The widespread use of cocaine by women of child-bearing age has resulted in a number of reports of adverse fetal and neonatal outcomes associated with in utero cocaine exposure. Specific causality is difficult to ascertain because of multiple confounding variables associated with substance abuse. In an effort to better define the effects of cocaine exposure, it is necessary to adequately document drug exposure and adjust for associated covariates. In this proposal, the syndromes produced by cocaine intoxication and withdrawal will be defined by measuring cord blood concentrations of cocaine and its metabolites (benzylecgonine, anhydroecgoninemethyl-ester and coca-ethylene). It is our hypothesis that there are clinical parameters available that can distinguish between intoxication and withdrawal. Using a detailed neurological and adaptive capacity examination that has been tested and defined previously, the correlation between signs on the examination and blood levels of cocaine and/or its metabolites will be made. Using the data obtained from patients with positive assays for coca-ethylene, which is a metabolite of cocaine in the presence of alcohol, we will attempt to separate effects of cocaine from fetal alcohol exposure. Recent reports of stroke and other central nervous system lesions suggest that cocaine may exert a teratogenic effect on the brain. Impaired cerebral blood flow, excitotoxic injury and impaired neuronal development have been implicated as possible mechanisms of injury. At one month of life, cocaine-exposed neonates will be reexamined to determine which signs persist beyond intoxication and withdrawal and may represent an embryopathic effect. In addition, the incidence of delayed visual maturation will be determined and will be analyzed to see if its occurrence can be used as a marker for cocaine effects on the developing nervous system. The identification of these neonates who are cocaine exposed will allow the development of a cohort for longitudinal studies on the incidence and types of neurological complications seen. The ability to define these syndromes and recognize complications will enable us to understand better the mechanisms of ischemic injury to the developing central nervous system. The identification of clinical signs and symptoms in the neonatal period in cocaine-exposed babies will help determine which infants are at risk for developmental disabilities. With this information, clinical recommendations regarding followup care and assessment can be made more accurately.

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National Institute of Neurological Disorders and Stroke (NINDS)
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