Page 833 - Robbins Basic Pathology by Vinay Kumar, Abul K. Abbas, Jon C. Aster
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Figure 22–11 Arteriovenous malformation. Cerebrovascular Diseases 819
vascular channels (Fig. 22–11). Microscopic examination
shows enlarged blood vessels separated by gliotic tissue, location, lacunes can be silent clinically or cause signifi-
often with evidence of previous hemorrhage. Some vessels cant neurologic impairment.
can be recognized as arteries with duplicated and fragmented • Rupture of the small-caliber penetrating vessels may occur,
internal elastic lamina, while others show marked thickening leading to the development of small hemorrhages.
or partial replacement of the media by hyalinized connective In time, these hemorrhages resorb, leaving behind a
tissue. slitlike cavity (slit hemorrhage) surrounded by brownish
discoloration.
Cavernous malformations consist of distended, loosely • Acute hypertensive encephalopathy most often is associated
organized vascular channels with thin collagenized walls with sudden sustained rises in diastolic blood pressure
without intervening nervous tissue. They occur most often in to greater than 130 mm Hg. It is characterized by
the cerebellum, pons, and subcortical regions, and have a low increased intracranial pressure and global cerebral dys-
blood flow without significant arteriovenous shunting. Foci of function, manifesting as headaches, confusion, vomit-
old hemorrhage, infarction, and calcification frequently sur- ing, convulsions, and sometimes coma. Rapid therapeutic
round the abnormal vessels. intervention to reduce the intracranial pressure is essen-
tial. Postmortem examination may show brain edema,
Capillary telangiectasias are microscopic foci of dilated with or without transtentorial or tonsillar herniation.
thin-walled vascular channels separated by relatively normal Petechiae and fibrinoid necrosis of arterioles in the gray
brain parenchyma that occur most frequently in the pons. and white matter may be seen microscopically.
Venous angiomas (varices) consist of aggregates of ectatic
venous channels. These latter two types of vascular malfor- Vasculitis
mation are unlikely to bleed or to cause symptoms, and most
are incidental findings. A variety of inflammatory processes involving blood
vessels may compromise blood flow and cause cerebral
infarction. Infectious arteritis of small and large vessels
was previously seen mainly in association with syphilis
and tuberculosis, but is now more often caused by oppor-
tunistic infections (such as aspergillosis, herpes zoster, or
CMV) arising in the setting of immunosuppression. Some
systemic forms of vasculitis, such as polyarteritis nodosa,
may involve cerebral vessels and cause single or multiple
infarcts throughout the brain. Primary angiitis of the CNS is
a form of vasculitis involving multiple small to medium-
sized parenchymal and subarachnoid vessels that is char-
acterized by chronic inflammation, multinucleate giant
cells (with or without granuloma formation), and destruc-
tion of vessel walls. Affected persons present with a diffuse
encephalopathy, often with cognitive dysfunction. Treat-
ment consists of an appropriate regimen of immunosup-
pressive agents.
Other Vascular Diseases S U M M A RY
Hypertensive Cerebrovascular Disease Cerebrovascular Diseases
Hypertension causes hyaline arteriolar sclerosis of the deep • Stroke is the clinical term for acute-onset neurologic defi-
penetrating arteries and arterioles that supply the basal cits resulting from hemorrhagic or obstructive vascular
ganglia, the hemispheric white matter, and the brain stem. lesions.
Affected arteriolar walls are weakened and are more vul-
nerable to rupture. In some instances, minute aneurysms • Cerebral infarction follows loss of blood supply and can
(Charcot-Bouchard microaneurysms) form in vessels less than be widespread or focal, or affect regions with the least
300 µm in diameter. In addition to massive intracerebral robust vascular supply (“watershed” infarcts).
hemorrhage (discussed earlier), several other pathologic
brain processes are related to hypertension. • Focal cerebral infarcts are most commonly embolic; with
• Lacunes or lacunar infarcts are small cavitary infarcts, just subsequent dissolution of an embolism and reperfusion, a
nonhemorrhagic infarct can become hemorrhagic.
a few millimeters in size, found most commonly in
the deep gray matter (basal ganglia and thalamus), the • Primary intraparenchymal hemorrhages typically are due
internal capsule, the deep white matter, and the pons. to either hypertension (most commonly in white matter,
They are caused by occlusion of a single penetrating deep gray matter, or posterior fossa contents) or cerebral
branch of a large cerebral artery. Depending on their amyloid angiopathy.
• Spontaneous subarachnoid hemorrhage usually is caused
by a structural vascular abnormality, such as an aneurysm
or arteriovenous malformation.
