Regional homogeneity alterations in multi-frequency bands in tension-type headache: a resting-state fMRI study

ABSTRACT:

Objectives

In this study, we aimed to investigate the spontaneous neural activity in the conventional frequency band (0.01−0.08 Hz) and two sub-frequency bands (slow-4: 0.027–0.073 Hz, and slow-5: 0.01–0.027 Hz) in tension-type headache (TTH) patients with regional homogeneity (ReHo) analyses.

Methods

Thirty-eight TTH patients and thirty-eight healthy controls (HCs) underwent resting-state functional magnetic resonance imaging (RS-fMRI) scanning to investigate abnormal spontaneous neural activity using ReHo analysis in conventional frequency band (0.01−0.08 Hz) and two sub-frequency bands (slow-4: 0.027–0.073 Hz and slow-5: 0.01–0.027 Hz).

Results

In comparison with the HC group, patients with TTH exhibited ReHo increases in the right medial superior frontal gyrus in the conventional frequency band (0.01−0.08 Hz). The between group differences in the slow-5 band (0.01–0.027 Hz) highly resembled the differences in the conventional frequency band (0.01−0.08 Hz); even the voxels with increased ReHo were spatially more extensive, including the right medial superior frontal gyrus and the middle frontal gyrus. In contrast, no region showed significant between-group differences in the slow-4 band (0.027–0.073 Hz). The correlation analyses showed no correlation between the ReHo values in TTH patients and VAS scores, course of disease and number of seizures per month in conventional band (0.01−0.08 Hz), slow-4 band (0.027–0.073 Hz), as well as in slow-5 band (0.01–0.027 Hz).

Conclusions

The results showed that the superior frontal gyrus and middle frontal gyrus were involved in the integration and processing of pain signals. In addition, the abnormal spontaneous neural activity in TTH patients was frequency-specific. Namely, slow-5 band (0.01–0.027 Hz) might contain additional useful information in comparison to slow-4 band (0.027−0.073 Hz). This preliminary exploration might provide an objective imaging basis for the understanding of the pathophysiological mechanism of TTH.

Supplementary Information

The online version contains supplementary material available at 10.1186/s10194-021-01341-4.

SUBMITTER: Zhang S 

PROVIDER: S-EPMC8555254 | biostudies-literature |

REPOSITORIES: biostudies-literature