RESUMO
Introduction: The most common cause of sudden isolated and prolonged global aphasia is acute stroke, affecting the cortical or subcortical language network. However, an aphasic status epilepticus (ASE) has to be considered as a possible differential diagnosis in awake patients presenting with acute and prolonged language impairment. ASE is suggestive of a localized dysfunction of language processing in the dominant hemisphere. ASE is a rare phenomenon and few cases are reported in the current literature. In the differential diagnosis between ASE and stroke with aphasia, FDG-PET imaging could be used when EEG shows no clear evidence of epileptic activity. Case Presentation: We described a case of a 74 year-old woman who presented sudden onset of isolated and prolonged global aphasia; she suffered 5 months before of a left temporo-occipital hemorrhage and 20 days before a left hemispheric ischemic stroke. A new ischemic or hemorrhagic event was excluded by neuroimaging (CT and MRI, including DWI). Since several EEGs did not show ictal epileptic pattern, but only inter-ictal slow waves in the left temporal region, an FDG-PET was performed, resulting in two hypermetabolic areas in the left temporal and occipital lobes. The aphasia improved after anti-epileptic therapy. Discussion and Conclusion: In conclusion, this is a case of post-stroke ASE, in which the evidence of hypermetabolism on FDG-PET allowed a definite diagnosis of epilepsy, despite the non-ictal EEG pattern.
RESUMO
We report herein a patient with aphasic status epilepticus (ASE) who underwent serial brain magnetic resonance imaging (MRI) including diffusion-weighted imaging (DWI), perfusion imaging (PI), and magnetic resonance angiography (MRA) in the peri-ictal phase. The initial DWI revealed a high signal intensity in the left medial temporal area and PI demonstrated hyperperfusion in the left temporoparietal area. MRA revealed an increased flow signal in the ipsilateral intracranial arteries. PI signal changes had normalized by the follow-up MRI. The DWI, PI, MRA, and clinical manifestation of ASE are described herein.