This document summarizes pathology related to cerebrovascular disease. It discusses different types of strokes including ischemic, hemorrhagic, and transient ischemic attacks. Specific factors that can contribute to tissue damage in ischemic strokes are explained. Locations and appearances of infarcts over time are described. Causes and presentations of hemorrhagic strokes including those from aneurysms and arteriovenous malformations are covered.

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