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06.03.2019 | Head and Neck

Effects of thalamic infarction on the structural and functional connectivity of the ipsilesional primary somatosensory cortex

Zeitschrift:
European Radiology
Autoren:
Li Chen, Tianyou Luo, Kangcheng Wang, Yong Zhang, Dandan Shi, Fajin Lv, Yang Li, Yongmei Li, Qi Li, Weidong Fang, Zhiwei Zhang, Juan Peng, Hanfeng Yang
Wichtige Hinweise

Electronic supplementary material

The online version of this article (https://​doi.​org/​10.​1007/​s00330-019-06068-0) contains supplementary material, which is available to authorized users.

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Abstract

Objectives

To identify regions causally influenced by thalamic stroke by measuring white matter integrity, cortical volume, and functional connectivity (FC) among patients with thalamic infarction (TI) and to determine the association between structural/functional alteration and somatosensory dysfunction.

Methods

Thirty-one cases with TI-induced somatosensory dysfunction and 32 healthy controls underwent magnetic resonance imaging scanning. We reconstructed the ipsilesional central thalamic radiation (CTR) and assessed its integrity using fractional anisotropy (FA), assessed S1 ipsilesional changes with cortical volume, and identified brain regions functionally connected to TI locations and regions without TI to examine the potential effects on somatosensory symptoms.

Results

Compared with controls, TI patients showed decreased FA (F = 17.626, p < 0.001) in the ipsilesional CTR. TI patients exhibited significantly decreased cortical volume in the ipsilesional top S1. Both affected CTR (r = 0.460, p = 0.012) and S1 volume (r = 0.375, p = 0.049) were positively correlated with somatosensory impairment in TI patients. In controls, the TI region was highly functionally connected to atrophic top S1 and less connected to the adjacent middle S1 region in FC mapping. However, T1 patients demonstrated significantly increased FC between the ipsilesional thalamus and middle S1 area, which was adjacent to the atrophic S1 region.

Conclusions

TI induces remote changes in the S1, and this network of abnormality underlies the cause of the sensory deficits. However, our other finding that there is stronger connectivity in pathways adjacent to the damaged ones is likely responsible for at least some of the recovery of function.

Key Points

• TI led to secondary impairment in the CTR and cortical atrophy in the ipsilesional top of S1.
• TI patients exhibited significantly higher functional connectivity with the ipsilateral middle S1 which was mainly located within the non-atrophic area of S1.
• Our results provide neuroimaging markers for non-invasive treatment and predict somatosensory recovery.

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