DIFFUSION CHANGES SUGGESTING VASOGENIC EDEMA IN PARTIAL STATUS EPILEPTICUS
Abstract number :
1.251
Submission category :
Year :
2002
Submission ID :
96
Source :
www.aesnet.org
Presentation date :
12/7/2002 12:00:00 AM
Published date :
Dec 1, 2002, 06:00 AM
Authors :
Keun-Sik Hong, Yong-Jin Cho, Won-Kyu Kim, Sung-Wook Park, Sang Kun Lee. Department of Neurology, Inje University Ilsan Paik Hospital, Koyang, Gyeong-Ki do, Korea; Department of Neurology, Seoul National University College of medicine, Seoul, Seoul, Korea
RATIONALE: During partial status epilepticus (PSE), diffusion-weighted imaging (DWI) have demonstrated focal hyperintensity lesion with decreased apparent diffusion coefficient (ADC). These findings are suggestive of cytotoxic edema due to energy failure of Na+/K+-ATPase pump. However, signal intensity on DWI could be influenced by another factors such as vasogenic edema developed during seizure. We hypothesize that the DWI findings other than cytotoxic edema can be observed during PSE.
We report DWI abnormalities suggestive of vasogenic edema in a patient with EEG-confirmed PSE.
METHODS: We reviewed the DWI findings in a 76-year old woman who presented with PSE developed after the successful thrombolysis for the presumed left middle cerebral artery (MCA) occlusion. Initial MRI (T2-weighted, DWI, ADC map, MR angiography) performed on the next day of thrombolysis revealed unremarkable finings despite sensory aphasia with decreasing severity. One month later, she showed prolonged confusion, sensory aphasia, right hemiparesis of mild degree, and sometimes, brief attacks of focal clonic movement in right upper extremity without generalized tonic-clonic seizure. EEG and MRI were performed on the same day during PSE. Follw-up EEG and MRI were performed 3 months later.
RESULTS: EEG performed during PSE showed ictal discharge localized in left temporo-parieto-occipital area. DWI and T2-weighted imaging (T2WI) showed the hyperintense signal in left parieto-temporal cortex. The ADC map also showed increased signal in the corresponding area, suggestive of vasogenic edema. MR angiography showed increased signal in the MCA branches of the epileptic hemisphere. Follow-up EEG and MRI were performed 3 months later on the same day. EEG showed diffuse slowings in left parieto-temporo-occipital areas. T2WI showed some regional brain atrophy in left parieto-temporal cortex with increased signal in the underlying white matter. However, DWI and ADC map did not reveal any significant signal changes. Follow-up MRA no longer showed signal asymmetry of both MCA.
CONCLUSIONS: During PSE, diffusion changes seen on MRI can be variable dependent upon the severity of cytotoxic edema, vasogenic edema, and blood flow. We report a very rare case of PSE presenting vasogenic edema on DWI.