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  • Title: Functional connectivity disruption of the substantia nigra associated with cognitive impairment in acute mild traumatic brain injury.
    Author: Lu L, Li F, Ma Y, Chen H, Wang P, Peng M, Chen YC, Yin X.
    Journal: Eur J Radiol; 2019 May; 114():69-75. PubMed ID: 31005180.
    Abstract:
    PURPOSE: Mild traumatic brain injury is known to have frequent cognitive impairment. Accumulating evidence is pointing to the malfunctioning of the substantia nigra (SN) as an important factor for head trauma. However, it remains unknown whether changes in the SN-based resting state functional connectivity following mTBI at acute stage and its relationship with cognitive function. MATERIALS AND METHODS: 58 patients with mTBI and 30 age-, gender-, and years of education-matched healthy controls were enrolled in the current study. All of participants received resting state functional magnetic resonance imaging as well as neuropsychological assessment. The resting state functional MR imaging data were analyzed by using a standard seed-based whole-brain correlation method to characterize SN resting state networks. Student t tests were used to perform comparisons. The association between SN resting state networks and performance on neuropsychological measures was also investigated in patients with mTBI by using Pearson rank correlation. RESULTS: Patients with mTBI at acute stage exhibited reduced left SN-based functional connectivity with right insula and caudate and increased left SN-based functional connectivity with left precuneus and left middle occipital gyrus, and reduced right SN-based functional connectivity with left insula. Increased functional connectivity of left precuneus was negatively associated with neurocognitive functions as well (r = -0.266; P =  0.049). CONCLUSION: The present study indicated that patients with acute mTBI suffer from disruption in their SN resting state networks. Moreover, abnormal functional connectivity significantly correlated with cognitive function. Taking together, these results may better improve our understanding of the neuropathological mechanism underlying the neurocognitive symptoms associated with acute mTBI.
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