Screening sleep disordered breathing in stroke unit

Resea ch A icle Sc eening Sleep Diso de ed B ea hing in S oke Uni Ki si Väy ynen,1,2 Ka i Ko elainen,2Heikki Numminen,2Ka ja Mie inen,3Anna Keso,3 Mi ja Tenhunen,1Heini Huh ala,4and Sa i-Leena Himanen1,3 1Depa men o Clinical Neu ophysiology, Medical Imaging Cen e and Hospi al Pha macy, Tampe e Uni e si y Hospi al, 33521 Tampe e, Finland 2Depa men o Neu oscience and Rehabili a ion, Tampe e Uni e si y Hospi al, 33521 Tampe e, Finland 3School o Medicine, Uni e si y o Tampe e, 33520 Tampe e, Finland 4School o Heal h Sciences, Uni e si y o Tampe e, 33520 Tampe e, Finland Co espondence should be add essed o Sa i-Leena Himanen; sa i-leena.himanen@u a. i Recei ed 25 Ma ch 2014; Re ised 12 May 2014; Accep ed 14 May 2014; Published 27 May 2014 Academic Edi o : Ma co Zucconi Copy igh © 2014 Ki si V¨ ay ynen e al. This is an open access a icle dis ibu ed unde he C ea i e Commons A ibu ion License, which pe mi s un es ic ed use, dis ibu ion, and ep oduc ion in any medium, p o ided he o iginal wo k is p ope ly ci ed. In acu e s oke, OSA has been ound o impai ehabili a ion and inc ease mo ali y bu he e ec o cen al apnea is mo e unclea . The aim o he p esen s udy was o e alua e he easibili y o using limi ed ambula o y eco ding sys em (sleep ma ess o e alua e noc u nal b ea hing and EOG-elec odes o sleep s aging) in sleep diso de ed b ea hing (SDB) diagnos ics in mild acu e ce eb al ischemia pa ien s and o disco e he p e alence o a ious SDB-pa e ns among hese pa ien s. 42 pa ien s wi h mild ischemic s oke o ansien ischemic a ack we e s udied. OSA was ound in 22 pa ien s (52.4%). Cen al apnea was ound in wo pa ien s (4.8%) and sus ained pa ial obs uc ion in only one pa ien (2.4%). Sleep s aging wi h EOG-elec odes only yielded a simila ou come as sco ing wi h s anda d ules. OSA was ound o be common e en a e mild s oke. I s ea ly diagnosis and ea men would be a ou able in o de o imp o e eco e y and educe mo ali y. Ou esul s sugges ha OSA can be assessed by a limi ed eco ding se ing wi h EOG-elec odes, sleep ma ess, and pulse oxime y. 1. In oduc ion Sleep diso de ed b ea hing (SDB) is common in ce eb o as- cula disease [1]. In pa icula , obs uc i e sleep apnea (OSA) cons i u es a isk ac o o ce eb o ascula e en s, and i is equen ly seen in pa ien s wi h bo h s oke and ansien ischemic a ack (TIA) [1,2]. OSA is known o inc ease s oke mo ali y and i wo sens he ou comes o ehabili a ion [3– 5]. Con inuous posi i e ai way p essu e (CPAP) ea men o OSAins okepa ien shasbeen ound odec easemo ali y, imp o e unc ional eco e y, inc ease subjec i e well-being and mood, and inhibi ecu en s okes [6–10]. The e ec o cen alapneasonmo ali yand unc ional eco e yins oke pa ien s is less s udied, bu in one s udy cen al apnea did no inc ease mo ali y a e s oke as OSA did [11]. E en hough ou ine sc eening o OSA in he s oke uni s is becoming mo e common, i is no usually pe o med in he s oke uni s in Finland. One eason o his migh be ha pa ien s wi h bo h s oke and OSA do no p esen he ypical clinical pic u e o sleep apnea; hey a e o en nei he obese no sleepy [4,12,13]. In addi ion, i migh be ha sleep s udies a e conside ed cumbe some in acu e hospi al wa ds. Pa ien s in s oke uni s may ha e many di e en moni o ing de ices, as well as nasal supplemen a y oxygen he apy, and pe o ming noc u nal polyg aphy wi h addi ional senso s is pe haps no a o ed. Sleep ma esses p o ide a nonin asi e means o diagnose SDB. Bo h he SCSB (s a ic cha ge sensi i e bed) and he Em i mo emen senso ha e been p o en o be sui able in de ec ing sleep apnea [14,15]. SDB diagnos ics wi h he mo emen senso is pa ien - iendly, and he manual sco ing p ocedu e, pe o med in 3 min epochs, is easy and apid. Howe e , in limi ed polyg aphy se ings wi hou EEG, he apnea-hypopnea index (AHI) ends o be lowe han in ull polysomnog aphy (PSG) eco dings [16]. In acu e wa ds pa ien s o en sleep poo ly due o he nu sing and ea men Hindawi Publishing Co po a ion Sleep Diso de s Volume 2014, A icle ID 317615, 7 pages h p://dx.doi.o g/10.1155/2014/317615 2Sleep Diso de s ime schedules. The e o e some es ima ion o o al sleep ime would be bene icial. Wi h his s udy we aim o disco e he p e alence o obs uc i e and cen al sleep apnea as well as p olonged pa ial obs uc ion, among mild s oke and TIA pa ien s in Finland. P olonged pa ial obs uc ion is associa ed wi h con inuous inc ease in espi a o y esis ance wi hou apneas o hypopneas [17–19]. I is easily de ec ed by he SCSB and heEm i senso s,andi sp e alenceins okepa ien shas no been p e iously s udied. In addi ion we aim o de e mina e whe he limi ed polyg- aphy consis ing o mo emen senso and pulse oxime y in o de o e alua e noc u nal b ea hing combined wi h elec ooculog aphy-signal (EOG) in o de o e alua e sleep ime will p o ide a diagnos ic means o adequa e quali y in de ec ing SDB. 2. Ma e ials and Me hods Pa ien s we e ec ui ed om he S oke Uni o Tampe e Uni- e si y Hospi al be ween May and Oc obe , 2010. All pa ien s we e hospi alized due o ischemic ce eb al s oke o ansien ischemic a ack (TIA). The ini ial eligibili y c i e ia o he s udy we e as ollows: (a) TIA o mild ischemic s oke, he se e i y de ined as Na ional Ins i u es o Heal h S oke Scale (NIHSS) sco e <12, and (b) no p e ious CPAP ea men o OSA. The esea che e alua ed he NIHSS sco e a he wa d and he ollowing demog aphic da a we e ga he ed: age, sex, BMI, neck ci cum e ence, p e ious diseases, smoking, use o alcohol, subjec i e sleep p oblems (sno ing and apnea) in he weeks be o e he s oke, and inc eased day ime sleepiness. Fo sleepiness he ollowing ques ion was p esen ed: “we e yousleepie hanusualacoupleo daysbe o e hes oke?” The s udy was app o ed by he E hical Commi ee o he Pi kanmaa Hospi al Dis ic and all he subjec s ga e hei w i en in o med consen . I OSA was ound, he subjec was e e ed o he Sleep Cen e o e alua e he need o CPAP ea men . The pulmonologis hen began CPAP ea men acco ding o he s anda ds o ou hospi al. 2.1. Reco ding Mon age. The polyg aphic eco dings we e pe o med du ing he i s nigh in he hospi al, whene e possible. The eco dings we e made in he s oke uni o a he neu ologic wa d. The limi ed polyg aphy se ing consis ed o wo EOG channels (EOG P8-A2, EOG P18-A2), elec o- ca diog aphy, pulse oxime y, and he Em i senso (32 cm × 62 ×0.4 cm, placed unde he ho acic a ea o he pa ien ). In 14 andomly selec ed pa ien s noc u nal sleep quali y and b ea hing we e assessed wi h ull polysomnog aphy, which consis ed o he same senso s as he limi ed polyg aphy and addi ionally six EEG channels (F3-A2, C3-A2, O1-A2, F4- A1, C4-A1, and O2-A1), submen al and an e io ibialis mus- cle elec omyog aphy, ho acic and abdominal espi a o y mo emen s by induc i e bel s, and posi ion. Ai low was measu ed wi h a he mis o and also wi h a nasal p essu e ansduce i he pa ien did no ha e nasal supplemen a y oxygen he apy. A sampling a e o 2 Hz was used o pulse oxime y, 10 Hz o espi a o y mo emen s, 500 Hz o ECG, and 200 Hz o he Em i senso and he o he signals. 2.2. Visual Analysis. The ull polysomnog aphies (PSG) we e classi ied in o he sleep s ages acco ding o he s anda d c i e ia. The apnea-hypopnea index (AHI) was calcula ed as he numbe o obs uc i e apneas and hypopneas (hypopnea ule 4b in [20]) pe hou o sleep. A ousals we e sco ed acco ding o he c i e ia o he ASDA [21]. To e alua e he easibili y o he in ended EOG sleep s aging we classi ied he ull polysomnog aphies in o he sleep s ages by means o he EOG-signals, wi hou EEG o EMG, oo [22]. The amoun s o sleep and sleep s ages comp ised by he wo di e en me hods we e hen compa ed. The limi ed polyg aphs (POL) we e classi ied in o he sleep s ages u ilizing only he EOG signals. The espi a o y analysis o he limi ed polyg aphs was pe o med by he Em i signal. Em i signal was sco ed in o one o en ca ego ies in 3 min epochs as in ou p e ious wo k [15,19]. The ma ess signal ca ego ies used we e as ollows: no mal b ea hing (NB), pe iodic b ea hing ype 1 (P1), obs uc i e pe iodic b ea hing ypes 1–3 (OP1–3), cen al pe iodic b ea hing (CP), p olonged pa ial obs uc ion (inc eased espi a o y esis ance, IRR), la ge mo emen a i ac s las ing >40 s (M), epochs wi h a leas ou sho pe iodic mo emen s in all channels wi hou espi a o y a ia ion (pe iodic mo emen s, PM), and wake epochs (W) wi h EEG-de ined wake ulness o mo e han 50% o ime. The wake ulness epochs we e no included in he u he analyses. The espi a o y esul s o he ma ess b ea hing analyses a e p esen ed in pe cen ages o o al sleep ime de i ed om he EOG sco ing. The EEG sco ings we e pe o med by wo clinical neu- ophysiologis s. The median sco ing ag eemen was 84.1% (76.4–86.7%)wi h hemedianKappa aluebeing0.71( ange 0.67–0.81). The consensus sco ings we e used in he inal analyses. The u he analyses o he eco dings we e pe - o med om he i s sleep onse a e 8 PM o he inal awakening in he mo ning. Obs uc i e AHI ≥15/h was selec ed o designa e ma ked obs uc i e sleep apnea. Based on ou p e ious s udy an obs uc i e AHI o 15/h co esponds well wi h obs uc i e pe iodic b ea hing ime (%OP1 + %OP2 +%OP3)o 21%inEm i sco ing[15]. Thus he cu -o alues o obs uc i e AHI ≥15/h and obs uc i e pe iodic ime pe cen age o ≥21 we e selec ed o de ine ma ked OSA and such pa ien s we e classi ied in o he OSA g oup. The same cu -o alues we e used o de ine he cen al apnea g oup(cen alAI≥15/h o cen al pe iodic b ea hing o ≥21%). The hi d g oup was comp ised o he pa ien s ha ing a p olonged pa ial obs uc ion (IRR) pe cen age ≥21%, wi h bo h obs uc i e AHI and cen al AI less han 15/h (IRR g oup). The emaining pa ien s composed he non-SDB g oup. 2.3. S a is ics. In he s a is ical compa isons, nonpa ame - ic es s we e used, since all he a iables we e no no - mallydis ibu ed.Thecompa isonbe ween he wosleep s aging p ocedu es (s anda d sco ing e sus EOG sco ing) was pe o med by Spea man’s co ela ion coe icien and Sleep Diso de s 3 Cohen’s Kappa-analysis [23]. Pai -wised compa isons o ela ed pa ame e s we e conduc ed by using he Wilcoxon es . The pa ien g oups we e compa ed wi h he Mann- Whi ney es . The demog aphic da a (sex, age, BMI, p e ious dep ession, p e ious s oke, p e ious hea ailu e, hype en- sion, hype choles e olemia, diabe es melli us, hypo hy eosis, as hma, COPD, p e ious o he lung diseases, use o obacco, use o alcohol, NIHSS-sco e, sno ing, wi nessed apneas, and inc eased sleepiness) we e e alua ed wi h he bina y logis ic eg ession analysis. In s a is ical analyses 𝑃 alues <0.05 we e conside ed s a is ically signi ican . 3. Resul s Al oge he 46 pa ien s olun ee ed o he s udy. Fou een pa ien s we e ec ui ed o ull polysomnog aphy bu only wel e eco dings we e comple ed (86%). One pa ien wan ed he senso s o be de ached soon a e s a ing he eco ding, and one eco ding e mina ed unexpec edly a 11 p.m. Thi y- wo pa ien s we e examined by using he limi ed polyg aphy. Two o hese eco dings (6%) we e excluded om he analyses; one pa ien wan ed he eco ding o be s opped jus be o e alling asleep and in one eco ding bo h he Em i and pulse oxime y signals we e missed. In o al, 42 pa ien s we e accep ed in o he analyses. The polysomnog aphy g oup (PSG) consis ed o one emale pa ien and ele en male pa ien s, whe eas in he limi ed polyg aphy (POL) g oup, 17 pa ien s we e emale and 13 we e male. The analysis s a imes a ied be ween 20 : 06 and 02 : 45, wi h median o 21 : 19. In o de o ensu e he easibili y o he sleep s age sco ing basedon heEOGelec odes,wecompa ed hesleeps age esul s de i ed by using he wo sco ing me hods in he PSG g oup. The sleep s aging ag eemen be ween he s anda d sco ingme hodand heEOGsco ingwas82.2%(median, ange 56.3–88.2%). The median Kappa alue was 0.72 (0.41– 0.80), indica ing subs an ial ag eemen [23]. The o al sleep ime (TST) es ima ed by he EOG sco ing co ela ed well wi h he TST measu ed by s anda d sco ing (Spea man’s co ela ion coe icien 0.964). The sleep s age pa ame e s a e p esen ed in Table 1. The o al amoun o sleep was highe by heEOGsco ing hanby hes anda dsco ing(353.5min e sus 321 min, esp., Table 1), bu he di e ence emained a he edge o s a is ical signi icance. The pe cen ages in he amoun s o a ious sleep s ages be ween he wo sco ing p ocedu es did no yield o s a is ically signi ican di e ences. Figu e 1 depic u es he hypnog ams wi h he lowes sleep s aging ag eemen be ween he s anda d sco ing and he EOG sco ing (56.3%, Kappa 0.41 = mode a e conco dance). The sleep s age pa ame e s o all 42 pa ien s a e p esen ed in Table 2. The median sleep e iciency, as well as he amoun s o deep sleep and REM-sleep, was in gene al qui e low e en i mos o he subjec s slep subjec i ely well o ai ly well du ing he s udy nigh (45% and 36%, esp.). Se en een pe cen o he pa ien s slep poo ly and one pa ien (2%) el ha hehadno slep a all(his o alsleep imewas3h). Eigh ou o he wel e subjec s in he PSG g oup had AHI ≥15/h (one emale, 7 men). In he POL g oup 14 pa ien s had obs uc i e pe iodic b ea hing ≥21% o TST (8 emale, 6 male). The espi a o y pa ame e s o he PSG g oup and he POL g oup a e p esen ed in Table 3.Wealsocalcula ed he AHI o sleep pe iod ime in he PSG g oup (sleep pe iod ime, ime omsleeponse o he inalawakeningwi h wake ulness ime inside he sleep pe iod included). The AHI o he sleep pe iod ime was signi ican ly lowe han he AHI de i ed om TST (13.3/h, ange 0.5–48.5, e sus 18.1/h ange 1.2–67.9, 𝑃 alue0.002).Whileeigh pa ien sou o wel ehad AHI >15/h when TST was applied, only h ee pa ien s had AHI >15/h i sleep pe iod ime was used. Al oge he 17 subjec s (40.5%, 9 males, 8 emales) did no ha e sleep diso de ed b ea hing (non-SDB g oup, Table 4) when hePSGand hePOLg oupswe epooled.The emaining pa ien s had ei he obs uc i e o cen al b ea h- ing diso de ; no one had bo h abno mal obs uc i e and abno mal cen al indices. OSA was ound in 22 pa ien s (52.4%, OSA g oup). Nine o hese pa ien s we e emale (41%). Cen al apnea was ound in wo male pa ien s (4.8%, cen al g oup). IRR was ound only in one emale pa ien (2.4%, IRR g oup). In gene al he s udy subjec s had e y mild s oke as assessed by he NIHSS and hey we e no e y o e weigh . S a is ical compa isons we e made be ween henon-SDBand heOSAg oupsonlyas hecen alg oup and he IRR g oup emained so small. The e we e only ew s a is ically signi ican di e ences be ween he non-SDB and OSA g oups; he subjec s in he non-SDB g oup had mo e slow wa e sleep (N3), and hei oxygen desa u a ion indices (ODI4) we e lowe . Mo e demog aphic pa ame e s a e p esen ed in Table 5. Hype ension, sno ing, and inc eased sleepiness we e e- quen in all subjec g oups. The demog aphic a iables we e e alua ed wi h he bina y logis ic eg ession analysis. Only inc eased sleepiness was iden i ied as an independen p edic o o hes okein henon-SDBg oupwi hOR=5.33 (CI 1.32–21.53). 4. Discussion In he p esen s udy he p e alence o SDB among mild s oke and TIA pa ien s was 59.5%. Ou esul o he p e alence o OSA (52.3%) in pa ien s wi h TIA o mild s oke is in conco dance wi h hose o a p e ious s udy [24]. Only wo subjec swe e ound oha ema kedcen alapnea(4.8%), bu his co esponds wi h he indings in a p e ious me a- analysis [25]. The p e alence o IRR in he p esen s udy was lowe (2.4%) han he p e alence among ou sleep labo a o y pa ien s (10.2%) [15]. The cu -o limi we p e iously used was lowe (≥15%)bu e eni he aluehadbeenused, henumbe o IRR-pa ien s in he p esen s udy would no ha e changed. OSA inc eases sympa he ic one [26], inducing hype - ension which may be a p edisposing ac o o s oke. Howe e , he e a e many physiologic mechanisms behind he inc ease in blood p essu e in OSA. Fo example, he hypoxia associa ed wi h pe iodic apnea augmen s sympa he ic ac i i y and blood p essu e wi h an addi ional inc ease caused by epe i i e a ousals, es o ing he uppe ai way pa ency [27– 29]. IRR ep esen s a di e en SDB en i y since he pe iods wi h pa ial obs uc ion may las se e al minu es wi hou 4Sleep Diso de s Table 1: Sleep s age pa ame e s o he PSG g oup wi h he wo di e en sco ing sys ems. S anda d sco ing EOG sco ing 𝑃 alue Median (min–max) Median (min–max) TST (min) 321 (48.5–506.5) 353.5 (49.5–498.5) 0.051 SEI (%) 72.2 (42–90.9) 69.1 (42.9–89.4) 0.48 % N1 12.8 (6.5–41.2) 15.4 (6.8–48.5) 0.068 % N2 69.5 (36.1–83.2) 66.2 (37.4–82.4) 0.33 % N3 7.0 (0–23.6) 5.9 (0–17.7) 0.17 % REM 11.2 (0–22.3) 12.9 (0–25.4) 0.61 S anda d sco ing: sleep s age sco ing acco ding o he s anda d ules; EOG sco ing: sleep s age sco ing based on he wo EOG (elec ooculog aphy) channels only; TST: o al sleep ime; SEI: sleep e iciency index e e ed o analysis ime; % N1–N3: pe cen age o N1–N3 sleep e e ed o TST; % REM: pe cen age o REM sleep e e ed o TST. S a is ical compa isons wi h he Wilcoxon es . Wake REM N1 N2 N3 (a) Wake REM N1 N2 N3 22:00 23:00 0:00 1:00 2:00 3:00 4:00 5:00 (b) Figu e 1: Example o he hypnog ams o he same pa ien de i ed by he wo di e en sleep s aging p ocedu es. The uppe hypnog am ep esen s s anda d sleep s aging and he lowe hypnog am ep esen s EOG sco ing. The hypnog ams esemble each o he bu he e a e di e ences in bo h sleep e iciency (69% by s anda d sleep s aging, 59% by EOG-sco ing) and he a angemen o he sleep s ages. The pa ien had mode a e OSA (AHI 18.8/h). Table 2: The sleep quali y pa ame e s o he 42 pa ien s. Median Min Max TST (min) 368.5 48.5 510.5 SEI (%) 70.8 27.5 97.6 % N1 8.8 1.8 41.2 % N2 46.9 3.3 83.2 % N3 6.5 0 26.2 %REM 7.1 0 31.2 TST: o al sleep ime; SEI: Sleep E iciency Index e e ed o analysis ime; % N1–N3: pe cen age o N1–N3 sleep e e ed o TST; % REM: pe cen age o REM sleep e e ed o TST. a ousals. In ha way he inc ease in sympa he ic ac i i y induced by a ousals does no eme ge. In addi ion he p e- ailing ai low agains esis ance du ing IRR is capable o ac i a ing he pulmona y s e ch ecep o s, which leads o he inhibi ion o sympa he ic ac i a ion [30]. Thus, i migh be ha IRR does no cons i u e a ma ked isk ac o o hype ension. Indeed, i has been p esen ed ha women wi h IRR ha e less hype ension han women in he gene al popula ion [31]. I is possible ha he isk o ca dio ascula e en s o IRR pa ien s migh be educed as compa ed o OSA pa ien s. Thus he p esen s udy inc eases ou knowledge o IRR, bu i s p o ound signi icance s ill emains somewha obscu e and equi es u he e alua ion. In he p esen s udy, he neck ci cum e ence measu e- men did no di e be ween he OSA g oup and he non- SDB g oup. This migh be due o he ac ha he BMI o ou pa ien s was no high in gene al. Simila esul s ha e been ound ea lie [13,24]. In addi ion, ou OSA pa ien s did no p esen inc eased day ime sleepiness be o e s oke, unlike hose who did no ha e OSA. The absence o excessi e day ime sleepiness has been no ed be o e [13]. I may be ha pa ien s wi h OSA do no necessa ily ecognize inc eased Sleep Diso de s 5 Table3:The espi a o ypa ame e so hePSGg oupand hePOLg oup. PSG g oup POL g oup Median Min Max Median Min Max AHI obs uc i e (𝑛/h) 18.1 1.2 67.9 AHI cen al (𝑛/h) 0 0 1.2 ODI4 4.5 0 32.5 6.0 0 64.8 % OP1–OP3 27.2 2.6 69.3 14.1 0 45.8 % CP 0 0 4.7 0 0 51.6 % IRR 0.8 0 9.6 0.5 0 25.4 SaO2min (%) 87.5 79.0 93.0 85.0 75.0 91.0 SaO2mean (%) 93.7 90.7 96.5 93.2 89.5 97.1 Pulse (bpm) 55 46 73 58 46 86 AHI obs uc i e: numbe o obs uc i e apneas and hypopneas pe hou o sleep; AHI cen al: numbe o cen al apneas pe hou o sleep; ODI4: numbe o desa u a ions pe hou o sleep; % OP1–OP3: pe cen age o ime wi h obs uc i e pe iodic b ea hing as de ec ed by Em i senso ; % CP: pe cen age o imewi h cen al pe iodic b ea hing as de ec ed by Em i senso ; % IRR: pe cen age o ime wi h p olonged pa ial obs uc ion as de ec ed by Em i senso ; SaO2min: minimum oxygen sa u a ion pe cen age; SaO2mean:a e ageoxygensa u a ionpe cen age;Pulse:meanpulsepe minu e. Table 4: Some demog aphic and sleep pa ame e s o he di e en subjec g oups. Non-SDB, 𝑛=17 OSA, 𝑛=22 Cen al, 𝑛=2 IRR, 𝑛=1 Non-SDB e sus OSA Median (min–max) Median (min–max) Median (min–max) Value 𝑃 alue BMI 26.0 (19.9–32.7) 26.6 (21.9–37.4) 25.3 (25.2–25.3) 27.5 0.705 AGE 62 (45–79) 69 (37–82) 77 (75–78) 68 0.131 TST 426 (49–511) 321 (105–490) 300 (282–318) 416 0.116 SEI 72.8 (42.0–97.6) 70.3 (27.5–95.7) 65.2 (61.3–69.1) 67.2 0.236 % N1 8.9 (2.6–41.2) 9.0 (1.8–23.0) 12.5 (11.9–13.1) 8.2 0.962 % N2 45.9 (33.1–73.9) 57.8 (3.3–83.2) 44.7 (42.7–46.7) 53.6 0.168 % N3 12.4 (3.3–26.2) 4.3 (0–23.6) 1.5 (1.1–1.8) 2.4 0.005 % REM 6.9 (0–22.3) 10.8 (1.0–31.2) 6.9 (5.2–8.5) 3.1 0.539 ODI4 1.8 (0–8.2) 16.4 (0–64.8) 9.7 (4.2–15.1) 0.7 0.000 SaO2min (%) 87 (80–91) 85 (75–93) 87 (84–89) 85 0.053 SaO2mean (%) 93.6 (90.7–97.1) 93.3 (89.5–96.8) 94.5 (93.3–95.7) 91.7 0.975 Pulse (bpm) 61 (50–86) 58 (46–78) 51 (50–52) 51 0.133 NIHSS 2 (0–6) 1 (0–4) 3 (2–4) 1 0.138 Neck (cm) 40 (34–44) 41 (38–53) 41 (40–42) 39 0.231 NIHSS: Na ional Ins i u es o Heal h S oke Scale; Neck: neck ci cum e ence in cen ime e s. The es o he abb e ia ions a e as in Tables 1and 3. S a is ical compa isons be ween he Non-SDB g oup and he OSA g oup wi h he Mann-Whi ney es . sleepiness due o he ch onic sleepiness induced by OSA. The p oblem wi h ou s udy is ha sleepiness was no e alua ed s uc u ally, so i is no possible o d aw s ong conclusions. In a p e ious me a-analysis he p e alence o emale pa ien s wi h OSA and s oke was ound o be 35.4% [25]. In ou s udy, he pe cen age o emales wi h OSA was 41%. In ha way, he po ion o emale pa ien s is clea ly la ge han he p e alence o OSA in emales in gene al [32]. I hasbeenshown ha emalesmayp esen a ypicalSDB- ela ed symp oms, o example, insomnia and dep ession [33],and he ema kablepo iono emalepa ien samong he OSA + s oke pa ien s may, in pa , accoun o he a ypical subjec i e complain s among hese pa ien s. I is possible ha ou ine anamnesis as i con en ionally ela es o OSA does no necessa ily e eal SDB in s oke pa ien s, which s esses he need o OSA sc eening in s oke uni s. Pa ien s end o sleep poo ly in he hospi al, and also he objec i e sleep quali y o ou pa ien s was poo , as assessed by sleep e iciency. In mos o he sleep eco d- ings we u ilized only he wo EOG channels in he sleep s age sco ing (EOG sco ing) o achie e an es ima e o TST. As a esul , he o al sleep ime ob ained by he EOG sco ing co ela ed well wi h he s anda d sco ing esul s. Acco ding o p e ious s udies sleep s aging by EOG sig- nal seems ela i ely eliable and p omising [22,34]and because heEOGsignalscanbe eco dedbydisposable elec odes, he a achmen o he elec odes is easy. Ou esul s sugges ha sleep s aging wi h EOG esul s in mo e alid diagnos ic SDB ou come han con en ional espi a o y polyg aphy wi hou sleep s aging e en i he EOG sco ing p ocedu e may o e es ima e he amoun o sleep. 6Sleep Diso de s Table 5: Demog aphic pa ame e s o he 42 pa ien s. Non-SDB OSA Cen al IRR Dep ession (%) 5.9 4.5 0 0 P e ious s oke (%) 5.9 13.6 0 0 Hea ailu e (%) 23.5 27.3 0 0 Hype ension (%) 47.1 63.6 50 100 Hype choles e olemia (%) 11.8 13.6 0 0 Diabe es melli us (%) 5.9 4.5 0 0 Hypo hy eosis (%) 5.9 4.5 0 100 As hma (%) 5.9 0 0 0 COPD (%) 17.6 4.5 0 0 Tobacco use (%) 47 18.1 50 0 Alcohol use (%) 29.4 22.7 0 0 Sno ing (%) 52.9 54.5 50 100 Wi nessed apneas (%) 5.9 22.7 50 0 Inc eased sleepiness 76.5 40.9 0 100 COPD: ch onic obs uc i e pulmonal disease. Ou o he aim was o e alua e he easibili y o limi ed polyg aphy wi h a sleep ma ess in sc eening SDB. The clinical e alua ion o ma ess signal is easy and as and, depending on he eco ding de ice used, adding di e en addi ional signals is o en simple. In he p esen s udy, he pe cen age o success ul eco dings was highe in he POL g oup han in he PSG g oup, which suppo s he use o he limi ed eco ding mon age in acu e wa ds. I he numbe o eco ded pa ame e s is kep low, he sys em does no dis u b he pa ien , enabling eco dings o se e al nigh s when needed. 5. Conclusion In hep esen s udyweconcen a edonmilds okeand TIA pa ien s only, and he eco dings we e made soon a e he s oke. In gene al, pa ien s wi h TIA and mild s oke eco e well, bu , acco ding o he cu en knowledge, hey ha e an inc eased isk o s oke ecu ence [35]. As ecu en s oke migh be inhibi ed by he p ope ea men o SDB [6], sc eening o SDB should be a ou ed in he s oke uni s. Ou esul s sugges ha limi ed and less dis u bing eco ding se ing is su icien o e eal OSA in s oke uni s. Con lic o In e es s The au ho s decla e ha he e is no con lic o in e es s ega ding he publica ion o his pape . Acknowledgmen s The s udy was inancially suppo ed by Tekes, he Na ional Technology Agency o Finland, and by he Compe i i e Resea ch Financing o he Expe Responsibili y a ea o Tampe e Uni e si y Hospi al G an nos. 9M014 and 9P013. 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