Research Reports - Prefrontal cortical thickening after mild traumatic brain injury

J Neurotrauma. 2017 Aug 28. doi: 10.1089/neu.2017.5124. [Epub ahead of print]

Dall'Acqua P(1)(2), Johannes S(3), Mica L(4), Simmen HP(5), Glaab R(6), Fandino

J(7), Schwendinger M(8), Meier C(9), Ulbrich EJ(10), Müller A(11), Jäncke
L(1)(12)(13), Hänggi J(14).

OBJECTIVE: To evaluate group-by-time interactions between gray matter morphology
of healthy controls and that of patients with mild traumatic brain injury (mTBI)
as they transitioned from acute to chronic stages and to relate these findings to
long-term cognitive alterations to identify distinct recovery trajectories
between good (GO) and poor outcome (PO).
METHODS: High-resolution T1-weighted MR images were acquired in 49 mTBI patients
within 7 days and 1 year post-injury and at equivalent times in 49 healthy
controls. Using linear mixed-effects models, we performed mass-univariate
analyses and associated the results of the interaction with changes in cognitive
performance. Morphological alterations indexed by increased or decreased cortical
thickness have been expected mainly in frontal, parietal and temporal brain
RESULTS: A significant interaction was found in cortical thickness, spatially
restricted to bilateral structures of the prefrontal cortex showing thickening in
mTBI and normal developmental thinning in controls. A discrete thickness increase
that can interpreted as the absence of cortical thinning typically seen in the
healthy population was associated with cognitive recovery in the GO subgroup, but
the exaggerated cortical thickening in the PO patients was linked to worsening
cognitive performance.
CONCLUSIONS: Thickness of the prefrontal cortex is subject to structural
alterations during the first year after mTBI. Beside beneficial neuroplasticity,
a prolonged state of neuroinflammation for symptomatic patients (maladaptive
neuroplasticity) cannot be excluded. If the underlying cellular processes
responsible for cortical thickening following mTBI have been determined, brain
stimulation or even pharmacological intervention targeting the prefrontal cortex
might promote endogenous neural restoration. 

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