ECTRIMS eLearning

The spectrum of acute cardiopulmonary events associated with multiple sclerosis exacerbations
ECTRIMS Learn. Valencia-Sanchez C. 10/25/17; 199403; EP1382
Cristina Valencia-Sanchez
Cristina Valencia-Sanchez
Contributions
Abstract

Abstract: EP1382

Type: ePoster

Abstract Category: Clinical aspects of MS - 7 MS symptoms

Introduction: Acute neurological injuries may cause acute cardiopulmonary (CP) events including neurogenic pulmonary oedema (NPO) and Takotsubo cardiomyopathy (TTC). Sympathetic overstimulation is an important mechanism underlying central nervous system (CNS) deleterious effects on pulmonary and cardiac function. Focal CNS lesions, including demyelinating lesions in multiple sclerosis (MS), may cause CP disturbances.
Objective: Describe acute CP events associated with acute MS relapses.
Methods: We present the case of a 32 year-old woman with TTC after a brainstem MS exacerbation. We review the literature on acute CP events, specifically NPO and TTC, associated with MS relapses.
Results: A 32 year-old woman with a 3-year history of relapsing MS treated with subcutaneous interferon beta-1a presented with a brainstem exacerbation and active MS lesions in the cerebellum, cerebral peduncles, pons, right frontal and left occipital lobes on brain magnetic resonance imaging (MRI). After a 3-day course of intravenous (IV) methylprednisolone her deficits improved partially. Three weeks later, she presented with lethargy and chest tightness. Her electrocardiogram showed inverted T waves and she had elevated serum troponin levels. Echocardiography showed basal left ventricular (LV) akinesia consistent with TTC. Brain MRI revealed a new enhancing lesion in the left medulla. She completed a 3-day course of IV methylprednisolone with improvement of her symptoms and resolution of LV dysfunction.
Our literature review identified 30 relapsing MS patients with acute CP events in the setting of MS exacerbations. They presented with NPO (n=8), TTC (n=12), or concurrent unclassified myocardial dysfunction and pulmonary oedema (n=10). 26 patients had acute demyelinating lesions in the brainstem. In 21 cases, these lesions involved the medulla. 24 patients received treatment with high dose IV steroids. Three patients died but most survivors had a favourable outcome after treatment.
Discussion: NPO and TTC are increasingly recognized complications associated with acute brainstem MS relapses. Active demyelinating lesions involving the medulla may damage vasomotor centers at the dorsomedial medulla leading to autonomic dysfunction with profound sympathetic overstimulation. Clinicians should be aware that new cardiac or pulmonary symptoms may accompany MS relapses that involve the brainstem; the risk of CP complications of such attacks requires further systematic study.
Disclosure:
Cristina Valencia-Sanchez: nothing to disclose
Dean M. Wingerchuk: nothing to disclose

Abstract: EP1382

Type: ePoster

Abstract Category: Clinical aspects of MS - 7 MS symptoms

Introduction: Acute neurological injuries may cause acute cardiopulmonary (CP) events including neurogenic pulmonary oedema (NPO) and Takotsubo cardiomyopathy (TTC). Sympathetic overstimulation is an important mechanism underlying central nervous system (CNS) deleterious effects on pulmonary and cardiac function. Focal CNS lesions, including demyelinating lesions in multiple sclerosis (MS), may cause CP disturbances.
Objective: Describe acute CP events associated with acute MS relapses.
Methods: We present the case of a 32 year-old woman with TTC after a brainstem MS exacerbation. We review the literature on acute CP events, specifically NPO and TTC, associated with MS relapses.
Results: A 32 year-old woman with a 3-year history of relapsing MS treated with subcutaneous interferon beta-1a presented with a brainstem exacerbation and active MS lesions in the cerebellum, cerebral peduncles, pons, right frontal and left occipital lobes on brain magnetic resonance imaging (MRI). After a 3-day course of intravenous (IV) methylprednisolone her deficits improved partially. Three weeks later, she presented with lethargy and chest tightness. Her electrocardiogram showed inverted T waves and she had elevated serum troponin levels. Echocardiography showed basal left ventricular (LV) akinesia consistent with TTC. Brain MRI revealed a new enhancing lesion in the left medulla. She completed a 3-day course of IV methylprednisolone with improvement of her symptoms and resolution of LV dysfunction.
Our literature review identified 30 relapsing MS patients with acute CP events in the setting of MS exacerbations. They presented with NPO (n=8), TTC (n=12), or concurrent unclassified myocardial dysfunction and pulmonary oedema (n=10). 26 patients had acute demyelinating lesions in the brainstem. In 21 cases, these lesions involved the medulla. 24 patients received treatment with high dose IV steroids. Three patients died but most survivors had a favourable outcome after treatment.
Discussion: NPO and TTC are increasingly recognized complications associated with acute brainstem MS relapses. Active demyelinating lesions involving the medulla may damage vasomotor centers at the dorsomedial medulla leading to autonomic dysfunction with profound sympathetic overstimulation. Clinicians should be aware that new cardiac or pulmonary symptoms may accompany MS relapses that involve the brainstem; the risk of CP complications of such attacks requires further systematic study.
Disclosure:
Cristina Valencia-Sanchez: nothing to disclose
Dean M. Wingerchuk: nothing to disclose

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