Obstructive sleep apnoea: an underestimated cause of peripheral neuropathy

Short abstract

Patients with cryptogenic polyneuropathies should be screened for OSA

Chronic sensory or sensorimotor polyneuropathy is a common clinical problem referred to neurologists. Even with modern diagnostic approaches, up to one third of them remain unclassified.¹,² Recent studies have provided insight into their clinical spectrum and course. The age of onset tends to be in the sixth to seventh decade of life. Symptoms progress slowly, and most patients present with paraesthesias or pain. Cryptogenic polyneuropathies are almost exclusively axonal on clinical, electrophysiological and histological grounds.¹,²

In this volume of the Journal of Neurology, Neurosurgery, and Psychiatry, Dziewas et al³(see page 295) report the results of the treatment of obstructive sleep apnoea (OSA) on peripheral nerve function.³ In a previous study, the authors observed an increased prevalence of axonal sensory polyneuropathy in patients with OSA, but this association may be incidental as OSA is a frequent disorder with an estimated prevalence of 2–5% in the general population.³,⁴ The observation of an increased sensory nerve action potential after nasal continuous airway pressure, especially in patients with good compliance, argues for a link between the two pathologies. As pointed out by the authors, the limitation of this study is that thyroid function, vitamin B₁₂ and folic acid have not been systematically studied.

From a clinical point of view, this observation is of particular interest as firstly, it may be possible to reduce the number of cryptogenic polyneuropathies, and secondly, this could lead to a therapeutic approach—that is, nasal continuous airway pressure. Patients with cryptogenic polyneuropathies should be systematically clinically screened for OSA; if positive, they should undergo polysomnography.