A Diagnostic Crossroads: Bulbar Weakness Mimicking ALS in a Seropositive Myasthenia Gravis Patient— A Case Report

A Diagnostic Crossroads: Bulbar Weakness Mimicking ALS in a Seropositive Myasthenia Gravis Patient— A Case Report | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Case Report A Diagnostic Crossroads: Bulbar Weakness Mimicking ALS in a Seropositive Myasthenia Gravis Patient— A Case Report Beruk Ketema, Feryat Leul This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-6895607/v1 This work is licensed under a CC BY 4.0 License Status: Posted Version 1 posted You are reading this latest preprint version Abstract Bulbar-onset Amyotrophic Lateral Sclerosis (ALS) and Myasthenia Gravis (MG) may present with overlapping clinical features, complicating early diagnosis. We report the case of a 30-year-old woman with progressive dysarthria, dysphagia, and tongue fasciculations initially suggestive of bulbar-onset ALS. However, positive anti-acetylcholine receptor (anti-AChR) antibodies and a dramatic clinical response to anticholinesterase therapy and corticosteroids confirmed a diagnosis of bulbar-predominant MG. This case underscores the diagnostic challenge of differentiating bulbar MG from ALS and emphasizes the critical role of serologic evaluation and treatment response in avoiding misdiagnosis. Neurology Bulbar Myasthenia Gravis Amyotrophic Lateral Sclerosis (ALS) Differential Diagnosis Tongue Fasciculations Anti-Acetylcholine Receptor Antibodies Neuromuscular Junction Disorders Introduction Amyotrophic Lateral Sclerosis (ALS) is a fatal neurodegenerative disorder characterized by progressive loss of motor neurons. Bulbar-onset ALS accounts for approximately 25% of all ALS cases and is associated with early dysarthria, dysphagia, tongue fasciculations, and rapid functional decline [ 1 ]. Myasthenia Gravis (MG), on the other hand, is a chronic autoimmune disorder of the neuromuscular junction, typically presenting with ocular symptoms such as ptosis and diplopia, but can occasionally present with bulbar involvement, particularly in seropositive forms [ 2 ]. When bulbar symptoms occur in isolation—especially in the absence of ocular or limb involvement—MG may closely mimic ALS, posing a significant diagnostic challenge. Though fasciculations and pseudobulbar features are more characteristic of ALS, several reports have described MG patients being misdiagnosed with ALS [ 3 – 6 ]. In rarer scenarios, the two conditions may even coexist [ 7 , 8 ]. We present a diagnostically challenging case of a young woman with isolated bulbar symptoms and tongue fasciculations, ultimately diagnosed with anti-AChR positive MG. Case Presentation Patient A 30-year-old woman Chief Complaint 2 month history of progressive dysarthria, nasal speech, dysphagia, and intermittent blurring of vision. She noted diurnal fluctuation of symptoms, with worsening toward the evening. Medical and Family History No significant past medical history. No family history of neuromuscular disease. Neurological Examination: Cranial nerves : Nasal speech and tongue fasciculations were noted. She had difficulty with eyelid closure, but extraocular movements were intact. No facial weakness or ptosis was observed. Motor : Normal tone and strength in all four limbs. No muscle atrophy or fasciculations outside the tongue. Reflexes : Symmetric and normoreflexic. No Babinski sign. Sensation and coordination : Intact. Initial Investigations: Brain CT, chest X-ray, and barium swallow : Unremarkable. Thyroid ultrasound : Multinodular goiter without compressive features. Basic labs : CBC, renal, liver, and thyroid function tests were within normal ranges. Nerve conduction studies (NCS) : Showed mildly reduced compound muscle action potential (CMAP) amplitudes without conduction block. Repetitive nerve stimulation and EMG : Not revealing for a decremental response or chronic denervation. Serology : Strongly positive for anti-AChR antibodies. Diagnosis Bulbar-predominant Myasthenia Gravis Treatment The patient was initiated on pyridostigmine (60 mg three times daily) and oral prednisolone at a starting dose of 20 mg/day. Outcome Remarkable clinical improvement was observed within days of treatment initiation. Speech clarity improved, swallowing normalized, and the patient reported no further bulbar symptoms. By the three-week follow-up, complete resolution of symptoms was achieved. Discussion This case demonstrates a diagnostically challenging presentation of MG masquerading as bulbar-onset ALS. Although tongue fasciculations and progressive bulbar symptoms strongly suggested ALS initially, several clinical features helped distinguish MG: Diurnal Fluctuation : Symptom variation with fatigue, particularly worsening later in the day, is typical of MG and not characteristic of ALS. Serologic Confirmation : Detection of anti-AChR antibodies provided strong diagnostic evidence in favor of MG. Therapeutic Response : The rapid and complete clinical response to pyridostigmine and corticosteroids is inconsistent with the progressive nature of ALS. Misdiagnosis Risk Misdiagnosis of MG as ALS can have profound implications. Multiple case reports have described similar scenarios where bulbar MG, especially without ocular symptoms, led to premature ALS diagnoses [ 3 , 4 ]. In some cases, hyperreflexia or tongue fasciculations were misleading [ 5 ]. The presence of such "false upper motor neuron signs" in MG has been attributed to disuse hyperreflexia or anxiety-related muscle activity. Isolated Bulbar Myasthenia Gravis Bulbar-predominant MG without ocular or limb involvement is uncommon but documented [ 6 ]. In these cases, electrodiagnostic studies may not reveal the classic decremental response, making serologic testing critical. Clinicians should maintain high suspicion in young patients presenting with bulbar dysfunction and consider antibody testing early. Coexistence of MG and ALS Rare reports describe coexisting ALS and MG, raising speculation about shared immune or degenerative mechanisms [ 7 , 8 ]. However, true overlap syndromes remain exceptional. In our case, the absence of denervation potentials on EMG, lack of upper motor neuron signs, and rapid clinical improvement excluded a dual diagnosis. Conclusion This case underscores the importance of a careful and thorough diagnostic approach when evaluating bulbar symptoms. Clinicians should be aware of the potential for MG to mimic ALS, particularly when fasciculations and dysphagia are present in isolation. Prompt recognition through antibody testing and therapeutic trials can prevent misdiagnosis, reduce patient anxiety, and ensure appropriate treatment. Distinguishing these conditions is vital, given the vastly different prognoses and management strategies. Declarations Patient Consent Written informed consent was obtained from the patient for publication of this case report. Ethical Approval Not required for single case reports per institutional policy. Data Availability All data supporting this report are included in the manuscript. Conflict of Interest The authors declare no conflicts of interest. Funding No financial support was received for this work. Author Contributions Beruk Ketema: Patient evaluation, clinical management, data collection, literature review, and manuscript preparation. Feryat Leul: Clinical evaluation, supportive management, data interpretation, and critical review of the manuscript. References StatPearls Bulbar ALS Subtype . Available at: https://www.ncbi.nlm.nih.gov/books/NBK559262/ Gilhus NE (2016) Myasthenia Gravis. N Engl J Med 375(26):2570–2581 Basiri K, Ansari B et al (2014) Misdiagnosis of Myasthenia Gravis as ALS: A Case Report. Iran J Neurol 13(4):255–257 Meriggioli MN, Sanders DB (2009) Autoimmune Myasthenia Gravis: Emerging Clinical and Biological Heterogeneity. Lancet Neurol 8(5):475–490 Padua L, Stålberg E et al (2001) Clinical Features of Atypical MG Mimicking ALS. Muscle Nerve 24(11):1520–1523 Okamoto M et al (2003) Bulbar Myasthenia without Ocular Involvement. J Clin Neurosci 10(5):599–601 Pecar-Malec E et al (2011) Overlap Syndrome of MG and ALS. Neurol Sci 32(6):1085–1087 Fang F et al (2015) Coexistence of Myasthenia Gravis and ALS: A Population-Based Cohort Study. JAMA Neurol 72(6):706–712 Additional Declarations The authors declare no competing interests. Cite Share Download PDF Status: Posted Version 1 posted You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. We do this by developing innovative software and high quality services for the global research community. Our growing team is made up of researchers and industry professionals working together to solve the most critical problems facing scientific publishing. Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-6895607","acceptedTermsAndConditions":true,"allowDirectSubmit":true,"archivedVersions":[],"articleType":"Case Report","associatedPublications":[],"authors":[{"id":471353123,"identity":"0f69466b-4827-4bb1-818d-e8066db356cb","order_by":0,"name":"Beruk Ketema","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAABCUlEQVRIiWNgGAWjYBACeyBmbGA4DOF9gFAGeLUYNoC1HGPgAemdgdCCW5vBAbCWM2AtzDzEaDFs730mOYPhhpw9e3fiZ5sau8QG9uZtEgwVf3D7hee4meQGhg/GPDxnN0vnHEtObOA5VibBcAaPLTPS2CQfMHxI7JHI3SCdw8ac2CCRYybB2IbHL/efgbTcqO+Rf7v5t8W/+sQG+TdALf/waLnBxgZ02JkEHgnebdKMbYeBtvAAtTTgcVhPGrPlDINjhj1ncrdZ9vYdN27jSSu2SDhmjNv77McYb/ZUHJZnbz+7+caPb9Wy/eyHN974UCOHUwvUeUhsNhCRQEDDKBgFo2AUjAL8AAAGMFILm5mCCwAAAABJRU5ErkJggg==","orcid":"https://orcid.org/0009-0003-9448-3313","institution":"Addis Ababa University","correspondingAuthor":true,"prefix":"","firstName":"Beruk","middleName":"","lastName":"Ketema","suffix":""},{"id":471353124,"identity":"a37c032a-3b6c-4bba-9dbb-ef4966c878aa","order_by":1,"name":"Feryat Leul","email":"","orcid":"","institution":"Addis Ababa University","correspondingAuthor":false,"prefix":"","firstName":"Feryat","middleName":"","lastName":"Leul","suffix":""}],"badges":[],"createdAt":"2025-06-14 20:26:33","currentVersionCode":1,"declarations":{"humanSubjects":true,"vertebrateSubjects":false,"conflictsOfInterestStatement":false,"humanSubjectEthicalGuidelines":true,"humanSubjectConsent":true,"humanSubjectClinicalTrial":false,"humanSubjectCaseReport":true,"vertebrateSubjectEthicalGuidelines":false},"doi":"10.21203/rs.3.rs-6895607/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-6895607/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":84753443,"identity":"ab68ab23-e1aa-4a14-8a01-708f7b2c3675","added_by":"auto","created_at":"2025-06-17 03:38:52","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":466562,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-6895607/v1/0824c91d-33d1-44d1-9846-ea25a6c2590a.pdf"}],"financialInterests":"The authors declare no competing interests.","formattedTitle":"\u003cp\u003e\u003cstrong\u003eA Diagnostic Crossroads: Bulbar Weakness Mimicking ALS in a Seropositive Myasthenia Gravis Patient— A Case Report\u003c/strong\u003e\u003c/p\u003e","fulltext":[{"header":"Introduction","content":"\u003cp\u003eAmyotrophic Lateral Sclerosis (ALS) is a fatal neurodegenerative disorder characterized by progressive loss of motor neurons. Bulbar-onset ALS accounts for approximately 25% of all ALS cases and is associated with early dysarthria, dysphagia, tongue fasciculations, and rapid functional decline [\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e]. Myasthenia Gravis (MG), on the other hand, is a chronic autoimmune disorder of the neuromuscular junction, typically presenting with ocular symptoms such as ptosis and diplopia, but can occasionally present with bulbar involvement, particularly in seropositive forms [\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eWhen bulbar symptoms occur in isolation\u0026mdash;especially in the absence of ocular or limb involvement\u0026mdash;MG may closely mimic ALS, posing a significant diagnostic challenge. Though fasciculations and pseudobulbar features are more characteristic of ALS, several reports have described MG patients being misdiagnosed with ALS [\u003cspan additionalcitationids=\"CR4 CR5\" citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e]. In rarer scenarios, the two conditions may even coexist [\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e, \u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eWe present a diagnostically challenging case of a young woman with isolated bulbar symptoms and tongue fasciculations, ultimately diagnosed with anti-AChR positive MG.\u003c/p\u003e"},{"header":"Case Presentation","content":"\u003cp\u003e \u003cstrong\u003ePatient\u003c/strong\u003e \u003cp\u003eA 30-year-old woman\u003c/p\u003e \u003c/p\u003e \u003cp\u003e \u003cstrong\u003eChief Complaint\u003c/strong\u003e \u003cp\u003e2 month history of progressive dysarthria, nasal speech, dysphagia, and intermittent blurring of vision. She noted diurnal fluctuation of symptoms, with worsening toward the evening.\u003c/p\u003e \u003c/p\u003e \u003cp\u003e \u003cstrong\u003eMedical and Family History\u003c/strong\u003e \u003cp\u003eNo significant past medical history. No family history of neuromuscular disease.\u003c/p\u003e \u003c/p\u003e \u003cdiv id=\"Sec3\" class=\"Section2\"\u003e \u003ch2\u003eNeurological Examination:\u003c/h2\u003e \u003cp\u003e \u003cul\u003e \u003cli\u003e \u003cp\u003e \u003cb\u003eCranial nerves\u003c/b\u003e: Nasal speech and tongue fasciculations were noted. She had difficulty with eyelid closure, but extraocular movements were intact. No facial weakness or ptosis was observed.\u003c/p\u003e \u003c/li\u003e \u003cli\u003e \u003cp\u003e \u003cb\u003eMotor\u003c/b\u003e: Normal tone and strength in all four limbs. No muscle atrophy or fasciculations outside the tongue.\u003c/p\u003e \u003c/li\u003e \u003cli\u003e \u003cp\u003e \u003cb\u003eReflexes\u003c/b\u003e: Symmetric and normoreflexic. No Babinski sign.\u003c/p\u003e \u003c/li\u003e \u003cli\u003e \u003cp\u003e \u003cb\u003eSensation and coordination\u003c/b\u003e: Intact.\u003c/p\u003e \u003c/li\u003e \u003c/ul\u003e \u003c/p\u003e \u003c/div\u003e\n\u003ch3\u003eInitial Investigations:\u003c/h3\u003e\n\u003cp\u003e \u003cul\u003e \u003cli\u003e \u003cp\u003e \u003cb\u003eBrain CT, chest X-ray, and barium swallow\u003c/b\u003e: Unremarkable.\u003c/p\u003e \u003c/li\u003e \u003cli\u003e \u003cp\u003e \u003cb\u003eThyroid ultrasound\u003c/b\u003e: Multinodular goiter without compressive features.\u003c/p\u003e \u003c/li\u003e \u003cli\u003e \u003cp\u003e \u003cb\u003eBasic labs\u003c/b\u003e: CBC, renal, liver, and thyroid function tests were within normal ranges.\u003c/p\u003e \u003c/li\u003e \u003cli\u003e \u003cp\u003e \u003cb\u003eNerve conduction studies (NCS)\u003c/b\u003e: Showed mildly reduced compound muscle action potential (CMAP) amplitudes without conduction block.\u003c/p\u003e \u003c/li\u003e \u003cli\u003e \u003cp\u003e \u003cb\u003eRepetitive nerve stimulation and EMG\u003c/b\u003e: Not revealing for a decremental response or chronic denervation.\u003c/p\u003e \u003c/li\u003e \u003cli\u003e \u003cp\u003e \u003cb\u003eSerology\u003c/b\u003e: Strongly positive for anti-AChR antibodies.\u003c/p\u003e \u003c/li\u003e \u003c/ul\u003e \u003c/p\u003e \u003cp\u003e \u003cstrong\u003eDiagnosis\u003c/strong\u003e \u003cp\u003eBulbar-predominant Myasthenia Gravis\u003c/p\u003e \u003c/p\u003e \u003cp\u003e \u003cstrong\u003eTreatment\u003c/strong\u003e \u003cp\u003eThe patient was initiated on pyridostigmine (60 mg three times daily) and oral prednisolone at a starting dose of 20 mg/day.\u003c/p\u003e \u003c/p\u003e \u003cp\u003e \u003cstrong\u003eOutcome\u003c/strong\u003e \u003cp\u003eRemarkable clinical improvement was observed within days of treatment initiation. Speech clarity improved, swallowing normalized, and the patient reported no further bulbar symptoms. By the three-week follow-up, complete resolution of symptoms was achieved.\u003c/p\u003e \u003c/p\u003e"},{"header":"Discussion","content":"\u003cp\u003eThis case demonstrates a diagnostically challenging presentation of MG masquerading as bulbar-onset ALS. Although tongue fasciculations and progressive bulbar symptoms strongly suggested ALS initially, several clinical features helped distinguish MG:\u003c/p\u003e \u003cp\u003e \u003col\u003e \u003cspan\u003e \u003cli\u003e \u003cp\u003e \u003cb\u003eDiurnal Fluctuation\u003c/b\u003e: Symptom variation with fatigue, particularly worsening later in the day, is typical of MG and not characteristic of ALS.\u003c/p\u003e \u003c/li\u003e \u003c/span\u003e \u003cspan\u003e \u003cli\u003e \u003cp\u003e \u003cb\u003eSerologic Confirmation\u003c/b\u003e: Detection of anti-AChR antibodies provided strong diagnostic evidence in favor of MG.\u003c/p\u003e \u003c/li\u003e \u003c/span\u003e \u003cspan\u003e \u003cli\u003e \u003cp\u003e \u003cb\u003eTherapeutic Response\u003c/b\u003e: The rapid and complete clinical response to pyridostigmine and corticosteroids is inconsistent with the progressive nature of ALS.\u003c/p\u003e \u003c/li\u003e \u003c/span\u003e \u003c/ol\u003e \u003c/p\u003e\n\u003ch3\u003eMisdiagnosis Risk\u003c/h3\u003e\n\u003cp\u003eMisdiagnosis of MG as ALS can have profound implications. Multiple case reports have described similar scenarios where bulbar MG, especially without ocular symptoms, led to premature ALS diagnoses [\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e, \u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e]. In some cases, hyperreflexia or tongue fasciculations were misleading [\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e]. The presence of such \"false upper motor neuron signs\" in MG has been attributed to disuse hyperreflexia or anxiety-related muscle activity.\u003c/p\u003e\n\u003ch3\u003eIsolated Bulbar Myasthenia Gravis\u003c/h3\u003e\n\u003cp\u003eBulbar-predominant MG without ocular or limb involvement is uncommon but documented [\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e]. In these cases, electrodiagnostic studies may not reveal the classic decremental response, making serologic testing critical. Clinicians should maintain high suspicion in young patients presenting with bulbar dysfunction and consider antibody testing early.\u003c/p\u003e \u003cdiv id=\"Sec8\" class=\"Section2\"\u003e \u003ch2\u003eCoexistence of MG and ALS\u003c/h2\u003e \u003cp\u003eRare reports describe coexisting ALS and MG, raising speculation about shared immune or degenerative mechanisms [\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e, \u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e]. However, true overlap syndromes remain exceptional. In our case, the absence of denervation potentials on EMG, lack of upper motor neuron signs, and rapid clinical improvement excluded a dual diagnosis.\u003c/p\u003e \u003c/div\u003e"},{"header":"Conclusion","content":"\u003cp\u003eThis case underscores the importance of a careful and thorough diagnostic approach when evaluating bulbar symptoms. Clinicians should be aware of the potential for MG to mimic ALS, particularly when fasciculations and dysphagia are present in isolation. Prompt recognition through antibody testing and therapeutic trials can prevent misdiagnosis, reduce patient anxiety, and ensure appropriate treatment. Distinguishing these conditions is vital, given the vastly different prognoses and management strategies.\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003ePatient Consent\u003c/strong\u003e\u003cbr\u003e\u0026nbsp;Written informed consent was obtained from the patient for publication of this case report.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eEthical Approval\u003c/strong\u003e\u003cbr\u003e\u0026nbsp;Not required for single case reports per institutional policy.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eData Availability\u003c/strong\u003e\u003cbr\u003e\u0026nbsp;All data supporting this report are included in the manuscript.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConflict of Interest\u003c/strong\u003e\u003cbr\u003e\u0026nbsp;The authors declare no conflicts of interest.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eFunding\u003c/strong\u003e\u003cbr\u003e\u0026nbsp;No financial support was received for this work.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAuthor Contributions\u003c/strong\u003e\u003cbr\u003e\u0026nbsp;Beruk Ketema: Patient evaluation, clinical management, data collection, literature review, and manuscript preparation.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eFeryat Leul:\u003c/strong\u003e Clinical evaluation, supportive management, data interpretation, and critical review of the manuscript.\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\u003cli\u003e\u003cspan\u003eStatPearls \u003cem\u003eBulbar ALS Subtype\u003c/em\u003e. Available at: \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://www.ncbi.nlm.nih.gov/books/NBK559262/\u003c/span\u003e\u003cspan address=\"https://www.ncbi.nlm.nih.gov/books/NBK559262/\" targettype=\"URL\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eGilhus NE (2016) Myasthenia Gravis. N Engl J Med 375(26):2570\u0026ndash;2581\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eBasiri K, Ansari B et al (2014) Misdiagnosis of Myasthenia Gravis as ALS: A Case Report. Iran J Neurol 13(4):255\u0026ndash;257\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eMeriggioli MN, Sanders DB (2009) Autoimmune Myasthenia Gravis: Emerging Clinical and Biological Heterogeneity. Lancet Neurol 8(5):475\u0026ndash;490\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003ePadua L, St\u0026aring;lberg E et al (2001) Clinical Features of Atypical MG Mimicking ALS. Muscle Nerve 24(11):1520\u0026ndash;1523\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eOkamoto M et al (2003) Bulbar Myasthenia without Ocular Involvement. J Clin Neurosci 10(5):599\u0026ndash;601\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003ePecar-Malec E et al (2011) Overlap Syndrome of MG and ALS. Neurol Sci 32(6):1085\u0026ndash;1087\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eFang F et al (2015) Coexistence of Myasthenia Gravis and ALS: A Population-Based Cohort Study. JAMA Neurol 72(6):706\u0026ndash;712\u003c/span\u003e\u003c/li\u003e\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":true,"hideJournal":true,"highlight":"","institution":"Addis Ababa University","isAcceptedByJournal":false,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true},"keywords":"Bulbar Myasthenia Gravis, Amyotrophic Lateral Sclerosis (ALS), Differential Diagnosis, Tongue Fasciculations, Anti-Acetylcholine Receptor Antibodies, Neuromuscular Junction Disorders","lastPublishedDoi":"10.21203/rs.3.rs-6895607/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-6895607/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003cp\u003eBulbar-onset Amyotrophic Lateral Sclerosis (ALS) and Myasthenia Gravis (MG) may present with overlapping clinical features, complicating early diagnosis. We report the case of a 30-year-old woman with progressive dysarthria, dysphagia, and tongue fasciculations initially suggestive of bulbar-onset ALS. However, positive anti-acetylcholine receptor (anti-AChR) antibodies and a dramatic clinical response to anticholinesterase therapy and corticosteroids confirmed a diagnosis of bulbar-predominant MG. This case underscores the diagnostic challenge of differentiating bulbar MG from ALS and emphasizes the critical role of serologic evaluation and treatment response in avoiding misdiagnosis.\u003c/p\u003e","manuscriptTitle":"A Diagnostic Crossroads: Bulbar Weakness Mimicking ALS in a Seropositive Myasthenia Gravis Patient— A Case Report","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2025-06-17 03:30:42","doi":"10.21203/rs.3.rs-6895607/v1","editorialEvents":[{"type":"communityComments","content":0}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"bfb6b061-6778-4655-b97b-716c53c52820","owner":[],"postedDate":"June 17th, 2025","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"posted","subjectAreas":[{"id":50056469,"name":"Neurology"}],"tags":[],"updatedAt":"2025-06-17T03:30:42+00:00","versionOfRecord":[],"versionCreatedAt":"2025-06-17 03:30:42","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-6895607","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-6895607","identity":"rs-6895607","version":["v1"]},"buildId":"8U1c8b4HqxoKbykW_rLl7","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}