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.