1. Pathogenesis and risk factors of cerebrovascular accidents (II)
Dr. Mamlook Elmagraby

2. Objectives of the lecture:
Upon completion of this lecture, students should be able to:
Identify the causes and consequences of subarachnoid and intracerebral hemorrhage
Build a list of the different causes that can lead to cerebrovascular accident

3. INTRACRANIAL HEMORRHAGE

4. Hemorrhages may occur at any site within the CNS
epidural hemorrhage
Subdural hemorrhage
intracerebral (intraparenchymal) hemorrhage
subarachnoid hemorrhage
They may be a primary or secondary phenomenon

5. Intracerebral (intraparenchymal) hemorrhage
Nontraumatic type occur commonly in middle to late adult life
Most are caused by rupture of a small intraparenchymal vessel
The etiologies include:
hypertension
cerebral amyloid angiopathy
systemic coagulation disorders
neoplasms
vasculitis
aneurysms
vascular malformations

7. Morphology
Hypertensive hemorrhage may originate in the putamen, thalamus, pons, cerebellar hemispheres
Acute hemorrhages are characterized by extravasation of blood with compression of the adjacent parenchyma
Old hemorrhages show cavity with a rim of brownish discoloration

8. Brain, primary parenchymal hemorrhage – Gross, horizontal section
This image of a brain sectioned in the horizontal plane demonstrates a massive, acute hemorrhage in the region of the right basal ganglia. The hemorrhage is a well-demarcated mass (hematoma) that compresses and displaces adjacent brain parenchyma

9. The early lesion consists of a central core of clotted blood surrounded by a rim of tissue showing anoxic neuronal and glial changes and edema
Eventually
the edema resolves
pigment- and lipid-laden macrophages appear
proliferation of reactive astrocytes is seen at the periphery of the lesion

10. Clinical Features
Intracerebral hemorrhage can be clinically distressing if it affects large portions of the brain and extends into the ventricular system
Over weeks or months there is a gradual resolution of the hematoma, sometimes with considerable clinical improvement
The location of the hemorrhage determines the clinical manifestations

11. Subarachnoid Hemorrhage
The causes of subarachnoid hemorrhage include:
rupture of a saccular aneurysm
extension of a traumatic hematoma
rupture of a hypertensive intracerebral hemorrhage into the ventricular system
vascular malformation
hematologic disturbances
tumors

12. Brain, right cerebral hemisphere, subarachnoid hemorrhage – Gross, medial surface

13. The clinical consequences of blood in the subarachnoid space can be separated into:
Acute events
An increased risk of additional ischemic injury from vasospasm affecting vessels bathed in the extravasated blood
Late sequelae
Meningeal fibrosis occur, sometimes leading to obstruction of CSF flow as well as interruption of the normal pathways of CSF resorption

14. Saccular aneurysms The most common type of intracranial aneurysms
They are found at an arterial branch point along the circle of Willis or a major vessel just around it
2% of the population have saccular aneurysms
Multiple aneurysms exist in 20% to 30% of cases

15. The etiology of saccular aneurysms is unknown
These aneurysms develop at the site of a congenital focal defect in the media of the vessel
The majority occur sporadically
Genetic factors may be important in their pathogenesis
The predisposing factors include:
cigarette smoking
hypertension

16. Morphology
Saccular aneurysms measure from a few millimeters to 2 or 3 cm in diameter
Brownish discoloration of the adjacent brain and meninges is evidence of prior hemorrhage
Rupture of the aneurysm → extravasation of blood into the subarachnoid space, the substance of the brain, or both

17. Brain, saccular aneurysm – Gross, ventral surface
The brainstem and cerebellum are distorted by a large saccular aneurysm, which lies near the junction of the left vertebral and basilar arteries.
The aneurysm was clipped surgically in an effort to prevent rupture.

18. The muscular wall and intimal elastic lamina are absent from the aneurysm sac The sac is made up of thickened intima and covering adventitia

19. Clinical Features
Rupture of an aneurysm with subarachnoid hemorrhage is most frequent in the fifth decade
The probability of rupture increasing with the size of the lesion
Rupture is associated with acute increases in intracranial pressure in about one third of cases
25% - 50% of patients die with the first rupture

20. Repeat bleeding is common in survivors With each episode of bleeding, the prognosis is worse

21. HYPERTENSIVE CEREBROVASCULAR DISEASE

22. The most important effects of hypertension on the brain:
lacunar infarcts
slit hemorrhages
hypertensive encephalopathy
massive hypertensive intracerebral hemorrhage

23. Lacunar Infarcts
Hypertension affects the deep penetrating arteries and arterioles
These cerebral vessels develop arteriolar sclerosis and may become occluded
These occur in the lenticular nucleus, thalamus, internal capsule, deep white matter, caudate nucleus, and pons

24. An important consequence is the development of single or multiple, small, cavitary infarcts They consist of areas of tissue loss with scattered lipid-laden macrophages and surrounding gliosis Lacunae can either be clinically silent or cause severe neurologic impairment

25. Brain, pons, remote lacunar infarct – Gross, horizontal section
The term lacunar is used to describe small infarcts - by convention, infarcts measuring less than 1.5 cm in greatest dimension. The cystic appearance of this infarct indicates that it is a remote (healed) lesion.  

26. Slit Hemorrhages
Rupture of the small-caliber penetrating vessels → the development of small hemorrhages
In time these hemorrhages resorb, leaving behind a slitlike cavity surrounded by brownish discoloration
These lesions show focal tissue destruction, pigment- laden macrophages, and gliosis

27. Hypertensive Encephalopathy
A clinicopathologic syndrome:
arising in an individual with malignant hypertension
characterized by diffuse cerebral dysfunction
Rapid therapeutic intervention is required
The patients show an edematous brain with or without herniation
Petechiae and fibrinoid necrosis of arterioles in the gray and white matter may be seen