Article

SHORT COMMUNICATION: Diffuse Changes in Cortical Thickness in Pediatric Moderate-to-Severe Traumatic Brain Injury

Department of Psychology, Brigham Young University, Provo, Utah 84602, USA.
Journal of Neurotrauma (Impact Factor: 3.71). 12/2008; 25(11):1343-5. DOI: 10.1089/neu.2008.0615
Source: PubMed

ABSTRACT

Generalized whole brain volume loss has been well documented in moderate-to-severe traumatic brain injury (TBI), as has diffuse cerebral atrophy based on magnetic resonance imaging (MRI) volumetric methods where white matter may be more selectively affected than gray matter. However, specific regional differences in gray matter thickness of the cortical mantle have not been previously examined. As such, cortical thickness was assessed using FreeSurfer software to identify regions of significant gray matter cortical thinning in MRI scans of 16 young TBI subjects (age range, 9-16 years) compared to 16 demographically matched controls. Significant cortical thinning was observed globally in the TBI group compared to the cohort of typically developing children. Reduced cortical thickness was related to reported deficits in working memory. TBI-induced cortical thickness reductions are probably due to a combination of focal and diffuse effects and have implications for the neurobehavioral sequelae of TBI.

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    • "In keeping with expectations, we found that severe paediatric TBI is associated with global and local gray matter structural change in the SBN as early as 2-months post-injury. Moreover, group-level reductions in ToM fully mediated the relationship between structural change in the SBN and long-term behavior problems, indicating that morphological changes in the SBN prospectively predict chronic behavioral symptoms through impaired ToM.Wilde et al., 2005;Spanos et al., 2007;Fearing et al., 2008;Merkley et al., 2008;Bigler et al., 2010;Wu et al., 2010a;Beauchamp et al., 2011a;Beauchamp et al., 2011b;Levin et al., 2011Wilde et al., 2005;Bigler et al., 2010;McAllister, 2011;Bigler, 2013;Bigler et al., 2013Blatter et al., 1997;Adams et al., 2011;Bigler, 2013).In partial support of our hypotheses, we found evidence for post-acute social cognitive dysfunction among children with severe TBI, as well as children classified with mild complicated TBI on the basis of positive research MR findings. While these findings are consistent with previous reports of social cognitive dysfunction after severe pediatric TBI (ChertkoffWalz et al., 2010;Tlustos et al., 2011;Dennis et al., 2013b;Dennis et al., 2013c;Ryan et al., 2014b), we provide preliminary evidence that social cognitive functions are vulnerable to the effects of milder generalized injuries in mid-late childhood and adolescence. "
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    ABSTRACT: Childhood and adolescence coincide with rapid maturation and synaptic reorganization of distributed neural networks that underlie complex cognitive-affective behaviors. These regions, referred to collectively as the ‘social brain network’ (SBN) are commonly vulnerable to disruption from pediatric TBI; however, the mechanisms that link morphological changes in the SBN to behaviour problems in this population remain unclear. In 98 children with mild to severe TBI, we acquired 3D T1 weighted MRIs at 2-8 weeks post injury. For comparison, 33 typically developing controls of similar age, sex and education were scanned. All participants were assessed on measures of Theory of Mind (ToM) six months post-injury and parents provided ratings of behavior problems 24-months post-injury. Participants with severe TBI showed abnormal SBN morphology, as well local gray matter structural change in multiple component cortical regions of the SBN. Compared to controls and children with milder injuries, the severe TBI group had significantly poorer ToM, which was associated with more frequent behavior problems and abnormal SBN morphology. Mediation analysis indicated that impaired social cognition mediated the relationship between structural change in the SBN and more frequent behavior problems. Our findings suggest that sub-acute alterations in SBN morphology indirectly contribute to long-term behavior problems via their influence on ToM. Structural change in the SBN and its putative hub regions may represent a useful imaging biomarker for prediction of post-acute social cognitive impairment, which may in turn elevate risk for chronic behaviour problems.
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    • "This can be interpreted as growth retardation due to the trauma. Indeed, generalized atrophic changes resulting in reduced overall brain volume has been documented in moderate-to-severe pediatric traumatic brain injury [39]–[40]. In addition to this focal effect on brain, a general growth retardation due to post-traumatic endocrine disturbance [41] could be raised here. "
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    • "This is perhaps not surprising, given that the social brain involves a broad array of spatially-remote regions thought to interact as a network (Adolphs, 2001; Johnson et al., 2005). Individual differences in overall brain maturation should involve many of these regions, as should the diffuse atrophy that occurs after more severe TBI (Bigler et al., 2010; Merkley et al., 2008). "
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    ABSTRACT: This study examined the associations among brain volumes, theory of mind (ToM), peer relationships, and psychosocial adjustment in children with traumatic brain injury (TBI). Participants included 8- to 13-year-old children, 82 with TBI and 61 with orthopedic injuries (OIs). Children completed three measures of ToM. Classmates provided ratings of participants’ peer relationships, acceptance, and friendships. Parents rated children’s psychosocial adjustment. MRI was used to determine brain volumes. Brain volumes were associated with ToM, which in turn was associated with peer rejection/victimization. Peer rejection/victimization in the classroom was associated with peer acceptance, friendship, social withdrawal, and general psychopathology. Brain volumes, ToM, peer relationships, and social adjustment show significant links among children with TBI and those with OI. The findings support a multilevel model of social competence in childhood TBI.
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