激症経過をとった大脳基底核部出血の臨床病理学的研究

Since we proposed the extremely early operation or the operation within 7 hours after the apoplectic attack for the lateral type of hypertensive intracerebral hemorrhage in 1973, the excellent surgical results could have been obtained for them. But there are still fulminant cases in approximately 10% of the lateral type, in which even if they are admitted in a short period of time after the attack, they progress too rapidly and develop into the irreversible state due to damage of the brainstem. In these fulminant cases cerebral herniation is not caused by the secondary edema of the brain but by the direct compression of huge hematoma possibly caused by the rupture of the large caliber of the artery.<BR>This is the first report, at least in our investigation, as the clinicopathological study on these fulminant hemorrhage in the basal ganglia.<BR>We reviewed 13 autopsy cases of the fulminant type clinically and pathologically, particularly regarding to the midbrain lesion.<BR>During the past 6 years, a total of 650 cases of cerebrovascular accident have been admitted in our hospital. Of these cases the hypertensive intracerebral hematoma was located laterally in 145 cases, medially (thalamic hemorrhage) in 48 cases and 18 cases of them took the fulminant course in the former (10 autopsy cases) and 11 cases in the latter (autopsy cases). The clinical findings in 13 autopsy cases were presented in Table 1. 11 cases admitted within 3 hours were not indicated for operation at that time, because they already showed the damage of the brainstem. Some types of respiratory disturbance were always observed from the onset of the attack until the death in every case.<BR>In the neuroradiological examination, carotid angiography was performed in 5 cases which revealed findings of huge hematoma and CT was performed in other 5 cases, which showed huge high density area with marked midline shift and ventricular perforation of hematoma. The sign of downward transtentorial herniation was observed in every case. In the rest of 3 cases, no neuroradiological examination could be done because of the too rapid progression.<BR>In autopsy findings, all brains were extremely edematous. Schemata of the extension of hemorrhage is presented in Fig. 1. The ventricular perforation of hematoma were observed in all cases of the lateral type, either into the anterior horn, the trigone or the body of the lateral ventricle. In the thalamic hemorrhage, the hematoma extended downward and destructed the hypothalamus and the midbrain directly. (Secondary lesion of the brainstem was presented in Table 1.) In the lateral type, there were 7 cases of secondary midbrain hemorrhage, 4 cases of upper pontine hemorrhage. But we could not find out any damage to the medulla macroscopically. Other lesions of the midbrain which was proposed by Blackwood et al. (Fig. 5) were checked in our cases as Table 1.<BR>As a conclusion, 1) In this type of the fulminant lateral hemorrhage, cerebral herniation and secondary midbrain lesion were caused by the hematoma itself in a short period of time. 2) In the fulminant thalamic hemorrhage the midbrain were damaged directly by the extension of hemorrhage. 3) In these fulminant types of basal ganglionic hemorrhage, there were secondary hemorrhage, squeezing or destruction of the midbrain in all cases, but could not find any lesion in the medulla. 4) Therefore, we were strongly impressed that the cause of death in these fulminant basal ganglionic hemorrhage could be destruction of the midbrain.