Rationale: Cancer-associated myositis (CAM) is a rare autoimmune disease linked to underlying malignancies and classified as an idiopathic inflammatory myopathy. It is characterized by a complex pathogenesis, poor prognosis, and diverse symptoms such as muscle weakness and myalgia, which may be accompanied by extramuscular manifestations. The presence of comorbidities in elderly patients can mask these symptoms, posing significant diagnostic and treatment challenges. Early recognition of CAM and detection of malignancy are crucial for improving patient outcomes. Patient concerns: A 71-year-old male presented with progressive symmetrical proximal muscle pain as the sole manifestation, without typical extramuscular manifestations. Initial tests revealed negative muscle enzyme results, but electromyography indicated myogenic damage in the proximal muscles of the limbs. Further serological testing detected positive anti-TIF1γ and anti-PL-7 antibodies. Diagnoses: The patient was diagnosed with CAM based on the presence of specific autoantibodies and a rapid clinical response to corticosteroids. Interventions: Treatment with low-dose hormone therapy resulted in significant improvement of symptoms. A comprehensive malignancy screening was performed. Outcomes: Subsequent surgical pathology confirmed the presence of colon cancer. The patient’s condition improved markedly with timely intervention and targeted treatment. At 6-month follow-up, he remained symptom-free. Lessons: This case underscores the importance of considering CAM in patients with unexplained symmetrical proximal muscle pain, even in the absence of typical extramuscular symptoms. The detection of myositis-specific autoantibodies is critical for accurate diagnosis. Early identification and treatment of the underlying malignancy can significantly improve prognosis. Future research should focus on elucidating the pathogenesis of CAM, identifying more specific biomarkers, and developing standardized diagnostic and therapeutic guidelines to enhance early diagnosis and treatment outcomes.

Introduction: Glutamic acid decarboxylase 65 (GAD65) antibody-associated autoimmune encephalitis is an uncommon immune-mediated neurological disorder with heterogeneous neuropsychiatric manifestations. Diagnosis is particularly challenging in older adults when symptoms of recent traumatic brain injury (TBI) overlap with structural or metabolic conditions. Case presentation: We report a 79-year-old man who developed recurrent headache, progressive confusion, abnormal behavior, poor oral intake, intermittent myoclonic jerks, and low-grade fever after TBI complicated by chronic subdural hematoma. Initial laboratory testing revealed hyponatremia, and the working diagnosis was post-traumatic brain syndrome with syndrome of inappropriate antidiuretic hormone secretion (SIADH). Although serum sodium was corrected and nocturnal agitation partially improved, persistent daytime confusion, cognitive impairment, behavioral abnormalities, and low-grade fever prompted further investigation. Cerebrospinal fluid (CSF) analysis showed mild inflammatory changes with pleocytosis and elevated protein. CSF metagenomic next-generation sequencing (mNGS) and paraneoplastic antibody testing were negative, whereas the autoimmune encephalitis panel was positive for GAD65 antibody at a titer of 1:32. Whole-body positron emission tomography-computed tomography (PET-CT) did not reveal malignancy. The diagnosis was therefore revised to GAD65 antibody-associated autoimmune encephalitis. Because high-dose corticosteroids were considered unsuitable owing to his history of gastric ulcer and previous gastrointestinal bleeding, he was treated with intravenous immunoglobulin (IVIG) at a total dose of 2 g/kg divided over 3 consecutive days followed by oral azathioprine 50 mg daily. His fever resolved within 1 week, and his mental status and responsiveness gradually improved. At 6-month follow-up, he had achieved near-baseline mental status, was able to walk with a cane, and was almost fully independent in daily activities, without relapse or serious treatment-related adverse events. Discussion: This case highlights the diagnostic difficulty of recognizing autoimmune encephalitis after TBI. The clinical overlap between post- traumatic syndrome and immune-mediated brain injury often delays diagnosis, emphasizing the value of targeted CSF autoantibody testing in atypical cases. Conclusion: Traumatic brain injury may obscure the onset of GAD65-associated autoimmune encephalitis. Early recognition and a corticosteroid-sparing immunotherapy strategy (IVIG and azathioprine) can yield favorable outcomes in elderly patients with medical comorbidities.