Acute Bilateral Vocal Cord Immobility Secondary to Acute Myopathy

Pharyngolaryngeal dysfunction associated with myopathy is not well characterized. We present a case of toxic or inflammatory myopathy causing severe vocal fold hypomobility and dysphagia, with complete recovery. A 47-year-old female with tuberous sclerosis, lymphangioleiomyomatosis, and a recent upper respiratory infection, taking atorvastatin and, until recently, everolimus, presented with several weeks of myalgias and 10 days of dyspnea. Examination demonstrated full extremity strength and inspiratory stridor. Flexible laryngoscopy revealed severely hypomobile bilateral vocal folds with pooled pharyngeal secretions. Creatine phosphokinase (CK) was >40,000 U/L at presentation. Rheumatology workup was negative. Magnetic resonance imaging of the brain demonstrated enhancement of facial and cervical musculature. Computed tomography of the neck showed new laryngeal muscle heterogeneity. Neither identified vagal or laryngeal nerve pathology. Treatment included high-dose dexamethasone, racemic epinephrine, albuterol, intravenous fluids, a temporary feeding tube, and discontinuation of atorvastatin and lisinopril. By hospital day 14, CK decreased to 1,420 U/L, and vocal fold motion had significantly improved. At one-month follow-up, vocal fold mobility normalized, symptoms resolved, and CK was 320 U/L. Extended myositis antibody panel at four-month follow-up was negative. Recovery was sustained at seven months. This case suggests pharyngolaryngeal musculature can be preferentially affected in acute myopathy.