Abstracts

Rationale: MRI changes are well-known in the setting of ischemic stroke, status epilepticus and focal recurrent seizures. Similarly, transient MR signal changes in the splenium of the corpus callosum and parenchyma have been described in the setting of AED withdrawal, frequent seizures and from partial status epilepticus. These MRI changes have been shown to be reversible over time. Episodes preceding these changes that resemble typical seizure semiology, increase suspicion for lesion being secondary to seizure. Abrupt onset of neurological symptoms different from a patient’s typical seizure semiology must raise suspicion for a vascular insult. A patient with chronic temporal lobe epilepsy with acute onset of homonymous hemianopsia, and an unusual pattern of MRI signal abnormalities is presented. Methods: A 36 year old man with intractable epilepsy since age 10 years old, left mesial temporal sclerosis, and independent bilateral mesial temporal lobe seizure onset by video-EEG monitoring presented with chief complaint of headache and double vision. The patient denied any breakthrough seizures for more than a month prior to admission. He was found to have right homonymous hemianopsia and a valproic acid level of 146. The differential diagnosis included valproic acid toxicity, encephalitis, acute young stroke and occipital seizure. Results: On presentation, this patient’s CT showed a left occipital hypodensity and brain MRI showed areas of hyperintensity on diffusion-weighted images (DWI) and T2 FLAIR images over the left Occipital and Temporal cortex as well as the left Thalamus, suggestive of ischemic lesions. His apparent diffusion coefficient (ADC) images showed an atypical mixed increased and decreased signal pattern. An initial routine EEG showed sharply contoured slowing over the left occipital region on a background of mild diffuse slowing. As part of the evaluation for a possible ischemic stroke, the patient underwent an echocardiogram and was found to have two findings associated with ischemia, an atrial septal aneurysm and patent foramen ovale (PFO). A repeat brain MRI seven days later showed interval evolution of the three discrete lesions, which raised the concern for multiple emboli. A repeat extended EEG then showed infrequent left temporal-occipital discharges and left temporal-occipital focal slowing. His visual deficit remained static confirmed by ophthalmology. Due to the multiple MRI signal changes interpreted as possible ischemia his PFO was closed. His valproic acid was tapered gradually and he was converted to levitiracetam monotherapy. Conclusions: Although diffusion-weighted MRI changes in patients with epilepsy are frequently related to either seizures or status epilepticus, this unusual case highlights the diagnostic difficulty in evaluation and treatment of patients with acute presentation of focal neurological signs, equivocal MRI abnormalities and risk factors for cerebrovascular disease. A follow up MRI will be presented to hopefully clear up the issue of ictal versus ischemic event.