The spectrum of acute cardiopulmonary events associated with multiple sclerosis exacerbations

2019 ◽  
Vol 25 (6) ◽  
pp. 758-765 ◽  
Author(s):  
Cristina Valencia-Sanchez ◽  
Brent P Goodman ◽  
Jonathan L Carter ◽  
Dean M Wingerchuk
Keyword(s):  
Multiple Sclerosis ◽  
Nervous System ◽  
Cardiac Function ◽  
Pulmonary Edema ◽  
Myocardial Dysfunction ◽  
Case Reports ◽  
Systemic Blood Pressure ◽  
Stunned Myocardium ◽  
Neurogenic Pulmonary Edema ◽  
Demyelinating Lesions

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.

scholarly journals Immunology and Oxidative Stress in Multiple Sclerosis: Clinical and Basic Approach

2013 ◽  
Vol 2013 ◽  
pp. 1-14 ◽  
Author(s):  
Genaro G. Ortiz ◽  
Fermín P. Pacheco-Moisés ◽  
Oscar K. Bitzer-Quintero ◽  
Ana C. Ramírez-Anguiano ◽  
Luis J. Flores-Alvarado ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Multiple Sclerosis ◽  
Central Nervous System ◽  
Nervous System ◽  
Tissue Injury ◽  
Autoimmune Disorder ◽  
Demyelinating Lesions ◽  
The Central Nervous System ◽  
The Brain ◽  
And Oxidative Stress

Multiple sclerosis (MS) exhibits many of the hallmarks of an inflammatory autoimmune disorder including breakdown of the blood-brain barrier (BBB), the recruitment of lymphocytes, microglia, and macrophages to lesion sites, the presence of multiple lesions, generally being more pronounced in the brain stem and spinal cord, the predominantly perivascular location of lesions, the temporal maturation of lesions from inflammation through demyelination, to gliosis and partial remyelination, and the presence of immunoglobulin in the central nervous system and cerebrospinal fluid. Lymphocytes activated in the periphery infiltrate the central nervous system to trigger a local immune response that ultimately damages myelin and axons. Pro-inflammatory cytokines amplify the inflammatory cascade by compromising the BBB, recruiting immune cells from the periphery, and activating resident microglia. inflammation-associated oxidative burst in activated microglia and macrophages plays an important role in the demyelination and free radical-mediated tissue injury in the pathogenesis of MS. The inflammatory environment in demyelinating lesions leads to the generation of oxygen- and nitrogen-free radicals as well as proinflammatory cytokines which contribute to the development and progression of the disease. Inflammation can lead to oxidative stress and vice versa. Thus, oxidative stress and inflammation are involved in a self-perpetuating cycle.

scholarly journals Rapid but not slow spinal cord compression elicits neurogenic pulmonary edema in the rat

2009 ◽  
pp. 269-277 ◽  
Author(s):  
J Šedý ◽  
J Zicha ◽  
J Kuneš ◽  
P Jendelová ◽  
E Syková
Keyword(s):  
Spinal Cord ◽  
Heart Rate ◽  
Pulmonary Edema ◽  
Slow Rate ◽  
Systemic Blood Pressure ◽  
Cord Compression ◽  
Neurogenic Pulmonary Edema ◽  
Balloon Inflation ◽  
Thoracic Spinal Cord ◽  
Thoracic Spinal

The development of neurogenic pulmonary edema (NPE) can be elicited by an immediate epidural balloon compression of the thoracic spinal cord. To evaluate whether a slower balloon inflation could prevent NPE development, we examined the extent of NPE in animals lesioned with a rapid (5 μl - 5 μl - 5 μl) or slow rate (3 μl - 2 μl - 2 μl - 2 μl - 2 μl - 2 μl - 2 μl) of balloon inflation. These groups were compared with the NPE model (immediate inflation to 15 μl) and with healthy controls. Slow balloon inflation prevented NPE development, whereas the pulmonary index and histology revealed a massive pulmonary edema in the group with a rapid rate of balloon inflation. Pulmonary edema was preceded by a considerable decrease in heart rate during the inflation procedure. Moreover, rapid inflation of balloon in spinal channel to either 5 μl or 10 μl did not cause NPE. Thus, a slow rate of balloon inflation in the thoracic epidural space prevents the development of neurogenic pulmonary edema, most likely due to the better adaptation of the organism to acute circulatory changes (rapid elevation of systemic blood pressure accompanied by profound heart rate reduction) during the longer balloon inflation period. It should be noted that spinal cord transection at the same level did not cause neurogenic pulmonary edema.

Role of central nervous system nitric oxide in the development of neurogenic pulmonary edema in rats

2001 ◽  
Vol 29 (6) ◽  
pp. 1222-1228 ◽  
Author(s):  
Ossama Hamdy ◽  
Hiroshi Maekawa ◽  
Yasuhiro Shimada ◽  
Guo Gang Feng ◽  
Naohisa Ishikawa
Keyword(s):  
Nitric Oxide ◽  
Central Nervous System ◽  
Nervous System ◽  
Pulmonary Edema ◽  
Neurogenic Pulmonary Edema

Fatal neurogenic pulmonary edema in a patient with progressive multiple sclerosis

2008 ◽  
Vol 14 (5) ◽  
pp. 711-715 ◽  
Author(s):  
S Bramow ◽  
JC Faber-Rod ◽  
C Jacobsen ◽  
A Kutzelnigg ◽  
P Patrikios ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Pulmonary Edema ◽  
Progressive Disease ◽  
Progressive Multiple Sclerosis ◽  
Neurogenic Pulmonary Edema ◽  
Unexpected Death ◽  
Respiratory Centers ◽  
Lymphocytic Infiltrates ◽  
The Brain ◽  
Neuropathological Examination

We report a case of fatal neurogenic pulmonary edema in progressive multiple sclerosis (MS). The patient had one isolated relapse-like episode. Six years later progressive disease began, lasting 5 years until unexpected death during sleep. Medico-legal autopsy revealed pulmonary edema and neuropathological examination showed infiltrations with lymphocytes and microglia in the respiratory centers of the medulla. More classical demyelinated lesions were found in the white matter of spinal cord and in the gray matter of the brain along with disseminated perivascular lymphocytic infiltrates. Medullary inflammation in progressive MS may result in sudden fatal respiratory failure.

scholarly journals Central Nervous System Demyelination Associated With Immune Checkpoint Inhibitors: Review of the Literature

2020 ◽  
Vol 11 ◽  
Author(s):  
Marcos C. B. Oliveira ◽  
Marcelo H. de Brito ◽  
Mateus M. Simabukuro
Keyword(s):  
Multiple Sclerosis ◽  
Central Nervous System ◽  
Nervous System ◽  
Adverse Events ◽  
Immune Checkpoint ◽  
Immune Checkpoint Inhibitors ◽  
Checkpoint Inhibitors ◽  
Case Reports ◽  
Cell Mediated Immune Response ◽  
Central Nervous System Demyelination

Immune checkpoint inhibitors (ICI) are a novel class of antineoplastic treatment that enhances immunity against tumors. They are associated with immune adverse events, and several neurological syndromes have been described, including multiple sclerosis and atypical demyelination. We performed a systematic literature review of case reports with neurological immune adverse events that presented with central nervous system demyelination, up to December 2019. We found 23 cases: seven with myelitis, four isolated optic neuritis, one neuromyelitis optica spectrum disorder, five multiple sclerosis, and six with atypical demyelination. Ipilimumab was the most frequently used ICI (11/23). The median time to develop symptoms from the onset of ICI was 6.5 weeks [range 1.0–43.0], and from last ICI dose was 14 days [range 0–161]. Anatomopathological examination was performed in four cases, with the finding of a T-cell mediated immune response. Outcomes were generally favorable after immunosuppression: 18 patients had improvement or a full recovery, three patients did not respond to treatment, three patients died, and in one, treatment was not reported. We describe the patients' clinical presentation, treatment administered, and outcomes. We further speculate on possible pathophysiological mechanisms and discuss potential treatments that may be worth investigating.

scholarly journals Acute demyelinating lesions with restricted diffusion in multiple sclerosis

2012 ◽  
Vol 18 (12) ◽  
pp. 1745-1753 ◽  
Author(s):  
Konstantin E Balashov ◽  
Eric Lindzen
Keyword(s):  
Multiple Sclerosis ◽  
Vasogenic Edema ◽  
Case Reports ◽  
Case Series ◽  
Restricted Diffusion ◽  
Retrospective Case ◽  
Stroke In Young Adults ◽  
Case Series Study ◽  
New Variant ◽  
Demyelinating Lesions

Background and objectives: It is widely accepted that typical acute demyelinating lesions in relapsing–remitting multiple sclerosis (RRMS) exhibit vasogenic edema with increased diffusion, as demonstrated by an increased apparent diffusion coefficient on MRI. In contrast, acute ischemic lesions demonstrate cytotoxic edema with restricted diffusion. Recent reports have documented selected cases of acute demyelinating lesions exhibiting restricted diffusion (ADLRD) in MS. We aimed to assess the morphologies, distributions, signal characteristics and changes over time of nine ADLRD. An additional goal was to obtain clinical correlations and relate our findings to all previously published case reports describing ADLRD. Methods: A retrospective case series study was performed at two academic centers. MRI characteristics of nine ADLRD found in six RRMS patients were compared with typical active symptomatic contrast-enhancing lesions with increased or normal diffusion in control RRMS patients. Results: The average size of ADLRD was not significantly different from typical lesions. A periventricular location and faint signal on T2-weighted images were significantly more common for ADLRD compared with typical lesions. Two patients with ADLRD on initial MRI exhibited new ADLRD on their follow up scans. Conclusion: Our results and review of prior published cases suggest that ADLRD represent a new variant of MS lesion. The restricted diffusion that is a characteristic of ADLRD on MRI is a new challenge in the differential diagnosis of stroke in young adults. The pathogenesis of ADLRD remains to be understood.

Neurogenic pulmonary edema: a presenting symptom in multiple sclerosis

1992 ◽  
Vol 13 (5) ◽  
pp. 435-438 ◽  
Author(s):  
N. Gentiloni ◽  
D. Schiavino ◽  
Corte F. Della ◽  
E. Ricci ◽  
C. Colosimo
Keyword(s):  
Multiple Sclerosis ◽  
Pulmonary Edema ◽  
Neurogenic Pulmonary Edema

Tumor-Like Multiple Sclerosis: Report of Four Cases and Literature Review

2006 ◽  
Vol 92 (6) ◽  
pp. 559-562 ◽  
Author(s):  
Emanuela Caroli ◽  
Maurizio Salvati ◽  
Luigi Ferrante
Keyword(s):  
Multiple Sclerosis ◽  
Central Nervous System ◽  
Nervous System ◽  
Demyelinating Disease ◽  
Brain Lesion ◽  
Mri Scan ◽  
Cerebral Tumor ◽  
Demyelinating Lesions ◽  
The Central Nervous System ◽  
Demyelinating Process

Aims and background Classical multiple sclerosis plaques usually have typical features on gadolinium-enhanced MRI scan. This non-neoplastic demyelinating process of the central nervous system generally does not produce focal space-occupying lesions associated with ring enhancement. However, atypical appearance of demyelinating lesions simulating a brain tumor is a possible well-known phenomenon. Methods We present our experience with 4 cases of multiple sclerosis indistinguishable clinically and neuroradiologically from a cerebral tumor. All patients underwent surgery. Results Histological examinations of all cases were positive for multiple sclerosis plaques. Conclusions The presented cases demonstrate the importance of considering a demyelinating disease in the differential diagnosis of a tumor-like brain lesion.

scholarly journals Neurogenic Pulmonary Edema

2018 ◽  
Vol 21 (1) ◽  
pp. 49-52
Author(s):  
Carlos Eduardo Romeu De Almeida ◽  
Eberval Gadelha Figueiredo ◽  
Bernardo Assumpção De Monaco ◽  
Arthur Maynart Pereira Oliveira ◽  
Manoel Jacobsen Teixeira
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Subarachnoid Hemorrhage ◽  
Lung Injury ◽  
Pulmonary Edema ◽  
Patient Management ◽  
Acute Onset ◽  
Neurogenic Pulmonary Edema ◽  
Alveolar Space ◽  
Pulmonary Vasoconstriction

Neurogenic Pulmonary Edema (NPE) is defined as the acute onset of dyspnea or a decrease in PaO2/FiO2 ratio, following an acute central nervous system (CNS) insult, in the absence of other obvious causes of lung injury. The most important cause of NPE is subarachnoid hemorrhage (SAH), followed by cerebraltrauma and epilepsy. The incidence of NPE after SAH in the literature may vary from 4 to 23% in greater studies, with SAH accounting for 43-73% of cases of NPE. It is postulated that an excessive adrenergic discharge would lead to pulmonary vasoconstriction and a rapid increase in pulmonary capillaryhydrostatic pressure, thus promoting fluid leakage to the alveolar space. NPE is generally treated in a supportive and conservative fashion, and patient management should be focused in the primary insult.

scholarly journals Mechanisms of neurogenic pulmonary edema development

2008 ◽  
pp. 499-506
Author(s):  
J Šedý ◽  
J Zicha ◽  
J Kuneš ◽  
P Jendelová ◽  
E Syková
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Intracranial Pressure ◽  
Pulmonary Edema ◽  
Current Knowledge ◽  
Experimental Models ◽  
Neurogenic Pulmonary Edema ◽  
Life Threatening ◽  
Life Threatening Complication ◽  
Sympathetic Discharge

Neurogenic pulmonary edema is a life-threatening complication, known for almost 100 years, but its etiopathogenesis is still not completely understood. This review summarizes current knowledge about the etiology and pathophysiology of neurogenic pulmonary edema. The roles of systemic sympathetic discharge, central nervous system trigger zones, intracranial pressure, inflammation and anesthesia in the etiopathogenesis of neurogenic pulmonary edema are considered in detail. The management of the patient and experimental models of neurogenic pulmonary edema are also discussed.

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