Why the study?
Focal central nervous system demyelinating lesions in multiple sclerosis may cause cardiopulmonary disturbances, prompting a review of acute cardiopulmonary events associated with relapses.
Acute brainstem multiple sclerosis relapses with medullary lesions can present with acute cardiopulmonary events such as neurogenic pulmonary edema and Takotsubo cardiomyopathy due to sympathetic hyperstimulation.
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Acute MS relapses may trigger neurogenic cardiopulmonary events; leaves open whether routine monitoring improves outcomes.
Diverse acute neurological injuries may cause acute cardiopulmonary events including neurogenic pulmonary edema (NPE) and neurogenic stunned myocardium (NSM). The mechanism is probably mediated by sympathetic nervous system activation. Focal central nervous system (CNS) lesions, such as demyelinating lesions in multiple sclerosis (MS), may also cause cardiopulmonary disturbances. We aim to review the acute cardiopulmonary events associated with MS relapses. We performed a literature search using PubMed, and selected case reports of acute cardiac and/or pulmonary events related to MS exacerbations. We grouped these events into three categories: 1) NPE with normal cardiac function; 2) NSM and Takotsubo cardiomyopathy (TTC); 3) coexisting myocardial dysfunction and pulmonary edema. In some cases, cardiac and pulmonary symptoms preceded the onset of neurological symptoms. The majority of cases were associated with acute demyelinating lesions located in the medulla. Acute brainstem MS relapses, with demyelinating lesions affecting the medulla, may cause acute cardiac and pulmonary events presumably secondary to sympathetic hyperstimulation. Specific regions in the medulla that regulate cardiac function, systemic blood pressure and pulmonary hydrostatic pressure seem to be responsible for these events.
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Valencia-Sánchez et al. (2019) studied this question.
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