Acute cerebral infarct complicated by history of prothrombin mutation
Presentation
Sudden onset left sided facial droop, upper and lower limb hemiparesis and hemisensory loss. Associated intermittent slurred speech, disorientation and a witnessed, self terminating, 30 sec tonic clonic seizure. Relevant past medical history included a known prothrombin genetic mutation on low dose aspirin. Nil previous strokes or similar presentations.
Patient Data
There is no evidence of intra or extra-axial hemorrhage, mass or collection identified. Normal grey/white matter differentiation. Normal appearance of the ventricles, sulci and basal cisterns. Suboptimal opacifications of the vessels and no signs of a vertebral or carotid dissection. No definite aneurysm is identified. There is possible filling defect seen within the right MCA with loss of enhancement distal to this region which may be in keeping with thrombo-emboic disease.
Multiple areas of restricted diffusion are noted in the right MCA territory. These areas include the right insular cortex, external capsule and lentiform nucleus extending up to the centrum semiovale and right periventricular frontal lobe. Multiple other foci are noted within the cortical frontal lobe and the cortical right parietal lobe. This pattern of restricted diffusion likely represents an infarct from an embolic shower.
There is hemorrhagic transformation of the largest of these infarcted areas in the deep grey matter on the right and subcortical insular cortex.
This is the repeat CT scan 3/52 weeks following her initial presentation.
There is a hypodensity in the right midzone and the middle portion. The features suggest gliosis related to infarction. There is no evidence of hemorrhagic transformation or hemorrhage and no significant mass effect. The findings suggest evolving gliosis at the sites of infarction.
Case Discussion
CT brain shows findings suggestive of ischemia in the right middle cerebral artery territory and this is confirmed on MRI images above.
This patient was admitted under the Neurology team and recovered with no significant residual deficits. A full stroke work up during admission found no evidence of a haemodynamically significant stenosis on carotid doppler ultrasound and no overt evidence of cardioembolic source was found on a transoesphageal echocardiogram. Nil specific intervention was instituted. Hematology discussed options for consideration of lifelong anticoagulation in the context of her prothrombin genetic mutation but this was not deemed appropriate. She was advised to continue with daily, low dose aspirin.
A repeat CT brain three weeks following initial imaging showed evidence of evolving gliosis at the sites of infarction but no further progression of the region of hemorrhagic transformation.