Social cognition and traumatic brain injury: current knowledge

Background: Many patients with moderate to severe traumatic brain injury have deficits in social cognition. Social cognition refers to the ability to perceive, interpret, and act upon social information. Few studies have investigated the effectiveness of treatment for impairments of social cognition in patients with traumatic brain injury. Moreover, these studies have targeted only a single aspect of the problem. They all reported improvements, but evidence for transfer of learned skills to daily life was scarce. We evaluated a multifaceted treatment protocol for poor social cognition and emotion regulation impairments (called T-ScEmo) in patients with traumatic brain injury and found evidence for transfer to participation and quality of life. Purpose: In the current paper, we describe the theoretical underpinning, the design, and the content of our treatment of social cognition and emotion regulation (T-ScEmo). Theory into practice: The multifaceted treatment that we describe is aimed at improving social cognition, regulation of social behavior and participation in everyday life. Some of the methods taught were already evidence-based and derived from existing studies. They were combined, modified, or extended with newly developed material. Protocol design: T-ScEmo consists of 20 one-hour individual sessions and incorporates three modules: (1) emotion perception, (2) perspective taking and theory of mind, and (3) regulation of social behavior. It includes goal-setting, psycho-education, function training, compensatory strategy training, self-monitoring, role-play with participation of a significant other, and homework assignments. Recommendations: It is strongly recommended to offer all three modules, as they build upon each other. However, therapists can vary the time spent per module, in line with the patients’ individual needs and goals. In future, development of e-learning modules and virtual reality sessions might shorten the treatment.

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Independent contributions of social cognition and depression to functional status after moderate or severe traumatic brain injury

Neuropsychological Rehabilitation ◽

10.1080/09602011.2020.1749675 ◽

2020 ◽

pp. 1-17 ◽

Cited By ~ 2

Author(s):

Umesh M. Venkatesan ◽

Katie Lancaster ◽

Jean Lengenfelder ◽

Helen M. Genova

Keyword(s):

Traumatic Brain Injury ◽

Social Cognition ◽

Brain Injury ◽

Functional Status ◽

Severe Traumatic Brain Injury

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The mentalizing network and theory of mind mediate adjustment after childhood traumatic brain injury

Social Cognitive and Affective Neuroscience ◽

10.1093/scan/nsaa006 ◽

2019 ◽

Vol 14 (12) ◽

pp. 1285-1295 ◽

Cited By ~ 1

Author(s):

Kristen R Hoskinson ◽

Erin D Bigler ◽

Tracy J Abildskov ◽

Maureen Dennis ◽

H Gerry Taylor ◽

...

Keyword(s):

Traumatic Brain Injury ◽

Executive Function ◽

Social Cognition ◽

Brain Injury ◽

Theory Of Mind ◽

Psychosocial Adjustment ◽

Right Hemisphere ◽

Brain Networks ◽

The United States ◽

Severe Tbi

Abstract Childhood traumatic brain injury (TBI) affects over 600 000 children per year in the United States. Following TBI, children are vulnerable to deficits in psychosocial adjustment and neurocognition, including social cognition, which persist long-term. They are also susceptible to direct and secondary damage to related brain networks. In this study, we examine whether brain morphometry of the mentalizing network (MN) and theory of mind (ToM; one component of social cognition) mediates the effects of TBI on adjustment. Children with severe TBI (n = 15, Mage = 10.32), complicated mild/moderate TBI (n = 30, Mage = 10.81) and orthopedic injury (OI; n = 42, Mage = 10.65) completed measures of ToM and executive function and underwent MRI; parents rated children’s psychosocial adjustment. Children with severe TBI demonstrated reduced right-hemisphere MN volume, and poorer ToM, vs children with OI. Ordinary least-squares path analysis indicated that right-hemisphere MN volume and ToM mediated the association between severe TBI and adjustment. Parallel analyses substituting the central executive network and executive function were not significant, suggesting some model specificity. Children at greatest risk of poor adjustment after TBI could be identified based in part on neuroimaging of social brain networks and assessment of social cognition and thereby more effectively allocate limited intervention resources.

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The Role of Free Radicals in Traumatic Brain Injury

Biological Research For Nursing ◽

10.1177/1099800411431823 ◽

2012 ◽

Vol 15 (3) ◽

pp. 253-263 ◽

Cited By ~ 24

Author(s):

Karen M. O’Connell ◽

Marguerite T. Littleton-Kearney

Keyword(s):

Traumatic Brain Injury ◽

Free Radicals ◽

Free Radical ◽

Brain Injury ◽

Current Knowledge ◽

Cellular Level ◽

Secondary Brain Injury ◽

Secondary Injury ◽

The Military

Traumatic brain injury (TBI) is a significant cause of death and disability in both the civilian and the military populations. The primary impact causes initial tissue damage, which initiates biochemical cascades, known as secondary injury, that expand the damage. Free radicals are implicated as major contributors to the secondary injury. Our review of recent rodent and human research reveals the prominent role of the free radicals superoxide anion, nitric oxide, and peroxynitrite in secondary brain injury. Much of our current knowledge is based on rodent studies, and the authors identified a gap in the translation of findings from rodent to human TBI. Rodent models are an effective method for elucidating specific mechanisms of free radical-induced injury at the cellular level in a well-controlled environment. However, human TBI does not occur in a vacuum, and variables controlled in the laboratory may affect the injury progression. Additionally, multiple experimental TBI models are accepted in rodent research, and no one model fully reproduces the heterogeneous injury seen in humans. Free radical levels are measured indirectly in human studies based on assumptions from the findings from rodent studies that use direct free radical measurements. Further study in humans should be directed toward large samples to validate the findings in rodent studies. Data obtained from these studies may lead to more targeted treatment to interrupt the secondary injury cascades.

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