Reduced sleep quality defines a subtype of obsessive-compulsive disorder with lower Glx levels in the resting thalamus and worse response inhibition.

BACKGROUND: The aim of this study was to investigate the differences between resting and active thalamic neurometabolite levels and inhibitory function in obsessive compulsive disorder (OCD) patients with poor sleep quality (PSQ was defined as Pittsburgh Sleep Quality Index >5 and sleep efficiency ≤85%) compared to OCD patients with good sleep quality (GSQ) and healthy controls (HCs), as well as the relationship of these indices to obsessive compulsive symptoms. METHODS: Functional magnetic resonance spectroscopy (fMRS) was used to measure resting and active thalamic neurometabolite levels in 72 subjects (20 HCs and 38 OCD patients included in study analysis). Response inhibition function was measured by the Go-Nogo task before and during MRS recording. Subjective sleep quality was assessed using the Pittsburgh Sleep Quality Index (PSQI). The symptoms of OCD, anxiety and depression were evaluated using relevant clinical scales. RESULTS: OCD patients exhibited significantly reduced Glx/Cr levels in the resting thalamus. The levels of resting thalamic Glu/Cr and Glx/Cr in OCD patients with PSQ were significantly lowest. OCD patients had significantly lower correct rates on Go tasks, higher error rates on Nogo tasks, and longer error average response times (EART) to the Nogo task. OCD patients with PSQ demonstrated the highest Nogo task error rate and the longest EART to Nogo task. Furthermore, PSQI scores exhibited negative correlations with Glu/Cr and Glx/Cr in the resting thalamus. CONCLUSION: OCD patients with PSQ demonstrated reduced levels of thalamic resting Glx and more pronounced response inhibitory function impairment. Aberrant neurometabolite levels in critical brain regions, coupled with heightened response inhibition function deficits, may be a neurobiological basis for the PSQ that OCD patients generally exhibit.

Glutamatergic neurotransmission is affected by low-frequency repetitive transcranial magnetic stimulation over the supplemental motor cortex of patients with obsessive-compulsive disorder.

OBJECTIVE: In obsessive-compulsive disorder (OCD), glutamatergic neurotransmission dysfunction played key roles in pathophysiology. The current research assessed changes of neurometabolites in the bilateral striatum of OCD patients receiving low-frequency repetitive transcranial magnetic stimulation (rTMS) using 1H proton magnetic resonance spectroscopy (1H-MRS). METHODS: 52 OCD patients were divided into rTMS treatment group (29) and the control group (medication only) (22). The levels of neurometabolites in the bilateral striatum of patients with OCD were measured using MRS before and after treatment. All participants were taking medication prior to the treatment and the process. RESULTS: Following rTMS treatment, Yale-Brown Obsessive-Compulsive Scale (YBOCS) score was significantly decreased in the rTMS group compared with the control group. Glutamate (Glu) and glutamate and glutamine complexes (Glx) in the bilateral striatum of the rTMS treatment response group increased significantly with the improvement of OCD. Glu in the bilateral striatum and Glx in the right striatum were positively correlated with compulsion after the treatment. CONCLUSIONS: The physiopathological mechanism of OCD may be related to the glutamatergic dysfunction, and the low-frequency repetitive transcranial magnetic stimulation applied to the supplementary motor area can improve OCD symptoms by modulating glutamatergic levels in the bilateral striatum of patients with OCD.