{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T11:42:15Z","timestamp":1790336535869,"version":"4.1.0"},"reference-count":34,"publisher":"Oxford University Press (OUP)","issue":"5","license":[{"start":{"date-parts":[[2020,11,29]],"date-time":"2020-11-29T00:00:00Z","timestamp":1606608000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2021,5,14]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Study Objectives<\/jats:title>\n                    <jats:p>Hypocretin deficient narcolepsy (type 1, NT1) presents with multiple sleep abnormalities including sleep-onset rapid eye movement (REM) periods (SOREMPs) and sleep fragmentation. We hypothesized that cortical arousals, as scored by an automatic detector, are elevated in NT1 and narcolepsy type 2 (NT2) patients as compared to control subjects.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We analyzed nocturnal polysomnography (PSG) recordings from 25 NT1 patients, 20 NT2 patients, 18 clinical control subjects (CC, suspected central hypersomnia but with normal cerebrospinal (CSF) fluid hypocretin-1 (hcrt-1) levels and normal results on the multiple sleep latency test), and 37 healthy control (HC) subjects. Arousals were automatically scored using Multimodal Arousal Detector (MAD), a previously validated automatic wakefulness and arousal detector. Multiple linear regressions were used to compare arousal index (ArI) distributions across groups. Comparisons were corrected for age, sex, body-mass index, medication, apnea-hypopnea index, periodic leg movement index, and comorbid rapid eye movement sleep behavior disorder.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>NT1 was associated with an average increase in ArI of 4.02 events\/h (p = 0.0246) compared to HC and CC, while no difference was found between NT2 and control groups. Additionally, a low CSF hcrt-1 level was predictive of increased ArI in all the CC, NT2, and NT1 groups.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>The results further support the hypothesis that a loss of hypocretin neurons causes fragmented sleep, which can be measured as an increased ArI as scored by the MAD.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/sleep\/zsaa255","type":"journal-article","created":{"date-parts":[[2020,11,28]],"date-time":"2020-11-28T20:26:45Z","timestamp":1606595205000},"source":"Crossref","is-referenced-by-count":19,"title":["Cortical arousal frequency is increased in narcolepsy type 1"],"prefix":"10.1093","volume":"44","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2872-0929","authenticated-orcid":false,"given":"Andreas","family":"Brink-Kjaer","sequence":"first","affiliation":[{"name":"Department of Health Technology, 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