Abstract

To quantify clinical and structural white matter tract changes over six months, in patients with mild traumatic brain injury (mTBI) following early structured cognitive therapy. This was a non-randomized quasi-experimental study design. All patients with mTBI received written information and education on symptom(s) management before being assigned to structured cognitive therapy or conventional cognitive therapy at two weeks post injury. Structured therapy was one hour per week session by using computer-based and metacognitive training for the first three months followed by one hour per month session for the remaining three months. Conventional therapy was patient focused symptom(s) management and coping strategies. Neuropsychological assessment and Diffusion Tensor Imaging (DTI) were performed at baseline and six months post injury. Each group consisted of four male participants ( n = 8). Mean cognitive therapy duration was 7 hours (SD ± 1.8). There was no demographic, Glasgow Coma Scale, Post Traumatic Amnesia and loss of consciousness duration statistical difference between groups. Although all cognitive domains tested were not statistically significant, the scores for Attention, Memory, Language, and Executive Function domains were higher than conventional group at six months. We analysed nine white matter tracts. Almost all Fractional Anisotropy mean values were lower (Corpus Callosum genu: P = 0.03; splenium: P = 0.05) whereas Mean Diffusivity and Radial Diffusivity mean values were higher at six months. We quantified deficits in various cognitive domains as early as two weeks following mTBI, with higher normal scores in the structured therapy group as compared to conventional group at six months. Abnormal values of DTI parameters may suggest chronic axonal damage of various white matter locations and bundles. We did not yield statistical significance in our analysis due to small sample size caused by high drop-out rate. However, we concluded that early structured cognitive therapy may improve cognitive deficits beyond spontaneous recovery, despite persistent microstructural brain damage.

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