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From the Stanford Stroke Center (Drs. Lansberg, O’Brien, and Albers), the Stanford Department of Radiology (Drs. Moseley and Norbash), and the Stanford Comprehensive Epilepsy Center (Dr. Morrell), UCSF Stanford Health Care, Palo Alto, CA.
Address correspondence and reprint requests to Dr. Maarten G. Lansberg, Stanford Stroke Center, 701 Welch Road, Building B, Suite 325, Palo Alto, CA 94304-1705.
OBJECTIVE: To report neuroimaging findings in patients with complex partial status epilepticus.
BACKGROUND: During status epilepticus, neuroimaging may be used to exclude other neurologic conditions. Therefore, it is important to identify the neuroimaging features that are associated with status epilepticus. In addition, MRI characteristics may provide insight into the pathophysiologic changes during status epilepticus.
METHODS: The history and neuroimaging examination results of three patients with complex partial status epilepticus were reviewed. Studies obtained during status epilepticus included diffusion-weighted MRI (DWI), MR angiography (MRA), postcontrast T1-weighted MRI, T2-weighted MRI, and CT. Follow-up MRI was obtained in two patients, and autopsy results were available for the third.
RESULTS: Some of the MRI and CT findings during partial status epilepticus mimicked those of acute ischemic stroke: DWI and T2-weighted MRI showed cortical hyperintensity with a corresponding low apparent diffusion coefficient, and CT showed an area of decreased attenuation with effacement of sulci and loss of gray-white differentiation. However, the lesions did not respect vascular territories, there was increased signal of the ipsilateral middle cerebral artery on MRA, and leptomeningeal enhancement appeared on postcontrast MRI. On follow-up imaging, the abnormalities had resolved, but some cerebral atrophy was present.
CONCLUSIONS: The radiologic characteristics of status epilepticus resemble those of ischemic stroke but can be differentiated based on lesion location and findings on MRA and postcontrast MRI. The MRI abnormalities indicated the presence of cytotoxic and vasogenic edema, hyperperfusion of the epileptic region, and alteration of the leptomeningeal blood–brain barrier. These changes reversed, but they resulted in some regional brain atrophy.
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