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D. Tarsy, MD
Dept of Neurology Boston VA Hospital 150 S Huntington Ave Boston, MA 02130

Arch Neurol. 1977;34(11):723.

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

In Reply.—

My colleagues and I agree with Dr Young that our report can offer only tenuous indication that a single discrete brain lesion can produce asterixis in the absence of toxicmetabolic factors. We did, in fact, state that stereotactic ventrolateral thalamotomy can produce contralateral asterixis, but unfortunately a footnote to the cited reference by Shahani and Young¹ was inadvertantly omitted. We were unaware of their earlier reference,² while the more recent one³ was in press simultaneously with our own report.

We continue to doubt that, in the absence of other proprioceptive deficits, minimal reduction of two-point discrimination can be considered relevant for asterixis and, like Shahani and Young,¹ have not been impressed with an association between proprioceptive sensory loss and asterixis in general.

We agree that the role of mild weakness in asterixis can be uncertain. However, since in our patient prominent asterixis persisted after resolution of weakness, and since it . . . [Full Text PDF of this Article]

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