Background
In necrotising myositis, the emergence of atypical features such as ophthalmoplegia and fatigable weakness should raise the possibility of myasthenia gravis.
Case
An 81-year-old right-handed man presented with a four-month history of progressive limb weakness. He had noted difficulty climbing stairs and could not rise from a chair without using his arms. He eventually could not stand unaided and had difficulty elevating his arms above the head.  There was no fatigable weakness. He had taken simvastatin 20mg daily 11 years previously, for a period of 19 months. 
Initial investigations revealed an elevated serum creatinine kinase and alanine transaminase. Electromyography revealed increased frequency of short duration polyphasic motor unit action potentials recruited early with a rapid firing rate in addition to spontaneous fibrillations and positive sharp waves. MRI showed patchy T1-weighted hyperintensities in the forearm, hip, thigh, and leg muscles. A biopsy of the left quadriceps muscle was performed which showed features of a necrotising myopathy.
Muscle-specific autoantibody tests were sent. Four weeks later, the patient presented to the emergency department with worsening, now fatigable, weakness, horizontal binocular diplopia, right ptosis, and dysphagia. His creatine kinase was unchanged (2108 iu/l).  Stimulation single fibre electromyography study of right orbicularis oculi showed significant abnormality (66% increased jitter and 32% block, mean jitter MCD of 73.7µs). Repetitive nerve stimulation of right nasalis and left trapezius at 3Hz was abnormal with decrement of 26% and 12% respectively.
His antibody assay revealed elevated anti-3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR) at 125 units (reference range <15).  No other myositis-specific antibodies were detected. Additionally, the anti-acetylcholine receptor antibody was elevated (>20 nmol/l, reference range 0-0.45). Computed tomography of his chest revealed no evidence of thymoma. 
He was treated with intravenous immunoglobin (2g/kg over 5 days) and physiotherapy.  His diplopia and dysphagia resolved, and his limb weakness improved. He was started on daily prednisolone (30mg), azathioprine (50mg), and pyridostigmine (60mg four times daily). At the time of this report, his myasthenic symptoms remained well controlled, with no recurrence of eye complaints.
Conclusion
Our case is relevant to the clinical care of similar patients. First, corticosteroids treat both diseases but require more cautious titration in MG. Second, the co-occurrence of both diseases should prompt careful evaluation for a common underlying cause, such as a thymoma. Clinicians should consider concurrent MG in a patient with myositis who develops typical features of MG- such as ptosis, ophthalmoplegia and fatigable weakness.