Psychomotor Stimulants – Your Brain on Cocaine

In 1987, the Partnership for a Drug-Free America unveiled a national ad campaign depicting an egg frying in a skillet and stating ominously that “This is your brain on drugs.”Well, obviously drugs don’t literally fry your brain, but can they cause serious damage? Later in this post we will see that certain amphetamine analogs do cause damage to specific neurotransmitter systems in experimental animals and probably also in high-dose human users.The situation is less clear for cocaine. Nevertheless, there is substantial evidence that chronic cocaine exposure can lead to biochemical, physiological, and structural abnormalities in the brain,as well as neurological deficits.

Several research groups have looked for changes in the DA system in chronic cocaine users.This has been accomplished by means of both brain imaging methods in living subjects and postmortem brain studies, including some instances in which the subjects died from drug overdose. A number of changes in dopaminergic functioning have been reported, although the results are not entirely consistent. Such discrepancies are probably due to differences in subject populations and experimental methodology.

In one important study,Volkow and her colleagues used PET imaging with [18F]N-methylspiroperidol to determine D2 receptor availability in cocaine-dependent freebase or crack users (Volkow et al., 1993). Receptor availability in the cocaine group was significantly decreased compared to normal controls, and this difference persisted even in subjects who were retested following 3 months of cocaine abstinence.This finding could reflect either reduced D2 receptor density or increased levels of DA competing with the radiolabeled drug for access to the receptors.Volkow and coworkers (1997) subsequently examined the DA response to methylphenidate, a drug that increases synaptic DA levels by blocking reuptake.

Two PET scans were performed, the first under baseline conditions and the second after methylphenidate administration.The drug was given by IV injection, which is noteworthy because unlike standard oral dosing, this route of methylphenidate administration produces a subjective high. D2 receptors were again imaged, but this time with ["C]raclopride,a drug that is particularly known to be sensitive to changes in synaptic levels of DA. Consequently, the reduction in radiolabeled raclopride binding in the second scan compared to the first was taken as a measure of the methylphenidate- induced increase in DA. Compared with controls, the cocaine-dependent subjects showed a lower response to methylphenidate in the striatum, and they also reported a less intense drug high. In contrast,a greater methylphenidate response occurred in the thalamus, which was statistically correlated with self-reported cocaine craving.These results indicate that chronic cocaine use is associated with alterations in DA availability that vary with brain region.

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Other kinds of imaging techniques have enabled researchers to look for possible abnormalities in regional cerebral blood flow, utilization of glucose (the brain’s primary metabolic fuel), brain volume, and gray-matter density in chronic cocaine users. Although such measures do not tell us about neurotransmitter systems, they do provide important information about the structural and functional integrity of the brain areas being scanned.Therefore, it is noteworthy that several research groups have reported small, localized regions (varying from one subject to another) of hypoperfusion (abnormally low blood flow) in cocaine abusers that persist even during abstinence from the drug.There is also some evidence that chronic cocaine use leads to long-term deficits in glucose utilization by the frontal lobes as well as in frontal lobe volume. Finally, Franklin and coworkers (2002) found decreased gray matter concentration in select brain regions of cocaine- dependent compared to control subjects.The affected areas are important in a number of processes including decision making, behavioral inhibition, and emotional responses to environmental stimuli.

Do these brain abnormalities have functional consequences?This question has been addressed in a number of studies comparing neuropsychological test performance of abstinent cocaine-abusing subjects with that of control subjects.Overall, the results indicate that cocaine abuse is associated with significant impairment in many different cognitive functions, including verbal memory, attention, and motor function (Toomey et al„ 2003; Browndyke et al., 2004).These cognitive deficits could be related to some combination of neurotransmitter-related (for example, dopamine) dysfunction, deficits in regional blood flow or glucose utilization, and structural abnormalities.

Before closing, we need to mention two significant limitations of the research just discussed. First, the study designs do not permit a determination of whether the brain abnormalities and cognitive deficits were caused by cocaine or were preexisting in the subjects. People who become dependent on cocaine may have abnormal brains before they begin their cocaine use. Indeed, some of these abnormalities could predispose the individuals to substance use and eventual dependence.This important issue can only be resolved by longitudinal studies of the same subjects that encompass time points prior to and following the development of their cocaine dependence.

The second limitation is that most cocaine users also routinely take other drugs of abuse; that is, they are polysubstance users. Consequently, some of the findings may be difficult to attribute specifically to cocaine. Even with these limitations in mind, there is good reason to believe that “a brain on cocaine”is not a normal,healthy brain, even though it may not actually resemble an egg in a frying pan.

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