CEREBROVASCULAR ACCIDENT/BRAIN

ATTACK

GIDEON GACHIHI
Associate faculty, MKU
Anatomy
3
 Definition
• Rapidly developing episode of focal or
at times global loss of cerebral
functions with symptoms lasting more
than 24 hours ,or leading to death,
and with no apparent cause other
than that of a vascular origin
• Infarction 85%
• Primary intracerebral/Haemmorhagic15%
 Risk Factors
• Non -modifiable
– Age
– Family history
– Male sex
– Previous history of stroke
 Hypertension
– Increases stroke risk 3 fold
– Accelerates atherosclerosis
– Most strokes occur in borderline hypertension
– Reduction in blood pressure -50% RRR of stroke
– reduction of stroke rates among those with
isolated systolic hypertension
– Framingham study showed borderline with 42%
increase in stroke
 Risk Factors
• Diabetes 3 times risk
• Physical activity
• Cigarette smoking
– 50% increase in the risk of stroke
– Nurses health study showed reduction after
quit smoking
 Risk Factors
• Hyperlipidemia
• Hyperhomocysteinemia
• Excessive alcohol intake
• Contraceptive pills
• Cardiac embolic source
 Common causes of cardiac emboli
• Cardiomyopathy
• Valvular heart disease
• Cardiac arrthymmia
• Intracardiac tumours
• Intracardiac defects with paradoxical emboli
– ASD, PFO
• Acute myocardial infarction
• Left ventricular aneurysm
• Congenital heart diseases
 Ischemic cerebrovascular disease
• Large –artery stenosis or occlusion
• Small artery occlusion( lacunes)
• Cardioembolic
• Hemodynamic( watershed infarcts
• Non atherosclerotic vasculopathies
• Hypercoagulable states
• Infarcts of undetermined cause
• Dissection of the carotid artery
 Pathogenesis
• Presence of collaterals
• Circle of Willis
– Internal external orbit
– Meningeal anastomosis
– Neck occipital , ascending pharygeal muscular
branches deep and ascending cervical arteries
• Rapidity of occlusion
• Cellular death occurs via two distinct pathways:
-(1) a necrotic pathway in which cellular
cytoskeletal breakdown is rapid, due principally to
energy failure of the cell; and
- (2) an apoptotic pathway in which cells
become programmed to die.
• Ischemia produces necrosis by starving neurons of
glucose
• mitochondria fail to produce ATP.
• Membrane ion pumps stop functioning and
neurons depolarize,and intracellular ca2+ rises.
 Thrombosis
• Elderly
• Presence of atheroma markers
• Occurs at night
• May be progressive
• No loss of consciousness
• No vomiting
 Embolic
• Young patient
• Embolic source
• Maximum deficit at onset
• Distal territory
• Quick Recovery
 Lacunar syndrome
• Pure motor stroke
• Pure sensory
• Sensorimotor
• Ataxic hemiparesis
 Transient Ischemic Attack

• Acute loss of focal or cerebral or monocular

function with symptoms lasting less than 24
hours and which, after adequate
investigations is presumed to be due to
embolic or thrombotic vascular disease
• 10% of risk of stroke within 3mo but
highest risk is within the first 2days
 Ddx
•   Seizure with postictal Todd's paresis
•   Tumor
•   Migraine
•   Metabolic encephalopathy
•     Fever/infection and old stroke
•     Hyperglycemia
•     Hypercalcemia
•     Hepatic encephalopathy
• Sagittal sinus thrombosis
 Investigation

• Hemogram ESR, HB electrophoresis

• Coagulation profile
• Glucose levels
• Lipid profile
• VDRL
• Vasculitic screen antinuclear factor
• Antiphospholipid antibodies
• Echocardiography
• Holter ECG monitoring
 Radiological Investigation
• CXR
• Ct scan
• MRI
• Carotid doppler Ultrasound
 Deterioration
• Propagation of the thrombus
• Recurrent embolism
• Seizures
• Hemorrhagic transformation
• Infections, metabolics, medications
• Fever
• Hyperglycemia>11.1mmol/L
 Management
• Treatments designed to reverse or lessen the
amount of tissue infarction fall within five
categories:
(1) medical support,
(2) thrombolysis,
(3) anticoagulation,
(4) antiplatelet agents,
(5) neuroprotection.
 Medical
• immediate goal is to optimize cerebral perfusion
in the surrounding ischemic penumbra
• preventing the common complications of
bedridden pts—infections (pneumonia, urinary
tract, and skin) and DVT and PTE
• BP should be lowered if:-
- -there is malignant
hypertension(220/120mmHg)
- -concomitant myocardial ischemia
- -it is >185/110 mmHg and thrombolytic therapy
 medical
• Fever is detrimental and should be treated
with antipyretics.
• Serum glucose should be monitored and kept
at <11.1 mmol/L (200 mg/dL)
• Edema peaks on the second or third day but
can cause mass effect for ~10 days.
• Water restriction and intravenous mannitol
may be used to raise the serum osmolarity
 thrombolysis

• Rx with iv rtPA within 3 h of the onset of

ischemic stroke improves clinical outcomes.
• dose of 0.9 mg/kg administered(safe)
• There is risk of hemorrhage
• Contraindications:-
-Sustained BP > 185/110 despite treatment
-Platelets < 100,000; HCT < 25%; glucose < 50
or > 400 mg/dL
 Contraindications of
thrombolysis
- Use of heparin within 48 h and prolonged
PTT, or elevated INR
-Rapidly improving symptoms
-Prior stroke or head injury within 3 months;
prior intracranial hemorrhage
- Major surgery in preceding 14 days
-Minor stroke symptoms
-Gastrointestinal bleeding in preceding 21 days
- Recent myocardial infarction
 Antiplatelet agents

• Aspirin is the only antiplatelet agent that

has been proved for the Rx of acute
ischemic stroke
• Asa given preferably within 48h
• Early results from ongoing studies show
that iv abciximab can be used safely within
6 h of stroke onset.
• Heparin is avoided but can be used for DVT
prophylaxis in ischemic strokes
 Intracerebral hemmorrhage
• 10 to 15% of CVA
• More in blacks and Japanese
• Zimbabwe 29% of CVA
 Pathology
• Segmental lipohyalinosis
Microaneursym(Charcot Bouchard)
• Haematoma pressure on the reticular
activating system
• Surrounding edema
• Signs depend on the site
 Risk factors
• Acute or chronic hypertension
• Amyloid angiopathy
• Bleeding diathesis
• Tumours
– Astrocytoma, oligodendroglioma, melanoma,
choriocarcinoma
 Risk factors
• AVMs
• cavernous angioma
• Venous thrombosis
• Trauma
• Aneurysm
• Pregnancy related eclampsia
 Clinical presentation
• Sudden onset
• Headache
• Vomiting
• Convulsions
 Clinical presention
• Pons quadriplegia
– Pin point pupils, fever
• Cerebellar dizziness vomiting ataxia
• Lobar
– Hemianopia
– aphasia
 Prognosis
• Location of haematoma
• Size of haematoma
• Level of consciousness at admission
• Increase in intracranial pressure
 Subarachnoid Haemorrhage
• Avm
• Saccular aneursym
– developmental
– 25% multiple
• 85% carotid artery territory
 Association
• Coarctation of aorta
• Fibromuscular dysplasia
• Polycystic kidney disease
 Commonest sites
• Junction of anterior communicating and
anterior cerebral artery
• Origin of posterior communicating artery
• Bifurcation of middle cerebral artery
 Clinical presentation
• Sudden onset of severe headache(thunder
clap)
• Meningism
• Focal signs rare except for postcom 3rd nerve
palsy
 Complications
• Focal cerebral ischaemia
• Rebleed(Rerapture-highest risk in the first 1wk)
• Hydrocephalous-acute causes stupor and
coma,subacute-progressive drowsiness/abulia
with incontinence
• Hyponatremia –Brain wasting syndrome due to
ADH/ANP and BNP-Should not be treated with
free water restriction as it may lead to stroke
• vasospasm
 Diagnosis
• History/P/E
• Ct scan
• Csf xanthochromia
• 4 vessel angiography
 Treatment
• Neurosurgical
• Nimodipine to reduce risk of vasospasm
• Treat hypertension
THANKS