Acute stressors and clinical characteristics differentiate death by suicide, accident, or natural causes among illicit and prescription opiate users.

BACKGROUND: Opiate misuse has reached epidemic levels. Prevention efforts depend on distinguishing opiate users from abusers. The current study compared opioid users who died by natural cases, accidents, and suicide using psychological autopsy methods. Groups were compared on substance use characteristics, treatment history, experiences of negative life events, and circumstances at the time of death. METHODS: Substance use and suicide risk were evaluated using psychological autopsy methods in 63 decedents with positive toxicology for opiates at death divided into three groups: adults dying by suicide (n = 19), accident (n = 19), and natural causes (n = 25). Groups were compared on several dependent measures, using chi-square analyses to examine categorical variables and one-way analyses of variance (ANOVA) to examine continuous variables. RESULTS: Individuals who died by suicide were similar in many ways to adults who died by an accidental overdose. However, suicide completers were more likely to have struggled with severe depression, and previously attempted suicide, whereas the accidental overdose sample was more likely to display a chronic pattern of severe drug abuse. CONCLUSIONS: The current study helps to distinguish between opiate users who are at risk for death by an accidental or intentional overdose. In the ongoing opiate crisis, clinicians must understand the risk of overdose and the nuances of accidental behaviors compared to purposeful ones. Signs of suicidal planning, relevant psychopathology, and ongoing life stress may be useful points of intervention for stopping the increasing number of deaths among opiate users.

Acute change in anterior cingulate cortex GABA, but not glutamine/glutamate, mediates antidepressant response to citalopram.

Little is known about the acute effects of antidepressant treatments on brain glutamate and gamma-amino-butyric acid (GABA) levels, and their association with clinical response. Using proton magnetic resonance spectroscopy (1H-MRS) we examined longitudinally the effects of citalopram on glutamine/glutamate ratios and GABA levels in the pregenual anterior cingulate cortex (pgACC) of individuals with major depressive disorder (MDD). We acquired 1H-MRS scans at baseline and at days 3, 7, and 42 of citalopram treatment in nineteen unmedicated individuals with MDD. Ten age- and sex-matched non-depressed comparison individuals were scanned once. The association between 1) baseline metabolites and 2) change in metabolites from baseline to each time point and clinical response (change in Montgomery-Åsberg Depression Rating Scale (MADRS) score from baseline to day 42) was assessed by longitudinal regression analysis using generalized estimating equations. Contrary to our hypotheses, no significant associations emerged between glutamate metabolites and clinical response; however, greater increases (or smaller decreases) in pgACC GABA levels from baseline to days 3 and 7 of citalopram treatment were significantly associated with clinical response. These findings suggest that an acute change in GABA levels in pgACC predicts, and possibly mediates, later clinical response to citalopram treatment in individuals with MDD.

REDUCED DISGUST PROPENSITY IS ASSOCIATED WITH IMPROVEMENT IN CONTAMINATION/WASHING SYMPTOMS IN OBSESSIVE-COMPULSIVE DISORDER.

OBJECTIVES: Disgust is a well-established phenomenon with known neurobiological correlates. However, it remains unclear how or whether disgust changes with clinical treatment, because few longitudinal studies have tracked the association of disgust vulnerability and clinical symptoms in patient populations. METHODS: We assessed disgust propensity and symptoms of obsessive-compulsive disorder (OCD) in 134 patients receiving intensive residential treatment for OCD. Using linear regression with adjustment for age, sex, and depression severity, we tested the association between change in disgust propensity and change in OCD symptoms from admission to discharge. RESULTS: Change in disgust propensity was significantly associated with improvement in contamination/washing symptoms (ß = 0.25 [95% confidence interval: 0.11-0.39]; P = .001). No significant association was found between change in disgust propensity and change in other OCD symptom dimensions. CONCLUSIONS: In patients with OCD undergoing intensive residential treatment, disgust propensity appears to improve in parallel with contamination/washing symptoms.

An Examination of Rostral Anterior Cingulate Cortex Function and Neurochemistry in Obsessive-Compulsive Disorder.

The anterior cingulate cortex is implicated in the neurobiology of obsessive-compulsive disorder (OCD). However, few studies have examined functional and neurochemical abnormalities specifically in the rostral subdivision of the ACC (rACC) in OCD patients. We used functional magnetic resonance imaging (fMRI) during an emotional counting Stroop task and single-voxel J-resolved proton magnetic resonance spectroscopy ((1)H-MRS) in the rACC to examine the function and neurochemistry of the rACC in individuals with OCD and comparison individuals without OCD. Between-group differences in rACC activation and glutamine/glutamate ratio (Gln/Glu), Glu, and Gln levels, as well as associations between rACC activation, Gln/Glu, Glu, Gln, behavioral, and clinical measures were examined using linear regression. In a sample of 30 participants with OCD and 29 age- and sex-matched participants without OCD, participants with OCD displayed significantly reduced rACC deactivation compared with those without OCD in response to OCD-specific words versus neutral words on the emotional counting Stroop task. However, Gln/Glu, Glu, and Gln in the rACC did not differ between groups nor was there an association between reduced rACC deactivation and Gln/Glu, Glu, or Gln in the OCD group. Taken together, these findings strengthen the evidence for rACC dysfunction in OCD, but weigh against an underlying association with abnormal rACC glutamatergic neurotransmission.