The aim of this single-center prospective study was to assess the presence of Cheyne-Stokes respiration (CSR) and CSR-related variables in 68 consecutive patients with radiologically proven first-ever lacunar stroke undergoing a respiratory sleep study using a portable respiratory polygraph within the first 48 hours of stroke onset. CSR was diagnosed in 14 patients (20.6%). Patients with CSR as compared with those without CSR showed a significantly higher mean (standard deviation, SD) apnea-hypopnea index (AHI) (34.9 (21.7) versus 18.5 (14.4), ) and central apnea index (13.1 (13.8) versus 1.8 (3.4), ) as well as higher scores of the Barthel index and the Canadian Neurological scale as a measure of stroke severity, and longer hospital stay. CSR was present in one of each five patients with lacunar stroke. The presence of CSR was associated with a trend towards a higher functional stroke severity and worse prognosis. 1. Introduction Central sleep apnea and Cheyne-Stokes respiration are frequently observed during sleep in patients with stroke affecting large areas of the cerebral parenchyma [1–5] and in patients with congestive heart failure and low ventricular ejection fraction [6–10]. In a previous study carried out in a nonselected sample of patients with cerebral infarction, Parra et al. [11] reported the presence of Cheyne-Stokes respiration in 26% of patients, a percentage higher than 6% of observed in the study of Bassetti and Aldrichet [12]. To date, Cheyne-Stokes respiration in stroke patients has been related to a worse prognosis probably because this abnormal breathing pattern is found in more extensive cerebral lesions and is also more common in hemorrhagic strokes than in ischemic infarctions [11, 13]. However, the traditional relationship between nocturnal Cheyne-Stokes respiration and large cerebral lesions is a matter of controversy given that Cheyne-Stokes respiration has been occasionally described in patients with transient ischemic attack (TIA) [11]. Lacunar infarctions are very homogeneous cerebral lesions regarding infarct size (maximal diameter of the lesion <20？mm), topography (affecting subcortical structures or the pons), and clinical features (limited neurological deficit and favorable neurological recovery on hospital discharge). In this respect, patients with lacunar stroke may constitute an intermediate group of stroke severity between TIA and extensive cardioembolic or atherothrombotic infarctions. Given that the presence of Cheyne-Stokes respiration in patients with lacunar infarction has not been previously examined, a
References
[1]
J. J. M. Askenasy and I. Goldhammer, “Sleep apnea as a feature of bulbar stroke,” Stroke, vol. 19, no. 5, pp. 637–639, 1988.
[2]
A. Nachtmann, M. Siebler, G. Rose, M. Sitzer, and H. Steinmetz, “Cheyne-Stokes respiration in ischemic stroke,” Neurology, vol. 45, no. 4, pp. 820–821, 1995.
[3]
N. S. Cherniack, G. Longobardo, and C. J. Evangelista, “Causes of Cheyne-Stokes respiration,” Neurocritical Care, vol. 3, no. 3, pp. 271–279, 2005.
[4]
D. M. Hermann, M. Siccoli, P. Kirov, M. Gugger, and C. L. Bassetti, “Central periodic breathing during sleep in acute ischemic stroke,” Stroke, vol. 38, no. 3, pp. 1082–1084, 2007.
[5]
A. M. Rowat, J. M. Wardlow, and M. S. Dennis, “Abnormal breathing patterns in stroke—relationship to acute stroke lesion location and prior cerebrovascular disease,” Journal of Neurology, Neurosurgery & Psychiatry, vol. 78, pp. 277–279, 2007.
[6]
V. K. Somers, D. P. White, R. Amin et al., “Sleep apnea and cardiovascular disease,” Circulation, vol. 118, no. 10, pp. 1080–1111, 2008.
[7]
C. Nopmaneejumruslers, Y. Kaneko, V. Hajek, V. Zivanovic, and T. D. Bradley, “Cheyne-stokes respiration in stroke: relationship to hypocapnia and occult cardiac dysfunction,” American Journal of Respiratory and Critical Care Medicine, vol. 171, no. 9, pp. 1048–1052, 2005.
[8]
D. Yumino and T. D. Bradley, “Central sleep apnea and Cheyne-Stokes respiration,” Proceedings of the American Thoracic Society, vol. 5, no. 2, pp. 226–236, 2008.
[9]
T. Brack, I. Thüer, C. F. Clarenbach et al., “Day time Cheyne-Stokes respiration in ambulatory patients with severe congestive heart failure is associated with increased mortality,” Chest, vol. 132, no. 5, pp. 1463–1471, 2007.
[10]
A. Garcia-Touchard, V. K. Somers, L. J. Olson, and S. M. Caples, “Central sleep apnea: implications for congestive heart failure,” Chest, vol. 133, no. 6, pp. 1495–1504, 2008.
[11]
O. Parra, A. Arboix, S. Bechich, et al., “Time course of sleep-related breathing disorders in first-ever stroke or transient ischemic attack,” American Journal of Respiratory and Critical Care Medicine, vol. 161, no. 2, pp. 375–380, 2000.
[12]
C. Bassetti and M. S. Aldrich, “Sleep apnea in acute cerebrovascular diseases: final report on 128 patients,” Sleep, vol. 22, no. 2, pp. 217–223, 1999.
[13]
M. M. Siccoli, P. O. Valko, D. M. Hermann, and C. L. Bassetti, “Central periodic breathing during sleep in 74 patients with acute ischemic stroke—neurogenic and cardiogenic factors,” Journal of Neurology, vol. 255, no. 11, pp. 1687–1692, 2008.
[14]
A. Arboix, V. Cendrós, M. Besa et al., “Trends in risk factors, stroke subtypes and outcome. Nineteen-year data from the Sagrat Cor Hospital of Barcelona Stroke Registry,” Cerebrovascular Diseases, vol. 26, no. 5, pp. 509–516, 2008.
[15]
M. W. Johns, “A new method for measuring daytime sleepiness: the Epworth sleepiness scale,” Sleep, vol. 14, no. 6, pp. 540–545, 1991.
[16]
M. Bonnin-Vilaplana, A. Arboix, O. Parra, L. García-Eroles, J. M. Montserrat, and J. Massons, “Sleep-related breathing disorders in acute lacunar stroke,” Journal of Neurology, vol. 256, no. 12, pp. 2036–2042, 2009.
[17]
O. Parra, A. Sánchez-Armengol, M. Bonnin, et al., “Early treatment of obstructive apnoe and stroke outcome: a randomized controled trial,” European Respiratory Journal, vol. 37, pp. 1128–1136, 2011.
[18]
F. I. Mahoney and D. W. Barthel, “Functional evaluation of the Barthel index,” Maryland State Medical Journal, vol. 14, pp. 61–65, 1965.
[19]
R. C？te, V. C. Hachinski, B. L. Shurvell, J. W. Norris, and C. Wolfson, “The Canadian neurological scale: a preliminary study in acute stroke,” Stroke, vol. 17, no. 4, pp. 731–737, 1986.
[20]
J. C. van Swieten, P. J. Koudstaal, M. C. Visser, H. J. A. Schouten, and J. van Gijn, “Interobserver agreement for the assessment of handicap in stroke patients,” Stroke, vol. 19, no. 5, pp. 604–607, 1988.
[21]
S. Javaheri, “Central sleep apnea,” Clinics in Chest Medicine, vol. 31, no. 2, pp. 235–248, 2010.
[22]
A. Arboix and J. L. Martí-Vilaita, “Lacunar stroke,” Expert Review of Neurotherapeutics, vol. 9, no. 2, pp. 179–196, 2009.
[23]
B. A. Chaudhary, A. S. Elguindi, and D. W. King, “Obstructive sleep apnea after lateral medullary syndrome,” Southern Medical Journal, vol. 75, no. 1, pp. 65–67, 1982.
[24]
D. W. Hudgel, P. Devadatta, and H. Hamilton, “Pattern of breathing and upper airway mechanics during wakefulness and sleep in healthy elderly humans,” Journal of Applied Physiology, vol. 74, no. 5, pp. 2198–2204, 1993.
[25]
C. Jackson and C. Sudlow, “Are lacunar strokes really different? A systematic review of differences in risk factor profiles between lacunar and nonlacunar infarcts,” Stroke, vol. 36, no. 4, pp. 891–901, 2005.
[26]
D. C. Good, J. Q. Henkle, D. Gelber, J. Welsh, and S. Verhulst, “Sleep-disordered breathing and poor functional outcome after stroke,” Stroke, vol. 27, no. 2, pp. 252–259, 1996.
[27]
S. Yan-Fang and W. Yu-Ping, “Sleep-disordered breathing: impact on functional outcome of ischemic stroke patients,” Sleep Medicine, vol. 10, no. 7, pp. 717–719, 2009.
