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Serious neuropsychological impairments are seen in a minority of addiction treatment clients, and, theoretically, these impairments should undermine behavioral changes targeted by treatment; however, little evidence supports a direct influence of impairment on treatment response. To address this paradox, the authors used structural equation modeling and Project MATCH data (N=1,726) to examine direct, mediated, and moderated paths between cognitive impairment, therapeutic processes, and treatment outcome. Mediated relations were found, wherein impairment led to less treatment compliance, lower self-efficacy, and greater Alcoholics Anonymous Involvement, which, in turn, more proximally predicted drinking. Impairment further moderated the effect of self-efficacy, making it a poor predictor of drinking outcomes in impaired clients, thereby suggesting that impaired and unimpaired clients traverse different pathways to addiction recovery.

Using the mitochondrial membrane potential (⌬⌿ m )-sensitive fluorescent dyes 5,5Ј,6,6Ј-tetrachloro-1,1Ј,3,3Ј-tetraethylbenzimidazolocarbocyanine iodide (JC-1) and tetramethylrhodamine methyl ester (TMRM), we have observed spontaneous changes in the ⌬⌿ m of cultured forebrain neurons. These fluctuations in ⌬⌿ m appear to represent partial, transient depolarizations of individual mitochondria. The frequency of these ⌬⌿ m fluctuations can be significantly lowered by exposure to a photo-induced oxidant burden, an ATP synthase inhibitor, or a glutamate-induced sodium load, without changing overall JC-1 fluorescence intensity. These spontaneous fluctuations in JC-1 signal were not inhibited by altering plasma membrane activity with tetrodotoxin or MK-801 or by blocking the mitochondrial permeability transition pore (PTP) with cyclosporin A. Neurons loaded with TMRM showed similar, low-amplitude, spontaneous fluctuations in ⌬⌿ m . We hypothesize that these ⌬⌿ m fluctuations are dependent on the proper functioning of the mitochondria and reflect mitochondria alternating between the active and inactive states of oxidative phosphorylation. Mitochondria have been implicated in excitotoxic injury pathways, as well as injury mechanisms manifested as apoptotic or necrotic death processes. The mitochondrial membrane potential (⌬⌿ m ) has often been used as a marker for mitochondrial activity and neuronal viability during the various cell death cascades (for review, see Kroemer et al., 1998;Nicholls and Ward, 2000). Injurious stimuli, leading to either excitotoxicity or apoptosis, can lead to profound depolarization of ⌬⌿ m resulting from abnormalities in neuronal processes, including alterations in intracellular calcium dynamics and the opening of the mitochondrial permeability transition pore (PTP) (Ankarcrona et al., 1995;Nieminen et al., 1996;Schinder et al., 1996;White and Reynolds, 1996;Vergun et al., 1999;Budd et al., 2000). Although a loss of ⌬⌿ m may be linked to various inducers of cell death, these are observed as large and possibly catastrophic changes in mitochondrial function.Mitochondria under physiological conditions also play active roles in the maintenance of normal cellular functioning. A key feature of mitochondria that allows them to participate in cell survival is proton pumping across the impermeable inner membrane. This generates an electrochemical gradient, composed of ⌬⌿ m and ⌬pH, which is used for ATP synthesis, ADP-ATP exchange, uptake of respiratory substrates and inorganic phosphate, transport of K ϩ , Na ϩ , and anions to regulate volume, and regulation of protons to control heat production (for review, see Bernardi, 1999). Mitochondria also play protective roles by buffering cells against high concentrations of calcium (Budd and Nicholls, 1996;White and Reynolds, 1997;Stout et al., 1998) and sequestering proapoptotic agents, such as cytochrome c (for review, see Green and Reed, 1998;Desagher and Martinou, 2000). Compared with the catastrophic changes in acute injury states, healthy mitochondria...

Neurocognitive impairments are prevalent in persons seeking treatment for alcohol use disorders (AUDs). These impairments and their physical, social, psychological and occupational consequences vary in severity across persons, much like those resulting from traumatic brain injury; however, due to their slower course of onset, alcohol-related cognitive impairments are often overlooked both within and outside of the treatment setting. Evidence suggests that cognitive impairments can impede treatment goals through their effects on treatment processes. Although some recovery of alcohol-related cognitive impairments often occurs after cessation of drinking (time-dependent recovery), the rate and extent of recovery is variable across cognitive domains and individuals. Following a long hiatus in scientific interest, a new generation of research aims to facilitate treatment process and improve AUD treatment outcomes by directly promoting cognitive recovery (experience-dependent recovery). This review updates knowledge about the nature and course of cognitive and brain impairments associated with AUD, including cognitive effects of adolescent AUD. We summarize current evidence for indirect and moderating relationships of cognitive impairment to treatment outcome, and discuss how advances in conceptual frameworks of brain-behavior relationships are fueling the development of novel AUD interventions that include techniques for cognitive remediation. Emerging evidence suggests that such interventions can be effective in promoting cognitive recovery in persons with AUD and other substance use disorders, and potentially increasing the efficacy of AUD treatments. Finally, translational approaches based on cognitive science, neurophysiology, and neuroscience research are considered as promising future directions for effective treatment development that includes cognitive rehabilitation.

Objective-The authors compared the prevalence and pattern of substance use in undergraduate student athletes and nonathletes from 2005-2006. Participants-Authors collected data from male (n = 418) and female (n = 475) student athletes and nonathletes from [2005][2006]. Methods-The authors administered self-report questionnaires to assess prevalence, quantity, and frequency of alcohol and drug use, and to determine patterns of student athletes' alcohol and drug use during their athletic season versus out of season.Results-Male student athletes were at high risk for heavy drinking and performance-enhancing drug use. Considerable in-season versus out-of-season substance use fluctuations were identified in male and female student athletes.Conclusions-Additional, and possibly alternative, factors are involved in a student athlete's decision-making process regarding drug and alcohol use, which suggests that the development of prevention programs that are specifically designed to meet the unique needs of the college student athlete may be beneficial. Keywordsalcohol; athletics; college students; other drugs; performance-enhancing drugs; sex The use of alcohol and drugs by students is one of the most serious problems facing colleges today. Student athletes may be particularly at risk for substance use-related problems in the college setting due to their unique social environments, the increased physical demands of athletics, and the heightened stress and time constraints placed upon them by fulfilling the dual role of athlete and student. 1,2 Therefore, the college experience of student athletes may be distinct from nonathletes, 2 which raises the question of whether substance use interventions geared toward the general student body are equally effective for college student athletes. 1 In this study, we assessed the prevalence, quantity, and frequency of alcohol and drug use by male and female undergraduate student athletes and nonathletes. We also evaluated patterns of use, such as student athletes' alcohol and drug use during their athletic season versus out of season. Comprehensively assessing the prevalence and patterns of substance use in male and female student athletes and how it differs from nonathletes of the same sex may inform the development of prevention interventions that focus on the specific needs of student athletes.For comments and further information, address correspondence to Dr Helene R. White, Center of Alcohol Studies, Rutgers, the State University of New Jersey, 607 Allison Road, Piscataway, NJ 08854, USA (hewhite@rutgers.edu). NIH Public Access NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author ManuscriptIn the United States, the rates of heavy drinking, tobacco use, and illicit substance use peak between ages 18 and 25 years. 3 This age range coincides with a period of major transition out of high school and, for many, into college. In the college setting, frequent and heavy drinking is common. Using data collected from 5 national surveys, O'Malley and Johnston 4 estimat...

Cognitive recovery in the first 6 weeks of treatment is possible, but, with the possible exception of memory, improvement may be minor in terms of clinical relevance.

Background-Impaired neuropsychological test performance, especially on tests of executive function and attention, is often seen in children diagnosed with autism spectrum disorders (ASD). Structures involved in fronto-striatal circuitry, such as the caudate nucleus, may support these cognitive abilities. However, few studies have examined caudate volumes specifically in children with ASD, or correlated caudate volumes to cognitive ability.