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the process of receiving the feedback can itself actually damage the solitary tract nuclei.7,8 The excitatory return-messaging is believed to significantly increase the metabolic rate of parenchymal tissue in dendritic areas of the solitary tract nuclei, where much of that parenchyma is perfused by only a limited watershed vasculature. The result is focal areas of ischemia and occasionally infarction.7,8 These medullary ischemic lesions often then cause further problems by triggering violent autonomic discharges, which are life-threatening.9 The specific mechanisms are unknown.9 Ischemic lesion formation in the solitary tract nuclei of patients with central sleep apnea and/or heart failure disrupts medullary brain autonomic regulation, and may induce severe cardiac arrhythmias.7–9 The failure of the various recent clinical trials1–3 to prevent life-threatening cardiac events possibly lies in their failure to address the focal physiological mismatch causing medullary brain ischemia.7–9 The improvement in nocturnal systemic blood gasses probably has little overall effect on this focal physiological mismatch, which is often localized primarily to the solitary tract nuclei.

Ischemic Lesion Formation in Solitary Tract Nuclei During Central Sleep Apnea With Heart Failure