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Validation of the emotional Hayling test

The purpose of this systematized review is to review evidence within current peer reviewed literature relating to therapeutic claims of mood regulation including reduction of agitation and aggression, enhancing relaxation, and, improving overall wellbeing.

Supplemental material, sj-docx-1-tpp-10.1177_20451253211045248 for CoMET: a randomised controlled trial of co-commencement of metformin versus placebo as an adjunctive treatment to attenuate weight gain in patients with schizophrenia newly commenced on clozapine by Dan Siskind, Anthony W. Russell, Shuichi Suetani, Dylan Flaws, Steve Kisely, Vikas Moudgil, Korinne Northwood, Gail Robinson, James G. Scott, Terry Stedman, Nicola Warren, Karl Winckel, Peter Cosgrove and Andrea Baker in Therapeutic Advances in Psychopharmacology

The deleted in colorectal cancer (DCC) gene encodes the netrin-1 (NTN1) receptor DCC, a transmembrane protein required for the guidance of commissural axons. Germline DCC mutations disrupt the development of predominantly commissural tracts in the central nervous system (CNS) and cause a spectrum of neurological disorders. Monoallelic, missense, and predicted loss-of-function DCC mutations cause congenital mirror movements, isolated agenesis of the corpus callosum (ACC), or both. Biallelic, predicted loss-of-function DCC mutations cause developmental split brain syndrome (DSBS). Although the underlying molecular mechanisms leading to disease remain poorly understood, they are thought to stem from reduced or perturbed NTN1 signaling. Here, we review the 26 reported DCC mutations associated with abnormal CNS development in humans, including 14 missense and 12 predicted loss-of-function mutations, and discuss their associated clinical characteristics and diagnostic features. We provide an update on the observed genotype-phenotype relationships of congenital mirror movements, isolated ACC and DSBS, and correlate this to our current understanding of the biological function of DCC in the development of the CNS. All mutations and their associated phenotypes were deposited into a locus-specific LOVD (https://databases.lovd.nl/shared/genes/DCC).

Initiation and suppression deficits are documented in patients with frontal lesions although this has typically been with different tasks that are hard to compare. The Hayling Sentence Completion Test (Burgess & Shallice, 1997) was designed to tap initiation, suppression and strategy use within the same sentence completion task. There are few studies specifically investigating the neural correlates of initiation and suppression using the same task in frontal patients. We investigated initiation, suppression and strategy use on the Hayling Test in 40 frontal patients, 30 posterior patients and 40 matched healthy controls. Lesions were analysed with a finer-grained frontal localisation method (Right/Left Lateral, Medial) and traditional methods (i.e., anterior/posterior). We analysed the standard clinical measures (Initiation RT, Suppression RT, Suppression Errors and Overall Score), composite error scores and strategic responses. The results showed that all four Hayling Test clinical measures were sensitive to frontal lesions; however, only Suppression Errors and the Overall measure were specific to frontal lobe damage. All frontal patients produced blatant suppression failures but there was a specific Right Lateral frontal effect for producing subtly incorrect responses. In addition, Right Lateral patients produced fewer correct strategic responses and incurred longer response times in doing so. These findings suggest that the right lateral frontal cortex plays a role in suppression and strategic processes.

Background: Schizophrenia is a highly heritable disorder affecting approximately 1 in 100 people in Australia and worldwide. The emerging picture is of common and rare genetic variants, as well as environmental factors, contributing to risk. One such rare variant is chromosomal microdeletions, especially large rare deletions. However, little is known about how these deletions affect the phenotype and confer risk for schizophrenia. Method: Clinical data (N=633), cognitive data (N=78), and neuroimaging data (VBM, DTI, & fMRI) (N=35) were collected on patients with schizophrenia with existing genetic information available from a large genome-wide association study (GWAS) pertaining to the presence of large, rare deletions and deletion burden in general. Results: Rare deletions were associated with reduced rates of cannabis abuse, later age at onset of psychosis, greater cognitive dysfunction, and structural (VBM and DTI) profiles intermediate to those identified between healthy controls and schizophrenia patients in general. Rare deletions were associated with reduced functional connectivity between prefrontal cortex and striatum and between regions in the default mode network as identified in rs-fMRI. Conclusions: Rare deletions affect the schizophrenia phenotype across clinical, cognitive, and neuroimaging domains, suggesting an important role in the developmental pathway towards psychosis. Further investigation is warranted, especially in larger samples.