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Neuroimaging studies of vulnerability to Alcohol Use Disorder (AUD) have identified structural and functional variations which might reflect inheritable features in alcohol-naïve relatives of AUD individuals (FH+) compared to controls having no such family history (FH-). However, prior research did not simultaneously account for childhood maltreatment, any clinically significant disorder and maternal AUD. Therefore, we mainly aimed to investigate the brain structure and reward-related neural activations (fMRI), using whole-brain analysis in FH+ young adults with no prevalent confounders.
Methods:
46 FH+ and 45 FH- male and female participants had no severe childhood maltreatment exposure, neither any psychiatric disorder or AUD, nor a prenatal exposure to maternal AUD. We used a 3 T MRI coupled with a whole brain voxel-based method to compare between groups the grey matter volumes and activations in response to big versus small wins during a Monetary Incentive Delay task. The Childhood Trauma Questionnaire score was used as confounding variable in the analyses to account for the remaining variance between groups.
Results:
Compared to FH- controls, FH+ participants had smaller grey matter volumes in the frontal and cingulate regions as well as in the bilateral nucleus accumbens and right insula. The FH+ participants’ fMRI datasets denoted a blunted activation in the middle cingulum with respect to FH- controls’ during the processing of reward magnitude, and a greater activation in the anterior cingulum in response to anticipation of a small win.
Conclusions:
Family history of alcohol use disorder is linked to structural and functional variations including brain regions involved in reward processes.
Data on psychotropic medications of older patients with schizophrenia spectrum disorder are scarce. Specifically, information about the use of benzodiazepines among older patients with schizophrenia spectrum disorder is very limited. Because benzodiazepine use in older patients has been associated with many disabling side effects, its use in actual practice must be described and questioned. This study aimed at exploring the prevalence of benzodiazepine use and the clinical factors associated with such use among older patients with schizophrenia spectrum disorder.
Methods/Design:
Data from the Cohort of individuals with Schizophrenia Aged 55 years or more (CSA) were used to examine the prevalence of benzodiazepine use among older patients with schizophrenia spectrum disorder. Demographic and clinical characteristics associated with benzodiazepine prescription were also explored.
Results:
The prevalence of benzodiazepine use was 29.8% of older patients with schizophrenia spectrum disorder. These patients were significantly more likely to have medical comorbidities, cognitive and social functioning impairments, to report a lifetime history of suicide attempt, to be institutionalized, and to have been hospitalized in a psychiatric service in the past year compared to those without a benzodiazepine prescription (all p<0.05). There were no between-group differences in schizophrenia severity and psychiatric comorbidity.
Conclusions:
Although it can be hypothesized that benzodiazepine prescription is part of a short-term therapeutic strategy toward patients with more severe trouble or comorbid disorders, our results suggest a strong link between benzodiazepine prescription and a particularly vulnerable subpopulation of older patients with schizophrenia spectrum disorder.
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