Objective: Deep small basal ganglia infarction (DSBI) cannot be clearly classified as either lacune or striatocapsular infarction by their sizes only. We tried to elucidate clinical and other properties of DSBI to und...Objective: Deep small basal ganglia infarction (DSBI) cannot be clearly classified as either lacune or striatocapsular infarction by their sizes only. We tried to elucidate clinical and other properties of DSBI to understand better in pathophysiology of ischemic lesion of basal ganglia. Methods: We analyzed 36 patien ts with acute ischemic lesion of basal ganglia with the size varying from 1.5 to 3 cm in maximal diameters. We assessed clinical features, laboratory data, risk factors of stroke, and radiologic findings such as MRI and MR angiography. Resu lts: Patients with DSBI could be largely divided into two distinctive groups, sm all infarction with cortical sign (SICS) and lacunar syndrome (LS) according to their presence of cortical manifestations. Total of 11 patients were in SICS gro up and they showed cortical manifestations such as eyeball deviation, visual fie ld defect, aphasia and neglect. They also showed severer noncortical neurologic deficit compared with LS group. Whereas LS group showed various MRA patterns, 7 patients of SICS group (63.6%) showed proximal MCA stenosis in MRA. Conclusions : We found that many patients with DSBI could have the features of either lacune or striatocapsular infarction. Although they have similar morphologic character istics but they are presumed to have different pathophysiologic mechanism.展开更多
文摘Objective: Deep small basal ganglia infarction (DSBI) cannot be clearly classified as either lacune or striatocapsular infarction by their sizes only. We tried to elucidate clinical and other properties of DSBI to understand better in pathophysiology of ischemic lesion of basal ganglia. Methods: We analyzed 36 patien ts with acute ischemic lesion of basal ganglia with the size varying from 1.5 to 3 cm in maximal diameters. We assessed clinical features, laboratory data, risk factors of stroke, and radiologic findings such as MRI and MR angiography. Resu lts: Patients with DSBI could be largely divided into two distinctive groups, sm all infarction with cortical sign (SICS) and lacunar syndrome (LS) according to their presence of cortical manifestations. Total of 11 patients were in SICS gro up and they showed cortical manifestations such as eyeball deviation, visual fie ld defect, aphasia and neglect. They also showed severer noncortical neurologic deficit compared with LS group. Whereas LS group showed various MRA patterns, 7 patients of SICS group (63.6%) showed proximal MCA stenosis in MRA. Conclusions : We found that many patients with DSBI could have the features of either lacune or striatocapsular infarction. Although they have similar morphologic character istics but they are presumed to have different pathophysiologic mechanism.
