ObjectiveThis study was aimed to investigate the characteristics of the amplitude of low-frequency fluctuation (ALFF) at specific frequencies in severe obstructive sleep apnea (OSA) patients. A comparison was made between pre-CPAP treatment and one night after continuous positive airway pressure (CPAP) treatment.Methods30 severe OSA patients and 19 healthy controls (HC) were recruited. The ALFF method was used to assess the local features of spontaneous brain activity and calculated at different bands (slow-5 and slow-4). A correlation analysis was performed to evaluate the relationship between the changes of the ALFF and polysomnography data.ResultsCompared with HC, in slow-5 frequency band, OSA patients showed significantly decreased ALFF in the left inferior temporal gyrus, and significantly increased ALFF in the left middle frontal gyrus, left inferior frontal gyrus, triangular part, right superior frontal gyrus, dorsolateral and right middle temporal gyrus. In slow-4 frequency, there was significantly decreased ALFF in the right inferior temporal gyrus, and significantly increased ALFF in the left precuneus, right posterior cingulate gyrus and right median cingulate besides the slow-5 difference band showed. Compared with pre-CPAP, we found that after CPAP treatment, ALFF signals in the left insula in slow-5 and left caudate in slow-4 increased, but the calcarine in slow-4 significantly reduced. Correlation analysis showed that the left angular slow-4 band change was positively correlated with the slow wave sleep change (r = 0.4933, p = 0.0056). The left cerebellum 6 slow-5 band change was positively correlated with the duration of the REM sleep change (r = 0.4563, p = 0.0113), and the left cerebellum 6 slow-4 band change was also positively correlated with the mean blood oxygen change in the REM (r = 0.4591, p = 0.0107) and NREM sleep (r = 0.4492, p = 0.0128).ConclusionWe found that the use of slow-4 was more specific in OSA studies. These results suggested that the severe OSA patients have frequency-related abnormal spontaneous neural activity, which may contribute to a better understanding of the pathological basis of OSA-related diseases and provide a potential therapeutic target for OSA patients.