Current drug abuse reviews最新文献

Objective: To discuss the role of substance-related and addictive disorders (SRAD) that lead patients with attention-deficit hyperactivity disorder (ADHD) to suicide and homicide.

Method: Relevant articles were searched via PubMed using several keywords related to this issue. Most of the articles included in this review were published after 2000.

Results: Patients with ADHD often fall into crises of catastrophic life events such as suicide or homicide. SRAD play an important role in leading ADHD patients to such events. Because ADHD is characterized by inattentiveness and impulsivity, any kinds of substances, legal or illegal, can deteriorate ADHD symptoms, leading ADHD patients to such catastrophic events. There are several pathways that connect ADHD with SRAD, which are roughly divided into two ways: internalizing mental disorders and externalizing mental disorders. The former includes depression and anxiety disorders characterized by self-inhibition or withdrawal. The latter typically includes conduct disorder or oppositional defiant disorder, as well as antisocial personality disorder, characterized by aggressive or antisocial behaviors or emotions towards others. These comorbid psychiatric disorders are apt to lead ADHD patients to SRAD, and once these patients suffer from SRAD, risk of catastrophic life events seems to increase due to the irreversibility of their adverse mentality. Comorbid mental disorders with ADHD can act, at least partially, as mediators from ADHD to SRAD.

Conclusion: SRAD can be a critical risk factor of suicide and homicide among patients with ADHD. Early interventions for families with ADHD and psychiatric comorbidities may work as effective preventive strategies against such events.

Background: People commonly use psychoactive substances to increase physical and psychological pleasure. Neuroadaptations in the brain's reward system coupled with changes in social functioning and networking resulting from chronic substance use impede the ability to derive pleasure from non-substance related activities.

Objective: We elucidate and validate the hypothesis that treatments for substance use disorders would potentially have a stronger and broader impact by helping recipients to experience pleasure as part of an expansive focus of increasing adaptive functioning, well-being, and personal fulfillment and actualization.

Method: We have organized and integrated relatively sparse and disparate theory and research to describe a multi-stage model linking pleasure and substance use. We review research on pleasure in the context of treatment for substance use, and describe future research directions.

Results: Our model integrates several independent research programs with prominent theories and models of substance dependence that together provide evidence that pleasure, or lack thereof, is a risk or protective factor for initiating, escalating and maintaining substance use and substance use disorders. Pleasure is an overlooked but potentially high-yield target of existing evidence-based treatments.

Conclusion: Research is needed to investigate the relation between pleasure and substance use, and existing and newly developed treatments that have the potential to increase pleasure. By increasing pleasure such treatments have the potential to help recipients to live fuller and richer lives. Integration of pleasure into existing treatments has compelling transdiagnostic implications for individuals at any point along a substance use severity continuum.

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: 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.

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.