Impact of Intermittent Hypoxia on Peripheral Nervous Systems in Obstructive Sleep Apnea Syndrome

Abstract

Objectives: Intermittent hypoxia resulting in endothelial dysfunction in microvascular circulation constitutes one of the mechanisms underlying complications of obstructive sleep apnea syndrome (OSAS), such as hypertension and atherosclerosis. The role of intermittent hypoxia on peripheral nerves, however, is still debated. Here, we designed a study in patients with OSAS to investigate different levels of the central and peripheral nervous systems, in order to delineate what kind of pathologic substrate was present, if any, and at which level of the neuromuscular pathway. Methods: A total of 20 patients with OSAS and 18 sex- and age-matched healthy controls were enrolled in our study. All participants underwent nerve conduction studies (NCSs) to analyze peripheral nerves, evoked potentials for somatosensory, visual evoked potential (VEP) and brainstem auditory pathways, blink reflex studies to analyze brainstem and subcortical structures, and transcranial magnetic stimulation to analyze the motor cortex and corticospinal pathway. Results: A comparison of NCSs between the two groups showed that the motor amplitudes of the ulnar nerve (P = 0.015) and sensory amplitudes of the sural nerve (P = 0.026) were significantly smaller in the OSAS group than those in the control group. The mean P100 amplitudes of VEP responses were 7.11 ± 2.73 μV in the OSAS group and 9.75 ± 3.52 μV in the control group (P = 0.022). In correlation analysis, the amplitude of P100 responses was positively correlated with the lowest oxygen saturation (P = 0.026). Conclusion: Our results confirmed the presence of generalized axonal involvement in the peripheral nervous system in OSAS, probably secondary to chronic intermittent hypoxemia.

Brainstem impairment in obstructive sleep apnoea and the effect of CPAP treatment: an electrophysiological blink reflex study

“…In line with the present findings, the study by Urban et al (1996), although not showing significant changes in electrophysiological brainstem responses in a group of 18 patients with OSA, documented abnormalities in the left BR R1 component in one patient, suggesting a left pontine lesion [ 10 ]. However, more recently, Tavsanli and colleagues found no significant differences in BR response latencies between patients with OSA and controls [ 30 ]. Considering the paucity of studies investigating the BR responses in patients with OSA, further studies are needed for reaching a unequivocal conclusion, that currently cannot be postulated.…”