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There are known relationships between psychopathology, personality, and executive function (EF), though the association between personality and EF, independent of psychopathology, remains understudied. The present study investigated relationships between Five Factor Model personality traits and indices of response inhibition, sustained attention, and response variability on a continuous performance test (CPT) among 50 healthy adults (male = 27, female = 23; Mage = 19.9 years, range 18–24 years) of primarily Caucasian descent (58.0%). Participants performed an open-source CPT, the Psychology Experiment Building Language Battery Test of Attentional Vigilance (TOAV), and completed self-ratings of conscientiousness, extraversion, and neuroticism on an inventory developed from the public-domain International Personality Item Pool. After controlling for the influences of age, gender, and other personality traits, neuroticism was significantly associated with faster error reaction time and a higher frequency of multiple responses. Neuroticism was also nominally predictive of more frequent commission errors and faster correct and mean reaction time. The present findings indicate that neuroticism is associated with error-prone behavioral performance on a CPT, suggesting that a propensity to experience negative emotions may manifest as impulsivity and hyperactivity on performance-based measures of EF.

Low reward responsiveness (RR) is associated with poor psychological wellbeing, psychiatric disorder risk, and psychotropic treatment resistance. Functional MRI studies have reported decreased activity within the brain's reward network in individuals with RR deficits, however the neurochemistry underlying network hypofunction in those with low RR remains unclear. This study employed ultra-high field Glutamate Chemical Exchange Saturation Transfer (GluCEST) imaging to investigate the hypothesis that glutamatergic deficits within the reward network contribute to low RR. GluCEST images were acquired at 7.0T from 45 participants (ages 15-Users may view, print, copy, and download text and data-mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use:

Temporal lobe epilepsy is associated with impairment in episodic memory. A substantial subgroup, however, is able to maintain adequate memory despite temporal lobe pathology. Missing from prior work in cognitive reorganization is a direct comparison of temporal lobe epilepsy patients with intact status with those who are memory impaired. Little is known about the regional activations, functional connectivities, and/or network reconfigurations that implement changes in primary computations or support functions that drive adaptive plasticity and compensated memory. We utilized task fMRI on 54 unilateral temporal lobe epilepsy patients and 24 matched healthy controls during the performance of a paired associate memory task to address three questions: 1) which regions implement paired associate memory in temporal lobe epilepsy, and do they vary as a function of good versus poor performance, 2) is there unique functional connectivity present during memory encoding that accounts for intact status by preservation of primary memory computations or the supportive computations that allow for intact memory responses, and 3) what features during memory encoding are most distinctive: Is it the magnitude and location of regional activations, or the presence of enhanced functional connections to key structures such as the hippocampus? The study revealed non-dominant hemisphere regions (right posterior temporal regions) involving both increased regional activity and increased modulatory communication with the hippocampi as most important to intact memory in left temporal lobe epilepsy compared to impaired status. The profile involved areas that are neither contralateral homologues to left hemisphere memory areas, nor regions traditionally considered computationally primary for episodic memory. None of these areas of increased activation or functional connectivity were associated with advantaged memory in healthy controls. Our emphasis on different performance levels yielded insight into two forms of cognitive reorganization: Computational primacy, where left temporal lobe epilepsy showed little change relative to healthy controls, and computational support where intact left temporal lobe epilepsy patients showed adaptive abnormalities. The analyses isolated the unique regional activations and mediating functional connectivity that implements truly compensatory reorganization in left temporal lobe epilepsy. The results provided a new perspective on memory deficits by making clear that they arise not just from the knockout of a functional hub, but from the failure to instantiate a complex set of reorganization responses. Such responses provided the computational support to ensure successful memory. We demonstrated that by keeping track of performance levels, we can increase understanding of adaptive brain responses and neuroplasticity in epilepsy.