AUTHOR=Zhou Qianling , Li Meng , Fan Qisen , Chen Feng , Jiang Guihua , Wang Tianyue , He Qinmeng , Fu Shishun , Yin Yi , Lin Jinzhi , Yan Jianhao TITLE=Cerebral perfusion alterations in patients with trigeminal neuralgia as measured by pseudo-continuous arterial spin labeling JOURNAL=Frontiers in Neuroscience VOLUME=16 YEAR=2022 URL=https://www.frontiersin.org/journals/neuroscience/articles/10.3389/fnins.2022.1065411 DOI=10.3389/fnins.2022.1065411 ISSN=1662-453X ABSTRACT=Background

Accumulating evidence suggests that trigeminal neuralgia (TN) causes structural and functional alterations in the brain. However, only a few studies have focused on cerebral blood flow (CBF) changes in patients with TN. This study aimed to explore whether altered cerebral perfusion patterns exist in patients with TN and investigate the relationship between abnormal regional CBF (rCBF) and clinical characteristics of TN.

Materials and methods

This study included 28 patients with TN and 30 age- and sex-matched healthy controls (HCs) who underwent perfusion functional MRI (fMRI) of the brain using pseudo-continuous arterial spin labeling (pCASL) in the resting state. The regions of significantly altered CBF in patients with TN were detected using group comparison analyses. Then, the relationships between the clinical characteristics and abnormal rCBF were further investigated.

Results

Compared to the control group, patients with TN exhibited increased rCBF, primarily in the thalamus, middle frontal gyrus (MFG), and left insula. Furthermore, the CBF values of the thalamus were negatively correlated with the pain intensity of TN and positively correlated with pain duration in patients with TN.

Conclusion

Primary alterations in rCBF in patients with TN occurred in different brain regions related to pain, which are involved in cognitive-affective interaction, pain perception, and pain modulation. These results indicate that non-invasive resting cerebral perfusion imaging may contribute complementary information to further understanding the neuropathological mechanism underlying TN.