engleski

Obstructive sleep apnoea and sensomotor polyneuropathy

Obstructive sleep apnoea (OSA) is a major public health problem with increasing prevalence in parallel with the growing trend of obesity. It is unknown to what extent chronic intermittent hypoxemia in OSA causes damage to the motor peripheral nerves. We hypothesised that OSA patients would have bilaterally significantly impaired amplitudes of evoked potentials, not only in the sensory, but also in motor peripheral nerves. Objectives were to assess the relationship between OSA and peripheral motor neuropathy. We conducted an observational study on 43 OSA patients with AHI index>10 confirmed by the whole- night polysomnography (PSG), and 40 controls (without OSA). All subjects underwent standardised electroneurographic testing, with full assessment of amplitudes of evoked compound muscle action potentials (CMAP), sensory neural action potentials (SNAP), nerve conduction velocities, and distal motor and sensory latencies of peroneal and sural nerves, bilaterally. All subjects were tested with appropriate laboratory tests for known diseases that may affect the peripheral nervous system, and were excluded from the study if history of such diseases and/or tests values and/or clinical findings were positive. The averaged CMAP and SNAP amplitudes were significantly reduced in OSA patients compared with controls, before and after adjustment for BMI, age and gender (p<0.001). These results confirmed that OSA patients had significantly lower amplitudes of evoked action potentials of both motor and sensory peripheral nerves. The axonal damages of motor nerves clearly exist in OSA patients in lower limbs to a greater extent than previously thought.

obstructive sleep apnoea ; sensomotor polyneuropathy

nije evidentirano