Central periodic breathing during sleep in 74 patients with acute ischemic stroke - Neurogenic and cardiogenic factors

Dept. of Neurology, University Hospital of Zurich, Frauenklinikstrasse 26, 8091 Zurich, Switzerland.
Journal of Neurology (Impact Factor: 3.38). 12/2008; 255(11):1687-92. DOI: 10.1007/s00415-008-0981-9
Source: PubMed


The aims of our study were 1) to better characterize central periodic breathing during sleep (CPBS) and its clinical relevance in acute stroke, 2) to better define the role of brain damage in its pathogenesis.
We included 74 consecutive patients admitted within 96 hours after stroke onset. Stroke severity at admission, stroke outcome at discharge and stroke topography were assessed. ECG and transesophageal echocardiography were performed. Nocturnal breathing was assessed with an ambulatory device the first night after admission. CPBS severity was represented as absolute time and percentage of recording time.
Age was 63 +/- 13 (25-82), 49 (66 %) were male. Thirty (41 %) patients showed CPBS during >or= 10 % and 7 (9 %) during >or= 50 % of recording time. CPBS severity was associated with age (p = 0.017), stroke severity (p = 0.008), ECG abnormalities (p = 0.005) and lower left ventricular ejection fraction (p < 0.0001). CPBS severity was higher in patients with extensive hemispheric strokes (n = 6, p < 0.0001), and lower in patients with partial strokes involving the left insula (n = 5, p < 0.0001) and the mesencephalon (n = 5, p = 0.002).
CPBS is frequent in acute ischemic stroke and is associated with older age, stroke severity/extension, and lower left ventricular function. The lower occurrence of CPBS in left insular and mesencephalic stroke suggests a major role of distinct brain areas in the modulation of respiratory phenomena accompanying acute stroke.

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    • "Our finding of an association between frontal- and brainstem lesions and increasing length of CSR episodes is suggestive of disturbance or even more a damage of WM projections in frontal-brainstem pathways leading to central breathing dysregulation. These findings are supported by a study using functional MRI [64] and recent studies in stroke patients reporting patients with ischemic lesions in frontal areas to be particular affected by CSA-CSR [65]. "
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    ABSTRACT: The exact underlying pathomechanism of central sleep apnea with Cheyne-Stokes respiration (CSA-CSR) is still unclear. Recent studies have demonstrated an association between cerebral white matter changes and CSA. A dysfunction of central respiratory control centers in the brainstem was suggested by some authors. Novel MR-imaging analysis tools now allow far more subtle assessment of microstructural cerebral changes. The aim of this study was to investigate whether and what severity of subtle structural cerebral changes could lead to CSA-CSR, and whether there is a specific pattern of neurodegenerative changes that cause CSR. Therefore, we examined patients with Fabry disease (FD), an inherited, lysosomal storage disease. White matter lesions are early and frequent findings in FD. Thus, FD can serve as a "model disease" of cerebral microangiopathy to study in more detail the impact of cerebral lesions on central sleep apnea.
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    • "We performed our sleep study at 6.3±2.2 days after stroke onset using a simplified portable protocol that exclude TIA patients. We chose 17 articles reporting the prevalence of SDB,2-5,7-17,19-21 in which the sleep measurements were made within 24, 48, or 72 hours, within 1 or 2 weeks, and around 1 or 3 months after stroke onset. These can be grouped into hyperacute (≤3 days), acute (1-2 weeks), and subacute (1-3 months) periods, whose mean prevalence rates of SDB were 59% (range 51-71%), 57% (50-67%), and 59% (44-71%), respectively. "
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    ABSTRACT: Sleep-disordered breathing (SDB) is suggested to be strongly associated with ischemic strokes. Risk factors, stroke subtypes, stroke lesion distribution, and the outcome of SDB in stroke patients remain unclear in Korea. We prospectively studied 293 patients (159 men, 134 women; age 68.4±10.5) with acute ischemic stroke. Cardiovascular risk factors, stroke severity, sleep-related stroke onset, distribution of stroke lesions, and 3-month score on the modified Rankin Scale (mRS) were assessed. Stroke severity was assessed by the US National Institutes of Health Stroke Scale (NIHSS) and the mRS. The apnea-hypopnea index (AHI) was determined 6.3±2.2 days after stroke onset with the Apnea Link portable sleep apnea monitoring device. The prevalence of SDB (defined as an AHI of ≥10) was 63.1% (111 men, 74 women). Those in the SDB group were older, had higher NIHSS and mRS scores, greater bulbar weakness, and a higher incidence of sleep-associated stroke onset. Among risk-factor profiles, alcohol consumption and atrial fibrillation were significantly related to SDB. The stroke outcome was worse in patients with SDB than in those without SDB. The lesion location and specific stroke syndrome were not correlated with SDB. SDB is very common in acute cerebral infarction. Different risk-factor profiles and sleep-related stroke onsets suggest SDB as a cause of ischemic stroke. The higher NIHSS score and greater bulbar involvement in the SDB group seem to show the influence of ischemic stroke on the increased SDB prevalence.
    Full-text · Article · Jan 2013 · Journal of Clinical Neurology
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    • "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]. "
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