Ptosis and Diplopia in a 74-Year-Old With History of Stroke

Rod Foroozan, MD


December 02, 2015


Evaluation revealed that this patient developed ptosis and diplopia related to myasthenia gravis. This diagnosis was confounded by her prior clinical history from 4 years earlier, during which she was told a stroke was the cause of her symptoms. Review of the neuroimaging study from that time, however, did not reveal an abnormality that would cause diplopia.

Myasthenia gravis can cause an ocular misalignment in nearly any pattern and ptosis. Both the ocular misalignment and ptosis may be variable, which is the hallmark of the disease. Patients may have spontaneous relapses of symptoms and go years without problems before a recurrence prompts the diagnosis.

Systemic symptoms, such as difficulty with swallowing, breathing, and generalized weakness, may be helpful in making the diagnosis. In ocular myasthenia gravis, however, the systemic symptoms are absent and ptosis or diplopia occur in isolation.

Although the history and ocular examination may be suggestive, confirmation of the diagnosis is most commonly achieved by measuring antibodies to the acetylcholine receptor. These antibodies are positive more frequently in patients with generalized myasthenia gravis compared with ocular myasthenia gravis. Other antibodies, including those to the muscle-specific tyrosine kinase receptor and low-density lipoprotein receptor-related protein 4, have been thought to play a role in the pathophysiology in some patients.[1]

Medications, including statins typically used to treat hyperlipidemia, may aggravate or unmask the symptoms of myasthenia gravis.[2]

In patients with myasthenia gravis, there is also an increased incidence of other autoimmune disorders, such as thyroid disease, and an increased risk for thymoma.

Prior methods of treatment focused on increasing the availability of acetylcholine in the synaptic cleft using a medication such as pyridostigmine. However, as of late, more attention has been placed on the role of immunosuppression with corticosteroids, corticosteroid-sparing agents, plasmapheresis, and intravenous immunoglobulin. Randomized trials in this area are limited; therefore, the precise role of these treatment modalities has continued to evolve.

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