Anterior insula lesions and alexithymia reduce the endorsements of everyday altruistic attitudes.

Neuroimaging studies have reported a large network of brain regions involved in altruism. However, these studies are unable to determine if these regions are necessary for altruistic attitudes. Here, we examined the brain-basis of everyday altruistic attitudes ([Self-Report Altruism Scale]; e.g., helping a stranger with car troubles) and potential factors (i.e., alexithymia [Toronto Alexithymia Scale] such as empathic concern [Interpersonal Reactivity Index]) that may moderate this relationship. We carried out whole-brain voxel-based lesion-symptom mapping and region of interest analyses to study a large sample of patients (n = 130) with penetrating traumatic brain injuries. Our results showed that the effect of anterior insula (AI) lesions was moderated by alexithymia, but not empathic concern. The presence of AI lesions, as well as increased alexithymia, were associated with fewer endorsements of resource-costly altruistic attitudes. Empathic concern was positively correlated with endorsements of resource-costly altruistic attitudes. Taken together, our study provides direct evidence that the AI and alexithymia play crucial roles in everyday altruistic attitudes and reinforces the importance of the emotional experience in altruism.

Language and alexithymia: Evidence for the role of the inferior frontal gyrus in acquired alexithymia.

The clinical relevance of alexithymia, a condition associated with difficulties identifying and describing one's own emotion, is becoming ever more apparent. Increased rates of alexithymia are observed in multiple psychiatric conditions, and also in neurological conditions resulting from both organic and traumatic brain injury. The presence of alexithymia in these conditions predicts poorer regulation of one's emotions, decreased treatment response, and increased burden on carers. While clinically important, the aetiology of alexithymia is still a matter of debate, with several authors arguing for multiple 'routes' to impaired understanding of one's own emotions, which may or may not result in distinct subtypes of alexithymia. While previous studies support the role of impaired interoception (perceiving bodily states) in the development of alexithymia, the current study assessed whether acquired language impairment following traumatic brain injury, and damage to language regions, may also be associated with an increased risk of alexithymia. Within a sample of 129 participants with penetrating brain injury and 33 healthy controls, neuropsychological testing revealed that deficits in a non-emotional language task, object naming, were associated with alexithymia, specifically with difficulty identifying one's own emotions. Both region-of-interest and whole-brain lesion analyses revealed that damage to language regions in the inferior frontal gyrus was associated with the presence of both this language impairment and alexithymia. These results are consistent with a framework for acquired alexithymia that incorporates both interoceptive and language processes, and support the idea that brain injury may result in alexithymia via impairment in any one of a number of more basic processes.

Machiavellian tendencies increase following damage to the left dorsolateral prefrontal cortex.

Machiavellianism - a personality trait that is characterized by a tendency to distrust, deceive and exploit others - has been the focus of growing attention in psychological research. Neuroimaging studies of Machiavellianism highlight the influence of the dorsolateral prefrontal cortex (dlPFC) on Machiavellianism tendencies. However, knowledge regarding the causal role of the left and right dlPFC on Machiavellianism is still obscure. Here, we measured general Machiavellian tendencies, as well as two subscales (i.e., Machiavellian Views and Machiavellian Tactics) in a large sample of brain-injured patients (N = 129) and non-brain-injured control participants (N = 37) to determine whether Machiavellianism tendencies can be altered by brain damage. We analyzed Machiavellianism tendencies as a function of lesion location, with patients separated into four groups based on dlPFC damage: left dlPFC damage, right dlPFC damage, non-dlPFC damage, and healthy controls. We found that left dlPFC damage increased Machiavellianism in general, and Machiavellian perspective (views) in particular, but did not modulate behavior (tactics). Critically, left dlPFC damage predicted higher levels of Machiavellianism after controlling for general and emotional intelligence, linguistic abilities, empathy and psychopathology. These findings establish a causal role of the left dlPFC in modulating Machiavellian views, and indicate that one can hold Machiavellian views without necessarily endorsing Machiavellian tactics.

Impaired Valuation Leads to Increased Apathy Following Ventromedial Prefrontal Cortex Damage.

Apathy is defined by reduced goal-directed behavior, and is common in patients with damage to the ventromedial prefrontal cortex (vmPFC). Separately, in neuroeconomics research, the vmPFC has been shown to play a role in reward processing-namely, in "stimulus valuation," or the computation of the subjective reward value of a stimulus. Here, we used a sample of patients with focal brain lesions (N = 93) and matched healthy controls (N = 21) to determine whether the association between vmPFC damage and increased apathy is driven by impaired valuation. An auction task was used to measure valuation, and apathy was assessed via caregiver ratings of patients' day-to-day behavior. Lesion-symptom mapping identified the locus of impaired valuation in the vmPFC, and patients with damage to this region demonstrated increased apathy relative to patients with damage to dorsomedial prefrontal cortex (dmPFC), patients with damage to other brain regions, and healthy controls. Critically, the association between vmPFC damage and apathy was mediated by impaired valuation, with no effect as a function of dmPFC damage. Our results implicate a valuation-based mechanism underlying the relationship between vmPFC integrity and apathy, bridging findings from both the clinical literature and neuroeconomics research.

Networks underlying trait impulsivity: Evidence from voxel-based lesion-symptom mapping.

Impulsivity is considered a multidimensional construct that encompasses a range of behaviors, including poor impulse control, premature decision-making, and the inability to delay gratification. In order to determine the extent to which impulsivity and its components share a common network, a voxel-based lesion-symptom mapping (VLSM) analysis was performed in a large sample of patients (N = 131) with focal, penetrating traumatic brain injuries (pTBI). Impulsivity was assessed using the Barratt Impulsiveness Scale (BIS-11), a standard self-report measure that allows for unique estimates of global impulsivity and its factor analysis-derived components (e.g., "motor impulsivity"). Heightened global impulsivity was associated with damage to multiple areas in bilateral prefrontal cortex (PFC), left superior, middle and inferior temporal gyrus, and left hippocampus. Moreover, a cluster was identified within the left PFC associated specifically with motor impulsivity (defined as "acting without thinking"). The results were consistent with the existing literature on bilateral prefrontal cortical involvement in behavioral impulsivity, but also provided new evidence for a more complex neuroanatomical representation of this construct, characterized by left-lateralized temporal and hippocampal involvement, as well as a left-lateralized prefrontal network specifically associated with motor impulsivity. Hum Brain Mapp 38:656-665, 2017. © 2016 Wiley Periodicals, Inc.

Brain Regions Influencing Implicit Violent Attitudes: A Lesion-Mapping Study.

Increased aggression is common after traumatic brain injuries and may persist after cognitive recovery. Maladaptive aggression and violence are associated with dysfunction in the prefrontal and temporal cortex, but such dysfunctional behaviors are typically measured by explicit scales and history. However, it is well known that answers on explicit scales on sensitive topics--such as aggressive thoughts and behaviors--may not reveal true tendencies. Here, we investigated the neural basis of implicit attitudes toward aggression in humans using a modified version of the Implicit Association Task (IAT) with a unique sample of 112 Vietnam War veterans who suffered penetrating brain injury and 33 healthy controls who also served in combat in Vietnam but had no history of brain injury. We hypothesized that dorsolateral prefrontal cortex (dlPFC) lesions, due to the crucial role of the dlPFC in response inhibition, could influence performance on the IAT. In addition, we investigated the causal contribution of specific brain areas to implicit attitudes toward violence. We found a more positive implicit attitude toward aggression among individuals with lesions to the dlPFC and inferior posterior temporal cortex (ipTC). Furthermore, executive functions were critically involved in regulating implicit attitudes toward violence and aggression. Our findings complement existing evidence on the neural basis of explicit aggression centered on the ventromedial prefrontal cortex. These findings highlight that dlPFC and ipTC play a causal role in modulating implicit attitudes about violence and are crucially involved in the pathogenesis of aggressive behavior. SIGNIFICANCE STATEMENT: Maladaptive aggression and violence can lead to interpersonal conflict and criminal behavior. Surprisingly little is known about implicit attitudes toward violence and aggression. Here, we used a range of techniques, including voxel-based lesion-symptom mapping, to examine the causal role of brain structures underpinning implicit attitudes toward aggression in a unique sample of combat veterans with traumatic brain injury. We found that damage to the dorsolateral prefrontal cortex (dlPFC) led to a more positive implicit attitude toward violence that under most normal situations would be considered inappropriate. These results suggest that treatments aimed at increasing cognitive control using cognitive behavioral therapies dependent on the intact dlPFC could treat aggressive and violent behavior.

The effect of claustrum lesions on human consciousness and recovery of function.

Crick and Koch proposed that the claustrum plays a crucial role in consciousness. Their proposal was based on the structure and connectivity of the claustrum that suggested it had a role in coordinating a set of diverse brain functions. Given the few human studies investigating this claim, we decided to study the effects of claustrum lesions on consciousness in 171 combat veterans with penetrating traumatic brain injuries. Additionally, we studied the effects of claustrum lesions and loss of consciousness on long-term cognitive abilities. Claustrum damage was associated with the duration, but not frequency, of loss of consciousness, indicating that the claustrum may have an important role in regaining, but not maintaining, consciousness. Total brain volume loss, but not claustrum lesions, was associated with long-term recovery of neurobehavioral functions. Our findings constrain the current understanding of the neurobehavioral functions of the claustrum and its role in maintaining and regaining consciousness.

White and gray matter contributions to executive function recovery after traumatic brain injury.

OBJECTIVE: We investigated the association between regional white and gray matter volume loss and performance on executive functions (EFs) in patients with penetrating traumatic brain injury (pTBI). METHODS: We studied 164 pTBI patients and 43 healthy controls from the Vietnam Head Injury Study. We acquired CT scans for pTBI patients and divided them according to lesion localization (left and right prefrontal cortex [PFC]). We administered EF tests (Verbal Fluency, Trail Making, Twenty Questions) and used voxel-based lesion symptom mapping (VLSM) and group-based correlational and multiple regression analyses to examine the relative influence of gray and white matter lesions on EF recovery. RESULTS: The VLSM analysis revealed that white and gray white matter lesions were associated with impaired EFs. In the left PFC lesion group, damage to the PFC gray matter, anterior corona radiata, and superior longitudinal fasciculus (SLF) were most correlated with functional recovery. Verbal Fluency, which involves a broad fronto-temporo-parietal network, was best predicted by SLF lesion volume. Trail Making and Twenty Questions, which is associated with more focal left frontal damage, was better predicted by PFC lesions. CONCLUSIONS: Our results indicated that white matter volume loss can be a superior predictor of recovery and a crucial factor driving clinical outcome in functions involving a broad network such as Verbal Fluency. White matter damage may place additional burden on recovery by deteriorating signal transmission between cortical areas within a functional network.

The neural bases for devaluing radical political statements revealed by penetrating traumatic brain injury.

Given the determinant role of ventromedial prefrontal cortex (vmPFC) in valuation, we examined whether vmPFC lesions also modulate how people scale political beliefs. Patients with penetrating traumatic brain injury (pTBI; N = 102) and healthy controls (HCs; N = 31) were tested on the political belief task, where they rated 75 statements expressing political opinions concerned with welfare, economy, political involvement, civil rights, war and security. Each statement was rated for level of agreement and scaled along three dimensions: radicalism, individualism and conservatism. Voxel-based lesion-symptom mapping (VLSM) analysis showed that diminished scores for the radicalism dimension (i.e. statements were rated as less radical than the norms) were associated with lesions in bilateral vmPFC. After dividing the pTBI patients into three groups, according to lesion location (i.e. vmPFC, dorsolateral prefrontal cortex [dlPFC] and parietal cortex), we found that the vmPFC, but not the dlPFC, group had reduced radicalism scores compared with parietal and HC groups. These findings highlight the crucial role of the vmPFC in appropriately valuing political behaviors and may explain certain inappropriate social judgments observed in patients with vmPFC lesions.

Lesion mapping of social problem solving.

Accumulating neuroscience evidence indicates that human intelligence is supported by a distributed network of frontal and parietal regions that enable complex, goal-directed behaviour. However, the contributions of this network to social aspects of intellectual function remain to be well characterized. Here, we report a human lesion study (n = 144) that investigates the neural bases of social problem solving (measured by the Everyday Problem Solving Inventory) and examine the degree to which individual differences in performance are predicted by a broad spectrum of psychological variables, including psychometric intelligence (measured by the Wechsler Adult Intelligence Scale), emotional intelligence (measured by the Mayer, Salovey, Caruso Emotional Intelligence Test), and personality traits (measured by the Neuroticism-Extraversion-Openness Personality Inventory). Scores for each variable were obtained, followed by voxel-based lesion-symptom mapping. Stepwise regression analyses revealed that working memory, processing speed, and emotional intelligence predict individual differences in everyday problem solving. A targeted analysis of specific everyday problem solving domains (involving friends, home management, consumerism, work, information management, and family) revealed psychological variables that selectively contribute to each. Lesion mapping results indicated that social problem solving, psychometric intelligence, and emotional intelligence are supported by a shared network of frontal, temporal, and parietal regions, including white matter association tracts that bind these areas into a coordinated system. The results support an integrative framework for understanding social intelligence and make specific recommendations for the application of the Everyday Problem Solving Inventory to the study of social problem solving in health and disease.

Genetic polymorphisms and traumatic brain injury: the contribution of individual differences to recovery.

Recovery after Traumatic Brain Injury (TBI) is variable, even for patients with similar severity of brain injury. Recent research has highlighted the contribution that genetic predisposition plays in determining TBI outcome. This review considers the potential for genetic polymorphisms to influence recovery of cognitive and social processes following TBI. Limitations and considerations that researchers should make when assessing the potential impact of polymorphisms on TBI outcome are also discussed. Understanding the genetic factors that support neuroplasticity will contribute to an understanding of the variation in outcome following injury and help to identify potential targets for rehabilitation.

Cognitive decline in older adults with a history of traumatic brain injury.

Traumatic brain injury (TBI) is an important public health problem with potentially serious long-term neurobehavioural sequelae. There is evidence to suggest that a history of TBI can increase a person's risk of developing Alzheimer's disease. However, individuals with dementia do not usually have a history of TBI, and survivors of TBI do not invariably acquire dementia later in life. Instead, a history of traumatic brain injury, combined with brain changes associated with normal ageing, might lead to exacerbated cognitive decline in older adults. Strategies to increase or maintain cognitive reserve might help to prevent exacerbated decline after TBI. Systematic clinical assessment could help to differentiate between exacerbated cognitive decline and mild cognitive impairment, a precursor of Alzheimer's disease, with important implications for patients and their families.

Genetic polymorphisms influence recovery from traumatic brain injury.

Traumatic brain injury (TBI) is a major public health concern in both civilian and military populations. Recently, genetics studies have begun to identify individual differences in polymorphisms that could affect recovery and outcome of cognitive and social processes following TBI. This review considers the potential for polymorphisms to influence six specific cognitive and social functions, which represent the most prominent domains of impairment following TBI: working memory, executive function, decision making, inhibition and impulsivity, aggression, and social and emotional function. Examining the influence of polymorphisms on TBI outcome has the potential to contribute to an understanding of variations in TBI outcome, aid in the triaging and treatment of TBI patients, and ultimately lead to targeted interventions based on genetic profiles.