Cortical Thickness Changes and Their Relationship to Dual-Task Performance following Mild Traumatic Brain Injury in Youth

Abstract

Mild traumatic brain injury (mTBI) is common in youth, especially in those who participate in sport. Recent investigations from our group have shown that asymptomatic children and adolescents with mTBI continue to exhibit alterations in neural activity and cognitive performance compared with those without a history of mTBI. This is an intriguing finding, given that current return-to-learn and return-to-play protocols rely predominately on subjective symptom reports, which may not be sensitive enough to detect subtle injury-related changes. As a result, youth may be at greater risk for re-injury and long-term consequences if they are cleared for activity while their brains continue to be compromised. It is currently unknown whether mTBI also affects brain microstructure in the developing brain, particularly cortical thickness, and whether such changes are also related to cognitive performance. The present study examined cortical thickness in 13 asymptomatic youth (10-14 years old) who had sustained an mTBI 3-8 months prior to testing compared with 14 age-matched typically developing controls. Cortical thickness was also examined in relation to working memory performance during single and dual task paradigms. The results show that youth who had sustained an mTBI had thinner cortices in the left dorsolateral prefrontal region and right anterior and posterior inferior parietal lobes. Additionally, cortical thinning was associated with slower reaction time during the dual-task condition in the injured youth only. The results also point to a possible relationship between functional and structural alterations as a result of mTBI in youth, and lend evidence for neural changes beyond symptom resolution.

Differences in white matter structure and cortical thickness between patients with traumatic and idiopathic chronic neck pain: Associations with cognition and pain modulation?

“…In CINP patients, decreased precuneus thickness coincided with worse performance on the TMT part B, however decreased cortical thickness and worse cognitive performance could not be revealed in CINP patients compared with controls. The observed association between working memory capacity and cortical thickness in CINP patients is in line with studies reporting associations between regional GM morphology and working memory capacity or other features of cognition in patients with fibromyalgia (Luerding et al, 2008), patients with complex regional pain syndrome (Lee et al, 2015), and in mild TBI patients (Urban et al, 2017).…”

A systematic review of cross-sectional differences and longitudinal changes to the morphometry of the brain following paediatric traumatic brain injury

“…Morphometric investigations of the brain post-TBI were not limited to the volume of cortical regions, but also the cortical thickness. There were fewer investigations of cortical thickness, but early post-injury studies showed regions of dorso-lateral prefrontal cortex (dlPFC; McCauley et al, 2010; Urban et al, 2017; Wilde et al, 2011) and other prefrontal regions (McCauley et al, 2010; Wilde et al, 2011) as well as superior temporal sulcus (STS; McCauley et al, 2010; Wilde et al, 2011), cingulate regions (McCauley et al, 2010) and regions of the inferior parietal lobule (iPL; Urban et al, 2017) to be significantly thinner in the TBI group compared to controls. However, these differences were not replicated at a later timepoint post injury (Bigler et al, 2016) This is not to say that these differences have ‘recovered’ over time (due to the cross-sectional nature of this evidence) but more likely due to differences in methodology and samples.…”

“…This atrophy can vary in relation to injury factors such as mechanism, severity and pathology (Bigler, 2013; Cullen et al, 2011; Maxwell et al, 2010). This can be realised as changes to both brain volume (Bigler, 2016) and cortical thickness measures (Urban et al, 2017). Morphometric brain changes are also a feature of typical brain developing throughout childhood and adolescence (Batalle, Edwards and O'Muircheartaigh, 2018; Mills et al, 2016; Raznahan et al, 2011; Shaw et al, 2008).…”

“…Non-linear trajectories of grey matter (GM) and white matter (WM) maturation are apparent in measures of volume (Giedd, 2004; Gilmore et al, 2007; Knickmeyer et al, 2008), gyrification patterning (Dubois et al, 2008) and cortical thickness (Herting et al, 2015; Nie et al, 2014; Whitaker et al, 2016), usually showing reductions over time, in line with models of synaptic pruning and myelination (Whitaker et al, 2016). This means that the morphometric atrophy and developmentally-inappropriate apoptosis (Urban et al, 2017; Wilde et al, 2005) due to pTBI is occurring in the context of an already changing, age and development-dependent brain (Bigler, 2016; Maxwell, 2012). Therefore, long term effects of injury are likely due to these interactions of age, neuroinflammation and neurodegenerative effects (Bigler, 2013; Johnson et al, 2013).…”

Default Mode Network Oscillatory Coupling Is Increased Following Concussion

“…Preclinical work using optogenetics to stimulate neuronal (electrical) activity has shown that this promotes adaptive myelination ( 85 ), and a recent human study has proposed that there is a strong link between neural connectonomics, their dynamics, and cortical white matter structure [or “myeloarchitecture” ( 67 )]. It seems reasonable to posit, given these findings, that our observations in altered connectivity of cortical ICNs could be related to neuromorphological changes ( 86 ), and more specially microscopic white matter pathology following concussion, including demyelination and/or differentiation ( 87 , 88 ), reductions in cortical thickness ( 89 – 91 ), and Wallerian degeneration ( 92 , 93 ).…”