Cerebro Vascular Disease (CVD) vs Stroke

Budhi Suwarma SpS.

Definition
CVD : any abnormality of the brain resulting

from a pathologic process (occlusion, rupture,altered permeability,increase visco sity,other change in quality of the blood) of the blood vessels. Stroke : sudden focal/global neurological deficit cause by primary vascular disorders last more than 24 hr or death.There are temporal profiles

Stroke
Apoplexy, cerebrovascular accident (CVA)

50% of the neurologic ward admission

Third commonest cause of death after heart

disease and cancer Incidence 2 %o , prevalence 4 %o Every physician should at least know the common type One of the most instructive approaches

Stroke (cont.)
The neurologic deficit reflects both the location and

size of the lesion Temporal profile :

Abruptness neurologic deficit develop Deficit reaches its peak almost at once (emboli) More slowly saltatory fashion/series of step (thrombotic) Steadily progressive (intracerebral hemorrhage) Neurologic deficit arrest and then regression

Stroke (cont.)
To demonstrate of cerebral lesion and the offending

vessels : CT scan, MRI, Doppler/ ultra sound, TCD, Arteriography, MRA, LP, EEG Major risk factors (RF) :

Longterm controle of hypertension decreases the incidence of both atherothrombotic infarction and intracerebral hemorrhage Structural cardiac disease and arrhythmia particularly AF are the most important RF for embolic strokes DM hastens the atherosclerotic process (l/s arteries) Long duration cigarette smoking~develop a.sclerosis

CLASSIFICATION
Based on clinical appearance and temporal profile

FORMERLY
TIA RIND

RECENTLY ( CVD III )

Improving stroke

( Reversible ischemic neurological deficit )

S.I.E. Worsening stroke

( Stroke in evolution / Progressing stroke )

Completed stroke Stable stroke

Ischemic Stroke
The effects of occlusion vary depending upon

the location and available collateral and anastomotic channels

Prox. to the circ.Willis, acoma and pcoma are often adequate to prevent infarction ICA, retrograde anastomotic flow from ECA via ophthalmic a. VA,anastomotic flow via deep C, thyro C, occipital a. or retrograde from the other VA Stem of Cerebral/Cerebellar,meningeal anast.

Ischemic stroke (cont.Effects of occlusion depends upon :)

Capillary anastomotic system between adjacent

arterial branches Ischemic modifying factors Speed of occlusion Level of blood pressure 02 and C02 Viscosity and Osmolality Hyperglycemia Anomalies of vascular Previous vascular occlusion

Ischemic Stroke (pathophysiology)

Critical threshold of CBF in monkey 23 ml (N: 55

ml/100 gr/min) CBF 12-23 abolish function,EEG slowed, ischemic penumbra,EC K+, ATP & Creatine Phosphate depleted CBF 10-12 infarction regardless of its duration CBF 6-8 EC K+,IC Ca++,cellular acidosis, ne crosis.Free fatty acid/phospholipase activated destroy the phospholipid membrane. Prostaglandin ,leukotrienes,free radicals accumulated protein & enzym denaturatedcellular edema

Ischemic stroke (pathophysiology)

Excitatory neurotransmitter (GLU & ASP)

released by ischemic cellsinflux Na & Ca, irreversible injury Free radical productionperoxidation & destruction of the outer cell membrane Accumulation of lactic acid (neurotoxic) Reduction of body temperaturereduce metabolismincrease tolerance

Ischemic stroke (Neurovascular syndrome-Carotid system)

CCA Occlusion (only less than 1% of carotid

a.syndrome), mostly thrombotic. ICA Occlusion (most frequently in the first part/immediately beyond the bifurcation), mostly thrombotic,often silent

Embolus arising from thrombus (a to a embolism) Watershed/borderzone between their branches In case of no communication to the side of occluded via circ. Willis massive infarction involving 2/3 hemi sphere including basal ganglia

Ischemic stroke (Neurovascular syndrome-Carotid system cont.)

MCA occlusion,mostly embolic Stem (block the flow in deep penetrating & superficial cortical branches) : hemiplegi c.l., hemianesthesia c.l.,HH c.l.,deviation of the head and eyes toward the lesion,dull/stuporous,global aphasia (L),anosognosiaamorphosynthesis (R) Superior division : dense sensory-motor deficit face & arm c.l.,deviation of head & eyes toward the lesion, alert, predominantly motor aphasia Inferior division (less frequent) : Wernicke aphasia (L) superior quadrantopsia, left visual neglect, amorpho synthesis

Ischemic stroke (Neurovascular syndrome-Carotid system cont.)

ACA occlusion Stem prox to acoma is usually well tolerated Distal to acoma : sensory-motor deficit of the opposite foot and leg,deviation of head&eyes toward the lesion urinary incontinence, grasp & gegenhalten c.l.,symph athetic apraxia left arm/leg,left alien arm/hand,trans cortical motor aphasia (occlusion of Heubner a.), right hemiplegia leg>arm,grasping&groping right hand,bu ccofacial apraxia,absence of spontaneous speech, agraphia,telegraphic speech,dysnomia,able to repeat spoken/written sentences,abulia,whisper,distractable Penetrating branches : transient hemiparesis, dysar thria,abulia/agitation-hyperactivity

Ischemic Stroke (Neurovascular Syndrome-Carotid system cont.)

Ant Choroidal A.occlusion : hemiplegia

c.l.,hemihypesthesia c.l.,HH c.l.,cognitive function spared,left spatial neglect & con structional apraxia (R),dysphasia (L) NB : a branch from ICA just above the origin of pcoma

Ischemic Stroke (Neurovascular Syndrome-Vertebrobasilar System)

Anterior-proximal PCA occlusion: Thalamic syndrome Dejerine-Roussy:hemian esthesi c.l.,transitory hemiparesis c.l.,HH c.l. Central midbrain-subthalamic syndrome : III i.l., hemiplegia c.l., upgaze palsy, stupor/ coma, ataxia/tremor c.l. Antero-medial-inferior thalamic syndrome : hemibalismus,hemichoreoathetosis, hemiataxia, tremor, deep sensory loss.

Ischemic Stroke (Neurovasc.Synd.Vertebrobasilar System cont.)

Cortical syndrome : HH macular sparing,

visual hallucination, metamorphopsia, palinopsia. Dominant side : alexia +/agraphia, anomia, visual agnosia. Bilateral cortical syndrome : HH bilateral, unformed vis.hal.,Anton syndrome,gun barrel vision,altitudinal field defect, Balint syndrome, Korsakoff amnestic, prosopagnosia.

Ischemic Stroke (Neurovasc.Synd.Vertebrobasilar System cont.)

Vertebral a. : Lateral medullary syndrome

(Wallenberg), medial & posterior medullary syndrome. Basilar a.: Complete basilar (comatous, bi lateral long tract,cerebellar & cranial signs) Locked-in syndrome,Top of the basilar syndrome, Crossed syndrome

Ischemic Stroke (Lacunar)

Small cavity 3-15 mm

Occlusion of small arteries 50-200 m

Strong correlation with hypertension-arterio

sclerosis - DM Incidence 11% post mortem examination Pure motor,pure sensory,dysarthria-clumsi ness of one hand, hemiparesis-ataxic

Ischemic Stroke (The Major Types)

Atherothrombotic Brain Infarct (ABI) : 32%

Embolism (TES & CES)

Lacunes (LACI) Primary Intracerebral Hemorrhage

32% 18% 11%

7%

(PICH) Ruptured Aneurysm/AVM (SAH)

ABI
Risk Factors : Major-Minor / Modifiable-Non

modifiable.

Hypertension, Dyslipidemia, DM aggravate the atheromatous process. Age, gender, family history, genetic, cigarette smoking, obesity, satiety life.

The most frequent sites are : origin ICA,

cervical part VA/junction to form BA, stem/ main bifurcation MCA, PCA around midbrain, ACA curve over corpus callosum.

ABI
Atheromatous lesions develop silently 20-30 / more

years thrombotic complication May regress to some extent (diet/drug) but in the large majority a progressive disease Degeneration of / hemorrhage into the wall of a sclerotic vesseldamage the endothelium platelet & fibrin adheredelicate friable clot. Subintimal atheromatous deposit may slough, spewing crystalline cholesterol emboli. Thrombotic particles may break off repeatedly. (artery to artery emboli)

ABI (Clinical picture)

75% is preceded by minor signs 1 / > TIAs

lasts a few min to several hr;mostly<l0 min

Carotid system :amaurosis fugax,hemiparese, hemiesthesia,disturbance of speech/language VB system : dizziness, diplopia, numbness, impaired visual field, dysarthria

Step like/wise development, gradual fashion Onset during sleep/awakening

ABI (Clinical picture cont)

Hypertension +,DM+,Vascular diseases in

other parts + (coronary, angina, abn ECG, intermittent claudication, pulseless) Headache , seizure, fatiqability and depressed (left fr lobe), MID, Binswanger subcortical leukoencephalopathy. Detection by USG, CT, MRI-MRA, conventional angiography

TIA
Brief reversible episodes of focal non-con

vulsive neurologic disturbance,duration <24 hr Embolism : last only a few min, multiple episodes of different pattern Vascular occlusion : repeated ones of uni form type The 5-year cummulative rate of fatal/non fatal cerebral infarct 23%

TIA (mechanism)
Vascular stenosis ulcerated e.c. athero

sclerosis thrombus formation. Detection by USG & DSA Rheologic changes (anemia, polycythemia, thrombocythemia, hyperlipidemia, hyperviscosity, sickle-cell) Hypotension :orthostatik, awakening

TREATMENT OF ABI & TIA

Prevention of stroke by finding patients in the

asymptomatic stage of atherosclerosis Treat patients who have already symptom

Management in the acute phase Measures to restore the circulation and arrest the pathologic process Physical therapy and rehabilitation Measures to prevent further strokes and progression of the vascular disease

TREATMENT OF ABI & TIA(cont)

Management in the acute phase in Stroke

unit with specially trained clinical staff and technology to monitor BP, pulmonary func tion, blood gas, ICP Measures to restore the circulation and arrest the pathologic process :

Penumbra will survive if perfusion can be reestablished Major stroke : avoid upright position in the 1st day to maintain cerebral perfusion

TREATMENT OF ABI & TIA(cont)

Antihypertensive drug is preferably defered until neurologic deficit has stabilized Anemia corrected, polycythemia should be reduced r-TPA 0,9 mg/kgBW, 10% bolus, 90% infus 1h Acute surgical revascularization (clot removal, bypass procedure) Treatment of cerebral edema and raised ICP Hemicraniectomy.

TREATMENT OF ABI & TIA(cont)

Anticoagulant drugs (warfarin & heparin)

Fluctuating BA thrombosis Impending ICA occlusion CES possible need for immediate hepariniza tion No great value once the stroke is fully develop ed Check PT, BP <200/120, Exclude ICH

TREATMENT OF ABI & TIA(cont)

Antiplatelet drugs

Aspirin 325 mg Ticlopidine 250 twice daily Dipyridamole, sulfinpyrazone Clopidogrel

EMBOLIC INFARCTION
Most cases : fragment from thrombus within

the heart Less frequently : A to A from atheromatous plaque carotid / vertebral Any region of the brain may be affected most frequently MCA superior division Very rapid occlusion no collateral influx

EMBOLIC INFARCTION (con)

No warning, onset anytime

Chronic AF, paroxysmal AF/flutter, MCI,

cardiac cath/surgery, valvuloplasty, valve prothese, paradoxic embolism, MVP 30% produces hemorrhagic transformation of the infarct (HTI) ECG, Echocardiography TTE & TEE

Embolic Infarction & Prevention)

Physical therapy and rehabilitation

(Treatment

General medical management in acute phase

Measures directed to restoring the circulation

Prime importance is the prevention of CE Long term AC in AF, MCI, Valve prothesis Electrical cardioversion for recent AF Firm diagnosis of CE : begin heparin/ LMWH followed

by warfarin Risk of AC : large infarct, deep infarct

Primary Intracerebral Hemorrhage

Massive several cm , small 1-2 cm , slit

old collapsed hemorrhage Due predominantly to chronic hypertension and degenerative arterial changes Hematoma distort and compress the adjacent brain tissue midline shift ARAS and respiratory center are compromised Seepage into ventricle system usually occurs bloody CSF

PICH (cont)
Edema accumulates around the clot and adds to

mass effect hydrocephalus After 2-3 mo slit hemorrhage The most common sites :

Putamen-internal capsule Lobar Thalamus Cerebellar hemisphere Pons Intraventricular, midbrain, medullary

PICH (Pathogenesis)
Hypertensionsegmental lipohyalinosis

microaneurysm Symphatomimetic medication,cocaine, other circumstances Tensi Amyloidosis Anticoagulant Vascular malformation Hematologic disorder,liver,renal,lymphoma

PICH (Clinical picture)

The most dramatic stroke / apoplexy, obese,

plethoric, hypertensive male, while sane and sound falls impervious to shout, shaking, pinching, breaths stertorously dies in a few hours Smaller hemorrhages : abrupt onset evolve gradually and steadily over minutes, hours, headache and vomiting

PICH (Clinical picture)

Very small hemorrhages in silent region

escape clinical detection Average age is lower than in ABI Incidence > black people, Japanese Onset mostly while active , upright Neurologic deficit is never transitory Condition worses over a few hours there is enlargement of the hematoma

PICH (Clinical picture)

Summary :

Acute reactive hypertension far exceeding the patients chronic hypertension level Severe headache Nuchal rigidity Vomiting at the onset Seizure focal

PICH (Clinical picture)

Putaminal hemorrhage (usually extend to the

adjacent internal capsule)

Gradual progression a few min-30 min Headache Vomiting Hemiplegia c.l. Stupor,coma Deviation conjugae to the side of lesion

PICH (Clinical picture)

Thalamic hemorrhage (large/moderate size compress

the adjacent int.capsule)

Hemiplegia/hemiparese c.l. Hemihypesthesia c.l. Fluent aphasia (D),amorphosynthesis/neglect (ND) Extension to subthalamus and high midbrain: gaze palsy V&L, forced downward, anisocor, skew deviation c.l. eye, ptosis-miosis i.l., retraction nystagmus, compression 3rd ventricel 8 mm recovery, 9-30 mm survive, > 30 mm + sec IVH die

PICH (Clinical picture)

Pontin hemorrhage

Deep coma in a few minutes Tetraparesis Decerebrate rigidity Miosis 1 mm reactive Horizontal gaze palsy Death usually occurs within a few hours Small tegmental hemorrhagegood recovery

PICH (Clinical picture)

Cerebellar hemorrhage

Occipital headache Repeated vomiting Vertigo Deviation conjugae away from the lesion / ocular bobbing Inability to sit/stand/walk Small cases : nystagmus,cerebellar ataxia

PICH (Clinical picture)

Lobar hemorrhage

Progressively worsening headache Vomiting Drowsiness 40% occipital, 25% temporal, 15% frontal, 11% parietal

PICH (laboratory)
CT detects hemorrhage 1 cm

MRI is useful for brainstem hemorrhage or

residual hemorrhage (after 4-5 weeks) Era pra CT diagnosis depend on LP WBC 15.000-20.000

PICH (Course and Prognosis)

Large and medium size hematome 35% die

60 ml in the basal ganglia fatal, but may be

relatively benign in lobar Putaminal / thalamic hemorrhage

30 ml favorable outcome 60 ml, GCS 8 mortality 90%

PICH (Treatment)
Maintain adequate ventilation

Controlled HV PCO2 25-30 mmHg

Raised ICP mannitol (Osm 295-305; Na

145-150 mEq) Fluid intake 1200 ml/d NaCl 0,9% Reduction of hypertension 20-25% Surgical removal : deteriorating hemispheral > 30 mm. Cerebellar is a more urgent, > 30-40 mm evacuation

SUBARACHNOID HEMORRHAGE (SAH)

The 4th most frequent Stroke following ABI, Embolism

and PICH Cause by rupture of saccular / berry aneurysm

Development defects in the media&elastica, Focal destruction the int elastica memb. by hemodynamic forces Size 2 mm-30 mm 90-95% lie on the anterior part of the circle of Willis Co-incidence : Congenital polycystic kidney,Fibromus cular dysplasia of EC aa,Moya2,Coarctation of aorta

Peak incidence 35-60 yrs

SAH (Clinical Pictures)

Pre rupture : localized head pain 3rd CN (

2nd CN, Chiasm) (warning sign) Rupture : Excruciating generalized head ache,vomiting unconsciousness. Usually occurs while active, sexual intercourse, straining, lifting heavy object etc. Re rupture may occur at anytime, minutes 3 weeks later (unpredictable)

SAH (Clinical Pictures)

Less severe cases regained conciousness

within a few min/hr, drowsiness, confusion, amnesia, severe headache, stiff neck, few/ no lateralizing neurologic signs Vasospasm 3-l2 d after rupture delayed neurological deficit Hydrocephalus after 2-4 weeks, patient become confused / unconscious

SAH (Clinical Pictures)

Spontaneous IC hemorrhage with normal BP

should suggest ruptured aneurysm / AVM, bleeding diathesis, hemorrhage into tumor Nuchal rigidity occasionally absent (1st 4 hr or deep coma Interscapular/LB pain rather than headpain Pre retinal / subhyaloid retinal hemorrhage

SAH (Laboratory)
CT scan detect blood in SA/brain/ventricel

Coexistent hydrocephalus Clinical suggest SAH but CT normal LP (grossly bloody / deep xanthochromia, opening pressure 50 cm H2O Conventional angiography (MRA insuffic.) ECG changes, hypo Na, WBC 15.000 18.000

SAH ( Site of rupture)

Main clot on CT scan Anterior interhemisphere fissureacoma Sylvian fissureMCA Ant.perimidbrain cisternpcoma/distal basilar Clinical signs 3rd CN palsyjunction pcoma-ICA Transient paraparesisacoma Hemiparesis/aphasia1st major bifurcat MCA Akinetic mutism/abuliaacoma

SAH (Treatment)
Assess with Botterell & Hunt-Hess

Grade 1 : slight headache & stiff neck Grade 2 : moderate / severe headache + nuchal rigidity, rare focal / lateralizing sign Grade 3 : drowsy, mild focal deficit Grade 4 : stupor / semicoma Grade 5 : deep coma, decebrate rigidity

SAH (Treatment)
Bed rest, i.v.line, stool softener, systolic 150

mmHg, pain relieving headache Grade 1-2 : operate early within 36 hr then increase intravasc volume,BP N/ above N Grade 3 ? Grade 4 : ventricular drain Grade 5 : conservative

ARTERIOVENOUS MALFORMATION (AVM)

Developmental abn / abn communication

between the A and V system Size a few mm- large mass (SOL like, CO, intracerebral steal) Incidence 1/10 saccular aneurysm Men = women

AVM ( Clinical picture)

Pre rupture : chronic,recurrent headache (non

discript type, 10% migraineus), convulsion c.l. side, systolic bruit over carotid, mastoid process, eye ball in young adult, rarely retinal AVM,cutaneus AVM, naso- pharyngeal AVM Rupture : similar with SAH (aneurysm) + neurological deficit at the onset

AVM ( Laboratory)
95% AVM disclosed by CT, >95% by MRA

Conventional angiography AVM 5 mm

AVM (Treatment)
Surgical excission, mortality rate 2-5%,

morbidity rate 5-25% Ligation of feeding artery Endovascular embolization Low dose focused proton beam

COMPLICATIONS

A. Neurologic complications Brain edema Hemorrhage infarction

Vasospasm
Hydrocephalus

Hygroma

COMPLICATIONS ( cont )
B. Non neurologic complication

1. Due to intracranial process

Increase blood presure Hyperglicemia Pulmonary edema Cardiac disorders

2. Due to immobilitation
Bronchopneumonia

Thrombophlebitis
Bladder infection Decubitus Contracture