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Vicente J. Iragui, MD, PhD; Charlotte B. McCutchen, MD
Department of Neurosciences University of California-San Diego La Jolla, CA 92093 and Veterans Administration Medical Center San Diego, CA 92161

Arch Neurol. 1984;41(12):1236-1237.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

To the Editor.

—We read with interest the letter by Dr Jacome¹ on homolateral ataxia and crural paresis and the reply by Dr Fisher. Actually, the findings in Dr Jacome's patient more closely resemble those in the patient we described as having "capsular ataxic hemiparesis"² than those in the patient subsequently described by Ichikawa et al,³ since neither Dr Jacome's patient nor ours had a sensory deficit as did the patient of Ichikawa et al. The lesion in our patient was at a rostral level in the internal capsule near the corona radiata, whereas in Dr Jacome's patient the lesion was located at a more caudal level in the internal capsule.

Dr Fisher points out the shortcomings of the computed tomographic (CT) scan in the detection of small pontine infarcts and refers to one instance in which CT showed a lowdensity area in the internal capsule, whereas . . . [Full Text PDF of this Article]

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