J S Kim1, J H Lee, M C Lee. 1. Department of Neurology, University of Ulsan, Asan Medical Center, Seoul, South Korea.
Abstract
BACKGROUND: Although there have been sporadic reports of patients with small intracerebral hemorrhages presenting with discrete clinical features, the clinical and distributional characteristics of these hemorrhages have not been adequately investigated. CASE DESCRIPTIONS: We studied 28 patients who had primary intracerebral hemorrhage of a longest diameter < or = 1.5 cm as seen in computed tomographic scan and/or magnetic resonance imaging. Small primary intracerebral hemorrhages were found in the basal ganglia in 8 patients (2 with intraventricular hemorrhage), the posterior limb of the internal capsule in 8, the area of the fourth ventricle of the cerebellum in 7 (5 with intraventricular hemorrhage), the pontine tegmentum in 4, and the thalamomesencephalic area in 1. All patients except 3 were hypertensive, suggesting that most of the hemorrhages may have occurred because of rupture of small end arteries secondary to long-standing hypertension. Depending on their location, the hemorrhages clinically manifested as pure motor stroke in 7, pure sensory stroke in 6, vertigo/ataxia in 7, sensorimotor stroke in 4, and ataxic hemiparesis in 2 patients. One patient with thalamomesencephalic hemorrhage showed vertical gaze disturbance, and 1 with basal ganglionic hemorrhage presented with symptoms of acute hydrocephalus secondary to a relatively large amount of intraventricular hemorrhage. The prognosis of small intracerebral hemorrhage was generally excellent except for when patients were very old or when there was a significant amount of intraventricular bleeding. CONCLUSIONS: Small primary intracerebral hemorrhage has its predilection sites: basal ganglia, posterior limb of the internal capsule, area of the fourth ventricle of the cerebellum, and pontine tegmentum. Most of the hemorrhages are probably caused by rupturing of the small end arteries in the setting of chronic hypertension. They produce discrete clinical syndromes often mimicking classic lacunar syndrome, of which pure sensory stroke is relatively common.
BACKGROUND: Although there have been sporadic reports of patients with small intracerebral hemorrhages presenting with discrete clinical features, the clinical and distributional characteristics of these hemorrhages have not been adequately investigated. CASE DESCRIPTIONS: We studied 28 patients who had primary intracerebral hemorrhage of a longest diameter < or = 1.5 cm as seen in computed tomographic scan and/or magnetic resonance imaging. Small primary intracerebral hemorrhages were found in the basal ganglia in 8 patients (2 with intraventricular hemorrhage), the posterior limb of the internal capsule in 8, the area of the fourth ventricle of the cerebellum in 7 (5 with intraventricular hemorrhage), the pontine tegmentum in 4, and the thalamomesencephalic area in 1. All patients except 3 were hypertensive, suggesting that most of the hemorrhages may have occurred because of rupture of small end arteries secondary to long-standing hypertension. Depending on their location, the hemorrhages clinically manifested as pure motor stroke in 7, pure sensory stroke in 6, vertigo/ataxia in 7, sensorimotor stroke in 4, and ataxic hemiparesis in 2 patients. One patient with thalamomesencephalic hemorrhage showed vertical gaze disturbance, and 1 with basal ganglionic hemorrhage presented with symptoms of acute hydrocephalus secondary to a relatively large amount of intraventricular hemorrhage. The prognosis of small intracerebral hemorrhage was generally excellent except for when patients were very old or when there was a significant amount of intraventricular bleeding. CONCLUSIONS: Small primary intracerebral hemorrhage has its predilection sites: basal ganglia, posterior limb of the internal capsule, area of the fourth ventricle of the cerebellum, and pontine tegmentum. Most of the hemorrhages are probably caused by rupturing of the small end arteries in the setting of chronic hypertension. They produce discrete clinical syndromes often mimicking classic lacunar syndrome, of which pure sensory stroke is relatively common.