CEREBROVASCULAR DISEASES

FADARE B.A MBChB

OUTLINE
INTRODUCTION EPIDEMIOLOGY RISK FACTORS PATHOGENESIS CLINICAL FEATURES MANAGEMENT COMPLICATIONS DIFFERENTIAL DIAGNOSIS PROGNOSIS CONCLUSION

INTRODUCTION
Cerebrovascular disease(CVD) is a group of diseases which include some of the most common and devastating disorders: ischemic stroke,hemorrhagic stroke, and cerebrovascular anomalies such as intracranial aneurysms and arteriovenous malformations

 Cerebrovascular disease is defined as a sudden onset of a neurologic deficit that is attributable to a focal vascular cause.

CVD could be:

Stroke: sudden focal neurologic deficit of vascular origin that lasts more than 24hrs or results in the death of the patient. Transient Ischemic Attack(TIA):<24hrs Reversible Ischemic Neurologic Death(RIND):24hrs-1wk

Current thinking
Any neurologic deficit >1hr is not likely to be TIA Any demonstrable cerebral infarction, irrespective of the time=stroke=brain attack RIND= CITS(Cerebral Infarction with Transient Symptoms) CIND=Cerebral Infarction with No Deficit)

EPIDEMIOLOGY
3RD leading cause of death in the western countries & is the most common cause of severe physical disability Annual incidence of 180-300 per 100 000 3RD commonest neurological condition in Nigeria . 6-41% of neurological admission. 4-10% of hospital mortality in Nigeria. An important cause of mortality and morbidity affecting the patient, family, & society.

CLINICAL CLASSIFICATION
TIA STROKE PROGRESSING STROKE OR STROKE IN EVOLUTION COMPLETED STROKE

CLASSIFICATION Ischemic
Thrombotic Embolic

Hemorrhagic
Intracranial hemorrhage SAH

RISK FACTORS
NON-MODIFIABLE
Increasing age Male gender & PM women Black race +ve Family hx Past hx of TIA or stroke Genetics: deletion polymorphism of ACE gene

RISK FACTORS
MODIFIABLE
Undiagnosed Hypertension Diabetes Hrt dx [MI,IE,VHD,CMTy,CHD,AF] Hemoglobinopathy Smoking Heavy alcohol OCP Polycythemia Infections eg HIV Obesity sedentary lifestyle dyslipidemia protein C&S def thrombocytopenia homocystinuria

Common causes of ischemic stroke

Thrombosis:small vessel(lacunar), large vessel Embolic occlusion:Artery-to-artery(Carotid bifurcation,Aortic arch,Arterial dissection);Cardioembolic(Atrial fibrillation,Mural thrombus,MI,DCM,Valvular lesionS(MS,Mechanical valve,Bacterial endocarditis) Paradoxical embolus(ASD,Patent foramen ovale,Atrial septal aneurysm)

UNCOMMON CAUSES OF ISCHEMIC STROKE

Hypercoagulable disorders Protein C &S deficiency,Antithrombin III deficiency,Antiphospholipid syndrome,Factor V Leiden mutation,Systemic malignancy,Sickle cell anemia,BThalassemia,Polycythemia vera,SLE,Homocysteinemia,TTP,DIC,Dysproteinemias,Nephr otic syndrome,IBD,OCPs Fibromuscular dysplasia Vasculitis:Systemic vasculitis (PAN, Wegner s,Takayasu s, giant cell arteritis),PrimaryCNS vasculitis Meningitis (syphilis, tuberculosis, fungal, bacterial, zoster

CAUSES OF HEMORRHAGIC CVD

Charcot-Bouchard microaneurysms Amyloid angiopathy Impaired bld clotting(anticoagulant tx, bld dyscrasias, thrombolytic tx) Vascular anomaly( AV malformatn, carvernous hemangioma) Substance abuse(cocaine, amphetamines, alcohol)

CEREBRAL ARTERIAL SUPPLY

PATHOGENESIS
A fall in cerebral blood flow to zero causes death of brain tissue within 4 to 10 min; values 16 to 18 mL/100 g tissue per min cause infarction within an hour; and values 20 mL/100 g tissue per min cause ischemia without infarction unless prolonged for several hours or days.

 PENUMBRA: an area of ischemic tissue surrounding the core region of infarction that is reversibly dysfunctional. UMBRA: ischemic AND infarcted area Cellular death occurs via two distinct pathways:
Necrotic pathway Apoptotic pathway

Depolarization and glutamate release lead to the intracellular influx of calcium

 Worsens infarction: fever and hyperglycemia(bld glucose>11.1mmol/L) Neuroprotective: hypothermia; drugs that block the excitatory amino acid pathways

CLINICAL FEATURES
Neurological deficit: hx, examinatn Anosognosia:loss of appreciation that something is wrong Cerebral lesions: unilateral motor deficit, higher cerebral fxn deficit, visual field defect. Brain stem or cerebellar lesions:ataxia, diplopia,vertigo &/orbilateral weakness. Reduced conscious level: large volume lesion in cerebral hemisphere, brain stem lesion or complications.

GENERAL EXAMINATION OF STROKE PATIENTS

Skin: xanthelasma, rashes, limb ischemia Eyes: HTN, DM, retinal emboli, arcus senilis CVS: irregular pulse, BP, JVP, murmurs. Respiratory: pulmonary edema, respiratory infections Abdomen: urinary retentn locomotor

Ischemic stroke features

Thrombotic : usually occurs on waking up in the morning or while the px is resting with a gradual worsening of symptoms(stroke in evolution). Px may be completely paralyzed by the evening.

Ischemic stroke ctd Embolic stroke

Sudden onset Deficit complete at onset

Hemorrhagic stroke features

Occurs at the peak of activity Sever h/ache Vomiting Assotd with high BP Neck stiffness in SAH Maximal deficit at onset

WORLD HEALTH CRITERIA

Level of activity Headache Vomiting LOC Level of BP Blood in the CSF

SIRIRAJ CRITERIA
2.5(LOC)+2(h/ache)+2(vomiting)+0.5(DBP)3(atheroma marker)-12 Atheroma markers: DM, angina, intermittent claudication LOC:0=fully conscious 1=drowsy or stuporous 2=comatose h/ache or vommiting 0=absent 1=present

 Siriraj criteria
>/=1 : hemorrhagic stroke <1 : ischemic stroke 0 : borderline

Sensitivity of WH criteria is abt 65% while that of Siriraj is abt 60%.

Transient ischemic attack(TIA)

Symptoms <24hrs Hemiparesis and aphasia are the commonest symptoms AMAUROSIS FUGAX
Sudden transient mono-occular blindness ussually due to occlusion of the centrl retinal artery. Can also occur in migraine.

TRASIENT GLOBAL AMNESIA

Episodes of amnesia lasting several hours, occurring principally in people over 65, and followed by complete recovery.rarely recurrs.

STROKE SYNDROMES

STROKE SYNDROMES
Middle cerebral aa stroke
Hemiparesis Hemi-anaesthesia Homonymous hemianopia 7th&12th NN involvement: ipsilateral UMNL Dysphasia/aphasia in dominant lobe affectation Dysarthria:CN 7,9,9,10,cerebellum

Middle cerebral aa ctd

Gerstmann syndrome(non-dominant hemisphere affectation):
Acalculia Alexia Right leg disorientation Finger agnosia

hemineglect

Partial syndromes of MCA stroke

hand, or arm and hand, weakness alone (brachial syndrome) facial weakness with nonfluent (Broca) aphasia without arm weakness (frontal opercular syndrome). A combination of sensory disturbance, motor weakness, and nonfluent aphasia suggests that an embolus has occluded the proximal superior division and infarcted large portions of the frontal and parietal cortices.

 fluent (Wernicke s) aphasia without weakness, the inferior division of the MCA supplying the posterior part (temporal cortex) of the dominant hemisphere is probably involved. Hemineglect or spatial agnosia without weakness indicates that the inferior division of the MCA in the nondominant hemisphere is involve.

LACUNAR INFARCTION
Occlusion of a lenticulostriate vessel produces small-vessel (lacunar) stroke within the internal capsule producing pure motor stroke or sensory-motor stroke contralateral to the lesion.

MANIFESTATIONS OF LACUNAR INFARCTS

Pure motor hemiparesis from an infarct in the posterior limb of the internal capsule or basis pontis pure sensory stroke from an infarct in the ventrolateral thalamus ataxic hemiparesis from an infarct in the base of the pons a clumsy hand or arm due to infarction in the base of the pons or in the genu of the internal capsule pure motor hemiparesis with motor (Broca s) aphasia
parkinsonism and hemiballismus :affectation of globus pallidus and putamen

ACA STROKE SYNDROME

Weakness worse in LL Spincteric abnormalty Frontal lobe syndrome
Personality changes Intellectual impairmt Disinhibition Reappearance of primitive reflexes

ACA STROKE SPARES THE FACE

Brain stem infarction

Hemiparesis or tetraparesis Sensory loss Diplopia Facial numbness Facial weakness Nystagmus, vertigo Dysphagia, dysarthria Dysarthria, ataxia, hiccups,vomiting Horner's syndrome Altered consciousness

PCA STROKE
The lateral medullary syndrome, also called posterior inferior cerebellar artery (PICA) thrombosis,or Wallenberg's syndrome, is a common example of brainstem infarction presenting as acute vertigo with cerebellar and other signs:

 Weber's syndrome: This is ipsilateral third nerve paralysis with contralateral hemiplegia due to an infarct in one side of the midbrain. Paralysis of upward gaze may be present Claude syndrome: ipsilat 3rd nn palsy and contralat ataxia

INVESTIGATIONS
Neuroimaging : CT, MRI Carotid doppler US 4-vessel angiography Others
ECG, echo, FBC, ESR Urinalysis, FBS FLP

MANAGEMENT

Medical emergency Multidisciplinary Principles

Prevent or manage complications Tx stroke primarily Prevent repeat stroke

Prevent or manage complications

ABC of resuscitation Reduce cerebral dema
30 head tilt Hyperventilation Mannitol: 250-500ml of 20%mannitol, 1-2g/kg Add lasix Phenytoin/phenobarb Hypothermia Others:urea,glycerol,shunting of csf hemicraniectomy

 IV N/S 1L 8hrly Antihypertensives:indications for antiHTNsives in acute stroke Vit C 100mg TDS, vit E 300mg/day Physiotx Speech tx nutritn

Tx stroke primarily
THROMBOLYSIS :- Intravenous rtPA [0.9mg/kg to a 90mg max] 10% as a bolus, then the remainder over 60 mins within 3hrs of onset of ischemic stroke.

Eligibility criteria for thrombolysis

Eligibility Age > 18 years Clinical diagnosis of acute ischaemic stroke Assessed by experienced team Measurable neurological deficit Timing of symptom onset well established CT or MRI and blood test results available CT or MRI consistent with diagnosis Treatment could begin within 180 minutes of symptom onset

Exclusion criteria
Symptoms minor or improving rapidly Haemorrhage on pretreatment CT or MRI Suspected subarachnoid haemorrhage Active bleeding from any site Gastrointestinal or urinary tract haemorrhage in last 21 days Platelet count < 100 x 109/litre Recent treatment with heparin and activated partial thromboplastin time above normal Recent treatment with warfarin and INR elevated Major surgery or trauma in last 14 days Recent postmyocardial infarction pericarditis

 Neurosurgery,serious head trauma or stroke in last 3 months History of intracranial haemorrhage (any time) Known arteriovenous malformation or aneurysm Recent arterial puncture at non-compressible site Recent lumbar puncture Blood pressure consistently > 185 systolic or> 110 diastolic Abnormal blood glucose (< 3 mmol/litre or > 20 mmol/litre) Suspected or known pregnancy Active pancreatitis Epileptic,seizure at stroke onset

ANTIPLATELET AGENT:-Its been found that the use of aspirin within 48hrs of stroke onset reduce both stroke recurrence risk & mortality minimally. Clopidogrel,dipyridamole, ticlopidine

Prevent repeat stroke

Tx all modifiable factors

COMPLICATIONS

DIFFERENTIALS
Cerebral abscess Cerebral tumors Subdural hematoma SAH Todd s paralysis Conversion disorder Encephalitis Hypoglycemia Demyelination Migrainous aura Focal seizures

prognosis
About 1/5th of pxs will die within a month of the event and at least half of those who survive will be left with physical disability.

Conclusion