Sleep & breathing = Schlaf & Atmung · 2026
Selective prolongation of the long-latency reflex component in obstructive sleep apnea: Evidence for cortical sensorimotor slowing.
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Türkmen Nur, Akbal Çufalı Şeyda, Taş Ömer Faruk, Yurtsever Kum Nurcan
Аннотация
PURPOSE: Obstructive sleep apnea (OSA) is associated with neurocognitive impairment and central nervous system dysfunction. Long-latency reflexes (LLRs) provide a practical neurophysiological probe of cortical sensorimotor integration. This study investigated whether OSA selectively alters upper-limb LLR components.
METHODS: Thirty-nine patients with polysomnography-confirmed OSA and 21 healthy controls underwent Epworth Sleepiness Scale assessment and standardized median nerve stimulation at the wrist, with recordings from the abductor pollicis brevis during sustained contraction. H-reflex and LLR1-LLR3 onset latencies and response detectability were evaluated. Patients were stratified by OSA severity and REM/positional phenotype. Associations with polysomnographic indices, including minimum oxygen saturation, were explored.
RESULTS: H-reflex, LLR1, and LLR3 latencies did not differ significantly between groups. LLR2 latency was prolonged in moderate-to-severe OSA compared with controls in the unadjusted analysis (53.1 vs. 50.4 ms, p = 0.014), and the H-LLR2 interval was also longer (27.1 vs. 25.5 ms, p = 0.029). After adjustment for age and BMI, the group effect on LLR2 latency remained significant (F = 3.686, p = 0.032), whereas the adjusted group effect for the H-LLR2 interval was no longer significant. In an exploratory subgroup analysis of mild OSA, unadjusted inverse correlation was observed between LLR2 latency and minimum oxygen saturation (r = - 0.845, p = 0.008); however, this association did not persist after adjustment for age and BMI (partial r = 0.188, p = 0.378).
CONCLUSIONS: Moderate-to-severe OSA may be associated with selective prolongation of LLR2 latency, compatible with altered long-loop sensorimotor processing. LLR testing may represent a simple exploratory neurophysiological approach to complement conventional sleep metrics, pending validation in larger prospective cohorts.
METHODS: Thirty-nine patients with polysomnography-confirmed OSA and 21 healthy controls underwent Epworth Sleepiness Scale assessment and standardized median nerve stimulation at the wrist, with recordings from the abductor pollicis brevis during sustained contraction. H-reflex and LLR1-LLR3 onset latencies and response detectability were evaluated. Patients were stratified by OSA severity and REM/positional phenotype. Associations with polysomnographic indices, including minimum oxygen saturation, were explored.
RESULTS: H-reflex, LLR1, and LLR3 latencies did not differ significantly between groups. LLR2 latency was prolonged in moderate-to-severe OSA compared with controls in the unadjusted analysis (53.1 vs. 50.4 ms, p = 0.014), and the H-LLR2 interval was also longer (27.1 vs. 25.5 ms, p = 0.029). After adjustment for age and BMI, the group effect on LLR2 latency remained significant (F = 3.686, p = 0.032), whereas the adjusted group effect for the H-LLR2 interval was no longer significant. In an exploratory subgroup analysis of mild OSA, unadjusted inverse correlation was observed between LLR2 latency and minimum oxygen saturation (r = - 0.845, p = 0.008); however, this association did not persist after adjustment for age and BMI (partial r = 0.188, p = 0.378).
CONCLUSIONS: Moderate-to-severe OSA may be associated with selective prolongation of LLR2 latency, compatible with altered long-loop sensorimotor processing. LLR testing may represent a simple exploratory neurophysiological approach to complement conventional sleep metrics, pending validation in larger prospective cohorts.