Abstracts

Rationale: Todd s paralysis is a phenomenon attributed to neuronal exhaustation or inhibition . Few papers have determined its patophysiological explanation. Recent studies suggest that transient neuronal anoxia because of cortical hypoperfusion after epileptic seizures might be the cause of postictal paresis (1). Methods: We present a clinical case of an 80 year old woman who had relevant past medical history for hypertension, ischemic cardiopathy, atrial fibrillation, congestive heart failure, left middle cerebral artery stroke with sequela of mild right hemiparesis and dysphasia. Patient presented in a General Hospital with a cardiac infarct without ST changes and no significant repercussions, seven days after when she was going to be discharged from the hospital she was found in the bathroom with a left hemiparesis, due to high suspicion of stroke an emergency MRI was performed with STROKE-protocol and the patient was referred to our Neurological Center. Patient was received at the ER service of the Neurological Institute of Neurology and Neurosurgery, Mexico city, on clinical exam she was an 80 year old woman, vital signs were within normal limits, relevant neurological exam findings showed that patient was awake but disoriented and inattentive, left central facial paresis with left hemiparesis 3/5 in the arm and 4/5 in the leg with decrease muscular tone ipsilateral, sensibility and deep tendon reflexes were normal bilateral, absence of Babinski sign bilateral. Results: Capilar glucemia, general laboratory and CT were performed (figure1). MRI with STROKE-protocol on T1 and T2- weighted images showed an old left MCA artery infarct. Diffusion weighted imaging revealed no acute signs of ischemia on the left hemisphere. MR-angiography demonstrated right MCA occlusion (figure 2). Patient left hemiparesis recovered completely within 48 hours after the event so directed inquiry to patient s relatives was done and they described that the patient presented two events of left focal motor seizures followed by confusional state prior to developing the left hemiparesis. An EEG was performed that showed mild generalized slowing and epileptic discharges on the left frontotemporal (figure 3). Patient was started on levetiracetam (LEV) and she remains seizure free. Conclusions: Etiology of postictal paralysis is still unknown. This case, as one previously described (1), demonstrates the presence of hypoperfusion during postictal paresis however the role of these findings needs to be elucidated.