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Stroke Is Associated with Central Periodic (Cheyne-Stokes) Breathing
Abstract & Commentary
By Charles P. Pollak, MD, Professor of Clinical Neurology, Weill Cornell Medical College. Dr. Pollak reports no financial relationships relevant to this field of study.
Synopsis: Sleep disordered breathing occurs in most acute stroke patients and may contribute to morbidity
Source: Siccoli MM, Valko PO, Hermann DM, et. al. Central periodic breathing during sleep in 74 patients with acute ischemic stroke-Neurogenic and cardiogenic factors. J Neurol 2008;255:1687-1692.
Cheyne-Stokes breathing (CSB) is a type of periodic breathing that results from intracranial causes exacerbated by circulatory impairment (prolonged circulation time, congestive heart failure, hypoxiasee Plum and Posner, The Diagnosis of Stupor and Coma, 4th Ed, 2007). Respirographic tracings show alternating periods of hyperpnea, reflecting increased response to CO2, followed by apnea. The changes in depth of breathing are gradual, so the respirographic tracing has a spindle-like appearance. Unlike sleep apnea, CSB is not sleep dependent.
If the patient happens to be awake when respirations are normal or increased, he may lapse into sleep as they wane. Consciousness returns as respirations increase. The pathogenesis of CSB, then, involves overbreathing in response to CO2, alternating with posthyperventilation apnea. Arterial blood gases reflect mild overall hyperpnea. Classically, CSB implies bilateral dysfunction of the cerebral hemispheres or diencephalon, down to the upper pons. It is easy to see that circulatory impairments resulting in delayed feedback of CO2 or other blood gas information to the respiratory centers can cause or exacerbate respiratory instability such as periodic breathing.
Recently, Siccoli and colleagues at the University of Zurich investigated the brain lesions resulting from acute ischemic stroke that were responsible for CSB (termed "central periodic breathing," or CPB, in this report). Subjects were 74 patients admitted within 96 hours after first-ever stroke onset. Sleep-related breathing abnormalities assessed on the first night showed CPB in 53 patients (72%) during 10% of recording time. This may be compared with sleep apnea (obstructive or central), which was found in 41 (55%) patients. Of interest, the severity of CPB was strongly correlated with the severity of sleep apnea, suggesting that they may be pathogenetically related. CPB was much more frequent and severe in anterior circulation hemispheric strokes (six patients) and was milder in patients with strokes involving the left insula (n=5) and mesencephalon (n=5), as well as those with lower-left-ventricular ejection fraction.
Acute stroke is nearly always associated with a sleep-related breathing disorder, most often obstructive sleep apnea (OSA), which has been reported to occur in 69%-95% of patients. Because it is associated with transient ischemic attacks as often as completed stroke, CPB is more likely to be a predisposing condition rather than a cause of stroke. Risk factors that are shared by stroke and OSA include obesity, age, and hypertension. Furthermore, sleep fragmentation related to acute stroke may perpetuate and aggravate both central and obstructive sleep apnea.
Regardless of the mechanism, the astonishing frequency of OSA or CSB in stroke should make us wonder how much they may contribute to stroke morbidity and mortality and to what extent stroke burden might be lessened by treatment with continuous positive pressure ventilation (CPAP). Positive effects of CPAP have already been observed in individual patients, and a formal clinical trial of its potential benefits is warranted.