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Background: In scientific literature there are various treatment programs for people with alcohol dependence described, however, are psychosocial factors that promote recovery process described to a limited extent. Purpose: To describe the psychosocial factors that promotes recovery from alcohol dependence. Method: Literature study of ten scientific articles, published between 1999-2011 with both qualitative and quantitative design. Results: According to the literature, the recovery process can be considered to begin when a person with alcohol dependence reached his personal rock bottom. The longer the recovery progresses, the greater are the overall level of performance. Social support is described as an important factor to prevent relapse and reduce the need for professional help. Self-belief and support of self-help groups are described as important to maintaining sobriety. Social support and influence from family members was related to increased ability to analyze and assess their situation during the recovery. Therapeutic alliance and mutual goals are also important factors. Once treatment has been successfully described as a combination of self-motivation and willingness to initiate a radical change in behaviour. Conclusion: Psychosocial factors in the form of supportive relationships appear to promote recovery from alcohol dependence. Other conclusions drawn from this study is limited in scope and compiled by the studies of different design. Further studies need to be implemented in order to draw general conclusions, which can in turn be in support of clinical work.

Scientists have long wondered why some individuals are more sensitive to pain than others. While individual differences in pain have traditionally been discounted due to neuroticism, research has shown that individuals who are more sensitive to pain demonstrate real biological differences in pain perception (Coghill, McHaffie & Yen, 2003). However, individual differences in pain sensitivity remain under-explored in research and clinical settings that can provide further insights into clinical disorders such as addiction. The current research review is interested in examining the link between pain sensitivity and alcohol dependence. Investigating the relationship between pain sensitivity and alcohol addiction prompts many important peripheral questions such as whether increased pain sensitivity can serve as a useful biomarker for alcohol addiction, and how addiction to alcohol can cause changes in sensitivity to pain. Addiction potential or risk for addiction is a research area that is extremely important given that the high rate of addiction in this country is alarmingly high. The literature is sparse on the relationship between hyperalgesia or pain sensitization and risk for alcohol addiction. This literature review synthesizes current relevant research on pain and addiction, as well as addressing possible links between them. / text

Alcoholism is a devastating chronic relapsing disorder with significant costs to individuals and society. The mesolimbic dopamine (DA) system plays an important role in regulating reward and addiction. GABA neurons located in the ventral tegmental area (VTA) regulate VTA DA neuron activity, and are a relevant target for alcohol in the brain. VTA GABA neurons exhibit marked hyperexcitability during withdrawal from ethanol. Past research has demonstrated that the motivational effects of opiates cause a change in VTA GABA(A) receptors in opiate-dependent animals, which switch from a GABA-induced hyperpolarization of GABA neurons to a GABA-induced depolarization. The focus of this study was to characterize excitatory and inhibitory synaptic activity in VTA GABA neurons during withdrawal from acute and chronic alcohol, and to evaluate the function of the GABA(A) receptor in the pathway to dependence. Animals were either given injections of ethanol or saline, or were kept in ethanol vapor or air chambers for three weeks. We used standard whole-cell, perforated patch, and cell-attached mode electrophysiological techniques and pharmacology to obtain recordings of cellular activity. Results for excitatory and inhibitory synaptic events were somewhat mixed and inconclusive. There is evidence for a shift in function of the GABA(A) receptor after exposure to ethanol. We found that after a single injection of ethanol (4.0 g/kg) or a chronic intermittent ethanol vapor exposure, VTA GABA neuron firing rate is less sensitive to muscimol's inhibitory effects. The neural substrates of addiction studied here are important steps in the road to alcohol dependence, and a better understanding of them may lead to novel therapies.

There is growing research evidence and public concern over the burgeoning of disorders which share common features with substance addictions. In order to investigate the presence and role of addiction features in disorders outside of substance addictions, symptoms of addiction were explored within three addiction groups: alcohol dependence (AD), an established addiction (n = 24); pathological gambling (PG) a disorder with growing empirical support as an addiction (n = 20); and compulsive shopping (CS), a proposed 'novel' addiction(n = 20). Participants were recruited from either the general population, or from the Auckland Salvation Army Bridge residential alcohol and drug treatment programme; Salvation Army Oasis Gambling Service; Pacific Peoples Addiction Service Incorporated; or Te Kahui Hauora O Ngati Koata Trust. Participants completed a battery of self-report measures comprising a demographics questionnaire; Addictive Disorder Questionnaire (ADQ); anxiety and depression subscales of the Symptom Checklist 90 Revised (SCL-90R); Barratt Impulsivity Scale II-r; and substance specific adaptations of the Yale-Brown Obsessive Compulsive Scale (Y-BOCS). Three general categories of addiction symptoms: physiological, salience and dyscontrol, were identified as broad aspects of addiction, common across all three groups. Measurable aspects of addiction, including impulsivity, obsessions, anxiety and depression were found to be endorsed similarly across the three addictions, irrespective of the severity of their addiction. Compulsions were found to be higher in the AD group. Higher anxiety was found to be correlated with higher addiction in the behavioural addictions (CS and PG), whereas depression and anxiety were associated with higher addiction severity in the AD group. The results provide support for broadening addiction diagnostic definitions, to be more encompassing of the psychological and physiological experiences of each symptom; and developing different diagnostic categories for non-substance addictions that reflect the severity of the addiction. Results also provide evidence for developmental phases of addiction, from an early 'hedonistic' impulsive phase, to a compulsive phase, in which increased dyscontrol, mood and anxiety, marks the severity of the addiction.

Background: A dysfunctional mesocorticolimbic dopamine system has been reported in alcohol dependence and major depressive disorder. Probing mesocorticolimbic dopamine function in severe depression using dextroamphetamine revealed an altered behavioural response and a disrupted mesocorticolimbic circuitry in behavioural and functional magnetic resonance imaging (fMRI) studies. The purpose of this study was to use a similar approach in alcohol dependence. Behavioural Study: to assess dextroamphetamine subjective effects in alcohol-dependent and depressed alcohol-dependent participants. FMRI Study: to assess how the mesocorticolimbic circuitry would respond to a dextroamphetamine challenge in alcohol-dependent participants exposed to alcohol cues. Methods: In both studies, a single oral 30 mg dose of dextroamphetamine was the pharmacological intervention. Behavioural Study: randomized, double-blind, placebo-controlled, between-subject study. Eighteen alcohol-dependent and 22 depressed alcohol-dependent participants were compared using validated self-report drug effect tools (e.g. Addiction Research Center Inventory). FMRI Study: single-blind, between-subject study. FMRI blood oxygen level–dependent (BOLD) activation was measured in 14 alcohol-dependent and 9 healthy control participants during an alcohol-cue exposure task pre- and post-drug. Results: Behavioural Study: DRUG (F1,40=18.6; p<0.001) and GROUP (F1,40=16.6; p<0.001) main effects but no GROUPxDRUG interaction effects (F1,40=0.02; p=0.88) were detected, even when only severely depressed alcohol-dependent individuals were included (F1,30=0.04; p=0.84). FMRI Study: Alcohol-dependent participants exhibited greater ventral striatal activation compared to controls pre-drug and post-drug effect (F1,40=20.1; z=3.8; p<0.001; k>10; (x=10;y=-2;z=-14)). A GROUPxDRUG interaction effect was detected in the medial orbitofrontal cortex (mOFC) (F1,40=21.5; z=4.0; p<0.001; k>10; (x=-12;y=28;z=-20). The alcohol-dependent group exhibited a negligible mOFC response across both pre- and post-drug scanning sessions. In contrast, controls exhibited attenuation of mOFC response post-drug. Conclusion: The lack of significant GROUPxDRUG interaction effects in the Behavioural Study may suggest different neurobiological mechanisms underlying alcohol dependence and depression mesocorticolimbic dysfunction. Alcohol dependence appeared to mitigate the impact of depression severity on participants’ behavioural responses to dextroamphetamine. The FMRI Study data suggest there may be ventral striatal and mOFC disruption in alcohol-dependent participants. We suggest the mOFC may be involved in the reported loss of prefrontal modulation of dopamine cell activity in alcohol dependence. This supports a key role for the mOFC in mesocorticolimbic dysfunction in alcohol dependence.

Background: A dysfunctional mesocorticolimbic dopamine system has been reported in alcohol dependence and major depressive disorder. Probing mesocorticolimbic dopamine function in severe depression using dextroamphetamine revealed an altered behavioural response and a disrupted mesocorticolimbic circuitry in behavioural and functional magnetic resonance imaging (fMRI) studies. The purpose of this study was to use a similar approach in alcohol dependence. Behavioural Study: to assess dextroamphetamine subjective effects in alcohol-dependent and depressed alcohol-dependent participants. FMRI Study: to assess how the mesocorticolimbic circuitry would respond to a dextroamphetamine challenge in alcohol-dependent participants exposed to alcohol cues. Methods: In both studies, a single oral 30 mg dose of dextroamphetamine was the pharmacological intervention. Behavioural Study: randomized, double-blind, placebo-controlled, between-subject study. Eighteen alcohol-dependent and 22 depressed alcohol-dependent participants were compared using validated self-report drug effect tools (e.g. Addiction Research Center Inventory). FMRI Study: single-blind, between-subject study. FMRI blood oxygen level–dependent (BOLD) activation was measured in 14 alcohol-dependent and 9 healthy control participants during an alcohol-cue exposure task pre- and post-drug. Results: Behavioural Study: DRUG (F1,40=18.6; p<0.001) and GROUP (F1,40=16.6; p<0.001) main effects but no GROUPxDRUG interaction effects (F1,40=0.02; p=0.88) were detected, even when only severely depressed alcohol-dependent individuals were included (F1,30=0.04; p=0.84). FMRI Study: Alcohol-dependent participants exhibited greater ventral striatal activation compared to controls pre-drug and post-drug effect (F1,40=20.1; z=3.8; p<0.001; k>10; (x=10;y=-2;z=-14)). A GROUPxDRUG interaction effect was detected in the medial orbitofrontal cortex (mOFC) (F1,40=21.5; z=4.0; p<0.001; k>10; (x=-12;y=28;z=-20). The alcohol-dependent group exhibited a negligible mOFC response across both pre- and post-drug scanning sessions. In contrast, controls exhibited attenuation of mOFC response post-drug. Conclusion: The lack of significant GROUPxDRUG interaction effects in the Behavioural Study may suggest different neurobiological mechanisms underlying alcohol dependence and depression mesocorticolimbic dysfunction. Alcohol dependence appeared to mitigate the impact of depression severity on participants’ behavioural responses to dextroamphetamine. The FMRI Study data suggest there may be ventral striatal and mOFC disruption in alcohol-dependent participants. We suggest the mOFC may be involved in the reported loss of prefrontal modulation of dopamine cell activity in alcohol dependence. This supports a key role for the mOFC in mesocorticolimbic dysfunction in alcohol dependence.

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