• Holly E Hinson, Louis Puybasset, Nicolas Weiss, Vincent Perlbarg, Habib Benali, Damien Galanaud, Mike Lasarev, Robert D Stevens, and Neuro Imaging for Coma Emergence, Recovery (NICER) Consortium.
• Department of Neurology and Emergency Medicine, Oregon Health & Science University , Portland, OR , USA .
• Brain Inj. 2015 Jan 1;29(4):455-61.

Primary ObjectiveParoxysmal sympathetic hyperactivity (PSH) is observed in a sub-set of patients with moderate-to-severe traumatic brain injury (TBI). The neuroanatomical basis of PSH is poorly understood. It is hypothesized that PSH is linked to changes in connectivity within the central autonomic network.Research DesignRetrospective analysis in a sub-set of patients from a multi-centre, prospective cohort study Methods and procedures: Adult patients who were <3 weeks after severe TBI were enrolled and screened for PSH using a standard definition. Patients underwent multimodal MRI, which included quantitative diffusion tensor imaging.Main Outcomes And ResultsPrincipal component analysis (PCA) was used to resolve the set of tracts into components. Ability to predict PSH was evaluated via area under the receiver operating characteristic (AUROC) and tree-based classification analyses. Among 102 enrolled patients, 16 met criteria for PSH. The first principle component was significantly associated (p = 0.024, AUROC = 0.867) with PSH status even after controlling for age and admission GCS. In a classification tree analysis, age, GCS and decreased FA in the splenium of the corpus callosum and in the right posterior limb of the internal capsule discriminated PSH vs no PSH with an AUROC of 0.933.ConclusionsDisconnection involving the posterior corpus callosum and of the posterior limb of the internal capsule may play a role in the pathogenesis or expression of PSH.

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