Amplitude of low-frequency fluctuation after a single-trigger pain in patients with classical trigeminal neuralgia

Abstract

Objective: This study aimed to explore the central mechanism of classical trigeminal neuralgia (CTN) by analyzing the static amplitude of low-frequency fluctuation (sALFF) and dynamic amplitude of low-frequency fluctuation (dALFF) in patients with CTN before and after a single-trigger pain.

Methods: This study included 48 patients (37 women and 11 men, age 55.65 ± 11.41 years) with CTN. All participants underwent 3D-T1WI and three times resting-state functional magnetic resonance imaging. The images were taken before stimulating the trigger zone (baseline), within 5 s after stimulating the trigger zone (triggering-5 s), and in the 30th minute after stimulating the trigger zone (triggering-30 min). The differences between the three measurements were analyzed using a repeated-measures analysis of variance.

Results: The sALFF values of the bilateral middle occipital gyrus and right cuneus gradually increased, and the values of the left posterior cingulum gyrus and bilateral superior frontal gyrus gradually decreased in triggering-5 s and triggering-30 min. The values of the right middle temporal gyrus and right thalamus decreased in triggering-5 s and subsequently increased in triggering-30 min. The sALFF values of the left superior temporal gyrus increased in triggering-5 s and then decreased in triggering-30 min. The dALFF values of the right fusiform gyrus, bilateral lingual gyrus, left middle temporal gyrus, and right cuneus gyrus gradually increased in both triggering-5 s and triggering-30 min.

Conclusions: The sALFF and dALFF values changed differently in multiple brain regions in triggering-5 s and triggering-30 min of CTN patients after a single trigger of pain, and dALFF is complementary to sALFF. The results might help explore the therapeutic targets for relieving pain and improving the quality of life of patients with CTN.

Keywords: Amplitude of low-frequency fluctuation; Central mechanism; Classical trigeminal neuralgia; Pathophysiology; Resting-state magnetic resonance imaging.