Given the common use of glucocorticoid therapy in children, it is important that physicians and parents recognize the signs of steroid-induced psychosis and are aware of the data on treating this complication.
Background: Many reports have documented the relationship between previous traumatic experiences, including childhood trauma, and the development of later life psychopathology, including posttraumatic stress disorder (PTSD). Identification of individuals at greatest risk for the development of PTSD could lead to preventative interventions. The present study examined the developmental course of PTSD after trauma exposure, using histories of previous traumatic experiences and the severity of the reaction to the trauma as predictors. Methods: Participants (N = 713) were recruited from Emergency Departments in Miami and Atlanta immediately following a traumatic experience. Histories of previous traumatic experiences and the immediate reaction to the new trauma were examined at baseline. Follow-up assessments of PTSD severity were conducted at 1, 3, and 6 months. Results: Histories of child abuse and pre-existing trauma symptoms predicted the immediate response to stress (R 2 = .21, p < .001) and the initial trauma reaction (p < .005).) A mixed-model repeated-measures analysis of variance found that immediate stress response and a history of prior trauma (p < .001) significantly predicted the course of PTSD symptoms. Area under the curve (AUC) analyses suggested that the presence of PTSD at each successive assessment was predicted most substantially by the severity of PTSD at the immediately prior follow-up assessment (AUC > 0.86). Conclusions: The current findings suggest that previous traumatic experiences lead to a greater immediate reaction to trauma and combine to predict the development of PTSD, the maintenance of which is not moderated by these earlier experiences. The identification of people likely to develop PTSD may be aided by the assessment of prior experiences and immediate reactions.
Social cognition (SC) and neurocognition appear to predict different aspects of functional outcome in people with schizophrenia. However, the correlations between performance on these domains have not been tested extensively and compared cross-diagnostically with healthy controls. Further, some social cognitive measures appeared to have potential ceiling effects, particularly for healthy people, in previous research, so increasing their difficulty is of interest. In this paper we report on two studies wherein we examined the correlations between neurocognitive ability and performance on SC tests. In the first study the correlations between measures of social perception, emotion processing, and theory of mind and performance on a brief neuropsychological (NP) assessment were examined in 179 schizophrenia (SCZ) patients and 104 healthy controls (HC). In the second study, we instructed participants to perform a subset of the tasks as rapidly as possible in order to increase task difficulty, and we examined the effects of those instructions on task difficulty, task psychometrics, and correlations between SC and NP tests in 218 SCZ patients and 154 HC. In the first study, both HC and SCZ manifested a domain specific pattern of correlation between NP and SC test performance. Controlling for group differences in NP performance did not eliminate SC performance differences between the groups. In the second study, no differences in task performance, intercorrelations other SC tests, or test-retest stability were induced by the difficulty manipulation in the samples who performed the tasks with speed demands compared to the performance of the previous sample. These data suggest that simple manipulations aimed at increasing task difficulty may not have the desired effect and that despite consistent correlations between SC and NP test performance, impairments in social cognitive functioning are not fully explained by NP performance deficits.
Participants in this trial manifested retest effects on performance-based measures of cognition. Notably, they had minimal prior experience with performance-based assessments. Experiencing the structure and support of a clinical trial may have contributed to significant reductions in subject-reported and clinician-rated PTSD symptom levels. The improvement seen across all assessment domains was consistent with that seen in previous studies where the active treatments separated from placebo. Investigators conducting clinical trials treating PTSD patients should expect placebo effects and design studies accordingly.
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