Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS) [1]. In the majority of patients, MS begins with a relapsing–remitting course. It is characterized by unpredictable relapses followed by periods of months to years of clinical remission. MS relapses entail various clinical symptoms depending on the location of the inflammatory lesion within the CNS. Besides the common symptoms of optic neuritis, paresis, paraesthesia, and ataxic gait disorders, in some rare cases a relapse may alter cardiovascular and autonomic function [1]. Clinical studies have shown that acute cerebral lesions (e.g., stroke, hemorrhage) may induce changes in cardiac and respiratory function including hypertension, arrhythmias, myocardial necrosis, and sudden death [2, 3]. Moreover, experimental and clinical studies indicate that damage of the brainstem is likely to cause disturbances in either sympathetic or parasympathetic autonomic function with subsequent cardiac and respiratory dysfunction [4–6]. Neurogenic pulmonary edema (NPE) is usually defined as an acute pulmonary edema occurring shortly after various injuries of the central nervous system [7]. The most important vasomotor centers for NPE development are nuclei of the solitary tract, the dorsal motor vagus nucleus in the medulla oblongata and the medial reticulated nucleus. On the other hand, brainstem damage in the region of the solitary tract nuclei may result in a transient cardiomyopathy [8]. The exact mechanisms remain poorly understood because of the complexity of its pathophysiologic mechanisms, involving both hemodynamic and inflammatory aspects. There are two possible explanations: one presumes that neurological damage directly involves the pulmonary and cardiac vascular bed with disconnection of the central nervous system vasomotor centers. However, there are also data that brainstem dysfunction can cause changes of sympathetic vasomotor tone [7]. This case study describes a rare initial presentation of a MS relapse with pulmonary edema caused by left ventricular failure. A 48-year-old woman, diagnosed with clinically definite relapsing–remitting MS 3 years previously with a preexisting expanded disability status scale (EDSS) of 3.5, presented with increasing dyspnea and cough without chest pain to a department of internal medicine. She was on immunomodulatory treatment with glatiramer acetate. No clinically apparent atherosclerotic disease was known. On admission, laboratory testing showed that high-sensitivity troponin T was slightly elevated. An electrocardiogram showed no signs of myocardial infarction. In a coronary computed tomography angiogram, no significant changes in the coronary arteries were found. The next day, increases in high-sensitivity troponin T, C-reactive protein (CRP), and a massive increase of B-type natriuretic peptide (proBNP) were observed (Table 1). Pulmonary edema was initially not diagnosed (Fig. 1a) and according to the assumption of pneumonia the patient was treated with antibiotic therapy (amoxicillin) and furosemide. Due to the further worsening of respiratory conditions, intubation and mechanical respirator treatment became necessary. An echocardiogram showed acute left ventricular failure with apical wall motion abnormalities and a left ventricular ejection fraction of 35% in this patient without a history of cardiac disease. No abnormalities concerning the right ventricle and the atria were seen. With regard to her P. Wipfler (&) G. Pilz E. Broussalis S. M. Golaszewski A. Kunz E. Trinka J. Kraus Christian-Doppler-Klinik, University Hospital of Neurology, Paracelsus Medical University and Salzburger Landesklinken, Ignaz Harrerstrasse 79, 5020 Salzburg, Austria e-mail: p.wipfler@salk.at
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Jun 3, 2024
Christian Treat + 3
Open Access
