Sudden Onset Bilateral Carpal Tunnel Syndrome with Progressive Systemic Symptoms in a 57-Year-Old Man with Multiple Sclerosis

Background Myopathies in patients with pre-existing neurological disease pose significant diagnostic and management challenges. Distinguishing new musculoskeletal symptoms from manifestations of the underlying neurological disorder requires careful clinical and interdisciplinary assessment. Multiple sclerosis (MS) is primarily an autoimmune demyelinating condition, and its coexistence with autoimmune myopathies is rare. We present a unique case of myofasciitis in a patient with relapsing-remitting MS, highlighting the complexities of evaluation, diagnosis, and treatment in this setting. Case Report A 57-year-old man with relapsing-remitting MS on Tecfidera presented with a 1-year history of symptoms beginning with sudden-onset bilateral hand numbness, nocturnal heat sensations, plantar fasciitis, and mild foot drop while traveling internationally. Upon returning, nerve conduction studies confirmed bilateral carpal tunnel syndrome, and he underwent right carpal tunnel release without symptomatic improvement. Spinal MRI showed 2 new MS lesions at C4 and T3, though neither accounted for his symptoms. Over the following months, his musculoskeletal symptoms progressed to weakness, frequent dropping of objects, impaired fine motor control, stiffness in all extremities, and restricted mobility. He also reported a 3-month history of constitutional symptoms, including unintentional weight loss of 30 pounds, occasional night sweats, and generalized pruritus. On examination during his initial Rheumatology consultation, he was noted to have positive groove sign over the forearms and calves, lower extremity hyperpigmentation, erythema over the dorsum of the feet, flexor contractures of the fingers with a positive prayer sign, inability to make a fist, diminished bilateral grip strength, and restricted ability to kneel or cross the legs due to fascial tightening. In terms of investigations, comprehensive malignancy screening (pan-CT, PET, colonoscopy, esophagogastroduodenoscopy) was negative. Serologic testing revealed modest CRP elevation and weakly positive anti-Mup44 antibody. Muscle biopsy demonstrated myofasciitis, confirming the diagnosis. The patient provided consent for publication. Conclusion The patient was started on prednisone, resulting in prompt symptomatic improvement. In collaboration with Neurology, rituximab was initiated to manage both myofasciitis and MS concurrently. The weakly positive anti-Mup44 antibody, which is typically associated with inclusion body myositis (IBM), was considered to be clinically insignificant given that the clinical course and rapid response to prednisone were not in keeping with IBM. To our knowledge, this is the first report on a case of myofasciitis in an MS patient. This case highlights the importance of careful physical examination, expedited tissue diagnosis and close interdisciplinary collaboration between neurology and rheumatology for the workup of myopathies in patients with underlying neurological disease.