Prolonged Ictal Aphasia Presenting as Clinical-Diffusion Mismatch in a Patient with Acute Ischemic Stroke

permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. The presence of clinical-diffusion mismatch (CDM) in patients with acute ischemic stroke may represent the ischemic penumbra, which requires emergency reperfusion therapy to improve stroke outcomes. We report here our experience of treating a patient with acute ischemic stroke and CDM. Specifically , the patient had a small infarct in the left temporal cortex and presented with sensory aphasia, but did not require reper-fusion therapy. Magnetic resonance angiography and perfusion imaging findings were normal. Further investigation revealed that the aphasia was associated with ictal symptoms. Ictal apha-sia is a considerable cause of non-oligemic CDM, perfusion imaging and angiographic studies may help discriminate true isch-emic penumbra from non-oligemic CDM. A 44-year-old, right-handed male patient presented with sudden onset language disturbance and headache for 24 hours. Approximately 30 years prior, the patient had undergone surgery to removal a right cerebellar tumor, which resulted in a history of mild dysarthria, hearing difficulties, right-sided ataxia, left-sided facial palsy, and right exotropia. There was no history of tumor recurrence or seizure. Neurologic examination revealed Wernicke's aphasia in addition to the preexisting neurological deficits, with an initial score on the National Institutes of Health Stroke Scale of seven. Diffusion-weighted magnetic resonance imaging of the brain revealed a small, focal, and high-signal intensity (volume 1.3 mL) with the apparent diffusion coefficient restriction in the left temporal lobe, compatible with acute in-farction (Figure 1). Because there were no lesions that could explain the patient's aphasia, we diagnosed the condition to be significant neurological deficit with CDM and considered emergency revascularization. However, the revascularization procedure was not performed because we did not note any abnormal findings on magnetic resonance angiography or perfusion imaging. The results of the Korean version of the Western Aphasia Battery indicated severe Wernicke's aphasia (10/20 fluency, 1.9/10 auditory comprehension, 0.4/10 repetition, 0.5/10 naming, and 45.6/100 aphasia quotient). There were no abnormal laboratory results except a mild elevation in erythrocyte sedimenta-tion rate (23 mm/h). The electrocardiogram showed a normal sinus rhythm, and chest x-ray showed no active lesion in either lung fields. During hospitalization, the severity of aphasia and mild confusion fluctuated. Electroencephalography demonstrated intermittent theta slowing in the left temporal areas (Figure 1). Fluorodeoxyglucose positron emission tomography (FDG-PET) show ed hypermetabolism in the left temporal cortex (Figure 1). The aphasia was due to ictal and postictal symptoms following …