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Updated: May 5, 2026
Investigations on Alterations of Hippocampal Circuit Function Following Mild Traumatic Brain Injury
Published on: November 19, 2012
Linking Symptom Phenotypes to Patterns of White Matter Injury in Mild Traumatic Brain Injury: A Latent Class Analysis
Sohae Chung1,2, Seon-Hi Shin3,2, Alaleh Alivar3,2
1From the Department of Radiology, Center for Advanced Imaging Innovation and Research (CAI2R) (S. Chung, S.-H.S., A.A., S. Coelho, E.F., D.S.N., A.E.B., Y.W.L.), New York University Grossman School of Medicine, New York, New York sohae.chung@nyulangone.org.
Background And Purpose:
Mild traumatic brain injury (MTBI) is a common public health concern with potential long-term consequences, yet its underlying pathophysiology remains poorly understood. Clinical heterogeneity of individuals having diverse extent and array of symptoms has impeded the identification of reliable imaging biomarkers. Traditional group-level analyses may obscure biologically meaningful subtypes. This study uses latent class analysis (LCA) to classify MTBI subjects into symptom-defined subgroups and examines corresponding WM microstructural alterations using advanced diffusion MRI.
Materials And Methods:
Sixty-one patients with MTBI completed the Rivermead Post-Concussion Symptoms Questionnaire within 1 month of injury. LCA was used to identify symptom-based subgroups. Of these, 54 patients with MTBI underwent multishell diffusion MRI and were compared with 31 controls. WM changes were assessed across subgroups using ROI-based diffusion analyses.
Results:
LCA identified 3 distinct MTBI subgroups: those with minimal to no symptoms (31.5%), the cognitively symptomatic (38.9%), and the more globally symptomatic (29.6%). The 3 groups were associated with different patterns of diffusion MRI differences compared with controls. The cognitively symptomatic subgroup showed predominantly central WM differences, the globally symptomatic subgroup exhibited more peripheral differences with right-hemisphere predominance and sparing the corpus callosum, marked by reduced fractional anisotropy and kurtosis and elevated diffusivities, and the less symptomatic subgroup demonstrated focal differences in the callosal genu, with increased fractional anisotropy and kurtosis and decreased diffusivity measures.
Conclusions:
MTBI comprises biologically distinct phenotypes with subgroup-specific WM signatures on diffusion MRI. Even individuals with minimal to no symptoms show WM differences compared with controls, underscoring the limitations of symptom reporting alone. Integrating symptom-based classification with advanced diffusion MRI may improve diagnostic precision to help risk stratification and provide insight into mechanisms of injury.
