Delayed diagnosis of ocular myasthenia gravis in a patient with aponeurotic ptosis: A case report.

Acquired ptosis may result from multiple etiologies, including aponeurotic, neurogenic, myogenic, traumatic, and mechanical causes. When structural eyelid abnormalities are prominent, the clinical signs of underlying neuromuscular disorders may be physically masked and difficult to recognize. A patient in her 70s presented with an acute onset of unilateral ptosis. Neuroimaging revealed an incidental aneurysm of the left middle cerebral artery that was anatomically independent of the oculomotor nerve. Ophthalmic examination suggested aponeurotic ptosis, and surgical repair restored eyelid height immediately. However, fluctuating ptosis with diurnal variation was observed 1 week postoperatively. Electromyography showed a postsynaptic neuromuscular junction disorder. Together with positive acetylcholine receptor antibodies, ocular myasthenia gravis was diagnosed. Treatment with oral pyridostigmine resulted in marked clinical improvement. Severe aponeurotic disinsertion can obscure the fatigability typical of ocular myasthenia gravis and delay recognition of the underlying disorder. In patients with atypical presentations such as acute-onset ptosis, additional evaluation, including electrophysiological testing, is essential to identify coexisting neuromuscular dysfunction.