Cerebrovascular Disease:

 Most common forms of CVD =

o Cerebral thrombosis (40% of cases)
o Cerebral Embolism (30%)
o Cerebral Haemorrhage (20%)

Stroke (cerebrovascular accident)

“Neurological deficit of cerebrovascular cause that persists beyond 24 hours or is
interrupted by death within 24 hours”

- Rapid loss of brain function due to disturbance in blood supply to brain (ischemia,
embolism, thrombosis, haemorrhage)

(< 24 hours = transient ischemic attack)

2 major categories:
o Ischemic Stroke
 Blood supply to part of brain = decreased (dysfunction of brain tissue in that
area – no glucose / oxygen) – initiates ischemic cascade
 Brain tissue ceases to function if deprived of oxygen for more than 60 – 90
seconds (will suffer irreversible injury after +- 3 hours = death of tissue
(infarction))
 4 main causes:
1. Thrombosis
o blood clot forms around atherosclerotic plaques gradually &
blocks blood vessel
o onset of stroke = slower
o Vessel Size:
 large vessel disease
 common & internal carotids, vertebral & Circle
of Willis
 e.g. atherosclerosis – disrupt blood supply by
narrowing lumen of blood vessels = reduction
of blood flow by causing formation of blood
clots in vessel OR releasing showers of small
emboli through disintegration of
atherosclerotic plaques
 small vessel disease
 smaller arteries in brain
2. Embolism
 Blockage of an artery by arterial embolus (travelling particle /
debris in arterial bloodstream originating from elsewhere)
 Embolism = most commonly a thrombus BUT can also be fat,
air, cancer cells / clumps of bacteria (infectious endocarditis)
  Emboli most commonly arise from heart (high risk versus low
risk)
3. Systemic hypoperfusion
 Reduction of blood flow to all parts of body
 General decrease in blood supply
 Most commonly due to cardiac pump failure from arrest /
arrhythmias IR myocardial infarction, pulmonary embolism,
pericardial effusion / bleeding.
 Hypoxemia may precipitate hypo-perfusion.
 NB – because < blood flow = global ALL parts of brain may be
affected ESPECIALLY watershed areas (border zone regions
supplied by the major cerebral arteries) – ‘last meadow’
receives the least amount of ‘water’
4. Venous thrombosis
 Cerebral venous thrombosis = stroke due to locally increased
venous pressure – exceeds pressure generated by arteries.
 Infarcts = > likely to undergo haemorrhagic transformation
(leaking blood into damaged area) than other types of ischemic
stroke

 Cause of 87% of all strokes

o Haemorrhagic Stroke
 Intracranial haemorrhage = accumulation of blood anywhere in skull
vault
 Generally occurs in small arteries / arterioles – commonly due to
hypertension, intracranial vascular malformations, cerebral amyloid
angiopathy / infarcts into which 2ndary haemorrhage occur.
 Other potential causes: trauma, bleeding disorders, illicit drug use
(amphetamine / cocaine).
 Intra-axial haemorrhage
o Blood inside the brain
o Due to:
 Intra-parenchymal haemorrhage
 Intra-ventricular haemorrhage (blood in
ventricular system)
 Extra-axial haemorrhage
o Epidural hematoma (bleeding between dura mater &
skull)
o Subdural hematoma (bleeding in subdural space)
o Subarachnoid Haemorrhage (bleed between arachnoid
mater & pia mater)

Classification Systems:
 Oxford Community Stroke Project classification (OCSP / Bamford / Oxford)
o Based on xinitial symptoms – classified as 4 types:
 TACI – total anterior circulation infarct
  PACI – partial anterior circulation
 LACI – lacunar infarct
 POCI – posterior circulation infarct
o Predicts EXTENT of stroke, AREA of brain affected, underlying CAUSE,
PROGNOSIS.
 Trial of Org 10172 in Acute Stroke Treatment (TOAST)
o Based on clinical symptoms & further investigations
o Classified according to:
 Thrombosis / embolism (due to atherosclerosis or large artery)
 Embolism of cardiac origin
 Occlusion of small blood vessel
 Determined cause
 Undetermined cause (cryptogenic, 2 possible causes, incomplete
investigation)

Diagnosis
Stroke = diagnosed clinically with assistance from several techniques:

 Neurological exam (Nihss)

 CT scans (most often without contrast enhancements)
 MRI scans
 Doppler ultrasound
 Arteriography

Imaging techniques = assist in determining subtypes & cause of stroke.

Blood tests can help in finding cause of stroke BUT not commonly used in stroke diagnosis.

Physical Examination

 Medical history
 Neurological status
 Gives evaluation of location & severity of stroke

Imaging

 Ischemic Stroke Diagnosis in Emergency Settings

o CT scans (WITHOUT contrast)
 Sensitivity = 16%
 Specificity = 96%
o MRI scans
 Sensitivity = 83%
 Specificity = 89%
 Haemorrhagic Stroke Diagnosis in Emergency Settings
o CT scans (WITHOUT contrast)
 Sensitivity = 89%
 Specificity = 100%
o MRI scans
 Sensitivity = 81%
  Specificity = 100%
 NOTE: MRI = more sensitive in detecting chronic haemorrhages
 Assessment of stable stroke = SPECT ad PET/CT = helpful
o SPECT shows cerebral blood flow
o PET with FDG isotope show metabolic activity of neurons

Identifying Underlying Cause

 NB to determine whether there = peripheral source of emboli.

 Commonly used techniques:
o Ultrasound / Doppler study of carotid arteries
o ECG & echocardiogram – identify arrhythmias & resultant clots in heart which
may spread to brain vessels through bloodstream
o Holter monitor study – identify intermittent arrhythmias
o Angiogram
o Blood tests to determine hypercholesterolemia, bleeding diathesis & possible
homocysteinuria

Signs & Symptoms

Depends on area of brain affected:

- CNS Pathways (spinothalamic, corticospinal, dorsal column)

o Numbness
o < sensory / vibratory sensation
o Initial flaccidity (hypotonicity) – replaced by spasticity (hypertonicity)
o Hyperreflexia & obligatory synergies
o Hemiplegia & muscle weakness of face
- Brain stem & Cranial Nerves
o Altered smell, taste, hearing / vision (total / partial)
o Ptosis, weakness of ocular muscles
o < reflexes – gage, swallow, pupil reactivity to light
o < sensation & muscle weakness of face
o Balance problems
o Nystagmus
o Altered breating & heart rate
o Weakness – stenrocleidomastoid muscle (inability to turn head to one side)
o Weakness in tongue
- Cerebral Cortex
o Aphasia (difficulty with verbal expression, auditory comprehension, reading /
writing – typically involve Broca / Wernicke area)
o Dysarthria (motor speech disorder from neurological injury)
o Apraxia (altered voluntary movements)
o Visual field defect
o Memory deficits (temporal lobe involvement)
o Hemineglect (parietal lobe involvement)
o Disorganised thinking, confusion, hypersexual gestures (frontal lobe
involvement)
 o Lack of insight into stroke-related disability
- Cerebellum
o Altered gait
o Altered movement co-ordination
o Vertigo & / disequilibrium

Risk Factors
 Old age
 Hypertension
o 35-50% of stroke risk
o Most modifiable risk factor for stroke
o < blood pressure = shown to prevent ischemic & haemorrhagic strokes
o NB in 2ndary prevention
o Anti-hypertensive therapy = risk reduction
 Previous stroke / TIA
 Diabetes
o 2 – 3 X more likely to develop stroke
o Commonly have hypertension & hyperlipidemia
o Intensive disease control = < microvascular complications BUT NOT
macrovascular complications (e.g. stroke)
 High Cholesterol
o Inconsistently associated with ischemic stroke
o Statins = < stroke risk by 15% (through mechanisms other than lipid-lowering
effects)
 Smoking
 Atrial fibrillation
o 5% annual risk to develop stroke
o Anticoagulation medication (coumarins / aspirin) = stroke prevention

Prevention
 Stroke = burden of disease
 Primary prevention = LESS effective than 2ndary prevention
 Of recurrence
o = administration of antiplatelet drugs (aspirin & dipyridamole)
o Control & reduction of hypertension
o Use of statins
o Possible carotid endarterectomy & use of anticoagulants
 Surgery
o Carotid endarterectomy / carotid angioplasty – remove significant
atherosclerotic narrowing (stenosis)
 Nutrition
o ‘mediterranean-style diet’ – potential to decrease stroke risk by 50%
o Lower homocysteine – with folic acid & other supplements
o HeartScore

Management
 Treated in hospital with thrombolysis
 o Clot busting
o Dissolve clot & unblock artery (tissue plasminogen activator tPA)
 Some haemorrhagic strokes = benefit from neurosurgery
 Recover of lost function = ‘stroke rehabilitation’
o “Stroke Unit”
o Nurses & therapists with experience in stroke treatmetn
o Speech & language therapy, physical therapy, occupational therapy.
o People = > chance of surviving than those not admitted to stroke unit

Rehabilitation
 Includes:
o Therapy for communication disorders
o Strengthening motor skills
o Mobility training
o Range of motion therapy
o Psychological evaluation
o Constraint-induced therapy
o Electrical stimulation
o Robotic technology
o Virtual reality
 Should begin ASAP after stroke – sooner begin, more likely to regain lost abilities &
skills
o 1st stabilise condition
o Prevent another stroke
o Limit stroke-related complications
 Duration of rehab depends on severity of stroke & related complications
 Most = long term (months – years)
 Rehab plan = change during recovery as you relearn skills & needs change

Prognosis
 75% of stroke survivors = disabled
 Decreased employability
 Affect physical, mental, emotional / combination of three
 30-50% stroke survivors = post-stroke depression
o Lethargy
o Irritability
o Sleep disturbances
o Lowered self-esteem
o Withdrawal
 Depression = < motivation & worsen outcome – treated with antidepressants
 20% of stroke patients = Emotional lability – switch quickly between emotional highs
and lows / express emotions inappropriately
 Cognitive deficits
o Perceptual disorders
o Aphasia
o Dementia
o Attention
 o Memory
o Anosognosia
o Hemispatial neglect – Can’t attend to anything on opposite side to damage
hemisphere
 10% / > = develop seizures (most common in week subsequent to event) – severity
of stroke > likelihood of seizure.

Transient Ischemic Attack

 Transient episode of neurologic dysfunction
 Caused by ischaemia – loss of blood flow (focal brain, spinal cord / retinal) WITHOUT
acute infarction (tissue death)
 Share Etiology with stroke
 Same symptoms
o BUT RESOLVE within few minutes / 24 hours
 Brain injury = possible
 Risk factor for stroke
 Differs from silent stroke (silent cerebral infarct – no immediately observable
symptoms)

Signs & Symptoms

 Vary from person to person
 Depends on area of brain affected
 Most frequent symptoms:
o Temporary loss of vision (amaurosis fugax)
o Aphasia
o Hemiparesis
o Paresthesia (numbness / tingling) – usually one-sided
o Dizziness
o Lack of co-ordination
o Poor balance
 Short-lived } few seconds to few minutes – most disappear within 60 minutes

Causes
 Most common cause = embolus that occludes in artery in the brain
o Usually arises from dislodged atherosclerotic plaque in one of carotid arteries
/ from a thrombus in heart because of atrial fibrillation
 Blockage period = short-lived – hence no permanent damage
 Other causes:
o Excessive narrowing of large vessels (from atherosclerotic plaque)
o Increased blood viscosity (caused by some blood diseases)

Risk Factors
 Hypertension
 Heart disease (atrial fibrillation)
 Migraine
 Cigarette smoking
  Hypercholesterolemia
 Diabetes mellitus
 Family history of stroke
 > 55 years of age
 Men = slightly higher risk BUT females = more likely to die from a stroke
 Black – high risk of dying from stroke} due to hypertension & uncontrolled diabetes

Diagnosis
 Medical history
 Physical exam
 Imaging techniques (radiological tests)
o MRI / CT
o Ultrasound of neck
o Echocardiogram of heart
 Source of atherosclerosis = usually identified with ultrasound
 Other diagnoses with similar symptoms to TIA:
o Atypical migraine
o Partial seizure in parietal area of brain
o Glucose abnormalities
o Electrolyte abnormalities
o Hypertensive encephalopathy (headache, delirium, hypertension, cerebral
edema)
o Subdural hematoma (history of trauma, headache, loss of consciousness)
o Brain tumour (mode of onset, progressive headaches, increased intracranial
pressure)
o Demyelinating disease
o Conversion disorder

Prevention
 TIA = prevented by changes in lifestyle
o Avoid smoking
o Decrease fates & cholesterol – reduce plaque build up
o Healthy diet
o Limit sodium – reduce blood pressure
o Exercise regularly
o Moderate alcohol intake
o Maintain normal weight
o Control blood pressure & keep blood sugars under control

Treatment
 Diagnose & treat underlying cause
 Initial treatment = aspirin
 Second line = clopidogrel (plavix)
 Third line = ticlopidine
 ECG = show atrial fibrillation (common cause of TIAs)
 Echocardiogram = useful in detecting thrombus within heart chambers – benefit
from anticoagulation
  Anti-coagulant / anti-platelet medication may = warranted

Prognosis
 ‘warning for impending stroke’
 Blood supply impairment = > few minutes = permanent neurologic deficit
 1/3 people with TIA have later recurrent TIAs
 1/3 have stroke because of permanent nerve cell loss
 Risk of stroke occurring after TIA can = predicted using ABCD2 score