Severe traumatic brain injury (TBI) leads to physical, neuropsychological, and emotional deficits that interfere with the individual's capacity to return to his or her former lifestyle. This review focuses on social cognition, that is, the capacity to attend to, recognize and interpret interpersonal cues that guide social behavior. Social cognition entails “hot” processes, that is, emotion perception and emotional empathy and “cold” processes, that is, the ability to infer the beliefs, feelings, and intentions of others (theory of mind: ToM) to see their point of view (cognitive empathy) and what they mean when communicating (pragmatic inference). This review critically examines research attesting to deficits in each of these domains and also examines evidence for theorized mechanisms including specific neural networks, the role of simulation, and non-social cognition. Current research is hampered by small, heterogeneous samples and the inherent complexity of TBI pathology. Nevertheless, there is evidence that facets of social cognition are impaired in this population. New assessment tools to measure social cognition following TBI are required that predict everyday social functioning. In addition, research into remediation needs to be guided by the growing empirical base for understanding social cognition that may yet reveal how deficits dissociate following TBI. (JINS, 2013, 19, 1–16)

The object of this study was to evaluate the combined effect of body and facial feedback in adults who had suffered from a severe traumatic brain injury (TBI) to gain some understanding of their difficulties in the regulation of negative emotions. Twenty-four participants with TBI and 28 control participants adopted facial expressions and body postures according to specific instructions and maintained these positions for 10 s. Expressions and postures entailed anger, sadness, and happiness as well as a neutral (baseline) condition. After each expression/posture manipulation, participants evaluated their subjective emotional state (including cheerfulness, sadness, and irritation). TBI participants were globally less responsive to the effects of body and facial feedback than control participants, F(1,50) = 5.89, p = .02, η2 = .11. More interestingly, the TBI group differed from the Control group across emotions, F(8,400) = 2.51, p = .01, η2 = .05. Specifically, participants with TBI were responsive to happy but not to negative expression/posture manipulations whereas control participants were responsive to happy, angry, and sad expression/posture manipulations. In conclusion, TBI appears to impair the ability to recognize both the physical configuration of a negative emotion and its associated subjective feeling. (JINS, 2013, 19, 1–13)

This Short Review critically evaluates three hypotheses about the effects of emotion on memory: First, emotion usually enhances memory. Second, when emotion does not enhance memory, this can be understood by the magnitude of physiological arousal elicited, with arousal benefiting memory to a point but then having a detrimental influence. Third, when emotion facilitates the processing of information, this also facilitates the retention of that same information. For each of these hypotheses, we summarize the evidence consistent with it, present counter-evidence suggesting boundary conditions for the effect, and discuss the implications for future research. (JINS, 2013, 19, 1–9)

Functional magnetic resonance imaging (fMRI) studies have identified consistent age-related changes during various cognitive tasks, such that older individuals display more positive and less negative task-related activity than young adults. Recently, evidence shows that chronic physical exercise may alter aging-related changes in brain activity; however, the effect of exercise has not been studied for the neural substrates of language function. Additionally, the potential mechanisms by which aging alters neural recruitment remain understudied. To address these points, the present study enrolled elderly adults who were either sedentary or physically active to characterize the neural correlates of language function during semantic fluency between these groups in comparison to a young adult sample. Participants underwent fMRI during semantic fluency and transcranial magnetic stimulation to collect the ipsilateral silent period, a measure of interhemispheric inhibition. Results indicated that sedentary older adults displayed reductions in negative task-related activity compared to the active old group in areas of the attention network. Longer interhemispheric inhibition was associated with more negative task-related activity in the right and left posterior perisylvian cortex, suggesting that sedentary aging may result in losses in task facilitatory cortical inhibition. However, these losses may be mitigated by regular engagement in physical exercise. (JINS, 2013, 19, 1–10)

Recently, there has been renewed interest in the study of cognitive fatigue. It is known that fatigue is one of the most disabling symptoms in numerous neurological populations, including stroke, multiple sclerosis, Parkinson's disease, and traumatic brain injury. Behavioral studies of cognitive fatigue are hampered by lack of correlation of self-report measures with objective performance. Neuroimaging studies provide new insight about cognitive fatigue and its neural correlates. Impairment within the cortico-striatal network, involved in effort–reward calculation, has been suggested to be critically related to fatigue. The current review surveys the recent neuroimaging literature, and suggests promising avenues for future research. (JINS, 2013, 19, 1–5)

Postconcussion symptoms (PCS) and functional outcomes were evaluated in 91 OEF/OIF outpatient veterans with reported histories of blast-exposure, with the goal of evaluating (1) the association between these outcomes and a clinical diagnosis of mild traumatic brain injury (mTBI) with or without loss of consciousness (LOC); and (2) the influence of post-traumatic stress disorder (PTSD) and depression on PCS reporting and perceived functional limitations. Individuals who reported mTBI with LOC had greater PCS complaints than individuals who reported mTBI without LOC or individuals without mTBI. However, after adjusting for severity of PTSD and depression symptoms, this group difference disappeared. Functional limitations were particularly prominent in the psychosocial domain. Again, PTSD was significantly associated with functional outcomes, but the mTBI with LOC group had greater psychosocial limitations than the other two groups, even when PTSD and depression symptoms were taken into account. These findings highlight the role of mental health in both outcomes, but additionally point to the impact of mTBI with LOC on long-term psychosocial adjustment. (JINS, 2013, 19, 1–10)

The aim of this study was to determine whether naming difficulties arise in individuals as young as their 50s. Participants of 25–35, 50–59, 60–69, and above 70 years of age were given a picture naming task. To uncover subtle naming difficulties, latencies were analyzed in addition to accuracy. To control whether the expected slower naming latencies could be due to a general slowing affecting all cognitive tasks, participants were also given an odd/even judgment task to assess cognitive processing speed. The results confirmed that participants in their 50s presented decline in naming performance, reflected by an increase in naming latencies, whereas adults in their 60s and their 70s showed both a decrease in accuracy and an increase in latency. Moreover, the increase in naming latencies remained significant even after controlling for odd/even judgment latencies, suggesting a degradation specific to the picture naming task. We assumed that these slower latencies may result from a language-specific impairment. As a further test for language-specific degradation, participants’ semantic capacities were also assessed with a synonym judgment task and the Pyramids and Palm Trees test. The above-70 group showed semantic degradation. The contributions of multiple factors to naming difficulties in aging are discussed. (JINS, 2013, 19, 1–8)

Huntington disease (HD) is associated with decline in cognition and progressive morphological changes in brain structures. Cognitive reserve may represent a mechanism by which disease-related decline may be delayed or slowed. The current study examined the relationship between cognitive reserve and longitudinal change in cognitive functioning and brain volumes among prodromal (gene expansion-positive) HD individuals. Participants were genetically confirmed individuals with prodromal HD enrolled in the PREDICT-HD study. Cognitive reserve was computed as the composite of performance on a lexical task estimating premorbid intellectual level, occupational status, and years of education. Linear mixed effects regression (LMER) was used to examine longitudinal changes on four cognitive measures and three brain volumes over approximately 6 years. Higher cognitive reserve was significantly associated with a slower rate of change on one cognitive measure (Trail Making Test, Part B) and slower rate of volume loss in two brain structures (caudate, putamen) for those estimated to be closest to motor disease onset. This relationship was not observed among those estimated to be further from motor disease onset. Our findings demonstrate a relationship between cognitive reserve and both a measure of executive functioning and integrity of certain brain structures in prodromal HD individuals. (JINS, 2013, 19, 1–12).

Logopenic progressive aphasia (LPA) is a form of primary progressive aphasia (PPA) characterized by hesitant speech with marked impairment in naming and repetition. LPA is associated with brain atrophy in the left temporal and inferior parietal cortices and is predominantly associated with Alzheimer's disease (AD) pathology. In contrast to LPA, “typical” AD is commonly associated with episodic memory disturbance and bilateral medial temporal lobe atrophy. Recent evidence suggests verbal short-term memory is more impaired than visuospatial short-term memory in LPA. This study investigated verbal and visuospatial short-term memory in 12 LPA and 12 AD patients matched for disease severity, and in 12 age- and education-matched healthy controls. Overall, both patient groups showed significantly reduced verbal and visuospatial spans compared with controls. In addition, LPA patients performed significantly worse than AD patients on both forward and backward conditions of the Digit Span task. In contrast, no difference was present between patient groups on either version of the Spatial Span task. Importantly, LPA patients showed better visuospatial than verbal span whereas AD patients and controls did not differ across modality. This study demonstrates the specificity of the short-term memory disturbance in LPA, which arises from a breakdown of the phonological system. (JINS, 2012, 19, 1–7)

Core social interaction behaviors were examined in young children 0–36 months of age who were hospitalized for accidental (n = 61) or inflicted (n = 64) traumatic brain injury (TBI) in comparison to typically developing children (n = 60). Responding to and initiating gaze and joint attention (JA) were evaluated during a semi-structured sequence of social interactions between the child and an examiner at 2 and 12 months after injury. The accidental TBI group established gaze less often and had an initial deficit initiating JA that resolved by the follow-up. Contrary to expectation, children with inflicted TBI did not have lower rates of social engagement than other groups. Responding to JA was more strongly related than initiating JA to measures of injury severity and to later cognitive and social outcomes. Compared to complicated-mild/moderate TBI, severe TBI in young children was associated with less responsiveness in social interactions and less favorable caregiver ratings of communication and social behavior. JA response, family resources, and group interacted to predict outcomes. Children with inflicted TBI who were less socially responsive and had lower levels of family resources had the least favorable outcomes. Low social responsiveness after TBI may be an early marker for later cognitive and adaptive behavior difficulties. (JINS, 2013, 19, 1–11)

Childhood brain tumor survivors are at increased risk for neurocognitive impairments, including working memory (WM) problems. WM is typically assessed using performance measures. Little is known about the value of parent ratings for identifying WM difficulties, the relationship between rater and performance measures, or predictors of parent-reported WM problems in this population. Accordingly, the current study examined the utility of parent report in detecting WM difficulties among childhood brain tumor survivors treated with conformal radiation therapy (n = 50) relative to siblings (n = 40) and solid tumor survivors not receiving central nervous system-directed therapy (n = 40). Parents completed the Behavior Rating Inventory of Executive Function (BRIEF). Participants were administered WM measures (digit span, self-ordered search tasks). Findings revealed parents rated brain tumor survivors as having significantly more WM problems (p < .01) compared to controls. However, the BRIEF-WM scale demonstrated poor sensitivity and specificity for detecting performance-based problems. Significant, albeit modest, correlations were found between the BRIEF-WM scale and performance measures (r = −.24–.22; p < .05) for the combined group. Age at testing, socioeconomic status, and IQ were significant predictors of parent reported WM problems. Rater and performance measures offer complimentary yet different information in assessing WM, which reiterates the importance of using both within the context of clinical assessment. (JINS, 2013, 19, 1–10)

Adolescence is characterized by significant neuromaturation, including extensive cortical thinning, particularly in frontal regions. The goal of this study was to examine the behavioral correlates of neurostructural development in early adolescence. Participants were 185 healthy 12- to 14-year-olds (44% female) recruited from local schools. Participants completed a comprehensive neuropsychological test battery and magnetic resonance imaging session. Cortical surface reconstruction and thickness estimates were performed via FreeSurfer. Age and cortical thickness were negatively correlated in 10 brain regions, 7 of which were in frontal areas (β = −.15 to −.25, ps ≤ .05). Hierarchical linear regressions examined the influence of cortical thickness on working memory, attention, verbal learning and memory, visuospatial functioning, spatial planning and problem solving, and inhibition, controlling for age and intracranial volume. Thinner parietal cortices predicted better performances on tests of verbal learning and memory, visuospatial functioning, and spatial planning and problem solving (β = −.14 to −.24, ps ≤ .05). Age, spanning from 12 to 14 years, accounted for up to 6% of cortical thickness, suggesting substantial thinning during early adolescence, with males showing more accelerated thinning than females between ages 12 and 14. For both males and females, thinner parietal association cortices corresponded with better neurocognitive functioning above and beyond age alone. (JINS, 2013, 19, 1–9)

Previous studies suggest that task-activated functional magnetic resonance imaging (fMRI) can predict future cognitive decline among healthy older adults. The present fMRI study examined the relative sensitivity of semantic memory (SM) versus episodic memory (EM) activation tasks for predicting cognitive decline. Seventy-eight cognitively intact elders underwent neuropsychological testing at entry and after an 18-month interval, with participants classified as cognitively “Stable” or “Declining” based on ≥1.0 SD decline in performance. Baseline fMRI scanning involved SM (famous name discrimination) and EM (name recognition) tasks. SM and EM fMRI activation, along with Apolipoprotein E (APOE) ε4 status, served as predictors of cognitive outcome using a logistic regression analysis. Twenty-seven (34.6%) participants were classified as Declining and 51 (65.4%) as Stable. APOE ε4 status alone significantly predicted cognitive decline (R2 = .106; C index = .642). Addition of SM activation significantly improved prediction accuracy (R2 = .285; C index = .787), whereas the addition of EM did not (R2 = .212; C index = .711). In combination with APOE status, SM task activation predicts future cognitive decline better than EM activation. These results have implications for use of fMRI in prevention clinical trials involving the identification of persons at-risk for age-associated memory loss and Alzheimer's disease. (JINS, 2012, 18, 1–11)