A 62-year-old man with a history of migraine came to the emergency department with sudden onset of horizontal diplopia and, subsequently, bilateral ptosis. He noted feeling unsteady when walking. He reported that the diplopia worsened throughout the day. He had a history of hepatitis C infection. He had some vision loss in his left eye, which was thought to relate to a retinopathy. He disclosed that he had a history of cold feet and had notably high arches. He had a pacemaker because of syncope attributed to sick sinus syndrome. Computed tomography angiography of the head and neck were ruled negative for intracranial stenosis, occlusions, or aneurysms. Computed tomography of the head indicated a tiny lacunar infarct in the right caudate head. Magnetic resonance imaging of the brain identified a tiny, periaqueductal, enhancing abnormality in the right midbrain that was thought to be likely ischemic, but there was some concern for a demyelinating or inflammatory lesion. Cerebrospinal fluid evaluation indicated an increased protein concentration. Serologic evaluation for myasthenia gravis striational antibodies were positive at a titer of 1:240. Serum protein studies indicated the presence of polyclonal hypergammaglobulinemia. Myasthenia gravis was effectively ruled out. Given the hyperacute time course, the patient’s clinical disorder was most probably explained by an ischemic stroke that affected the oculomotor nuclei regions causing ptosis and ophthalmoparesis. On follow-up, the patient was discovered to have a patent foramen ovale. Whether the patent foramen ovale was a contributing factor to the stroke is uncertain. The recurrence rate in this setting is thought to be low relative to other causes of stroke. Ultimately it was decided to not close the patent foramen ovale and to maintain the patient on clopidogrel and adult low-dose aspirin. The onset of diplopia is typically sudden, but this occurs exclusively with vascular pathologic processes. Diplopia that appears intermittently with diurnal variation suggests the possibility of a neuromuscular junction disease such as myasthenia gravis.
Bilateral facial colliculus syndrome caused by pontine tegmentum infarction: a case report
