“…Clinical worsening after lacunar infarction has been extensively reported and may result from thrombi propagation, flow limiting arterial lesion supplying the ischemic zone, and perilesional edema. 9,10 We suspect that secondary neuronal degeneration, apoptosis, or abnormal plasticity involving local synaptic interconnections may explain the delay in the development of Ondine's curse after lateral medullary infarction, ranging several days to several months postinfarct. Likewise, hypoxemia secondary to altered automatic breathing in brainstem infarctions with hypercapnia-induced cerebral vasoconstriction can increase ischemia.…”