Current drug abuse reviews最新文献

Background: While chronic pain has been said to impact patient's response to methadone maintenance treatment for opioid dependence, the reported findings are inconsistent. These discrepancies may be a direct result of variations in the measurement of chronic pain or definitions of response to methadone treatment. The goal of this study is to evaluate the association between pain and substance use behaviour to determine the real impact of comorbid pain in the methadone population. We also aim to examine sources of variation across the literature with a specific focus on the measurement of pain.

Methods/design: We performed a systematic review using an electronic search strategy across CINAHL, MEDLINE, Web of Science, PsychINFO, EMBASE, and the Cochrane Library including Cochrane Reviews and the Cochrane Central Register of Controlled Trials databases. Title, abstract, as well as full text screening and extraction were performed in duplicate. Studies evaluating the association between chronic pain and methadone maintenance treatment response were eligible for inclusion in this review. Using a sample of 297 methadone patients from the Genetics of Opioid Addiction (GENOA) research collaborative, we assessed the reliability of patient self-reported pain and the validated Brief Pain Inventory (BPI) assessment tool.

Results: After screening 826 articles we identified five studies eligible for full text extraction, of which three showed a significant relationship between the presence of pain and the increase in substance abuse among patients on methadone for the treatment of opioid dependence. Studies varied largely in the definitions and measurement of both pain and response to treatment. Results from our validation of pain measurement in the GENOA sample (n=297) showed the use of a simple self-reported pain question is highly correlated to the use of the BPI. Simply asking patients whether they have pain showed a 44.2% sensitivity, 88.8% specificity, 84.4% PPV and 53.6% NPV to the BPI. The area under the ROC curve was 0.67 and the Pearson χ(2) was 37.3; (p<0.0001).

Discussion: The field of addiction medicine is at a lack of consensus as to the real effect of chronic pain on treatment response among opioid dependent patients. Whether it be the lack of a single "gold standard" measurement of response, or a lack of consistent measurement of pain, it is difficult to summarize and compare the results of these relatively small investigations. In comparison to the BPI, use of the simple self-reported pain has lower sensitivity for identifying patients with pain, suggesting the inconsistencies in these studies may result from differences in pain measurement. Future validation studies of pain measurement are required to address the predictive value of self-reported pain.

Given the large availability of nicotinic acetylcholine receptors (nAChRs) throughout the brain, and the wide range of neurotransmitter systems affected (norepinephrine, serotonin and dopamine), nicotine influences a wide variety of cognitive domains such as sensorial, motor, attention, executive function, learning and memory. This article reviews current state of the art research on the effects of nicotine upon cognition. There are different neurobiological mechanisms involved in acute/chronic smoking and nicotine abstinence. Smoking reinforcement could be due to the initial cognitive improvement, that is, individuals can learn that smoking temporarily increases cognitive functioning (improving some components of attention and memory). These acute nicotine effects improve (i) cognitive performance above smokers' normal levels, and (ii) cognitive disruption resulting from nicotine abstinence. Both neurobiological effects act as reinforcers to nicotine use, greatly contributing to the development of nicotine dependence. However, heavy smoking is associated with cognitive impairment and cognitive decline in middle age. Future clinical research should investigate the role of positive and negative cognitive effects of nicotine in smoking cessation treatment. This is clearly an important scientific issue, with insufficient current data from which to draw definitive conclusions.

Background: Laterality of brain activation is reported for tests of risk factors of addiction- impulsivity and craving-but authors rarely address the potential significance of those asymmetries.

Objective: The purpose of this study is to demonstrate this laterality and discuss its relevance to cognitive and neurophysiological asymmetries associated with drug abuse vulnerability in order to provide new insights for future research in drug abuse.

Method: From published reports, brain areas of activation for two tests of response inhibition or craving for drugs of abuse were compiled from fMRI activation peaks and were tabulated for eight sections (octants) in each hemisphere. Percent asymmetries were calculated (R-L/R+L) across studies for each area.

Results: For impulsivity, most activation peaks favored the right hemisphere. Overall, the percent difference was 32% (Χ2 = 16.026; p < 0.0001) with the greater asymmetry for anterior peaks (46.8%; Χ(2) = 17.329; p < 0.0001). The asymmetries for cue-induced craving were opposite, favoring the left hemisphere by 6.7% (Χ(2) = 4.028; p < 0.05). The consistency of left asymmetry was found for almost all drugs. For nicotine, studies where subjects were not allowed to smoke (deprived) prior to measurement had the same left hemisphere activation but those who smoked (satiated) before the fMRI measure showed right asymmetry.

Conclusion: Brain activation studies demonstrate different left/right hemispheric contributions for impulsivity versus craving-factors related to addiction. Failure to take laterality into consideration is a missed opportunity in designing studies and gaining insight into the etiology of drug abuse and pathways for treatment.

The literature on the two main models of addiction (dopamine-based positive reinforcement and stress-based negative reinforcement models) have made many important contributions to understanding this brain disorder. However, rarely has there been a comprehensive critique of the limitations of both models. This article seeks to resolve theoretical issues inherent to each model, as well as propose a more comprehensive psycho-neuro-endocrinological theory of addiction which reconciles important elements of both. We suggest that there is not only direct interaction of dopaminergic and stress systems throughout the addiction cycle, from initial use, via the abusing stage, to the endpoint of addiction, but that this interaction is present prior to initial use. A combination of genetic factors and/or experiences of adversity may result in a stress-triggered sensitisation of dopaminergic networks which is present before the onset of substance use, which cannot be explained solely in terms of dopaminergic (positive) reinforcement. Rather these processes are best explained by an allostatic model which reconciles aspects of both models of addiction and shows how dopamine/stress interactions become increasingly pathological in the addiction cycle. Our model suggests that chronic stress eventually creates baseline hypodopaminergic activity, but also prompts dopaminergic hyperactivity in cue reactivity. This is the neural marker of allostatic mechanisms observed at endpoint addiction. We propose a multi-circuit explanation of how this cumulative effect of stress increasingly impacts on dopaminergic networks of reward, affect, attention, memory and behavioural control. This revised model provides a useful frame of reference for further research and ultimately clinical practice.

Background: The most robust neurocognitive effect of marijuana use is memory impairment. Memory deficits are also high among persons living with HIV/AIDS, and marijuana is the most commonly used drug in this population. Yet research examining neurocognitive outcomes resulting from co-occurring marijuana and HIV is limited.

Objective: The primary objectives of this comprehensive review are to: (1) examine the literature on memory functioning in HIV-infected individuals; (2) examine the literature on memory functioning in marijuana users; (3) synthesize findings and propose a theoretical framework to guide future research.

Method: PubMed was searched for English publications 2000-2013. Twenty-two studies met inclusion criteria in the HIV literature, and 23 studies in the marijuana literature.

Results: Among HIV-infected individuals, memory deficits with medium to large effect sizes were observed. Marijuana users also demonstrated memory problems, but results were less consistent due to the diversity of samples.

Conclusion: A compensatory hypothesis, based on the cognitive aging literature, is proposed to provide a framework to explore the interaction between marijuana and HIV. There is some evidence that individuals infected with HIV recruit additional brain regions during memory tasks to compensate for HIV-related declines in neurocognitive functioning. Marijuana is associated with disturbance in similar brain systems, and thus it is hypothesized that the added neural strain of marijuana can exhaust neural resources, resulting in pronounced memory impairment. It will be important to test this hypothesis empirically, and future research priorities are discussed.

Up to now, there is no adequate definition of the alcohol hangover. The purpose of the current study was to develop a useful definition, and consensus among those who will use it in scientific publications. A survey was conducted among N=1099 social drinkers who recently had a hangover. They were asked to provide their definition of the alcohol hangover. Text mining and content analysis revealed 3 potential definitions. These were submitted to members of the Alcohol Hangover Research Group, who were asked to give their expert opinion on the proposed definitions. Taking into account their comments and suggestions, the following definition for the alcohol hangover was formulated: "The alcohol hangover refers to the combination of mental and physical symptoms, experienced the day after a single episode of heavy drinking, starting when blood alcohol concentration approaches zero."

High impulsivity in children with attention deficit/hyperactivity disorder (ADHD) plays a key role in their vulnerability to substance abuse disorders (SUDs). Although impulsivity is increasingly recognized as a multidimensional construct, efforts to describe the contribution of different impulsivity aspects to the development of SUD have been hindered by conceptual and experimental inconsistencies. This review seeks to map potential trajectories from childhood ADHD to SUD by examining the hypothesized mediating role of three different impulsivity-related constructs: disinhibition, impulsive choice, and sensation seeking. Integration of data from developmental, cognitive, and neurophysiological research suggests that childhood ADHD and SUD are both associated with behavioural and neurophysiological deficits in all three impulsivity-related constructs. Examination of brain mechanisms related to the three impulsivity-related constructs indicates that ADHD share neurophysiological deficits with SUD, such as abnormal brain activity in areas involved in inhibition and complex cognitive-emotional processes. We conclude that different impulsivity constructs operate independently and interact with each other to affect adult risk taking behaviour and SUD in patients with childhood ADHD. This review highlights the current theoretical and methodological challenges in the study of impulsivity and discusses clinical implications and directions for future research.

Ethanol is the most abused psychoactive substance. Accordingly to World Health Organization ethanol ranks among the top five risk factors for disease, disability and death (3.3 million/year) throughout the world. This manuscript highlights and critically analyses clinical and forensic signs related to hepatoxicity of ethanol that may lead to suspected of abuse. Namely, steatosis, jaundice, cirrhosis, hemorrhoids, esophageal varices caput medusae, ascites, petechiae, ecchymoses, splenomegaly, hemochromatosis, xanthelasma, nutritional deficiency, testicular atrophy, gynecomastia and dilated congestive cardiomyopathy are discussed and related to the toxic mechanism of ethanol.