1970 Volume 7 Issue 5 Pages 275-283
Sixty-six cases with bilateral cerebrovascular lesions among 141 autopsy cases examined at Harunaso Hospital during the past four years were analysed from a clinico-pathological point of view with special reference to the degree and mode of onset of motor disturbance.
These cases (84.6% of cases with cerebrovascular lesion) were classified into three groups I, II and III, depending on the state of motor disturbance.
Group I:
Cases with tetraplegia (or paresis) were designated as group I, which was further divided into four types, A, B, C and D, according to the mode of development of motor disturbance.
Type A: Separate attacks of hemiplegia on both sides with resulting tetraplegia (or paresis).
Type B: Acute onset of hemiplegia on one side with gradual development of motor paresis on the other side.
Type C: Gradual development of tetraparesis (or plegia)
Type D: Acute onset of tetraplegia (or paresis)
Group II:
This group comprised cases showing hemiplegia without motor disturbance on the other side (Hemiplegia with contralateral silent type).
Group III:
Cases with no motor disturbance were included in group III (silent group).
Pathological findings revealed that all cases of type A had their lesions in the basal ganglia including the internal capsule and 25% of these had lesions in the pons too.
Lesions of type B were chiefly of lacunes of basal ganglia and the responsible lesions for the evident hemiplegia were small softenings in the pons.
Cases belonging to type C were observed to have small softenings in the basal ganglia. In type D, acute onset of tetraplegia was caused by intracranial hemorrhage, i. e. cerebral (2 cases), cerebellar (1 case), pontine (1 case) and subarachnoid (3 cases) hemorrhages.
Lacunes in the claustrum were the main lesions of neurologically silent side of cases belonging to group II.
In group III, lacunar softenings or the cortical lesions in the silent area of the non-dominant hemisphere were the main lesions, while the other factors including diseases other than CVD, or secondary changes such as deformities of the limbs, edema or malnutrition made the diagnosis difficult in this group.
