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.

Methods: We examined medical records from a single central database for 65 patients receiving surgical treatment for ASD. Statistical comparisons were made between patients who experienced postoperative POH and those who did not, by examining patient and operative characteristics, such as age, sex, comorbidities, functional status, preoperative neurological function, vertebral fractures, three-column osteotomy, total operative time, estimated blood loss, length of stay, and radiographic parameters. The determinants of POH were assessed using multiple logistic regression. Results: We showed that postoperative POH was a complication of ASD surgery, with a 9% incidence rate. Patients with POH were statistically considerably more likely to require supported walkers due to partial paralysis and to have comorbidities including diabetes and neurodegenerative disease (ND). Furthermore, ND was an independent risk factor for postoperative POH (odds ratio, 4.073; 95% confidence interval, 1.094–8.362; p =0.020). Moreover, perioperative evaluation of the inferior vena cava showed that patients with postoperative POH had preoperative congestive heart failure and had hypovolemia lower postoperative diameter of the inferior vena cava than patients without POH. Conclusions Postoperative POH is a potential complication of ASD surgery. The most pertinent risk factor is having an ND. According to our study, patients who have surgery for ASD may experience alterations in their hemodynamics.