Contingency management (CM) treatments are usually applied individually for drug abstinence, but CM can also be targeted toward health behaviors and implemented in groups. HIV-positive patients with cocaine or opioid use disorders (n = 170) were randomized to weekly CM or 12 step (TS) groups for 24 weeks (mean (SD) attendance was 10.8 ± 8.1 sessions for CM participants and 9.0 ± 6.9 session for TS participants). During the treatment period, both groups received compensation for attendance ($10 per session) and submission of urine samples (about $2 per sample). In addition, participants received $25 for submitting samples and completing evaluations at months 1, 3, 6, 9, and 12, with 65 to 75 of the 81 participants assigned to TS and 71 to 80 of the 89 participants assigned to CM completing these evaluations. During the treatment period, patients in the CM group only received chances to win prizes contingent upon completing health activities and submitting substance-free specimens (mean = $260, SD = $267). CM participants submitted a significantly greater number of consecutive drug-free specimens than TS participants (5.2 ± 6.0 versus 3.7 ± 5.6), but proportions of negative samples did not differ between groups during treatment or at follow-up evaluations. From pre-to post-treatment, CM participants showed greater reductions in viral loads and HIV-risk behaviors than TS participants, but these effects were not maintained throughout the follow-up period. These data suggest the efficacy of group-based CM in HIV-positive substance abusers, but more research is needed to extend the long-term benefits.Keywords contingency management; group therapy; cocaine abuse; heroin abuse; HIV; AIDS; community settings Contingency management (CM) interventions are efficacious in enhancing participation in substance abuse treatment and reducing drug use. CM re-arranges the environment to frequently detect behaviors targeted for change and provides tangible reinforcers upon objective evidence of desired behaviors. Reinforcers are usually vouchers, exchangeable for retail goods and services (Higgins et al., 1994) or chances to win prizes (Petry, Martin, Cooney, *To whom all correspondence should be addressed. Nancy Petry, Ph.D., Calhoun Cardiology Center, Department of Medicine, University of Connecticut Health Center MC-3944, 263 Farmington Avenue, Farmington, CT 06030-3944, npetry@uchc.edu; phone: 860-679-2593; fax: 860-679-1312. Publisher's Disclaimer: The following manuscript is the final accepted manuscript. It has not been subjected to the final copyediting, fact-checking, and proofreading required for formal publication. It is not the definitive, publisher-authenticated version. The American Psychological Association and its Council of Editors disclaim any responsibility or liabilities for errors or omissions of this manuscript version, any version derived from this manuscript by NIH, or other third parties. The published version is available at http://www.apa.org/journals/ccp/ NIH Public Access & Kranzler, 2000). CM ...

Second generation studies of prenatal cocaine exposure failed to find gross deficits after controlling for confounders. Concern remained that exposure could cause subtle deficits. This prospective, cohort study evaluated effects of cocaine on development at 12, 18, 24, and 36 months. From 1991-1993, 361 mother-infant pairs were recruited from the Children's Hospital of New York, Presbyterian Medical Center's prenatal clinic or delivery room suite. Mothers were assigned to the cocaine group based on report of prenatal cocaine use or positive urine toxicology. Control mothers were enrolled from the same clinic and matched for age and socioeconomic status (SES). Women with serious medical problems were excluded from either group. Of the retained cohort, at 12 months, 147 infants were exposed and 89 were unexposed case controls. Both groups were raised in impoverished environments with few supports. Developmental evaluations were conducted blinded to group. Cross-sectional analysis revealed cocaine-related deficits in neurological exams and speech across all time periods, in spite of catch up in weight, length, and head circumference. Overall analysis of development was evaluated using Generalized Estimating Equations regression analysis. Bayley Mental [Badj = -6.5 (CI--9.4, -3.5, p < or = 0.001)] and Psychomotor [Badj = -3.9 (CI--7.4, -0.5, p = 0.02)] Developmental Indices showed deficits after controlling for confounders. Males were more vulnerable to cocaine exposure for height, motor development, and emotional regulation. Dose-response relationships existed for abnormal neurological exams (Ptrends < 0.08), Mental Development Index (MDI) (Ptrend < 0.001), and Psychomotor Development Index (PDI) (Ptrend < 0.001) deficits. Although nonexposed children performed poorly, cocaine-exposed children showed worse performance. Both groups showed declines at 18 months in mental and psychomotor development from which only nonexposed children rebounded. Overall, cocaine exposure adds an additional risk to disadvantaged children's development. Cocaine-exposed children are less resilient to effects of these multiple risks.

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