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Am J Psychiatry 1991; 148:292-305
Copyright © 1991 by American Psychiatric Association
Substance abuse and cerebral blood flow
RJ Mathew and WH Wilson
Department of Psychiatry, Duke University Medical Center, Durham, NC 27710.
OBJECTIVE AND METHOD: This paper reviews acute and chronic effects of drugs
of abuse on cerebral blood flow (CBF) and metabolism and their clinical
significance. The most important source of information for the review is
human research reports published in refereed journals. A few animal
studies, book chapters, and abstracts that are especially relevant are also
included. RESULTS: In humans, ethanol in small doses produces cerebral
vasodilation; higher doses induce cerebral vasoconstriction. Chronic
alcoholism is associated with reduced CBF and cerebral metabolism.
Sedatives and antianxiety drugs lead to global reduction in CBF and
cerebral metabolism. Caffeine, even in small doses, is a potent cerebral
vasoconstrictor. Cerebral vasodilation is seen immediately after cigarette
smoking, but chronic smokers show global reduction in CBF. Changes in CBF
after marijuana smoking are variable; both increases and decreases are
seen. Chronic marijuana smoking, however, seems to reduce CBF. Most
inhalants and solvents are vasodilators; chronic abuse is accompanied by a
decrease in CBF. A number of drugs of abuse, including ethanol,
amphetamines, cocaine, nicotine, and caffeine-phenylpropanolamine
combinations, increase the risk for stroke. Reduction in CBF associated
with chronic use of ethanol, nicotine, inhalants, and solvents is at least
partially reversible upon abstinence. CONCLUSIONS: Topics for future
research include regional brain function, which mediates drug-induced mood
changes (euphoria); CBF concomitants of psychological and physiological
characteristics that increase addiction potential; changes in CBF that
accompany withdrawal syndromes; mechanisms responsible for drug-induced
stroke; and effects of functional and organic complications on CBF.
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