Evidence map›Paper›PMID 42377633›Full record

ArticleSleep & breathing = Schlaf & Atmung2026

Selective prolongation of the long-latency reflex component in obstructive sleep apnea: Evidence for cortical sensorimotor slowing.

Nur Türkmen, Şeyda Akbal Çufalı, Ömer Faruk Taş, Nurcan Yurtsever Kum

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Article in Sleep & breathing = Schlaf & Atmung, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Nur TürkmenDepartment of Neurology, Division of Clinical Neurophysiology, Ankara Bilkent City Hospital, Ankara, Türkiye. nurnoroloji@gmail.com.ORCID http://orcid.org/0000-0001-5863-7010
Şeyda Akbal ÇufalıDepartment of Otolaryngology-Head and Neck Surgery, Ankara Bilkent City Hospital, Ankara, Türkiye.
Ömer Faruk TaşDepartment of Neurology, Ankara Bilkent City Hospital, Ankara, Türkiye.
Nurcan Yurtsever KumDepartment of Otolaryngology-Head and Neck Surgery, Ankara Bilkent City Hospital, Ankara, Türkiye.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeObstructive 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.

methodsThirty-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.

resultsH-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).

conclusionsModerate-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.

Indexed as

H-ReflexReaction TimeSensorimotor CortexSleep Apnea, ObstructiveAdultElectromyographyFemaleHumansMaleMedian NerveMiddle AgedPolysomnographyReference ValuesH-reflexHypoxemiaLLR2 latencyLong-latency reflexObstructive sleep apneaSensorimotor integration

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.