Pathogenesis and risk factors of cerebrovascular accidents (II)

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

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

INTRACRANIAL HEMORRHAGE

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

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

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

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

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

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

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

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

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

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

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

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

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.

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

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

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

HYPERTENSIVE CEREBROVASCULAR DISEASE

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

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

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

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.  

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

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