NCJ Number
141646
Date Published
1992
Length
12 pages
Annotation
This paper describes the neurologic and neuropsychiatric complications that accompany cocaine intoxication and discusses the possible mechanisms for these clinical changes, followed by a review of the abnormalities in cerebral blood flow demonstrated in cocaine abusers with Single Photon Emission Computerized Tomography (SPECT).
Abstract
Research into cocaine within psychiatry has focused on changes in neurotransmitters induced by cocaine abuse. Acutely, cocaine will block re-uptake of brain catecholamines and the "euphoria" associated with cocaine is probably secondary to increased activity in the central dopaminergic reward pathways. The increase in brain catecholamines caused by cocaine not only induces euphoria, but may also account for some of the toxicities of the drug. The chronic use of cocaine causes potentially reversible decreases in D-2 receptor density, which may be linked to the depression seen in these patients. Also, increases in catecholamines can lead to severe vasospasm in both peripheral and cerebral vessels. Cocaine acts as a local anesthetic, which may account for some of its toxicities. With the increased central and peripheral activity of dopamine and norepinephrine, hypertension, tachycardia, and excitation are seen. With higher doses, hyperthermia, acidosis, seizures, cardiovascular collapse, and death occur. With "crack" cocaine, lethal dosages are easily and unpredictably achieved. 19 references and 3 figures