Pathology+of+cerebrovascular+disease+dr+anim

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  • 1. Pathology of Cerebrovascular Disease By Prof. J.T. Anim Department of Pathology
  • 2. Cerebrovascular Disease
    • Affected blood vessels
      • Intracranial vessels
        • Middle cerebral artery
        • Anterior cerebral artery
        • Basilar artery (posterior cerebral arteries)
      • Extracranial vessels
        • Carotid artery
          • Common carotid artery
          • Internal carotid artery
          • (external carotid artery)
        • Vertebral artery
        • others
  • 3. Brain: Blood supply
  • 4. Brain: Blood supply
  • 5. Arterial blood supply to the brain
  • 6. Brain: Blood supply
  • 7. Cerebrovascular Disease
    • Transient 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
  • 8. Cerebrovascular Disease
    • Factors predisposing to TIA
      • Atherosclerosis
        • Superimposed hypotension
        • Spasm of diseased vessel
      • Disorders in the neck (spondylosis)
      • Other extracranial vascular diseases eg. embolism
  • 9. Cerebrovascular Disease
    • Stroke
      • 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
  • 10. 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
  • 11. Stroke: Causes
  • 12. Ischaemic Stroke
    • Atherosclerosis
      • Carotid artery
        • Common carotid
        • Internal carotid
        • (external carotid)
      • Vertebro-basilar system
        • Posterior cerebral
          • With normal BP, >90% cross sectional area reduction is necessary to impair blood flow
  • 13. Ischaemic Stroke
    • Factors affecting tissue survival
      • Adequacy of collateral circulation
      • State of systemic circulation
        • Reduced blood flow, cardiac pump failure, hypovolaemia, hyperviscosity
      • Serological factors
        • Low blood sugar, high blood sugar, hypoxia, elevated serum calcium, high blood alcohol
  • 14. Ischaemic Stroke
    • Factors affecting tissue survival contd .
      • Changes within obstructing vascular lesion
        • Fragmentation and advancing of embolus
        • Reactive vasoconstriction (spasm)
        • Reperfusion – stunned cells may recover
        • Propagation of thrombus – collateral occlusion
        • Embolisation from previous thrombus
  • 15. Ischaemic Stroke
    • Factors affecting tissue survival contd .
      • Resistance within microcirculatory bed
        • Hypertension
        • Diabetes mellitus – thickened vessel walls
        • Hyperviscosity
        • Diffuse thromboses (low microcirculatory flow)
      • Oedema and raised ICP
        • Increased resistance to blood flow
  • 16. Ischaemic Stroke
    • Intracranial vascular occlusion
      • Effects usually confined to area of supply of affected vessel
    • Extracranial vascular occlusion
      • Effects may be modified by collateral circulation
      • Watershed infarction may be seen
  • 17. Brain: Distribution of cerebral infarction
  • 18. CNS Ischaemia
    • Selective vulnerability of CNS cells
      • Neurons – most sensitive
      • Oligodendroglia
      • Astrocytes
      • Microglia
      • Blood vessels
          • In descending order of sensitivity
  • 19. Brain: Effect of global ischaemia
  • 20. Consequences of global ischaemia Effects of global ischaemia
  • 21. CNS Ischaemia
    • Mild hypoxia
      • Selective neuronal necrosis eg. respirator lung
    • Moderate hypoxia
      • Neuronal necrosis
      • Neuroglial necrosis
      • Blood vessels and microglia are spared
          • Partial cerebral infarction
  • 22. Ischaemic Stroke
    • Infarction (stroke)
      • Thrombotic – usually anaemic (may be haemorrhagic)
      • Embolic – usually haemorrhagic , often multiple. Haemorrhagic nature due to:
        • Necrosis of vessel wall
        • Lysis of embolus with restoration of some blood flow.
  • 23. CNS Infarction
    • Vascular occlusion causes:
      • Necrosis of neurons, neuroglia and blood vessels
      • 4-6 hrs. – coagulative necrosis
      • 12-15 hrs. – sharp demarcation (swelling of neuropil)
      • 24 hrs. – reactive changes
        • Proliferation of microglia, astrocytes, capillaries
        • Inflammatory reaction
  • 24. CNS Infarction
    • Infarction contd.
      • 1-2 weeks – Swelling resolves
        • Softening
        • Shrunken granular grey matter
        • Accumulation of lipid-laden phagocytes (gitter cells) in infarcted area
      • Several months – shrunken cystic lesion traversed by glial fibrils and small blood vessels
  • 25. Brain: Recent anaemic infarct
  • 26. Brain: Older infarct showing cavity formation
  • 27. Brain: Older infarct
  • 28. Bilateral posterior cerebral infarcts
  • 29. Brain: Recent haemorrhagic infarct
  • 30. Brain: Haemorrhagic infarct
  • 31. Brain: Haemorrhagic infarct
  • 32. Brain: Multiple haemorrhagic infarcts
  • 33. Brain: Relatively recent infarct - Histology
  • 34. Brain: Older infarct showing ‘gitter’ cells
  • 35. Brain: Older infarct - Histology
  • 36. Brain: Old infarct with cavity formation - Histology
  • 37. Brain: Laminar infarct
  • 38. Brain: Watershed infarct
  • 39. Brain: Very old infarct showing atrophy of hemisphere
  • 40. CNS Infarction
    • Vertebro-basilar occlusion
      • Infarction of brainstem
      • Infarction of cerebellum
      • Infarction of posterior cerebral arterial territory
  • 41. Clinical effects of basilar artery occlusion
  • 42. Brain: Haemorrhagic cerebellar infarcts
  • 43. Chronic CNS Ischaemia
    • Lacunae
      • Small cavities located deep within cerebral hemispheres (basal ganglia) and pons
      • Elderly subjects - >90% with hypertension
      • ? Small infarcts
      • ? Expanded perivascular spaces
      • ? Resolving haemorrhages
      • Associated with vascular dementia
        • Multi-infarct dementia
        • Binswanger’s disease
  • 44. Brain: Lacuna in pons
  • 45. Brain: Lacunar lesions
  • 46. CNS Infarction
    • Venous thrombosis
      • Primary – non-infectious
        • Pregnancy, puerperium and oral contraceptives
        • Haematological disorders
        • Extreme dehydration
          • Haemorrhagic infarction
      • Secondary – pyogenic infections
        • Infections from sinuses, middle ear
        • Compound fracture
          • Septic infarction
  • 47. Brain: Bilateral haemorrhagic infarct – Sup. Saggital sinus thrombosis
  • 48. Haemorrhagic Stroke
    • Brain and spinal cord substance (intraparenchymal)
    • Subarachnoid
    • Mixed
  • 49. Haemorrhagic Stroke
    • Major predisposing factors
      • Hypertension
      • Congenital anomalies
      • Vascular malformations
    • Minor predisposing factors
      • Vasculitis
      • Bleeding diatheses
  • 50. Haemorrhagic Stroke
    • Primary intraparenchmal haemorrhage
      • Predisposing vascular changes include:
        • Fibrinoid necrosis
        • Hyaline arteriolosclerosis (lipohyalinosis)
        • Microaneurysms (Charcôt-Bouchard)
      • Sizes of haemorrhage
        • Massive - >3cm diam. Cerebral hemisphere
            • > 1.5cm diam. brainstem
  • 51. Brain: Charcot-Bouchard microaneurysm
  • 52. Brain: Common sites of spontaneous haemorrhage
  • 53. Brain: Haemorrhage into basal ganglia
  • 54. Brain: Massive hemispheric haemorrhage
  • 55. Brain: Haemorrhage into basal ganglia
  • 56. Brain: Pontine haemorrhage
  • 57. Brain: Pontine haemorrhage
  • 58. Haemorrhagic Stroke
    • Subarachnoid haemorrhage
      • Saccular aneurysm 65%
          • Females = males
          • Developmental medial defect
          • Superimposed degenerative changes eg. atheroma
          • 15-20% multiple
      • A-V malformations 5%
      • Others (blood dyscrasias) 5%
      • No cause found 20%
  • 59. Haemorrhagic Stroke
    • Subarachnoid haemorrhage
      • Secondary effects include:
        • Rebleeding
        • Vasoconstriction (spasm)
        • hydrocephalus
  • 60. Brain: Distribution of saccular (berry) aneurysms
  • 61. Brain: Multiple berry aneurysms
  • 62. Brain: Berry aneurysm - arrow
  • 63. Brain: A large berry aneurysm
  • 64. Brain: Subarachnoid haemorrhage – ruptured berry aneurysm
  • 65. Brain: Giant atherosclerotic aneurysm
  • 66. Haemorrhagic Stroke
    • Mixed (intraparenchymal and subarachnoid) haemorrhage
      • A-V malformations
      • Capillary angiomas
        • Focal irritation may predispose to convulsions (epileptiform attacks)
  • 67. Brain: Causes of mixed subarachnoid and intracerebral haemorrhages
  • 68. Brain: Vascular malformations
  • 69. Brain: Vascular malformation – cerebral hemisphere
  • 70. Brain: Arterio-venous malformation
  • 71. Brain: Vascular malformation