pathology of cerebrovascular disease by prof. j.t. anim department of pathology
TRANSCRIPT
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Pathology of Cerebrovascular Disease
ByProf. J.T. Anim
Department of Pathology
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Cerebrovascular DiseaseAffected blood vessels
Intracranial vesselsMiddle cerebral arteryAnterior cerebral arteryBasilar artery (posterior cerebral arteries)
Extracranial vesselsCarotid artery
Common carotid arteryInternal carotid artery(external carotid artery)
Vertebral arteryothers
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Brain: Blood supply
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Brain: Blood supply
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Arterial blood supply to the brain
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Brain: Blood supply
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Cerebrovascular DiseaseTransient ischaemic attack (TIA)
A fully reversible neurological deficit often lasting for no more than a few minutes, but occasionally up to 24 hours.
No structural brain damage has occurred
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Cerebrovascular DiseaseFactors predisposing to TIA
AtherosclerosisSuperimposed hypotensionSpasm of diseased vessel
Disorders in the neck (spondylosis)Other extracranial vascular diseases eg. embolism
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Cerebrovascular DiseaseStroke
Rapid onset of a focal disturbance of cerebral function of presumed vascular origin and of more than 24 hours duration.
Permanent brain damage has occured
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STROKE
Ischaemic/Occlusive Haemorrhagic/Disruptive
Intraparenchymal
Subarachnoid
Mixed
Thrombosis Embolism Hypotension
Atherosclerosis
Fibromuscular dysplasia
Arteritis
Dissection
Cardiac
Extracranial vessels
Paradoxical
Other emboli
Pump failure
Hypovolaemia
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Stroke: Causes
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Ischaemic StrokeAtherosclerosis
Carotid arteryCommon carotidInternal carotid(external carotid)
Vertebro-basilar systemPosterior cerebral
With normal BP, >90% cross sectional area reduction is necessary to impair blood flow
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Ischaemic StrokeFactors affecting tissue survival
Adequacy of collateral circulationState of systemic circulation
Reduced blood flow, cardiac pump failure, hypovolaemia, hyperviscosity
Serological factorsLow blood sugar, high blood sugar, hypoxia, elevated serum calcium, high blood alcohol
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Ischaemic StrokeFactors affecting tissue survival contd.
Changes within obstructing vascular lesion
Fragmentation and advancing of embolusReactive vasoconstriction (spasm)Reperfusion – stunned cells may recoverPropagation of thrombus – collateral occlusionEmbolisation from previous thrombus
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Ischaemic StrokeFactors affecting tissue survival contd.
Resistance within microcirculatory bedHypertensionDiabetes mellitus – thickened vessel wallsHyperviscosityDiffuse thromboses (low microcirculatory flow)
Oedema and raised ICPIncreased resistance to blood flow
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Ischaemic StrokeIntracranial vascular occlusion
Effects usually confined to area of supply of affected vessel
Extracranial vascular occlusionEffects may be modified by collateral circulationWatershed infarction may be seen
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Brain: Distribution of cerebral infarction
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CNS IschaemiaSelective vulnerability of CNS cells
Neurons – most sensitiveOligodendrogliaAstrocytesMicrogliaBlood vessels
In descending order of sensitivity
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Brain: Effect of global ischaemia
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Consequences of global ischaemia
Effects of global ischaemia
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CNS IschaemiaMild hypoxia
Selective neuronal necrosis eg. respirator lung
Moderate hypoxiaNeuronal necrosisNeuroglial necrosisBlood vessels and microglia are spared
Partial cerebral infarction
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Ischaemic StrokeInfarction (stroke)
Thrombotic – usually anaemic (may be haemorrhagic)Embolic – usually haemorrhagic, often multiple. Haemorrhagic nature due to:
Necrosis of vessel wallLysis of embolus with restoration of some blood flow.
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CNS InfarctionVascular occlusion causes:
Necrosis of neurons, neuroglia and blood vessels4-6 hrs. – coagulative necrosis12-15 hrs. – sharp demarcation (swelling of neuropil)24 hrs. – reactive changes
Proliferation of microglia, astrocytes, capillariesInflammatory reaction
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CNS InfarctionInfarction contd.
1-2 weeks – Swelling resolvesSofteningShrunken granular grey matterAccumulation of lipid-laden phagocytes (gitter cells) in infarcted area
Several months – shrunken cystic lesion traversed by glial fibrils and small blood vessels
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Brain: Recent anaemic infarct
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Brain: Older infarct showing cavity formation
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Brain: Older infarct
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Bilateral posterior cerebral infarcts
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Brain: Recent haemorrhagic infarct
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Brain: Haemorrhagic infarct
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Brain: Haemorrhagic infarct
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Brain: Multiple haemorrhagic infarcts
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Brain: Relatively recent infarct - Histology
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Brain: Older infarct showing ‘gitter’ cells
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Brain: Older infarct - Histology
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Brain: Old infarct with cavity formation - Histology
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Brain: Laminar infarct
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Brain: Watershed infarct
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Brain: Very old infarct showing atrophy of hemisphere
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CNS InfarctionVertebro-basilar occlusion
Infarction of brainstemInfarction of cerebellumInfarction of posterior cerebral arterial territory
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Clinical effects of basilar artery occlusion
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Brain: Haemorrhagic cerebellar infarcts
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Chronic CNS IschaemiaLacunae
Small cavities located deep within cerebral hemispheres (basal ganglia) and ponsElderly subjects - >90% with hypertension? Small infarcts? Expanded perivascular spaces? Resolving haemorrhagesAssociated with vascular dementia
Multi-infarct dementiaBinswanger’s disease
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Brain: Lacuna in pons
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Brain: Lacunar lesions
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CNS InfarctionVenous thrombosis
Primary – non-infectiousPregnancy, puerperium and oral contraceptivesHaematological disordersExtreme dehydration
Haemorrhagic infarction
Secondary – pyogenic infectionsInfections from sinuses, middle earCompound fracture
Septic infarction
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Brain: Bilateral haemorrhagic infarct – Sup. Saggital sinus thrombosis
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Haemorrhagic StrokeBrain and spinal cord substance (intraparenchymal)SubarachnoidMixed
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Haemorrhagic StrokeMajor predisposing factors
HypertensionCongenital anomaliesVascular malformations
Minor predisposing factorsVasculitisBleeding diatheses
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Haemorrhagic StrokePrimary intraparenchmal haemorrhage
Predisposing vascular changes include:Fibrinoid necrosisHyaline arteriolosclerosis (lipohyalinosis)Microaneurysms (Charcôt-Bouchard)
Sizes of haemorrhageMassive - >3cm diam. Cerebral hemisphere
> 1.5cm diam. brainstem
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Brain: Charcot-Bouchard microaneurysm
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Brain:
Common sites of spontaneous haemorrhage
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Brain: Haemorrhage into basal ganglia
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Brain: Massive hemispheric haemorrhage
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Brain: Haemorrhage into basal ganglia
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Brain: Pontine haemorrhage
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Brain: Pontine haemorrhage
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Haemorrhagic StrokeSubarachnoid haemorrhage
Saccular aneurysm 65%Females = malesDevelopmental medial defectSuperimposed degenerative changes eg. atheroma15-20% multiple
A-V malformations 5%Others (blood dyscrasias) 5%No cause found 20%
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Haemorrhagic StrokeSubarachnoid haemorrhage
Secondary effects include:RebleedingVasoconstriction (spasm)hydrocephalus
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Brain: Distribution of saccular (berry) aneurysms
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Brain: Multiple berry aneurysms
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Brain: Berry aneurysm - arrow
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Brain: A large berry aneurysm
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Brain: Subarachnoid haemorrhage – ruptured berry aneurysm
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Brain: Giant atherosclerotic aneurysm
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Haemorrhagic StrokeMixed (intraparenchymal and subarachnoid) haemorrhage
A-V malformationsCapillary angiomas
Focal irritation may predispose to convulsions (epileptiform attacks)
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Brain:
Causes of mixed subarachnoid and intracerebral haemorrhages
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Brain:
Vascular malformations
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Brain: Vascular malformation – cerebral hemisphere
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Brain: Arterio-venous malformation
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Brain: Vascular malformation