ObjectivePsychiatry is a low-risk specialisation; however, there is a steady increase in malpractice claims against psychiatrists. Defensive psychiatry (DP) refers to any action undertaken by a psychiatrist to avoid malpractice liability that is not for the sole benefit of the patient's mental health and well-being. The objectives of this study were to assess the scope of DP practised by psychiatrists and to understand whether awareness of DP correlated with defensive behaviours.MethodsA questionnaire was administered to 213 Israeli psychiatry residents and certified psychiatrists during May and June 2015 regarding demographic data and experience with malpractice claims, medicolegal literature and litigation. Four clinical scenarios represented defensive behaviours and reactions (feelings and actions) to malpractice claims.ResultsForty-four (20.6%) certified psychiatrists and four (1.9%) residents were directly involved in malpractice claims, while 132 (62.1%) participants admitted to practising DP. Residents acknowledged the practice of DP more than did senior psychiatrists (p=0.038).Awareness of DP correlated with unnecessary hospitalisation of suicidal patients, increased unnecessary follow-up visits and prescribing smaller drug dosages than required for pregnant women and elderly patients.ConclusionsThis study provides evidence that DP is well established in the routine clinical daily practice of psychiatrists. Further studies are needed to reveal whether DP effectively protects psychiatrists from malpractice suits or, rather, if it impedes providing quality psychiatric care and represents an economic burden that leads to more harm for the patient.

Schizophrenia is a common, severe and debilitating psychiatric disorder. Despite extensive research there is as yet no biological marker that can aid in its diagnosis and course prediction. This precludes early detection and intervention. Imaging studies suggest brain volume loss around the onset and over the first few years of schizophrenia, and apoptosis has been proposed as the underlying mechanism. Cell-free DNA fragments (cfDNA) are released into the bloodstream following cell death. Tissue-specific methylation patterns allow the identification of the tissue origins of cfDNA. We developed a cocktail of brain specific DNA methylation markers, and used it to assess the presence of brain-derived cfDNA in the plasma of patients with a first psychotic episode. We detected significantly elevated neuron- (p=0.0013), astrocyte- (p=0.0016), oligodendrocyte- (p=0.0129) and whole brain-derived (p=0.0012) cfDNA in the plasma of patients during their first psychotic episode (n=29), compared with healthy controls (n=31). Increased cfDNA levels were not correlated with psychotropic medications use. Area Under the Curve (AUC) was 0.77, with 65% sensitivity at 90% specificity in patients with a psychotic episode. Potential interpretations of these findings include increased brain cell death, disruption of the blood-brain barrier or a defect in clearance of material from dying brain cells. Brain-specific cfDNA methylation markers can potentially assist early detection and monitoring of schizophrenia and thus allow early intervention and adequate therapy.

Objective STriatal-Enriched protein tyrosine Phosphatase (STEP) is a brain-specific member of the PTP family that has been implicated in learning and memory. In this study, we examined the association of the PTPN5 (protein-tyrosine-phosphatase non-receptor 5) gene, which encodes for STEP, with both schizophrenia and cognitive functioning in the Israeli Jewish population. Methods A 868 subjects schizophrenia (SZ) case-control study was performed (286 cases and 582 controls). Eleven STEP tagging SNPs were selected, and single markers and haplotypes association analyses were performed. A cognitive variability study included 437 healthy females who completed a computerized cognitive battery. We performed univariate associations between the SNPs and cognitive performance. The possible functional role of these variants was examined by studying their association with gene expression levels in the brain. Results In the SZ study, we found nominal association in the whole sample between rs4075664 and SZ. SZ males showed a more significant association for 3 SNPs (rs4075664, rs2278732, rs4757710). Haplotypes of the studied SNPs were associated with SZ both in the overall sample and within the male sub-sample. Expression analysis provided some support for the effects of the associated SNPs on PTPN5 expression level. The cognitive variability study showed positive associations between PTPN5 SNPs and different cognitive subtests. Principal component analysis demonstrated an “Attention Index” neurocognitive component that was associated with two SNP pairs (rs10832983*rs10766504 and rs7932938*rs4757718). Conclusion The results imply a model in which PTPN5 may play a role in normal cognitive functioning and contributes to aspects of the neuropathology of schizophrenia.

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