Swallowing and speech disturbances are frequent symptoms across a range of structural and neuromuscular disorders. Among them, multinodular goiter (MNG) and myasthenia gravis (MG) are distinct entities but may present with overlapping features, complicating diagnosis. MNG can cause compressive symptoms such as dysphagia and hoarseness through mass effect on the esophagus or recurrent laryngeal nerve. In contrast, MG is a neuromuscular junction disorder characterized by fatigable weakness of voluntary muscles, including those involved in speech and swallowing. 1 , 2 , 3
This case illustrates the diagnostic challenge posed by concurrent MNG and MG, emphasizing the importance of recognizing symptom patterns, especially fatigability, to distinguish between structural and neuromuscular causes.
Case Presentation
A 64‐year‐old woman presented with a 4‐day history of slurred, nasal speech and difficulty swallowing liquids, including nasal regurgitation. She had a known MNG for which thyroidectomy had been advised but not pursued. Neurological and otolaryngology (ENT) assessments were inconclusive. A noncontrast head CT showed only mild chronic ischemic changes, and flexible laryngoscopy revealed no vocal fold pathology.
She was discharged with plans for reflux treatment and outpatient imaging. However, she returned three days later with worsened dysphagia and nasal speech. A CT neck and chest showed a 3.7 × 3.5 cm thyroid nodule with mild tracheal deviation but no retrosternal extension or airway compromise. Thyroid function was normal. Surgery was recommended due to compressive symptoms.
She underwent total thyroidectomy without complications. Pathology revealed a 0.5 cm incidental papillary microcarcinoma. While her swallowing improved postoperatively, she continued to report hoarseness and progressive voice fatigue.
At her 1‐week postoperative endocrinology follow‐up, the patient described persistent hoarseness and increasing voice fatigue later in the day. This pattern of worsening with use prompted consideration of MG. Acetylcholine receptor antibody testing returned strongly positive (15 nmol/L; reference <0.50), confirming the diagnosis.
She began pyridostigmine with rapid symptom improvement. Later, prednisone and azathioprine were added for better bulbar control. Chest CT ruled out thymoma.
Discussion
This case highlights how concurrent structural and neuromuscular conditions can obscure diagnosis. Initial symptoms, including dysphagia and nasal speech, were attributed to MNG. However, subtle features such as fatigability and nasal phonation pointed toward bulbar MG. MNG causes symptoms through mechanical compression of adjacent structures. Dysphagia typically involves solids more than liquids, and voice changes result from stretch or injury to the recurrent laryngeal nerve. 4 In contrast, MG causes fatigable weakness of palatal and pharyngeal muscles, producing slurred, nasal speech and difficulty swallowing, especially liquids, with symptoms worsening throughout the day. 1 , 3
The absence of significant airway or esophageal compression on imaging raised suspicion that MNG alone could not explain the patient′s presentation. The persistence of dysarthria postthyroidectomy, along with symptom worsening in the evening and positive acetylcholine (AChR) antibodies, confirmed the presence of MG. Rapid response to pyridostigmine further validated the neuromuscular diagnosis.
This case underscores the importance of distinguishing dysphonia (voice production issues, often structural) from dysarthria (motor speech disorder, typically neurologic). The patient's symptoms, including nasal regurgitation and worsening speech with use, were more consistent with bulbar MG than with MNG‐related nerve involvement. 1 , 3 , 5
Accurate symptom characterization is essential. As shown in prior studies, bulbar symptoms are often the first or dominant manifestation of late‐onset MG and can mimic structural ENT or gastrointestinal disorders. 2 , 3 Misattribution of neuromuscular symptoms to coexisting structural pathology can delay appropriate treatment.
Conclusion
In the presence of thyroid disease, bulbar symptoms may be misattributed to structural compression, even when the clinical picture doesn't fully support a compressive mechanism. This reflects a common cognitive bias toward more familiar or visible diagnoses. Recognizing atypical features, like fatigability, is essential to avoid delays in diagnosing neurologic conditions such as MG.
Author Contributions
Yusef Hazime, case identification, consent coordination, manuscript review and finalization; Ms. Zeina El Zoert, literature review, initial manuscript draft, manuscript edit and submission; Dr. Pamela Howeiss and Dr. Mustapha El Lakis, manuscript review and finalization. All authors approved the final version and accept responsibility for the content.
Disclosures
Competing interests
None.
Funding source
None.
Acknowledgments
The authors would like to thank the patient and their family for their cooperation and for consenting to share this case.
References
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