4. cerebro vascular disease (cvd).ppt

Cerebro Vascular Disease (CVD) vs Stroke

Budhi Suwarma SpS.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 RECENTLY ( CVD III )

TIA

RIND 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),anosognosia-amorphosynthesis (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 Ø 3-15 mm Occlusion of small arteries Ø 50-200 μm 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) 32% Lacunes (LACI) 18% Primary Intracerebral Hemorrhage 11%

(PICH) Ruptured Aneurysm/AVM (SAH) 7%

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 mid- brain, 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 re-

established 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 (Treatment & Prevention) General medical management in acute phase Measures directed to restoring the circulation Physical therapy and rehabilitation 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 Ø several cm , small Ø 1-2 cm , slit old collapsed hemorrhage

Due predominantly to chronic hypertension and degenerative arterial changes

Hematoma distort and compress the adja- cent 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

patient’s 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 pro- cess, 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 Ø 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