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JSM Clinical Cytology and Pathology

Bulbar Dysfunction in Amyotrophic Lateral Sclerosis: A Case Report of a Rare Neurodegenerative Condition and Literature Review

[ ISSN : 2689-1549 ]

Abstract
Details

Received: 12-Dec-2019

Accepted: 26-Dec-2019

Published: 28-Dec-2019

Ange Ahoussougbemey Mele¹, Michael Sadej¹, Syeda Salman², Sunita Karki², Subhan Ata², and Mohamed Aziz¹*

¹ Department of Pathology, American University of the Caribbean, USA
² Department of Medicine, BronxCare Health System, USA

Corresponding Author:

Ange Ahoussougbemey Mele, Department of Pathology, American University of the Caribbean, 1 University Drive at Jordan Road Cupecoy, St Maarten., USA, Tel: 347-323-4704; Email: ange. mele@gmail.com

Keywords

Amyotrophic Lateral Sclerosis; Bulbar Dysfunction; Pathogenesis; Treatment

Abstract

Amyotrophic Lateral Sclerosis is a debilitating disorder characterized by degeneration of upper and lower motor neurons. Approximately 90% of all ALS cases are found to occur sporadically, whereas 10% of them are familial. ALS can characteristically present as bulbar dysfunction. We report the case of an 81-year-old female who presented with worsening dysarthria, dysphagia, and weight loss of one-year duration. She was later diagnosed with clinically possible to probable ALS based both on results of her laboratory tests and the diagnosis classification of Awaji-Shima Consensus Recommendations and the revised El Escorial Criteria. Riluzole and Edavarone are currently the only two drugs approved by the United States Food and Drug Administration (FDA) for ALS treatment. These drugs work mainly by delaying the course of the disease. Given the scant amount of treatment options available, further studies are warranted to better comprehend the pathogenesis of ALS and find novel and more efficacious ways of addressing it.

Citation

Mele AA, Sadej M, Salman S, Karki S, Ata S, et al. (2019) Bul bar Dysfunction in Amyotrophic Lateral Sclerosis: A Case Report of a Rare Neurodegenerative Condition and Literature Review. JSM Clin Cytol Pathol 4: 4.