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Thomas M. Hyde, MD, PhD; James C. Ziegler, MD; Daniel R. Weinberger, MD
Intramural Research Program National Institute of Mental Health 2700 Martin Luther King Jr Ave SE Washington, DC 20032

Arch Neurol. 1993;50(2):131.

	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.

—We appreciate the comments from Merriam and Hegarty regarding our recently published article about psychosis in metachromatic leukodystrophy.¹ We were aware of their case report and their other publications. Their case, however, was not included in our review because the age of clinical onset in their patient fell outside the age group (12 to 30 years) that we focused on in detail in our article.

The hypothesis that psychosis is related to disruption of neocortical regulation of limbic systems has a long history, with a variety of incarnations. If one were compelled to determine its origin, the task would be daunting at the least. It probably was first articulated clearly by MacLean,² who stressed neocortical-limbic connectivity as the neural substrate of psychosis. Nauta³ emphasized the role of the prefrontal cortex, suggesting that psychosis resulted from the loss of prefrontal control over limbic activity. More . . . [Full Text PDF of this Article]

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