Related Experiment Video
Updated: Apr 18, 2026

09:33
Diffusion Tensor Magnetic Resonance Imaging in the Analysis of Neurodegenerative Diseases
Published on: July 28, 2013
29.5K
Neuroanatomical basis of paroxysmal sympathetic hyperactivity: a diffusion tensor imaging analysis
Holly E Hinson1, Louis Puybasset, Nicolas Weiss
1Department of Neurology and Emergency Medicine, Oregon Health & Science University , Portland, OR , USA .
Brain Injury
|January 8, 2015
Summary
Paroxysmal sympathetic hyperactivity (PSH) after traumatic brain injury (TBI) may stem from disrupted brain connectivity. Specific white matter pathway changes in the corpus callosum and internal capsule predict PSH development.
Area of Science:
- Neuroscience
- Neurology
- Trauma Care
Background:
- Paroxysmal sympathetic hyperactivity (PSH) occurs in some moderate-to-severe traumatic brain injury (TBI) patients.
- The underlying neuroanatomy of PSH is not well understood.
- Connectivity changes in the central autonomic network are hypothesized to be involved.
Purpose of the Study:
- To investigate the neuroanatomical basis of PSH in TBI patients.
- To identify specific brain connectivity alterations associated with PSH.
Main Methods:
- Retrospective analysis of adult patients with severe TBI (within 3 weeks of injury).
- Screening for PSH using a standard definition.
- Multimodal MRI, including quantitative diffusion tensor imaging (DTI).
- Principal component analysis (PCA) and classification tree analysis for data interpretation.
Main Results:
- 16 out of 102 enrolled patients met PSH criteria.
- A significant association was found between the first principal component of DTI tracts and PSH status (AUROC = 0.867).
- Classification tree analysis identified decreased fractional anisotropy (FA) in the splenium of the corpus callosum and right posterior internal capsule as key predictors of PSH (AUROC = 0.933).
Conclusions:
- Disruptions in white matter tracts, particularly involving the posterior corpus callosum and posterior limb of the internal capsule, may contribute to PSH.
- These findings suggest a potential neuroanatomical basis for PSH in TBI.

