Gray matter abnormalities in pediatric mild traumatic brain injury
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Published on: February 7, 2025
Andrew R Mayer1, Faith M Hanlon, Josef M Ling
11 The Mind Research Network/Lovelace Biomedical and Environmental Research Institute , Albuquerque, New Mexico .
Insights
Pediatric mild traumatic brain injury (pmTBI) shows altered brain diffusion and atrophy over time. Standard assessments may underestimate recovery duration in children post-pmTBI.
Area of Science:
- Neuroscience
- Pediatric Neurology
- Radiology
Background:
- Pediatric mild traumatic brain injury (pmTBI) is common in children, leading to acute and chronic neuropsychiatric issues.
- The prospective pathophysiology of gray matter diffusion and atrophy in pmTBI remains poorly understood.
Purpose of the Study:
- To prospectively investigate changes in gray matter diffusion and atrophy in children following pmTBI.
- To correlate neuroimaging findings with clinical and cognitive assessments over time.
Main Methods:
- A prospective study involving 15 children with semi-acute pmTBI and 15 matched healthy controls.
- Clinical assessments included attention, processing speed, executive function, memory, and self-reported symptoms.
- Neuroimaging utilized fractional anisotropy (FA) for diffusion and atrophy measures in gray matter structures at baseline and 4 months.
Main Results:
- Patients showed reduced attention and processing speed with increased diffusion in the left superior temporal gyrus and right thalamus acutely.
- Increased diffusion persisted at 4 months, with partial cognitive recovery.
- Cortical atrophy in frontal and left-hemisphere regions emerged at 4 months post-injury.
Conclusions:
- Neurobehavioral, diffusion, and atrophy markers exhibit distinct recovery timelines after pmTBI.
- Patient self-report and standard clinical evaluations may not fully capture the extent or duration of recovery.
Abstract:
Pediatric mild traumatic brain injury (pmTBI) is the most prevalent neurological insult in children and is associated with both acute and chronic neuropsychiatric sequelae. However, little is known about underlying pathophysiology changes in gray matter diffusion and atrophy from a prospective stand-point. Fifteen semi-acute pmTBI patients and 15 well-matched healthy controls were evaluated with a clinical and neuroimaging battery, with a subset of participants returning for a second visit. Clinical measures included tests of attention, processing speed, executive function, working memory, memory, and self-reported post-concussive symptoms. Measures of diffusion (fractional anisotropy [FA]) and atrophy were also obtained for cortical and subcortical gray matter structures to characterize effects of injury as a function of time. Patients exhibited decreased scores in the domains of attention and processing speed relative to controls during the semi-acute injury stage, in conjunction with increased anisotropic diffusion in the left superior temporal gyrus and right thalamus. Evidence of increased diffusion in these regions was also present at four months post-injury, with performance on cognitive tests partially normalizing. In contrast, signs of cortical atrophy in bilateral frontal areas and other left-hemisphere cortical areas only emerged at four months post-injury for patients. Current results suggest potentially differential time-courses of recovery for neurobehavioral markers, anisotropic diffusion and atrophy following pmTBI. Importantly, these data suggest that relying on patient self-report or standard clinical assessments may underestimate the time for true injury recovery.
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