Cognitive function and cerebral perfusion during cocaine abstinence.

Abstract

Recovery from addiction requires motivation to change, understanding of the process of addiction, and the ability to form new, stable patterns of behavior. Cognitive behavior therapy is currently a mainstay of treatment for cocaine dependence. Its aim is to change behavior and affective responses by teaching coping skills and by addressing and modifying dysfunctional thought patterns. Through learning and practice, a patient can gain increasing control over urges and behaviors that were previously considered to be unmanageable and immutable. In most substance abuse treatment programs, counseling also includes disease-model education, anger management, and motivational enhancement in both individual and group settings to provide alternative responses when an addict is faced with unmanageable feelings, urges, or circumstances. The capacity to respond to such “psychosocial” intervention is largely dependent on a patient’s cognitive flexibility. Intellect, in the conventional sense, varies as a function of education and socioeconomic background. Educational history is relevant in cognitive therapy only as regards intellect in the intrinsic sense: the ability to learn and reason and abstract. The case reports presented here were chosen to illustrate the premise that intellect, in this less colloquial sense, changes over the period of early recovery from heavy drug exposure. We propose that this change in complex cognitive function is multidetermined, a product of effects of drug abuse at many levels of regulation of cerebral function, but focus on cerebral perfusion in these two cases. Cocaine induces constriction of coronary and cerebral vessels in both humans and in animal models (1, 2). Over the last 10 years, several groups of investigators using positron emission tomography and single photon emission computed tomography to measure brain perfusion have found that chronic cocaine use (usually in the context of polysubstance abuse) is associated with multiple focal decreases in cerebral blood flow (CBF) (3, 4). Magnetic resonance angiography has provided the first direct demonstration of acute, cocaine-induced cerebral vasospasm in humans (5). Previous investigations have demonstrated both deficits in neuropsychological performance and abnormalities in brain perfusion or metabolism in chronic cocaine abusers and that both of these deficits can improve during abstinence (4, 6, 7). Although prior studies have indicated that the severity of these flow deficits is related to the degree and duration of drug abuse, their pathophysiology is unknown, and their consequences on brain function are unclear. One corollary of these findings is that the degree of change in CBF during abstinence correlates with the degree of abnormality at the beginning of treatment. Figure 1 presents the baseline image of the patient in case 2, Ms. B, in relation to that of a typical comparison subject. These images have been scaled and colorcoded to show the same relative activity. Note that in addition to several cortical regions with markedly decreased perfusion, e.g., orbital and dorsal prefrontal, parieto-occipital and frontoparietal, CBF in the patient’s cortex is generally lower than that of a comparison subject. We have hypothesized that a measure of the change from baseline perfusion will correlate with a measure of the capacity to learn new behavior. The cases were chosen to highlight the role of cognitive function and its relation to cerebral perfusion in recovery from cocaine abuse and to demonstrate an association between the response to behavioral therapy and improvement in cerebral perfusion. Both patients were in drug-free residential care during the two neuroimaging and neuropsychological testing sessions. We suggest that this correlation provides a hypothesis for further clinical study of the relationship between cerebral perfusion and the response to cognitive behavior therapy in recovery from cocaine dependence.