Background and Purpose : Many cases of amnesia caused by thalamic hemorrhage involve anterior nucleus hemorrhage, dorsomedial nucleus hemorrhage, and intraventricular rupture. In the present study, intraventricular rupture was studied with a focus on cases with hematoma compression at the fornix. Methods : Of 116 patients with thalamic hemorrhage admitted to our hospital, 50 patients aged <70 years who had hemorrhage during their first stroke confined to the thalamus, internal capsule, and corona radiata, and who neither developed hydrocephalus nor showed dementia prior to onset were investigated. Thalamic hemorrhages were classified by CT findings and the extent of intraventricular rupture. Memory was studied by the FIM memory scores on admission and discharge. Results and Conclusion : Patients with dorsomedial nucleus hemorrhage showed no tendency toward amnesia and were equivalent to patients with posterolateral nucleus hemorrhage, which does not usually result in amnesia on its own. Of the 30 patients with posterolateral nucleus hemorrhage, a high degree of amnesia was observed in the 18 with intraventricular rupture. A high proportion of patients with dorsomedial nucleus hemorrhage experienced intraventricular rupture (5 of 6 patients). Equivalent degrees of amnesia were observed in patients with intraventricular rupture with dorsomedial nucleus hemorrhage and those with posterolateral nucleus hemorrhage. The present findings in conjunction with the fact that amnesia in thalamic hemorrhage involves episodic memory impairment suggest that amnesia in patients with dorsomedial or posterolateral nucleus hemorrhage or with intraventricular rupture does not stem from damage to the dorsomedial nucleus, which is part of the Yakovlev circuit involved in emotional memory. Instead, the primary cause appears to be the effects of intraventricular rupture on the Papez circuit surrounding the lateral ventricle and foramen of Monro.

Calcified amorphous tumor (CAT) is a non-neoplastic mass characterized by calcified nodules that was first reported in 1997. It is often associated with dialysis or mitral annular calcification (MAC). CAT is considered a risk factor for systemic embolism, but there has been no report of CAT damaging the native valve tissue and leading to valvular disease. An 81-year-old woman had shortness of breath on exertion starting 1 year previously, and was referred to our hospital with cardiac murmur detected on physical examination. Echocardiography showed evidence of severe mitral valve regurgitation with ruptured chordae tendineae of the posterior leaflet and a poorly mobile club-shaped structure protruding into the left ventricle and appearing to be continuous with MAC. She underwent elective mitral valve repair. A club-shaped calcification originating from MAC was found under the P2 segment, with ruptured P2 chordae tendineae immediately above it and mitral perforation in the contralateral A2 segment, which were likely to have resulted from direct damage by the hard structure. Mitral valve repair was successful with mass resection, triangular resection of the posterior leaflet P2 segment, and closure of the perforation. Histopathological findings of the mass were consistent with CAT, with no evidence of infection or malignancy. CAT may not only cause embolism but also grow while damaging the native valve tissue. It is important to closely follow-up and perform surgery in proper timing.