Ischemic lesions of the hippocampus and their relation to Ammon's horn sclerosis. A neuropathological study of two cases and a comparison to the vascular anatomy.

Two adult brains with small ischemic lesions in the hippocampus, due to impairment of the supply from the posterior cerebral artery, are presented. The first case corresponds to what is described in the literature as "incisural sclerosis" and shows no difference in vulnerability between the Sommer and the Spielmeyer sector. In the second case the hippocampal lesion is due to an embolic occlusion of the posterior cerebral artery and consists of selective necrosis of the subiculum, the Sommer sector and part of the endfolium of the pyramidal layer, the Spielmeyer sector remaining noninfarcted. The postmortem angiograms of 12l hippocampi of adults, as well as full term born and premature infants, show that the h1 and h2 sectors and part of the h3 sector of the hippocampus are supplied by the same "sulcus" arteries. Although there is a selective vulnerability to ischemia in some sectors of the hippocampus, which is typical for Ammon's horn sclerosis, this cannot be explained by a difference of arterial supply or by compression of arteries during the process of birth.

Cimetidine-induced liver injury. Report of three cases.

Cimetidine-induced liver injury has only very rarely been reported. Three patients are described who developed signs of hepatic damage after the institution of cimetidine therapy. Transient signs of acute liver failure were noticed in one patient. Histologically, a cytotoxic type of injury with centrilobular confluent and bridging portal-central necrosis, accompanied by a mixed mono- and polymorphonuclear infiltrate with signs of cholangiolitis in the portal tracts was observed in two patients, whereas a hepatocanalicular type of cholestatic hepatitis was noticed in another patient. It is proposed that the mechanism of cimetidine-induced liver injury may vary in different patients: it may be due either to a 'metabolic idiosyncrasy' because of the production of hitherto unknown toxic metabolites or to a hypersensitivity reaction.