Search for: All records

Despite the well-defined behavioral criteria for posttraumatic stress disorder (PTSD), clinical care is com- plicated by the heterogeneity of biological factors underly- ing impairment. Eye movement tasks provide an opportunity to assess the relationships between aberrant neurobiological function and non-volitional performance metrics that are not dependent on self-report. A recent study using an emotional variant of the antisaccade task demonstrated attentional control biases that interfered with task performance in Veterans with PTSD. Here we present a neuroanatomically-inspired com- putational model based on gated attractor networks that is designed to replicate oculomotor behavior on an affective anti- saccade task. The model includes the putative neural circuitry underlying fear response (amygdala) and top-down inhibitory control (prefrontal cortex), and is capable of generating testable predictions about the causal implications of changes in this circuitry on task performance and neural activation associated with PTSD. Calibrating the model with the results of behavioral and neuroimaging studies on patient populations yields a pattern of connectivity changes characterized by increased amygdala sensitivity and reduced top-down prefrontal control that is consistent with the fear conditioning model of PTSD. In addition, the model makes experimentally verifiable predictions about the consequences of increased prefrontal connectivity associated with cognitive reappraisal training. Keywords: posttraumatic stress disorder, antisaccade task, inhibitory control deficits, attentional bias, cognitive control. 

Abstract Non‐conscious processing of human memory has traditionally been difficult to objectively measure and thus understand. A prior study on a group of hippocampal amnesia (N= 3) patients and healthy controls (N= 6) used a novel procedure for capturing neural correlates of implicit memory using event‐related potentials (ERPs): old and new items were equated for varying levels of memory awareness, with ERP differences observed from 400 to 800 ms in bilateral parietal regions that were hippocampal‐dependent. The current investigation sought to address the limitations of that study by increasing the sample of healthy subjects (N = 54), applying new controls for construct validity, and developing an improved, open‐source tool for automated analysis of the procedure used for equating levels of memory awareness. Results faithfully reproduced prior ERP findings of parietal effects that a series of systematic control analyses validated were not contributed to nor contaminated by explicit memory. Implicit memory effects extended from 600 to 1000 ms, localized to right parietal sites. These ERP effects were found to be behaviorally relevant and specific in predicting implicit memory response times, and were topographically dissociable from other traditional ERP measures of implicit memory (miss vs. correct rejections) that instead occurred in left parietal regions. Results suggest first that equating for reported awareness of memory strength is a valid, powerful new method for revealing neural correlates of non‐conscious human memory, and second, behavioral correlations suggest that these implicit effects reflect a pure form of priming, whereas misses represent fluency leading to the subjective experience of familiarity.