Treatment for obstructive sleep apnoea: effect on peripheral nerve function

Background and objective

Obstructive sleep apnoea (OSA) is suggested to be associated with peripheral nerve damage. A case–control study was conducted to provide further support to this observation. In a longitudinal intervention study, it was examined whether treatment for OSA has a possible beneficial effect on peripheral nerve function.

Methods

Participants were 23 patients with OSA and 23 controls matched for age and body mass index (BMI), all without any known cause of peripheral nerve damage. The sensory nerve action potential (SNAP) amplitudes of both sural nerves were determined. After 6 months of treatment for OSA, treatment compliance was evaluated and nerve conduction studies were repeated.

Results

Patients with OSA had significantly lower mean (standard deviation) sural SNAP amplitudes than controls (6.3 (3.5) v 11.2 (5.0), p<0.001). Multivariate regression analysis including the variables age, BMI and Apnoea–Hypopnea Index (AHI) showed that both age (p<0.01) and AHI (p<0.05) were inversely related to the SNAP amplitude. On follow‐up, the sural SNAP showed an increase of 2.6 mV on average (p<0.001). Multivariate regression analysis including the variables age, BMI, AHI, pretreatment SNAP and treatment compliance identified only treatment compliance as being significantly related to the SNAP increase (p⩽0.005).

Conclusion

OSA is an independent risk factor for axonal dysfunction of peripheral sensory nerves. Impaired neural function is at least partly reversible with treatment for sleep apnoea.Obstructive sleep apnoea (OSA) is a common disorder with an estimated prevalence in the general population of 2–5%.¹ Its main clinical features are loud snoring and breathing stoppage during sleep. Owing to non‐restful sleep, patients with OSA experience excessive daytime sleepiness and related neuropsychological impairments.² By different pathophysiological mechanisms, OSA is known to be associated with arterial hypertension,³ a hypercoagulable state,⁴ decreased cerebral perfusion,⁵ arteriosclerosis⁶ and severe cardiac arrhythmias,⁷ all of which potentially contribute to the increased mortality and cerebrocardiovascular morbidity of patients with OSA.^8,9Apart from that, an association of OSA with damage to the peripheral nervous system has been described only recently.^10,11 Thus, we reported an increased prevalence of axonal sensory polyneuropathy in patients with OSA.¹¹ This study found a decreased sural sensory nerve action potential (SNAP) in patients with OSA compared with controls. Additionally, a correlation of axonal dysfunction with the extent of oxygen desaturation was observed. We hypothesised that intermittent hypoxaemia is an independent risk factor for axonal dysfunction of peripheral nerves.¹¹This study had two aims: (1) to replicate our previous results in another case–control study, thereby providing further support to the assumed pathophysiology; and (2) to examine a possible, beneficial effect of treatment for OSA on peripheral nerve function in a longitudinal intervention study.