Conclusion

Over the past 15 years, much has changed with regard to the use and our under standing of both amphetamines and cocaine. Most notably, cocaine depend ence now appears to be differentially affecting poor, minority individuals who live in the inner city. This same population is overrepresented in the AIDS population. This confluence is not surprising, because both sex risk (including sex workers) and needle risk are associated with chronic use of cocaine. It therefore appears that these two epidemics are interconnected in a way that deserves close attention.

At the same time, there may be reason for cautious optimism with regard to the long-term effects of prenatal exposure to cocaine. Some of the early claims of devastating physical consequences to "crack babies" have proven to be exaggerated; experts in the perinatal addiction field now consider that many factors (e.g., poverty, poor maternal nutrition/health, smoking, and exposure to violence) combine to influence development. Molecular mechanisms of developmental neuroadaptation are at the same time beginning to be studied. In the future, we hope to understand better the physiological basis for the observed clinical events.

In the basic sciences area, we have come to understand more about the interactions of various neurotransmitters, drug reinforcement, and the reward pathway. Receptors are being subtyped and cloned. Signal transduction pathways, with their longer range on protein synthesis and genetic regulation, are being explored. We are beginning to make inroads in our understanding of sen-sitization and tolerance. Although pharmacological treatments for cocaine addiction have not yet proven successful in clinical trials, there are many exciting new avenues of pursuit. These prospects for pharmacological intervention are based on the remarkable advances in neuroscience being made in this decade.

Researchers also have been hard at work testing psychotherapeutic solutions to this complex problem. Cocaine dependence should not be viewed in isolation from other psychiatric conditions and life problems. Rather, we must consider how best to address the problem in the presence of other psychoactive substance use and non-substance-use Axis I and Axis II disorders. Depending on the larger clinical picture, successful treatment may require multiple or highly select therapies that are matched to the patient's pathology and adaptive strengths and resources. It is clear that a "one size fits all" approach to treatment of cocaine dependence is inappropriate; instead, an array of assessment tools is necessary to determine patient needs, along with a menu of cost-effective and readily available therapeutic strategies. Although American Society of Addiction Medicine (Hoffman, Halikas, Mee-Lee, & Weedman, 1991) criteria facilitate patient placement in an appropriate treatment setting based on addiction severity, they provide little guidance in terms of specific interventions to be delivered within those settings. Clinical research aimed at developing therapies for specific subtypes of cocaine addicts in a variety of settings is the most promising approach we now have.

ACKNOWLEDGMENTS

Special thanks to Kenneth S. Kendler, MD, Rachel Brown Banks Distinguished Professor of Psychiatry and Professor of Human Genetics, Medical College of Virginia, Virginia Commonwealth University, Richmond, Virginia, for contributing to the genetic factors section of this chapter on genetic factors.

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