Progress in neuro-psychopharmacology & biological psychiatry · 2025
Thalamocortical structural connectivity with sleep oscillatory coupling in insomnia disorder.
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Shao Ziqiang, Du Zhe, Cai Suping, Liu Jiayi, Zhao Xumeng, Yu Dahua, Sheng Xiaona, Zhu Yifei, Yuan Kai
Аннотация
BACKGROUND: Thalamocortical interactions play a critical role in sleep oscillatory activities. However, in individuals with insomnia disorder (ID), the structural organization of these circuits, their relationship with sleep oscillatory coupling, and their potential modulation by repetitive transcranial magnetic stimulation (rTMS) remain unclear.
METHODS: In Study 1, we recruited 62 ID patients and 62 healthy controls and assessed white matter tract strength between thalamic subregions and cortical areas using probabilistic tractography. In Study 2, we administered 20 sessions of 1 Hz rTMS (active vs. sham) and evaluated changes in thalamocortical connectivity and sleep oscillations measured via polysomnography.
RESULTS: Abnormal thalamic structural connectivity was observed in tracts projecting to the left prefrontal cortex (PFC) and bilateral sensory cortex (SC). Following treatment, significant alterations in tract strength were detected between the right thalamus and both the PFC and SC, accompanied by improvements in slow wave (SW)-spindle coupling. Furthermore, changes in right thalamus-PFC tract strength were correlated with improved subjective sleep quality (Pittsburgh Sleep Quality Index, PSQI; r = 0.6143; 95 % CI, 0.24 to 0.83, p = 0.004), and right thalamus-SC tract strength was associated with SW-spindle coupling (post-rTMS: r = -0.59; 95 % CI, -0.83 to -0.17, p = 0.011).
CONCLUSION: These findings advance our understanding of the role of subdivided thalamocortical circuits and sleep oscillatory coupling in the pathophysiology of ID and suggest that rTMS can modulate these pathways, with concomitant improvements in PSQI.
METHODS: In Study 1, we recruited 62 ID patients and 62 healthy controls and assessed white matter tract strength between thalamic subregions and cortical areas using probabilistic tractography. In Study 2, we administered 20 sessions of 1 Hz rTMS (active vs. sham) and evaluated changes in thalamocortical connectivity and sleep oscillations measured via polysomnography.
RESULTS: Abnormal thalamic structural connectivity was observed in tracts projecting to the left prefrontal cortex (PFC) and bilateral sensory cortex (SC). Following treatment, significant alterations in tract strength were detected between the right thalamus and both the PFC and SC, accompanied by improvements in slow wave (SW)-spindle coupling. Furthermore, changes in right thalamus-PFC tract strength were correlated with improved subjective sleep quality (Pittsburgh Sleep Quality Index, PSQI; r = 0.6143; 95 % CI, 0.24 to 0.83, p = 0.004), and right thalamus-SC tract strength was associated with SW-spindle coupling (post-rTMS: r = -0.59; 95 % CI, -0.83 to -0.17, p = 0.011).
CONCLUSION: These findings advance our understanding of the role of subdivided thalamocortical circuits and sleep oscillatory coupling in the pathophysiology of ID and suggest that rTMS can modulate these pathways, with concomitant improvements in PSQI.