A 41-year-old military recruiter arrived at the clinic complaining of vision loss. On awakening that morning, he had noticed a slight headache and blurred vision in the left eye. A few minutes later, he had no peripheral vision. Within one hour of taking ibuprofen 400 mg, his headache was gone and his vision had improved. The patient felt well enough to go to work, but a few hours later, he noticed difficulty with his peripheral vision on the right side. He reported no nausea or vomiting. There was no past medical history of headaches or visual problems. The man’s surgical history included thyroidectomy and tonsillectomy. The patient was currently taking levothyroxine (Synthroid); he was allergic to penicillin.
The patient was 5 ft 10 in tall and weighed 214 lb. Vital signs included temperature 97.7°F, pulse 82 beats per minute, and BP 118/83 mm Hg. His visual acuity on the Snellen eye chart was 20/40 on the right and 20/25 on the left. Pupils were uniformly round and responded equally to light. Conjunctivae were clear. Fundoscopy revealed clear disc margins and showed no abnormalities of the blood vessels. Central vision in both eyes and peripheral vision on the left side were intact. However, peripheral vision on the right was decreased in the lateral, superior, and inferior fields. The patient’s tympanic membranes appeared normal. Cranial nerves were grossly intact. Deep tendon reflexes were equal bilaterally in the upper and lower extremities. A Romberg test was negative.
My first impression was that a pituitary tumor was causing temporal hemianopias. I discussed the case with my collaborating physician, who recommended consulting the ophthalmologist on call. Even though I had made up my mind that the patient needed to go to the emergency department (ED) for further workup, I placed a phone call to the ophthalmologist. He agreed with my impression and recommended a trip to the ED for an MRI, magnetic resonance angiography (MRA), complete blood count, erythrocyte sedimentation rate, and C-reactive protein. I discussed the plan with the patient and notified the ED.
3. Unexpected findings
The ED physician found no other neurologic deficits. However, MRI revealed: (1) acute infarcts in the medial and posterior left occipital lobe, with tiny infarcts in the deep left parietal and medial left temporal lobes; (2) a more subacute-to-chronic infarct in the anterior medial right occipital lobe; and (3) a chronic tiny infarct in the right cerebellum. MRA demonstrated an abnormal focal defect in the distal posterior cerebral artery.
The patient was admitted and started on anticoagulation therapy. During the hospitalization, he underwent an extensive workup. Carotid ultrasound was normal. Echocardiogram revealed a low ejection fraction of 45%-50% with findings of a positive right-to-left shunt on expiration. This ultimately led to a transesophageal echocardiogram, which showed low-normal to mild left ventricular systolic dysfunction with normal valves and a patent foramen ovale (seen in 25% of the population).
Prior to discharge, the patient had no sensorimotor deficits. His cognitive exam was unremarkable. At discharge, the only abnormal finding was a visual-field defect located mainly in the right superior quadrant. The patient was discharged on warfarin (Coumadin), which he was advised to continue for life. No surgery was recommended for his patent foramen ovale.
I checked on the patient’s recovery several months later. His vision had returned to normal. He had, however, had surgery for the foramen ovale, which was the source of the blood clots. Warfarin had been discontinued, and the patient now takes only a once-daily aspirin.
Clinical impressions can sometimes be deceiving. I always believed that patients with embolic strokes, especially in both hemispheres, would present with other clinical signs and symptoms. But this patient had no speech problems, peripheral weakness, or abnormal cognitive findings.