Prolonged fasting impairs neural reactivity to visual stimulation.

Previous literature has shown that hypoglycemia influences the intensity of the BOLD signal. A similar but smaller effect may also be elicited by low normal blood glucose levels in healthy individuals. This may not only confound the BOLD signal measured in fMRI, but also more generally interact with cognitive processing, and thus indirectly influence fMRI results. Here we show in a placebo-controlled, crossover, double-blind study on 40 healthy subjects, that overnight fasting and low normal levels of glucose contrasted to an activated, elevated glucose condition have an impact on brain activation during basal visual stimulation. Additionally, functional connectivity of the visual cortex shows a strengthened association with higher-order attention-related brain areas in an elevated blood glucose condition compared to the fasting condition. In a fasting state visual brain areas show stronger coupling to the inferior temporal gyrus. Results demonstrate that prolonged overnight fasting leads to a diminished BOLD signal in higher-order occipital processing areas when compared to an elevated blood glucose condition. Additionally, functional connectivity patterns underscore the modulatory influence of fasting on visual brain networks. Patterns of brain activation and functional connectivity associated with a broad range of attentional processes are affected by maturation and aging and associated with psychiatric disease and intoxication. Thus, we conclude that prolonged fasting may decrease fMRI design sensitivity in any task involving attentional processes when fasting status or blood glucose is not controlled.

Desvenlafaxine for the acute treatment of depression: a systematic review and meta-analysis.

INTRODUCTION: Desvenlafaxine, the active metabolite of venlafaxine, was approved in 2008 by the FDA for the treatment of depression. The aim of the present review is to provide an overview of the existing trials with desvenlafaxine and assess its overall efficacy and tolerability. METHODS: We searched in PubMed, EMBASE and the Cochrane Library for eligible studies (double-blind randomized control trials). A random effects model was used for the estimation of effect sizes. RESULTS: 17 trials were found in total. In the placebo-controlled trials the overall risk ratio for response was 1.24 (1.16-1.32, p<0.001), for remission 1.29 (1.16-1.43, p<0.001), for dropouts 1.16 (0.99-1.35, p=0.066) and for dropouts due to adverse events 1.98 (1.45-2.69, p<0.001). There were no differences between the various doses that were used (i. e., 50 mg, 100 mg, 200 mg, 400 mg). The mean risk ratio for response in the head-to-head trials was 0.90 (0.82-0.98, p=0.014) and for remission 0.82 (0.71-0.95, p=0.009). DISCUSSION: The risk ratios for response and remission were moderate. We further provide some evidence that desvenlafaxine might not be as efficacious as other antidepressants.

Reversible Amisulpride-induced Elevation of Creatine Kinase (CK): A Case Series from the German AMSP Pharmacovigilance Project.

The elevation of creatine kinase (CK) levels without neuroleptic malignant syndrome has been reported for several antipsychotics. We present here 4 cases with CK elevation induced by amisulpride, which have been registered for the German pharmacovigilance project, Arzneimittelsicherheit in der Psychiatrie (AMSP). The magnitude of the CK elevation ranged between 1, 498 IU/L and 21,018 IU/L. All 4 patients reported myalgia. In each case CK returned to normal after amisulpride discontinuation. In the fourth case, fluids were administered intravenously in order to prevent acute renal failure. None of the cases showed deterioration of renal function. Finally, we present recommendations for clinical practice.

In a sweet mood? Effects of experimental modulation of blood glucose levels on mood-induction during fMRI.

Glucose is the primary source of energy for the human brain. Previous literature has shown that varying blood glucose levels may have a strong impact on behaviour, subjective mood, and the intensity of the BOLD signal measured in fMRI. Therefore, blood glucose levels varying even within the normal range may interact with cognitive and emotional processing as well as BOLD signal. Here, in a placebo-controlled, double-blind crossover study on 20 healthy women, we show that overnight fasting, compared to an elevated glucose condition, influences brain activation and the affective state during mood induction. Results indicate that our brain may compensate for low glucose levels during fasting by stronger recruitment of the brain areas relevant to the task at hand. Additionally, we systematically tested the effect of prior cognitive effort on behavioural and neural patterns and found that elevated activation is only associated with maintained performance as long as no prior cognitively challenging task is administered. Prior cognitive effort leads to deteriorated performance and a further increase in emotion-associated brain activation in the pregenual anterior and posterior cingulate, the superior frontal gyrus, and the pre-SMA. These results are in line with the strength model of self-regulation. Our results corroborate the strength model of self-regulation and extend it to affect regulation processes. Additionally, our observations suggest that experimentally controlling for fasting state or glucose levels may be beneficial, especially when studying processes that involve self-regulation.