Capsular Infarcts (Clinical and Computed Tomographic Correlations)

ABSTRACT

Twenty patient's capsular lesions were detected by high resolution brain computed tomograhpy (CT). Eighteen of them had systemic hypertension. Two patients had prior stroke episodes that were of the same nature. All of the patients had sudden onset of neurologic deficits. Their neurologic syndromes were pure motor stoke (10 cases), ataxic hemiparesis (3 cases), pure motor stroke with dysphasia (1 cases), pure sensory-motor stroke (3 cases), pure motor stroke with tremor, locked-in syndrome, and hemiparesis with latered consciousness, each 1 case respectively. The CT showed capsular infarcts of ovolid or round hypodense lesion that was smaller than 20mm in diameter and that was seen on only two scan sections. The sites of capsular infarcts were genu(5 cases), posterior limb (9 cases), genu-posterior limb (3 cases), genu-anterior limb (3 cases), and anterior limb (4 cases) respectively. Large capsulo-putamino-caudate infarcts, or giants lacunes (type 1 of Rascol et al ) are seen in 3 cases only in pure motor stroke ; Posterior limb capsular Iacunes (type 2 of Rascol et al), 6 cases in pure motor stroke, 3 cases in ataxic hemiparesis, 2 cases in pure sensory-motor stroke, 1 case in modified pure motor stroke with tremor Anterior capsular lacunes (type 3 of Rascol et al), 1 case in pure motor stroke, 1 case in modified pure motor stroke with dysphasia, 1 case in modified pure motor stroke with memory and cognitive dysfunction. None of the capsular infarct caused mass effect. In five cases there was a relatively complete neurologic improvement, in 14 cases did the patients show mild residual neurologic deficit, and one patient expired. With the use of CT, the diagnosis of capsular infarcts has moderately increased.