A 42-year-old man presented to the emergency department after experiencing multiple episodes of difficulty in speaking. Over the past 24 hours, had been unable to formulate his speech for 1 to 2 minutes per episode but was aware of what he wanted to say. He had experienced a similar episode 2 weeks earlier when he lost the ability to verbalize his thoughts for nearly 5 minutes.
Three years earlier, the patient had a deep venous thrombosis (DVT) that was treated with anticoagulation. He had also sustained head trauma without loss of consciousness approximately 4 years earlier.
The patient was a competitive bicyclist and he maintained a rigorous training regimen year round. His social history was otherwise noncontributory. He denied any medication allergies and was not taking any medications on a routine basis. Review of systems was unremarkable.
Figure 1:
CT Head showing area of old infarct in the left parietal cortex.
On examination, the patient was alert and oriented to person, place, and time. Vital signs were within normal limits. Cardiovascular and pulmonary examinations were unremarkable. The neurologic examination was grossly non-focal except for speech, which was slow and lacking in fluency, and which required significant effort. Articulation was impaired, although semantics were appropriate. The patient occasionally used filler words to complete thoughts.
Examination of the lower extremities found varicose veins, but no tenderness or edema, and a negative Homan sign bilaterally.
Figure 2: MRA of neck with IV contrast.
Figure 3: MRI with IV contrast demonstrates focal diffusion restriction at the left posterior frontal lobe, which is suggestive of a subacute infarct. A CT scan of the head showed no acute infarct but revealed evidence of an old infarct in the left parietal cortex (Figure 1). MRI of the brain without contrast suggested an acute infarct in the left frontal supraventricular white matter; these images did rule out a solid lesion or signal abnormality that might be related to seizure activity. A neurology consult was requested.
CT angiography of the head was unremarkable and MRA of the neck (Figure 2) with contrast found no signs of stenosis, thrombosis, or dissection. Subsequent MRI of the brain with contrast indicated a subacute infarct (Figure 3). An infectious disease workup was normal and ruled out focal encephalitis. MRI spectroscopy (Figure 4) verified an ischemic infarct.
Additional studies were performed to identify the cause of infarct. Doppler ultrasonography of the carotid artery showed no blockage and results of a transthoracic echocardiogram were within normal limits. Cardiolipin IgG and IgM antibody levels were within normal limits, which ruled out antiphospholipid syndrome. Results of a lipid panel also were within normal limits, which further reduced the possibility of atherosclerosis in the carotid arteries.4 A workup for vasculitis also was negative.
The patient then underwent transesophageal echocardiography, which showed a patent foramen ovale (PFO) (Figure 4). Lower extremity venous Doppler ultrasonography was negative for DVT. Anticoagulation was initiated with enoxaparin(Drug information on enoxaparin) sodium, and the patient was discharged with a plan for outpatient closure of PFO. By the time of discharge, the patient’s speech had returned to baseline.
Because of our patient’s history of DVT, anticoagulation with enoxaparin and warfarin(Drug information on warfarin) was prescribed. After 6 months of anticoagulation therapy, he underwent an elective procedure to close the PFO. Anticoagulation therapy was discontinued after the procedure. He has been in follow-up care and has had no recurrence of original symptoms and has experienced no thrombotic events.
