{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T20:20:40Z","timestamp":1790799640112,"version":"4.1.0"},"reference-count":52,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Applied Physiology"],"published-print":{"date-parts":[[2014,2,1]]},"abstract":"<jats:p>\n                    Sleep-disordered breathing (SDB) is highly prevalent in patients with spinal cord injury (SCI); the exact mechanism(s) or the predictors of disease are unknown. We hypothesized that patients with cervical SCI (C-SCI) are more susceptible to central apnea than patients with thoracic SCI (T-SCI) or able-bodied controls. Sixteen patients with chronic SCI, level T6 or above (8 C-SCI, 8 T-SCI; age 42.5 \u00b1 15.5 years; body mass index 25.9 \u00b1 4.9 kg\/m\n                    <jats:sup>2<\/jats:sup>\n                    ) and 16 matched controls were studied. The hypocapnic apneic threshold and CO\n                    <jats:sub>2<\/jats:sub>\n                    reserve were determined using noninvasive ventilation. For participants with spontaneous central apnea, CO\n                    <jats:sub>2<\/jats:sub>\n                    was administered until central apnea was abolished, and CO\n                    <jats:sub>2<\/jats:sub>\n                    reserve was measured as the difference in end-tidal CO\n                    <jats:sub>2<\/jats:sub>\n                    (Pet\n                    <jats:sub>\n                      CO\n                      <jats:sub>2<\/jats:sub>\n                    <\/jats:sub>\n                    ) before and after. Steady-state plant gain (PG) was calculated from Pet\n                    <jats:sub>\n                      CO\n                      <jats:sub>2<\/jats:sub>\n                    <\/jats:sub>\n                    and V\n                    <jats:sub>E<\/jats:sub>\n                    ratio during stable sleep. Controller gain (CG) was defined as the ratio of change in V\n                    <jats:sub>E<\/jats:sub>\n                    between control and hypopnea or apnea to the \u0394Pet\n                    <jats:sub>\n                      CO\n                      <jats:sub>2<\/jats:sub>\n                    <\/jats:sub>\n                    . Central SDB was more common in C-SCI than T-SCI (63% vs. 13%, respectively; P &lt; 0.05). Mean CO\n                    <jats:sub>2<\/jats:sub>\n                    reserve for all participants was narrower in C-SCI than in T-SCI or control group (\u22120.4 \u00b1 2.9 vs.\u22122.9 \u00b1 3.3 vs. \u22123.0 \u00b1 1.2 l\u00b7min\n                    <jats:sup>\u22121<\/jats:sup>\n                    \u00b7mmHg\n                    <jats:sup>\u22121<\/jats:sup>\n                    , respectively; P &lt; 0.05). PG was higher in C-SCI than in T-SCI or control groups (10.5 \u00b1 2.4 vs. 5.9 \u00b1 2.4 vs. 6.3 \u00b1 1.6 mmHg\u00b7l\n                    <jats:sup>\u22121<\/jats:sup>\n                    \u00b7min\n                    <jats:sup>\u22121<\/jats:sup>\n                    , respectively; P &lt; 0.05) and CG was not significantly different. The CO\n                    <jats:sub>2<\/jats:sub>\n                    reserve was an independent predictor of apnea-hypopnea index. In conclusion, C-SCI had higher rates of central SDB, indicating that tetraplegia is a risk factor for central sleep apnea. Sleep-related hypoventilation may play a significant role in the mechanism of SDB in higher SCI levels.\n                  <\/jats:p>","DOI":"10.1152\/japplphysiol.00731.2013","type":"journal-article","created":{"date-parts":[[2013,10,11]],"date-time":"2013-10-11T09:24:55Z","timestamp":1381483495000},"page":"345-353","source":"Crossref","is-referenced-by-count":53,"title":["Tetraplegia is a risk factor for central sleep apnea"],"prefix":"10.1152","volume":"116","author":[{"given":"Abdulghani","family":"Sankari","sequence":"first","affiliation":[{"name":"Sleep Research Laboratory, John D. Dingell Veterans Affairs Medical Center, Wayne State University, Detroit, Michigan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Amy T.","family":"Bascom","sequence":"additional","affiliation":[{"name":"Sleep Research Laboratory, John D. 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