Long-latency reflex prolongation in obstructive sleep apnea suggests cortical sensorimotor slowing: a controlled neurophysiology study

Obstructive sleep apnea (OSA) is associated with neurocognitive impairment and diffuse brain dysfunction beyond sleep–wake regulation. Long-latency reflexes (LLRs) are transcortical responses that provide a practical probe of cortical sensorimotor integration. We aimed to determine whether OSA selectively alters upper-limb LLR components. Thirty-nine patients with polysomnography-confirmed OSA and 21 healthy controls underwent Epworth Sleepiness Scale (ESS) assessment and standardized median nerve stimulation at the wrist with recordings from the abductor pollicis brevis during sustained contraction. H-reflex latency and LLR1–LLR3 onset latencies and response detectability were evaluated. Patients were stratified by OSA severity (mild vs moderate-to-severe) and by REM/positional phenotype; associations with polysomnographic indices, including minimum oxygen saturation (minSpO₂), were explored. H-reflex, LLR1, and LLR3 latencies did not differ between groups (all p > 0.05). In contrast, LLR2 latency was prolonged in moderate-to-severe OSA compared with controls (53.1 vs 50.4 ms, p = 0.014), and the H–LLR2 interval was longer (27.1 vs 25.5 ms, p = 0.029). In mild OSA, LLR2 latency correlated strongly and inversely with minSpO₂ (r = − 0.845, p = 0.008). LLR detectability did not differ significantly across groups. OSA is associated with a selective delay of the LLR2 component, compatible with cortical sensorimotor slowing not readily explained by peripheral conduction or H-reflex changes. LLR testing may offer a simple, noninvasive neurophysiological marker to complement conventional sleep metrics in future studies.