Devin L Brown1, Ronald D Chervin, James Wolfe, Rebecca Hughes, MaryAnn Concannon, Lynda D Lisabeth, Kristen L Gruis. 1. From the Stroke Program (D.L.B., R.H., M.C., L.D.L.), Sleep Disorders Center (R.D.C.), EMG Laboratory, Department of Neurology (J.W.), and School of Public Health (L.D.L.), University of Michigan, Ann Arbor; and EMG Laboratory (K.L.G.), Department of Neurology, SUNY Upstate, Syracuse, NY.
Abstract
OBJECTIVE: This cross-sectional study of acute ischemic stroke patients examined relationships between hypoglossal nerve conduction, sleep-disordered breathing (SDB), and its severity. METHODS: Patients within 7 days of stroke underwent nocturnal respiratory monitoring with the ApneaLink device and hypoglossal nerve conduction studies. RESULTS: Eighteen of 52 subjects (35% [95% confidence interval: 22%, 49%]) had an abnormal hypoglossal amplitude and 23 (44% [95% confidence interval: 30%, 59%]) had an abnormal hypoglossal latency. No differences were identified in hypoglossal nerve latency or amplitude between those with (n = 26) and without (n = 26) significant SDB, defined by an apnea-hypopnea index ≥ 15. However, hypoglossal nerve conduction latency was associated (linear regression p < 0.05) with SDB severity as reflected by the apnea-hypopnea index. CONCLUSIONS: Acute ischemic stroke patients have a high prevalence of hypoglossal nerve dysfunction. Further studies are needed to explore whether hypoglossal nerve dysfunction may be a cause or consequence of SDB in stroke patients and whether this association can provide further insight into the pathophysiology of SDB in this population.
OBJECTIVE: This cross-sectional study of acute ischemic strokepatients examined relationships between hypoglossal nerve conduction, sleep-disordered breathing (SDB), and its severity. METHODS:Patients within 7 days of stroke underwent nocturnal respiratory monitoring with the ApneaLink device and hypoglossal nerve conduction studies. RESULTS: Eighteen of 52 subjects (35% [95% confidence interval: 22%, 49%]) had an abnormal hypoglossal amplitude and 23 (44% [95% confidence interval: 30%, 59%]) had an abnormal hypoglossal latency. No differences were identified in hypoglossal nerve latency or amplitude between those with (n = 26) and without (n = 26) significant SDB, defined by an apnea-hypopnea index ≥ 15. However, hypoglossal nerve conduction latency was associated (linear regression p < 0.05) with SDB severity as reflected by the apnea-hypopnea index. CONCLUSIONS: Acute ischemic strokepatients have a high prevalence of hypoglossal nerve dysfunction. Further studies are needed to explore whether hypoglossal nerve dysfunction may be a cause or consequence of SDB in strokepatients and whether this association can provide further insight into the pathophysiology of SDB in this population.
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