Cerebrovascular Disease Tumours
Cerebrovascular Disease Tumours
Cerebrovascular Disease Tumours
- Rapid loss of brain function due to disturbance in blood supply to brain (ischemia,
embolism, thrombosis, haemorrhage)
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
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:
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
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.
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