Functional Brain Activity Alterations in Type 1 Narcolepsy Patients with Anxiety and Depression: A 7-Tesla Resting State-Functional Magnetic Resonance Imaging Study.

Purpose: This study aimed to investigate abnormal changes in brain region functional activity in type 1 narcolepsy (NT1) patients comorbid with anxiety and depression.

Methods: Twenty NT1 patients and 20 healthy controls (HCs) underwent subjective/objective sleep assessments (polysomnography, SAS, SDS) and 7T rs-fMRI to analyze regional homogeneity (ReHo) and fractional amplitude of low-frequency fluctuations (fALFF).

Results: Compared with the HCs group, NT1 patients had higher SAS and SDS scores. Analysis of the correlation between sleep parameters and brain activity in NT1 patients showed that increased ReHo values in the right insula and right cerebellum were negatively correlated with the TST (r = -0.463, p = 0.040) and excessive day time sleepiness (r = -0.486, p = 0.041). The fALFF of the left lingual gyrus positively correlated with sleep efficiency (r = 0.582, p = 0.007). Additionally, altered brain activity in NT1 patients was associated with emotional disorders. ReHo and fALFF values of the right insula showed a positive correlation with SAS scores (ReHo: r = 0.583, p = 0.011; fALFF: r = 0.557, p = 0.016), and the fALFF value of the left postcentral region also correlated positively with SAS scores (r = 0.597, p = 0.009). Moreover, the ReHo values of the left and postcentral lingua were positively correlated with the SDS scores (left lingua: r = 0.478, p = 0.045; postcentral lingua: r = 0.499, p = 0.035). The fALFF values of the left occipital inferior and postcentral regions also exhibited positive correlations with the SDS scores (left occipital inferior: r = 0.541, p = 0.020; postcentral regions: r = 0.550, p = 0.018).

Conclusion: Abnormalities of rs-fMRI activities in NT1 patients, particularly those in the insula, calcarine, lingual gyrus, and postcentral regions, were closely associated with sleep disturbance and emotional disorders. These findings provide a better understanding the pathophysiology of NT1 with emotional disorders. Future longitudinal studies with independent cohorts are needed to explore the underlying neural mechanisms for neuropsychiatric comorbidities in NT1.