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Dialectical behaviour therapy is superior to usual treatment in reducing high-risk behaviours in patients with BPD.

BackgroundPrescription opioid use is highly associated with risk of opioid-related death, with 1 of every 550 chronic opioid users dying within approximately 2.5 years of their first opioid prescription. Although gabapentin is widely perceived as safe, drug-induced respiratory depression has been described when gabapentin is used alone or in combination with other medications. Because gabapentin and opioids are both commonly prescribed for pain, the likelihood of co-prescription is high. However, no published studies have examined whether concomitant gabapentin therapy is associated with an increased risk of accidental opioid-related death in patients receiving opioids. The objective of this study was to investigate whether co-prescription of opioids and gabapentin is associated with an increased risk of accidental opioid-related mortality.Methods and findingsWe conducted a population-based nested case–control study among opioid users who were residents of Ontario, Canada, between August 1, 1997, and December 31, 2013, using administrative databases. Cases, defined as opioid users who died of an opioid-related cause, were matched with up to 4 controls who also used opioids on age, sex, year of index date, history of chronic kidney disease, and a disease risk index. After matching, we included 1,256 cases and 4,619 controls. The primary exposure was concomitant gabapentin use in the 120 days preceding the index date. A secondary analysis characterized gabapentin dose as low (<900 mg daily), moderate (900 to 1,799 mg daily), or high (≥1,800 mg daily). A sensitivity analysis examined the effect of concomitant nonsteroidal anti-inflammatory drug (NSAID) use in the preceding 120 days. Overall, 12.3% of cases (155 of 1,256) and 6.8% of controls (313 of 4,619) were prescribed gabapentin in the prior 120 days. After multivariable adjustment, co-prescription of opioids and gabapentin was associated with a significantly increased odds of opioid-related death (odds ratio [OR] 1.99, 95% CI 1.61 to 2.47, p < 0.001; adjusted OR [aOR] 1.49, 95% CI 1.18 to 1.88, p < 0.001) compared to opioid prescription alone. In the dose–response analysis, moderate-dose (OR 2.05, 95% CI 1.46 to 2.87, p < 0.001; aOR 1.56, 95% CI 1.06 to 2.28, p = 0.024) and high-dose (OR 2.20, 95% CI 1.58 to 3.08, p < 0.001; aOR 1.58, 95% CI 1.09 to 2.27, p = 0.015) gabapentin use was associated with a nearly 60% increase in the odds of opioid-related death relative to no concomitant gabapentin use. As expected, we found no significant association between co-prescription of opioids and NSAIDs and opioid-related death (OR 1.11, 95% CI 0.98 to 1.27, p = 0.113; aOR 1.14, 95% CI 0.98 to 1.32, p = 0.083). In an exploratory analysis of patients at risk of combined opioid and gabapentin use, we found that 46.0% (45,173 of 98,288) of gabapentin users in calendar year 2013 received at least 1 concomitant prescription for an opioid. This study was limited to individuals eligible for public drug coverage in Ontario, we were only able to identify prescriptions reimbursed b...

Aims Neurocognitive functions in pathological gambling have relevance for the aetiology and treatment of this disorder, yet are poorly understood. This study therefore investigated neurocognitive impairments of executive functions in a group of carefully screened Diagnostic and Statistical Manual version IV (DSM-IV-TR) pathological gamblers. Performance was compared to a group of normal control participants. To study the specificity of these neurocognitive deficits, a substance dependence group (alcohol dependence) and an impulse control disorder group (Tourette syndrome) were included. Design Cross-sectional study. Setting Addiction and general mental health treatment centres. Participants Forty-nine pathological gamblers, 48 abstinent alcohol-dependent patients, 46 participants with Tourette syndrome and 49 normal control participants. Measurements A comprehensive neuropsychological battery measuring executive functions as well as basic cognitive functions. Findings Both the pathological gambling and the alcohol dependent groups were characterized by diminished performance on inhibition, time estimation, cognitive flexibility and planning tasks. The Tourette syndrome group showed deficits only on inhibition tasks. Basic cognitive functions were intact in all clinical groups. Comorbid attention deficit hyperactivity disorder, antisocial personality disorder and nicotine dependence influenced the impaired functions of the clinical groups only minimally. Conclusions Carefully screened groups of pathological gamblers and alcohol dependents were characterized by diminished executive functioning, suggesting a dysfunction of frontal lobe circuitry in these disorders. The resemblance between the pathological gambling group and the alcohol dependence group suggests a common neurocognitive aetiology for these disorders. Psychosocial treatment of these disorders could benefit from assessing and targeting deficits in executive functions, as they probably influence the course of these disorders negatively.

Little is known about the underlying neural mechanism of deep brain stimulation (DBS). We found that DBS targeted at the nucleus accumbens (NAc) normalized NAc activity, reduced excessive connectivity between the NAc and prefrontal cortex, and decreased frontal low-frequency oscillations during symptom provocation in patients with obsessive-compulsive disorder. Our findings suggest that DBS is able to reduce maladaptive activity and connectivity of the stimulated region.

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In this article, by reviewing the psychological, psychophysiological, neurobiological, and psychopharmacological literature on craving for alcohol, it is argued that converging evidence from several disciplines suggests a three-pathway psychobiological model of craving. Essential to this model is the appreciation of the role of individual differences in affect regulation strategies or personality styles, conditionability, sensitivity to alcohol's effects, and related dysregulations in distinct neural circuitries or neurotransmitter systems. These factors are of crucial importance to a proper understanding of the nature of craving, its underlying mechanisms and different manifestations. As a first pathway, it is suggested that reward craving or desire for the rewarding, stimulating and/or enhancing effects of alcohol might result from either dopaminergic/opioidergic dysregulation or a personality style characterized by reward seeking or a combination of both. As a second pathway, it is suggested that relief craving or desire for the reduction of tension or arousal might result from either gamma-aminobutyric acid (GABA)ergic/glutamatergic dysregulation or a personality style characterized by stress reactivity or a combination of both. Obsessive craving, the result of the third pathway, can be defined as lack of control over intrusive thoughts about drinking resulting in impaired functioning. This type of craving might result either from a serotonin deficiency or a personality style characterized by low constraint or disinhibition or a combination of both. The putative implications of this three-pathway model for the assessment of alcohol craving, diagnosis and treatment of alcoholism, and future research on craving, are discussed.