Search

Recent studies demonstrate that veterans exhibit higher suicide risk compared with the general U.S. population. A prior suicide attempt is a well-documented predictor of suicide death. Despite increased attention to clinical risk factors of suicide and efforts to develop psychosocial interventions to reduce suicide risk, the underlying biological factors that confer this risk are not well understood. This study examined affect-modulated startle (AMS) during a series of intermixed unpleasant, neutral, and pleasant pictures in a sample of 108 demographically-matched veterans at low (passive ideators: n = 26) and high risk (active ideators: n = 29; single attempters: n = 28; and multiple attempters: n = 25) for suicide based on the Columbia Suicide Severity Rating Scale. An exploratory aim involved a longitudinal component in a subset of the high-risk sample that went on to participate in a randomized 6-month clinical trial. We investigated whether baseline AMS predicts a subsequent suicide attempt at 12-month follow-up. Compared with the other three groups, multiple attempters showed greater startle potentiation during unpleasant pictures and deficient overall startle habituation from early to later trials. The groups did not differ in startle during neutral or pleasant pictures, or self-reported picture valence. Greater startle during unpleasant pictures was associated with greater emotion dysregulation as measured by the Difficulties in Emotion Regulation Scale and a future suicide attempt assessed prospectively at 12-month follow-up. These findings suggest that startle potentiation during unpleasant pictures in multiple-suicide attempters is a promising psychophysiological biomarker of suicide risk and underscore the clinical importance of targeting emotion dysregulation in the treatment of patients at-risk for suicide.

A model for personality dysfunction posits an interaction between inherited susceptibility and environmental factors such as childhood trauma. Core biological vulnerabilities in personality include dimensions of affective instability, impulsive aggression, and cognition/perceptual domains. For the dimension of impulsive aggression, often seen in borderline personality disorder (BPD), the underlying neurobiology involves deficits in central serotonin function and alterations in specific brain regions in the cingulate and the medial and orbital prefrontal cortex. The role of trauma in the development of personality disorder and especially for BPD remains unclear. Although recent studies suggest that BPD is not a trauma-spectrum disorder and that it is biologically distinct from posttraumatic stress disorder, high rates of childhood abuse and neglect do exist for individuals with personality dysfunction. Personality symptom clusters seem to be unrelated to specific abuses, but they may relate to more enduring aspects of interpersonal and family environments in childhood. Whereas twin and family studies indicate a partially heritable basis for impulsive aggression, studies of serotonin-related genes to date suggest only modest contributions to behavior. Gene-environment interactions involving childhood maltreatment are demonstrated in recent studies on antisocial behaviors and aggressive rhesus monkeys and highlight the need for further research in this important area.

To assess the relationship between two phenotypes in an extremely well-characterized population of personality disorder patients–impulsive aggression and prolactin response to fenfluramine–and tryptophan hydroxylase (TPH) genotype, TPH genotype (at an intronic polymorphic site) and prolactin response to fenfluramine were assessed in 40 Caucasian patients with personality disorder. Impulsive aggression was assessed by using the Buss-Durkee Hostility Inventory (BDHI). Twenty-one male patients with the “LL” genotype had higher BDHI scores than men with the “UL” or the “UU” genotype. No relationship between genotype and prolactin response to fenfluramine was found. It was concluded that impulsive-aggressive behavior in male personality disorder patients may be associated with the TPH genotype. Am. J. Med. Genet. (Neuropsychiatr. Genet.) 81:13–17, 1998. © 1998 Wiley-Liss, Inc.