Polysomnographic features of idiopathic central sleep apnea

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<ul><li><p>Psychiatry and Clinical Neurosciences (2002), 56, 323324</p><p>Sleep Breathing Disorder</p><p>Polysomnographic features of idiopathic central sleep apnea</p><p>MASAKAZU WAKAI, md,1 HIROFUMI NISHIKAGE, md,2 KAZUYUKI GOSHIMA, md2</p><p>AND JUNNOSUKE YAMAMOTO, md2Departments of 1Neurology and 2Internal Medicine, Kakegawa City General Hospital, Shizuoka, Japan</p><p>Abstract Two patients with idiopathic central sleep apnea (ICSA), which is an uncommon condition, wererecently encountered. This study examines the polysomnographic features of ICSA. The charac-teristic findings of ICSA are summarized as follows: (i) central apneas and hypopneas are pro-gressively less frequent as sleep state deepens from stage 1 to stage 2 to stage 3 + 4 to stage REM(rapid eye movement); (ii) desaturation related to apneas and hypopneas is mild; and (iii) peri-odic breathing is commonly observed. However, the two patients demonstrated apparently different findings. It is suggested that the mechanisms underlying apnea and hypopnea in ICSAare heterogeneous.</p><p>Key words idiopathic central sleep apnea, polysomnography, sleep architecture.</p><p>INTRODUCTION</p><p>Central sleep apnea (CSA) is a relatively uncommondisorder, occurring in fewer than 5% of all cases ofsleep apnea.1 The underlying diseases of CSA are het-erogeneous. Among those, congestive heart failure isthe most common cause. It is also seen, albeit less frequently, in cases in whom no apparent cardiac orneurological abnormalities can be identified, wherebyit is called idiopathic central sleep apnea (ICSA). It isbelieved that apneas occur mainly in the light stagesof non-rapid eye movement (NREM) sleep in ICSA.2</p><p>Recently, we encountered two patients with ICSA.Herein, we report these two cases, who did not mani-fest apneas dominantly in the light stages of NREMsleep.</p><p>SUBJECTS AND METHODS</p><p>Case 1</p><p>A 69-year-old woman had complained of chronicheadache, frequent awakening from sleep, and unre-freshing sleep for years. Physical and neurologicalexaminations showed no abnormalities. Blood exami-</p><p>nation, urinalysis, plain chest X-ray film, electrocar-diogram, and echocardiography were unremarkable.Brain magnetic resonance imaging (MRI) was normalfor her age.</p><p>Case 2</p><p>Ambulance brought a 69-year-old man to the hospi-tals emergency room at midnight because he wasexperiencing abrupt onset of gasp during sleep. Onarrival, he was confused and excited, and regainedconsciousness the next morning. Physical and neuro-logical examinations showed no abnormalities. Bloodexamination, urinalysis, plain chest X-ray film, electro-cardiogram, and echocardiography were unremark-able. Brain MRI was normal for his age.</p><p>Sleep stages were scored manually for periods of 30 s according to the criteria of Rechtschaffen andKales.3</p><p>RESULTS</p><p>Daytime arterial blood gas (ABG) examinationsshowed no abnormalities (pH 7.403, PaCO234.3 mmHg, PaO2 97.3 mmHg, HCO3 22.0 mmol/L) forcase 1, and showed mild hypoxia and normocapnea(pH 7.455, PaCO2 37.7 mmHg, PaO2 77.6 mmHg,HCO3 26.1 mmol/L) for case 2. The apneahypopneaindex (AHI), the central apnea index (CA), and the</p><p>Correspondence address: Masakazu Wakai, Department of Neurol-ogy, Kakegawa City General Hospital, 721 Sugiya, Kakegawa,Shizuoka 436-8502, Japan.</p></li><li><p>324 M. Wakai et al.</p><p>obstructive apnea index (OA) are shown in Table 1.The symptoms, the polysomnographic (PSG) results,and the ABG results fulfilled the diagnostic criteria ofICSA proposed by the American Academy of SleepMedicine Task Force2 and by Xie et al.4 Nasal continu-ous positive airway pressure was applied to case 1,but failed to decrease the AHI (AHI = 30.7).</p><p>Table 1 also shows the AHI and the desaturationindex (DSI) for each sleep stage. For case 1, the AHIwas highest during stage REM and lowest in stage 3 +4. For case 2, the AHI was highest during stage 2 andlowest in stage 1. For case 1, the DSI was highestduring stage REM and lowest in stage 3 + 4. For case2, the DSI was highest in stage 2 and lowest in stageREM. No episodes of hyperpnea alternating withthose of subsequent central apneas and hypopneas,which is called periodic breathing, was recognized ineither case.</p><p>DISCUSSION</p><p>Obstructive sleep apnea (OSA) resembles CSA whendecrement in intrathoracic pressure as the result ofinsufficient inspiratory effort. In the present study,complete cessation of respiratory effort was con-firmed in both cases. In addition, nasal CPAP provedto be ineffective in case 1. From these results, we con-cluded that the apnea presented by the two patients is CSA.</p><p>The characteristic findings of ICSA have been summarized recently as the following.2,4 First, centralapneas and hypopneas are progressively less frequent</p><p>as sleep state deepens from stage 1 to stage 2 to stage3 + 4 to stage REM. Second, desaturation related toapneas and hypopneas is mild and SaO2 rarely fallsbelow 90% in spite of frequent episodes of apneasand hypopneas. Third, periodic breathing is commonlyobserved.</p><p>The present study, however, showed different find-ings. Apneas occurred most frequently during stageREM in case 1 and most infrequently during stage 1in case 2. Desaturation index was comparable to thatpredicted from AHI. SaO2 sometimes fell below 90%.Periodic breathing was not observed in either case.Overall, the findings suggest that the mechanismsunderlying apnea and hypopnea in ICSA are hetero-geneous, resulting in various PSG profiles.</p><p>REFERENCES</p><p>1. Aldrich MS. Sleep Medicine. Oxford University Press,New York, 1999.</p><p>2. The Report of an American Academy of Sleep MedicineTask Force. Sleep-related breathing disorders in adults:Recommendations for syndrome definition and measure-ment techniques in clinical research. Sleep 1999; 22:667689.</p><p>3. Rechtschaffen A, Kales A (eds). A Manual of Standard-ized Terminology, Techniques and Scoring System forSleep Stages of Human Subjects. Public Health Service,US Government Printing Office, Washington, DC, 1968.</p><p>4. Xie A, Wong B, Phillipson EA et al. Interaction of hyper-ventilation and arousal in the pathogenesis of idiopathiccentral sleep apnea. Am. J. Respir. Crit. Care Med. 1994;150: 489495.</p><p>Table 1. Patients characteristics</p><p>Age/ BMI AHI AHI (No./h sleep) (% Total sleep time)gender (kg/m2) (No./h sleep) CA OA MA Hyp S1 S2 S3 + 4 REM</p><p>Case 1 69/F 20.0 24.0 10.3 0.0 0.0 13.7 17.8 (9.6) 24.6 (59.2) 4.0 (17.9) 52.5 (13.3)Case 2 69/M 21.9 28.7 15.7 1.2 1.2 10.6 17.7 (9.7) 35.0 (62.1) 18.1 (15.0) 20.7 (12.5)</p><p>DSI (No./h sleep)DSI S1 S2 S3 + 4 REM Low O2 (%) PBT</p><p>Case 1 19.1 7.4 19.3 2.4 49.3 83 0Case 2 19.9 14.0 23.6 18.1 9.8 88 0</p><p>BMI, body mass index; AHI, apneahypopnea index; CA, central apnea index; OA, obstructive apnea index; MA, mixedapnea index; Hyp, hypopnea index; DSI, desaturation index; Low O2, the lowest O2 saturation level associated with a respira-tory event, PBT, periodic breathing total time; S1, stage 1 sleep; S2, stage 2 sleep; S3 + 4, stage 3 + 4 sleep; REM, stage rapid eyemovement sleep.</p></li></ul>