

ECG ( LVH, MI, AF)

Carotid USG ( stenosis of carotid artery ) Angiography ( Carotid - Vertebrobasilar system.

 CT ( Computerized Tomography )Scanning : Infarction : Hypo density Hemorrhage : Hyper density MRI ( Magnetic Resonance Imaging ) Brainstem Lesion ( More sensitive)

LP ( Lumbar Puncture ) If CT Scan or MRI unavailable

ISCHEMIC / INFARCTION STROKE

Hemorrhagic STROKE

SAH

n engl j med 355;9

2. MANAGEMENT
Airway } important for Breathing } oxygenation Cardiovascular system : maintenance CBF Dont treat BP if : - Infarction < 220 / 120 mmHg - Hemorrhagic < 180 / 105 mmHg ( reactive Hypertension in acute phase)

 Water and electrolyte balance : - Infus : isotonic water haemodilution, - Maintenance input, food and drink, Diet basal metabolism 1500 cal. ( 23 cal/kg/weight ) : orally or NGT. - Output Control
Brain edema ( impending/ herniation ) Give antiedema (mannitol 20 %),

Max for 5 days ( rebound phenomen prohibition)

 Sign of impending herniation : - Decrease of consciousness - Pupil miosis and reactive - Cheynes stokes respiration - Bilateral Babinski (Pathologic Reflex) Sign of Herniation : - Decrease of consciousness - Pupil anisocor - Central Neurogenic Respiration - Bilateral Babinski

 Manitol Contraindication : - Hipotension - Renal Impairment - Dehydration - Decompensatio Cordis Head elevation 300
Hyperglycemia : if > 250 mg% give antidiabetic Control Complication and Underlying disease

 Control Vegetative function.

Passive Physiotherapy as soon as possible for preventing contracture, thrombophlebitis ( DVT ) Active Physiotherapy If No complication - Contraindication

 secondary prevention : Antiplatelet agent a. Asetilosalysilic acid ( ASA ) (cyclooxygenation enzyme inhibitor) decrease tromboxan A2, Inhibit platelet agregation

dose ( Varied ) : 250 mg/days

b. Clopidogrel

: 1 x 75 mg

 Cardio-embolic Infarction Prevention - Anticoagulant : first : heparin iv, continue with : oral anticoagulant (Coumarin)

 Recanalization thrombosis : - rTPa, Streptokinase. Complication : bleeding

Inhibition Vasospasme : (SAH Complication) 2 - 3 days after onset Clinically worsening, decrease level of consciousness neurological deficit

Vasospasme
Mechanism : Prostaglandin + cathecolamin accumulation. Therapy : Ca antagonist ( Nimodipin ) Within 3 days of onset

VERTIGO

Definitions
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

Symptoms
Pallor Sweating Nausea/Vomiting Auditory Symptoms :Hearing loss, Tinnitus,

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

Anatomy
Receptor Transduction : mechanic bio-elektro-kimia. Receptor : vestibulum, retina, proprioseptif (skin, muscle, joint) Saraf Aferen. Transmision : impuls equilibrium center through N.VIII, N. II, spino-vestibulo-serebelaris. Brain equilibrium center. Modulation, comparation, coordination, perception. Nucl.N.VIII, cerebellum, cortex cerebri (Limbik & Prefrontal), Hypothalamus, Brain stem otonomic center (Vomit center, Nucl. okulomotorius, Formatio reticularis )

FISIOLOGI
GERAKAN
Reseptor : Vestibularis ( 50 %) Visual (30%) Proprioseptif (20)

Gerakan endolimfe Menekuk cilia

INTI VESTIBULARIS PUSAT KESEIMBANGAN

Stimulus listrik kiri - kanan eksitator : Glu, Asp, Ach, His, Subst P inhibitor : GABA, GLY, NA, Dop, Ser

Patofosiologi
1. Sensory conflict Theory

Right Left sensory input imbalance. 2. Neural mismatch Theory New Type of Movement (Motoric Memory) 3. Autonomic imbalance Theory Sympatic parasympatic imbalance. 4. Neurohumoral Theory Physic/Psychic Stress Kortikotropin releasing factor from Hypothalamus. Sympatic dominacy : palour, cold skin, moist skin, panic, vertigo. Parasympatic dominacy : nausea, hipersalivation, vomitus.

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

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, nausea No nistagmus.

Etiologi
PERIPHERAL
Outer ear : cerumen, corp. alien Middle ear : Timpanic membrane, otitis media, labirintitis, cholesteatoma, trauma Inner ear : trauma, vasculer, alergy, hidrops labirin N.VIII : infection, trauma, thrombosis, tumor Nucl. vestibularis : infection, trauma, thrombosis, tumor, multiple sclerosis.

CENTRAL
CNS dis. : vasculer, infection, trauma, tumor, migraine, epilepsy. Endocrine : hypothyroid, hypoglicemia, adrenal tumor Psikiatri : depresion, neurosa, anxiety

NON VESTIBULER
Mata : refraktion, ocular muscle Proprioseptif : polineuropaty

Determine : a peripheral or a central problem

peripheral (99:100) refers to the inner ear or vestibular nerve up to the root entry zone in the brain stem central (1:100) refers to the brain, usually associated with focal neurologic findings, may be from cerebellar infarct

Peripheral vs Central Vertigo

Features Conscious Peripheral Vertigo Conscious Central Vertigo Unconscious Vertical typically changes direction toward the direction of gaze; not inhibited with fixation; last > 1-2 days No Nystagmus Horizontal/rotary always beats in one direction; inhibited with fixation; usually disappears within a few days
Related to position changing

Yes

Peripheral vs Central Vertigo

Features History & physical Peripheral Vertigo Ear / Auditory symptoms (aural fullness,tinnitus ,hearing loss, pain) Central Vertigo Neurologic symptoms (disequilibrium,gait) vascular risk fact. : age >60, HTN, smoking, atherosclerotic cardiac, peripheral vascular disease Degree of Pts prefer to lie Pts with cerebellar lesions imbalanc down, can get up and have severe imbalance that e walk if asked but tend they cannot stand up to veer to one side

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

peripheral lesions
siemicircular canal nystagmus otolith organs slight static eye displacement, use cover-uncover test

Central vertigo
Brainstem Lesions Intravascular: Vertebrobasilar insufficiency Tumors Intracranial infection Demyelinating diseases: Multiple Sclerosis, Syringobulbia

Peripheral Vertigo
1. BPPV (most common in adults) 2. Acute Labyrinthitis 3 Toxic Labyrinthitis. 4. Chronic Labyrinthitis (Menieres Syndrome) 4. Vestibular Neuronitis (viral labyrinthitis) 5. Otitis Media 6. Vestibular migraine 7. Senile vestibulopathy 8. Vestibular Neuronitis 9. Acoustic Nerve Lesions 10. Labyrinthine Ischemia

Benign Positional Vertigo

vertigo produced by change in position the most common cause of vertigo results from the free movement of dislodged utricle particulate debris calcium carbonate crystals - in the semicircular canals

BPV diagnostic testing

Dix-Hallpike test
positional testing using the head-hanging technique patients with benign positional vertigo will show a burst of nystagmus after a delay of 5 to 10 seconds, the nystagmus lasts about 30 seconds the test is never subtly positive

Dix-Hallpike Maneuver

Vertigo of Central Origin

Diagnotic clues
risk factors, focal neurologic findings

Diagnostic tests
MRI MR angiography

Treatment
Due to etiology

Neurologic exams
Nystagmus
Rombergs Gait Dix-Hallpike Maneuver

TREATMENT
CAUSAL
SYMPTOMATIC REHABILITATION

Symptomatic
Ca entry blocker Antihistamin Antikolinergik Monoaminergik Antidopaminergik Bensodiasepin Histaminik : Antiepileptic

Drug treatment of dizziness

Glutamate, GABA and ACh (Hist, 5HT, peptides, DA, NA) Prochlorperazine Betahistine (Serc) Cinnarazine Cyclizine Hyoscine promethazine

REHABILITATION
Brandt Daroff Methods Epley maneuvre : BPPV treatment. Visual vestibuler exercise Walking / gait exercise

Brandt Daroff

Epley Particle Repositioning Manoeuvre