Tagged: Biological Psychiatry

Ventral striatal-hippocampus coupling during reward processing as a (stratification) biomarker for psychotic disorders

Altered ventral striatal (vST) activation to reward expectancy is a well-established intermediate phenotype for psychiatric disorders, specifically schizophrenia. Preclinical research suggests that striatal alterations are related to a reduced inhibition by the hippocampal formation but its role in human transdiagnostic reward-network dysfunctions is not well understood.

Top-down control of appetite

The understanding of the neural control of appetite sheds light into the pathogenesis of eating disorders, such as anorexia nervosa and obesity. Both diseases are a result of maladaptive eating behaviors (overeating or undereating) and associated with life-threatening health problems. The fine regulation of appetite involves genetic, physiological and environmental factors which are detected and integrated in the brain by specific neuronal populations. For centuries, the hypothalamus has been the center of attention in the scientific community as a key regulator of appetite.

Longitudinal Changes of Local Field Potential Oscillations in Nucleus Accumbens and Anterior Limb of the Internal Capsule in Obsessive-Compulsive Disorder

Anterior limb of the internal capsule (ALIC) deep brain stimulation (DBS) shows stable efficacy in refractory obsessive-compulsive disorder (OCD) (1). Recently, several DBS connectivity studies in OCD have investigated the effect of DBS on the structural and functional connectivity in the nucleus accumbens (NAc) and ALIC (2–5). For electrophysiological effects, we attempt to examine the local effects of effective DBS in the NAc/ALIC by long-term recording the local field potentials (LFPs) in a case of OCD.

Does TBI Cause Risky Substance Use or Substance Use Disorder?

There is a high co-occurrence of risky substance use among adults with traumatic brain injury (TBI), although it is unknown if the neurological sequelae of TBI can promote this behavior. We propose that to conclude TBI can cause risky substance use, it must be determined that TBI precedes risky substance use, that confounders with the potential to increase the likelihood of both TBI and risky substance use must be ruled out, and that there must be a plausible mechanism of action. In this review, we address these factors by providing an overview of key clinical and preclinical studies, and list...

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