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Cerebrovascular
Disease
FM Brett , MD, FRCPath
~ In USA 0.5 million new strokes diagnosed
annually and 3 million survivors of a previous
stroke
~ Stroke 3rd most frequent cause of death
~ 2nd most frequent cause of dementia
~ Major reason for severe disability and long term
dependency
Epidemiological aspects of stroke
~ In the USA stroke is the third commonest cause
of death
~ Incidence increases with age
~ Major risk factors for stroke are hypertension,
cardiac disease, smoking, hyperlipidemia, and diabetes
~ Other causes OCP, sickle cell, coagulation disorders
~ In USA - brain infarction 10 times commoner than
haemorrhage
Blood supply to the brain
~ Human brain approx 2% of body
weight
~ Receives 15% of total cardiac
output O2 consumption
approximately 20% of whole body
(i.e high metabolic rate)
~ How long would the brain survive
if blood flow interrupted
Terminology
~ Ischaemia - arterial stenosis or occlusion
Infarction - perfusion territory of the affected vessel
~ Global brain ischaemia - < CPP below the
threshold for autoregulation i.e when systemic blood
pressure falls very low e.g cardiac tamponade, heroin
overdose, or ICP rises to a level that compromises cerebral
perfusion
Resultant brain damage or infarction is accentuated in the
WATERSHED REGIONS
CPP= SAP - ICP
CPP > 40 mmHg - necessary for autoregulation
If CPP < 40 mmHg CBF falls dramatically
Principal causes of hypoxia
Hypoxemic hypoxia - low O2 in blood
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Carbon monoxide poisoning
Near drowning
Respiratory arrest
Prolonged status epilepticus
Stagnant hypoxia - (inadequate supply of oxygenated O2
~ Cardiac arrest
~ Rise ICP
~ Respirator brain
Histotoxic hypoxia (inability of tissues to use O2)
~ Cyanide and sulphide exposure - inhibition of mitochondrial
enzymes involved in oxidative respiration
Selectively vulnerable zones
~ Hippocampus - CA1
~ Laminae 3 and 5 of cortex
~ Purkinje cells cerebellum
HYPOXIA - blood flow to the CNS may be
normal or increased
Damage occurs in selectively vulnerable
neurones
Hypoxic ischaemic encephalopathy
~ Variable clinical presentation
~ Clinical recovery generally better after hypoxemic
hypoxia than after global brain ischaemia
~ Severity and duration of HIE after transient cerebral
hypoxia depends on
I) duration of insult
2) completeness of insult
3) blood glucose level (high level poor outcome)
4) CNS temperature
~ Long term sequelae - difficult to predict
Persistent vegetative state
Clininical condition of complete unawareness of self and
environment, accompanied by sleep-wake cycles, with either
complete or partial preservation of hypothalamic and brainstem
autonomic functions
Occurs with;
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Diffuse cortical injury
Bilateral thalamic injury
Diffuse white matter
Major developmental abnormalitires
Infarct - region of cell death
Infarct may become secondarily haemorrhagic and may mimic a
primary haemorrhage
STROKE - rapid onset of focal disturbance of cerebral function
lasting > 24 hours
TIA - less than 24 hours
Infarcts may be caused by:
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Large vessel or macrovasculature disease
Small vessel or microvasculature disease
Emboli
Venous thrombosis
Types of vascular disease
Anterior circulation
A. Small vessel disease – e.g microangiopathy
B. Occlusive large vessel disease of pial arteries
C. Occlusive large- vessel disease of brain
supplying arteries in the neck
D. Embolising heart disease including aortic plaques
and R-L shunts
1 a, b – small vessel disease
2 a,b. Atherosclerotic or
embolic occlusion of
cerebellar artery
3 – intracranial thrombosis
4 – atheromatosis of
vertebro-basilar artery
5 – embolus sticking in
mid-basilar artery
6. In situ thrombosis of
basilar artery
Thalamic
infarction
Sensory or
sensiomotor hemideficits with
disassociated
sensory loss,
hemispasticity or
even severe
impairment of
position sense;
Segmental and
focal dystonia
without jerks and
abnormal dystonic
posture of affected
hand
Time after
infarction
Histological
changes
15-20 hrs
Defined margin between
ischaemiac and normal
brain
Early app of PML
Activation of microglia
and astrocytes
App of macrophages
Liquefaction of tissue;
gliosis
Cavitation and completion
of glial scar
24-30 hrs
24-36 hrs
36-48 hrs
1-2 weeks
Mths
~ Large vessel disease includes
atherosclerosis,
fibromuscular dysplasia,
arterial dissection,
giant cell arteritis
ATHEROSCLEROSIS IS THE
COMMONEST OF THESE
ATHEROSCLEROSIS - leading vasculopathy
producing brain infarcts. Affects intracranial and
extracranial large vessels
RISK FACTORS
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Hyperlipidemia
Hypertension
Cigarette smoking
Obesity
Age
Sex
Small vessel disease includes
cerebral vasulitides
PACNS
~ Isolated granulomatous or
primary angiitis of the CNS
(PACNS)
PACNS
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Recognised in the mid 1950’s
Diagnosis:
Clinical
Imaging
Biopsy
Case presentation
EMBOLIC DISEASE
Embolic stroke results when any solid material:
• forms within the aterial circulation
• is introduced into the arterial circulation
• forms within the venous and has a conduit to th
arterial circulation ì.e right to left shunt
Resultant infarct is :
• clinically abrupt
• haemorrhagic
Autopsy of a stroke patient
If infarction
1. Examine major cranial arteries i.e
carotid and vertebral arteries in the neck
2. Carefully examine heart for:
infective endocarditis
valvular abnormalities
septal defects
IF haemorrhage
Look for evidence of:
1. Hypertension i.e cardiomegaly, LVH,
nephrosclerosis
2. Neoplasia
3. Drug abuse
4. If dementia CAA
Blood in the cranial cavity
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Source?
Spread
Occur?
Cause?
Sufficient to cause death
Intracranial haemorrhage
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Extradural
Subdural
Subarachnoid
Intracerebral
SAH
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Berry aneurysm
Infectious
Fusiform aneurysm
AVM
CAA
CIRCLE OF WILLIS
Berry aneurysms
Congenital
Risk of bleeding inc;
• Hypertension
• AVM
• systemic vascular
disease
• defects collagen
• polcystic renal disease
ICH causes
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Hypertension
Trauma
CAA
Berry aneurysm
AVM
Bleeding diathesis
Vasculitides
Drugs
Neoplasm
Infective
Hypertension - major risk factor for brain
haemorrhage
Occurs due to rupture of arterioles that have
become
weakened
DUE TO
• Replacement of smooth muscle by
fibrocartilagenous material
• Fragmentation of elastic tissue
• Charcot-Bouchard aneurysms
Haemorrhages involving the basal gangliaputamen in particular
tend to be non-traumatic and caused by
hypertension
Chronic hypertension
leads to arteriolar sclerosis
resulting in small lacunar
infarcts
OCCUR
~ BASAL GANGLIA
~ PONS
~ DEEP WHITE
MATTER
AVM
• Commonest 3-4th decade
• Rarely familial
• Rarely multiple
• have a nidus
• commonest vascular malformation
identified in surgical specimens
End result of herniation is compression and Duret
haemorrhages as seen in the pons
Venous Thrombosis
~ Often secondary to infectious causes
~ Pregnancy
~ Puerperium
~ OCP
~ Haematological abnormalities