The Val158Met polymorphism of the catechol-O-methyltransferase (COMT) gene may be related to individual differences in cognition, likely via modulation of prefrontal dopamine catabolism. However, the available studies have yielded mixed results, possibly in part because they do not consistently account for other genes that affect cognition. We hypothesized that COMT Met allele homozygosity, which is associated with higher levels of prefrontal dopamine, would predict better executive function as measured using standard neuropsychological testing, and that other candidate genes might interact with COMT to modulate this effect. Participants were 95 healthy, right-handed adults who underwent genotyping and cognitive testing. COMT genotype predicted executive ability as measured by the Trail-Making Test, even after covarying for demographics and Apolipoprotein E (APOE), brain-derived neurotrophic factor (BDNF), and ankyrin repeat and kinase domain containing 1 (ANKK1) genotype. There was a COMT-ANKK1 interaction in which individuals having both the COMT Val allele and the ANKK1 T allele showed the poorest performance. This study suggests the heterogeneity in COMT effects reported in the literature may be due in part to gene–gene interactions that influence central dopaminergic systems. (JINS, 2011, 17, 1–7)

Theory of Mind (ToM) is the ability to attribute independent mental states to self and others to explain and predict behavior. Impairment of ToM is well established in developmental pathologies. In neurological populations, investigation of ToM is still rare but data suggest that ToM impairment could contribute to behavioral and social disturbances. In addition to neurological signs, multiple sclerosis (MS) presents with disorders of cognition and behavior directly related to brain damage. The aim of this study was to assess ToM abilities and recognition of facial emotional expression in adults with MS. We compared 64 patients with relapsing MS and 30 matched healthy controls on three levels of ToM tasks, a facial emotion recognition task, and a neuropsychological assessment. MS patients performed significantly worse than controls in emotion recognition and all ToM tasks (p < .02). These deficits were not correlated with demographic variables or neuropsychological test performance. These findings underscore the importance of assessing ToM and facial recognition in MS, as dysfunction in these areas may impact upon social interaction and, thus, impair quality of life for both patients with MS and their families. (JINS, 2011, 17, 1122–1131)

(JINS, 2011, 17, 751–752)

Difficulty in inhibition or cognitive control is a common and significant sequela of pediatric traumatic brain injury (TBI). The present study used functional MRI to examine one specific inhibitory function, interference control, in 11 adolescents, aged 12–16 years, (mean age, 15.7 years) with TBI who were at least 1 year postinjury and 11 age-matched typically developing control participants (TC) (mean age, 15.2 years). Participants completed a Counting Stroop task with 2 main conditions: (1) a neutral condition requiring the counting of animal words and (2) an interference condition in which mismatched number words were counted. Both TBI and TC adolescents activated similar networks of brain regions relevant to interference control, but the TBI group showed higher levels of activation relative to the TC group in multiple brain areas within this network, including predominantly right frontal and parietal regions. Findings of greater activation of the relevant neural network in the TBI group are consistent with recent fMRI findings using other interference control paradigms with individuals with a history of TBI. (JINS, 2011, 17, 000–000.)

A growing body of literature has documented evidence for emotion labeling (EL) deficits after traumatic brain injury (TBI); however, long-term effects of TBI on EL abilities, particularly among young children, are unclear. We investigated EL abilities and socio-emotional outcomes in 32 children with moderate–severe TBI, 23 with complicated-mild TBI, and 82 children with orthopedic injuries (OI), shortly after injury and at 18 months post-injury. All children were between 3:0 and 6:11 years of age at the time of injury. Repeated measures analyses indicated that all groups showed improved EL performance between acute and 18-month assessments, but that the moderate–severe TBI group improved at a slower rate than the OI group, so that the two groups showed significantly different performance at 18 months. Emotion labeling ability did not significantly contribute to the prediction of socio-emotional outcomes after controlling for pre-injury functioning. These results provide preliminary evidence of emerging EL deficits after early childhood TBI that are related to injury severity but that do not predict social and behavioral outcomes. (JINS, 2011, 17, 1132–1142)

The current pilot study examined functional magnetic resonance imaging (fMRI) activation in children with mild traumatic brain injury (mTBI) during tasks of working memory and inhibitory control, both of which are vulnerable to impairment following mTBI. Thirteen children with symptomatic mTBI and a group of controls completed a version of the Tasks of Executive Control (TEC) during fMRI scanning. Both groups showed greater prefrontal activation in response to increased working memory load. Activation patterns did not differ between groups on the working memory aspects of the task, but children with mTBI showed greater activation in the posterior cerebellum with the addition of a demand for inhibitory control. Children with mTBI showed greater impairment on symptom report and “real world” measures of executive functioning, but not on traditional “paper and pencil” tasks. Likewise, cognitive testing did not correlate significantly with imaging results, whereas increased report of post-concussive symptoms were correlated with increased cerebellar activation. Overall, results provide some evidence for the utility of symptom report as an indicator of recovery and the hypothesis that children with mTBI may experience disrupted neural circuitry during recovery. Limitations of the study included a small sample size, wide age range, and lack of in-scanner accuracy data. (JINS, 2011, 17, 1143–1152)

Both HIV and aging impact performance on neuropsychological testing; however, evidence for differences between HIV effects in younger compared to older subjects (interaction effects) is limited and the findings have been inconsistent. Coexisting morbidities that contribute to cognitive impairment in HIV include those not directly referable to infection, per se, and are more prevalent with advancing age, increasing the likelihood that HIV and age effects may be largely independent. As individuals survive with HIV into geriatric age groups, greater clarity on these relationships is essential. We present cross-sectional data from a large (n = 450) cohort designed to analyze HIV, age, and interaction effects using a well-matched cohort of HIV-negative individuals. Results reveal limited evidence for interaction effects between HIV and age on neuropsychological performance. We conclude that older age does not significantly influence neuropsychological performance among HIV patients when seronegative controls are largely composed of individuals from a similar socioeconomic background. (JINS, 2011, 17, 1–6)

Hemi-spatial neglect can manifest in both the horizontal and radial spatial plane. However, debate exists over how closely the two forms of neglect relate. Here we compared the ability of a neglect patient to bisect stimuli in horizontal versus radial orientation. When oriented horizontally, single lines were mis-bisected to the right, yet when surrounded by visual distracters, the lines were mis-bisected to the left. A leftward bias also emerged when horizontally aligned strings of symbols were bisected. Unexpectedly, an analogous pattern of bias appeared when the stimuli were bisected in radial orientation; stimuli that induced a leftward bias now induced a proximal bias, while stimuli that induced a rightward bias induced a distal bias. Spontaneous reversals in radial bias have not been previously reported, and given that they were coupled with the horizontal reversals, suggest that the spatial boundaries of horizontal and radial neglect are strongly constrained by common stimulus configurations. (JINS, 2011, 17, 943–947)

Clustering and switching strategies during phonemic and semantic verbal fluency tasks as defined by Troyer et al. (1997), Abwender et al. (2001), and Lanting et al. (2009) were compared using archival data to determine which scoring procedures best differentiate healthy older adults (n = 26) from individuals with early-stage Alzheimer's disease (AD, n = 26). Total word production showed the largest group difference, especially for semantic fluency. The AD group produced fewer switches when compared to the healthy control group, whereas the groups did not differ in cluster size. The AD group also accessed fewer novel semantic subcategories, presumably due to reduced access to semantic memory storage rather than lower processing speed. Clustering and switching scores on the phonemic task did not add information above total words produced, consistent with previous research indicating these variables are most informative in relation to semantic fluency. (JINS, 2011, 17, 1153–1157)

Sustained volitional attention and working memory capacity was examined for the first time in people with Friedreich ataxia (FRDA). We administered subtests of the Test of Everyday Attention to 16 individuals with molecularly confirmed FRDA and gender-, age-, and IQ-matched controls. Clinically significant impairment in working memory and sustained volitional attention was evident. Working memory deficits correlated significantly with GAA repeat number on the shorter allele of the FXN gene, and separately, with disease severity, as measured by the Friedreich Ataxia Rating Scale score. Sustained volitional attention was not correlated with disease parameters, suggesting that this impairment may not be related to the disease process in a simple way. The deficits observed may be the result of disruption to corticocerebellar pathways, or directly related to the cortical and/or cerebellar pathology evident in people with FRDA. (JINS, 2011, 17, 000–000)