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Donald J. Reis, MD

Arch Neurol. 1988;45(2):180-182.

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

Hypertension is one of the most common disorders affecting human health. It is the major cause of stroke, heart disease, and kidney failure. In the United States alone, it is estimated that 60 million individuals have blood pressure levels above the normal range. In the majority of patients with clinical hypertension the cause is unknown. In the majority of the remaining cases, the origin of the disorder lies within the kidney.¹

Over the past several years, there has been an increasing awareness that the central nervous system (CNS) may play a critical role in the expression of the cardinal sign of the disorder: the elevation of arterial pressure (AP). Largely working through the sympathetic nervous system, the evidence favors a view that, at the very least, the CNS plays a permissive role in sustaining the elevated AP. Conceivably, the role of the CNS may be causal.

The evidence in . . . [Full Text PDF of this Article]

Author Affiliations
From the Department of Neurology, Division of Neurobiology, Cornell University Medical College, New York.

Footnotes
Accepted for publication June 18, 1987.

Reprint requests to Department of Neurology, Division of Neurobiology, Cornell University Medical College, 411 E 69th St, New York, NY 10021 (Dr Reis).

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