Psychopathy is theorized as a disorder of personality and affective deficits while antisocial personality disorder (ASPD) diagnosis is primarily behaviorally based. While ASPD and psychopathy are similar and are highly comorbid with each other, they are not synonymous. ASPD has been well studied in community samples with estimates of its lifetime prevalence ranging from 1-4% of the general population.4,5 In contrast, psychopathy is almost exclusively investigated within criminal populations so that its prevalence in the general population has been inferred by psychopathic traits rather than disorder (1%). Differences in etiology and comorbidity with each other and other psychiatric disorders of these two disorders are also evident. The current article will briefly review the epidemiology, etiology, and comorbidity of ASPD and psychopathy, focusing predominately on research completed in community and clinical populations. This paper aims to highlight ASPD and psychopathy as related, but distinct disorders.

Background Differences between African Americans and European Americans in the prevalence and age at onset of alcohol use and alcohol use disorder (AUD) have been documented, but distinctions in the timing of early stage transitions and contribution of various psychiatric and psychosocial risk factors to the progression from initiation to AUD have yet to be investigated. The current study characterized progression from alcohol use initiation - defined alternatively as first drink, first intoxication, and regular drinking onset - to AUD in young African American and European American youth. Methods Psychiatric interviews were administered via telephone to 1,461 participants (56% African American, 44% European American) in a high-risk family study (50.3% female, mean age=17.6, SD=3.8). Cox proportional hazards regression analyses were conducted separately for the African American and European American subsamples to predict DSM-5 AUD as a function of age at alcohol use initiation, with age at first drink, age at first intoxication, and age at regular drinking onset as the point of origin in separate models. Results Across race/ethnicity, regardless of how it was measured, early alcohol use initiation predicted AUD, but hazard ratios (HRs) were lowest for first drink. Regular smoking and social anxiety disorder were significant predictors in both racial/ethnic groups but associations with conduct disorder (all 3 models: HR range=2.07–4.15) and major depressive disorder (regular drinking: HR=4.51, CI:1.60–12.69 for AUD onset age ≥20) were specific to African Americans. Posttraumatic stress disorder (HR=5.38, CI:1.44–20.08) and generalized anxiety disorder (HR=7.35, CI:2.31–23.34 for AUD onset ≤age 17) were strongly associated with progression from regular drinking to AUD exclusively in European Americans. Conclusions Early alcohol use initiation is a marker of risk for alcohol use disorder in both African American and European American youth, but the contributions of various psychiatric risk factors to the development of alcohol use disorder are not universal across racial/ethnic groups.

The human saphenous vein preincubated with [3H]noradrenaline was used to determine the pharmacological properties of the release-inhibiting presynaptic serotonin (5-HT) receptor on the sympathetic nerves. The overflow of tritium evoked by transmural electrical stimulation (2 Hz) was concentration-dependently inhibited by drugs known to stimulate 5-HT receptors in the following rank order: oxymetazoline greater than or equal to 5-HT greater than 5-carboxamidotryptamine = 5-methoxytryptamine = sumatriptan greater than tryptamine greater than N,N(CH3)2-5-HT = yohimbine = 8-hydroxy-2-(di-n-propylamino)-tetraline. The potencies of these agonists in inhibiting overflow were significantly correlated with their affinities for 5-HT1B and 5-HT1D binding sites, but not with those for 5-HT1A or 5-HT1C binding sites. 5-Aminotryptamine, methysergide, ipsapirone, cyanopindolol, SDZ 21009 and metergoline dit not produce a significant inhibition. Metitepine and methysergide antagonized the inhibitory effect of 5-HT, whereas spiroxatrine, propranolol, ketanserin and ICS 205-930 did not. These data exclude the idea that the inhibitory presynaptic 5-HT receptor on the sympathetic nerves belongs to the 5-HT2 and 5-HT3 receptor class; the pattern of agonist potencies suggests that the receptor is very similar to the 5-HT1D receptor subtype.

This study assessed the association between racial discrimination and suicidality (ideation, plan, or attempt) in African-American adolescents and young adults (n = 806, mean age = 17.9 years). Structured psychiatric phone interviews were conducted in offspring and their mothers in a high-risk alcoholism family study. Logistic regression analyses using offspring's own racial discrimination as a predictor revealed elevated odds of suicidality, even after adjusting for correlated psychiatric conditions (OR = 1.76) but was reduced to non-significance after adjusting for maternal experiences of racial discrimination (OR = 3.19 in males), depression, and problem drinking. Findings support a link between racial discrimination and suicidality in African-American youth that, for males, is partially explained by maternal racial discrimination.

Sleep disturbance may be the most often endorsed symptom of posttraumatic stress disorder (PTSD). Much of this research is based on subjective reports from trauma survivors; however, objective measures of sleep-related impairment have yielded findings inconsistent with self-report data. More studies investigating subjective and objective assessments concordantly are needed to understand sleep impairment in PTSD. The current study examined PTSD-related sleep disturbance in a female interpersonal violence cohort with full PTSD diagnoses (N = 51) assessing subjective (global and daily diary measures) and objective (actigraphy) sleep measures concurrently. PTSD severity was positively associated with global, subjective reports of sleep impairment and insomnia. Subjective measures of sleep (including global sleep impairment, insomnia, and daily sleep diary reports of total sleep time, sleep efficiency, and sleep onset latency) were moderately to strongly correlated. However, no significant correlations between subjective and objective reports of sleep impairment were found in this cohort. Analyses demonstrated an overall elevation in subjectively reported sleep impairment when compared to objective measurement assessed concurrently. Findings demonstrate a lack of agreement between subjective and objective measurements of sleep in a PTSD-positive female cohort, suggesting objective and subjective sleep impairments are distinct sleep parameters that do not necessarily directly co-vary.