Cavernous malformations consistofdistended,looselyorganizedvascularchannelswiththincollagenizedwallswithoutinterveningnervoustissue.Theyoccurmostofteninthecerebellum,pons,andsubcorticalregions,andhavealowbloodflowwithoutsignificantarteriovenousshunting.Fociofoldhemorrhage,infarction,andcalcificationfrequentlysurroundtheabnormalvessels.
Capillary telangiectasias aremicroscopicfociofdilatedthin-walledvascularchannelsseparatedbyrelativelynormalbrainparenchymathatoccurmostfrequentlyinthepons.Venous angiomas (varices)consistofaggregatesofectaticvenouschannels.Theselattertwotypesofvascularmalformationareunlikelytobleedortocausesymptoms,andmostareincidentalfindings.
Hypertension causes hyaline arteriolar sclerosis of the deep penetrating arteries and arterioles that supply the basal ganglia, the hemispheric white matter, and the brain stem. Affected arteriolar walls are weakened and are more vulnerable to rupture. In some instances, minute aneurysms (Charcot-Bouchard microaneurysms) form in vessels less than 300 µm in diameter. In addition to massive intracerebral hemorrhage (discussed earlier), several other pathologic outcomes are related to hypertension.
Fig. 23.10 Saccularaneurysms.(A)Viewofthebaseofthebrain,dissectedtoshowthecircleofWilliswithananeurysmoftheanteriorcerebralartery(arrow). (B)ThecircleofWillisisdissectedtoshowalargeaneurysm.(C)Sectionthroughasaccularaneurysmshowingthehyalinizedfibrousvesselwall.Hematoxylin-eosinstain.
http://ebooksmedicine.net
Fig. 23.11 Arteriovenousmalformation.
Lacunes or lacunar infarcts are small cavitary infarcts, just a few millimeters in size, that are found most commonly in the deep gray matter (basal ganglia and thalamus), the internal capsule, the deep white matter, and the pons. They are caused by occlusion of a single penetrating branch of a large cerebral artery. Depending on their location, lacunes can be silent clinically or cause significant neurologic impairment.
Rupture of the small-caliber penetrating vessels may occur, leading to the development of small hemorrhages. In time, these hemorrhages resorb, leaving behind a slit-like cavity (slit hemorrhage) surrounded by brownish discoloration.
Acute hypertensive encephalopathy most often is associated with sudden sustained increases in diastolic blood pressure to greater than 130 mm Hg. It is characterized by increased intracranial pressure and global cerebral dysfunction, manifesting as headaches, confusion, vomiting, convulsions, and sometimes coma. Rapid therapeutic intervention to reduce the blood pressure is essential. Postmortem examination may show brain edema, with or without transtentorial or tonsillar herniation. Petechiae and fibrinoid necrosis of arterioles in the gray matter and white matter may be seen microscopically.