• Rainer Dziewas, Matthias Schilling, Philipp Engel, Matthias Boentert, Hyon Hor, Angelika Okegwo, Peter Lüdemann, E Bernd Ringelstein, and Peter Young.
• Department of Neurology, University Hospital of Münster, Albert-Schweitzer-Strasse 33, 48129 Münster, Germany. dziewas@uni-muenster.de
• J. Neurol. Neurosurg. Psychiatr. 2007 Mar 1; 78 (3): 295297295-7.

Background And ObjectiveObstructive 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.MethodsParticipants 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.ResultsPatients 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 < or = 0.005).ConclusionOSA 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.

18 keywords...

hide…