Objectives: Intermittent hypoxia resulting in endothelial dysfunction inmicrovascular circulation constitutes one of the mechanisms underlyingcomplications of obstructive sleep apnea syndrome (OSAS), such as hypertensionand atherosclerosis. The role of intermittent hypoxia on peripheral nerves, however,is still debated. Here, we designed a study in patients with OSAS to investigatedifferent levels of the central and peripheral nervous systems, in order to delineatewhat kind of pathologic substrate was present, if any, and at which level of theneuromuscular pathway. Methods: A total of 20 patients with OSAS and 18sex‑ and age‑matched healthy controls were enrolled in our study. All participantsunderwent nerve conduction studies (NCSs) to analyze peripheral nerves, evokedpotentials for somatosensory, visual evoked potential (VEP) and brainstem auditorypathways, blink reflex studies to analyze brainstem and subcortical structures, andtranscranial magnetic stimulation to analyze the motor cortex and corticospinalpathway. Results: A comparison of NCSs between the two groups showed thatthe motor amplitudes of the ulnar nerve (P = 0.015) and sensory amplitudes of thesural nerve (P = 0.026) were significantly smaller in the OSAS group than those inthe control group. The mean P100 amplitudes of VEP responses were 7.11 ± 2.73μV in the OSAS group and 9.75 ± 3.52 μV in the control group (P = 0.022). Incorrelation analysis, the amplitude of P100 responses was positively correlatedwith the lowest oxygen saturation (P = 0.026). Conclusion: Our results confirmedthe presence of generalized axonal involvement in the peripheral nervous systemin OSAS, probably secondary to chronic intermittent hypoxemia.