PT  - JOURNAL ARTICLE
AU  - Takanashi, J.
AU  - Oba, H.
AU  - Barkovich, A. J.
AU  - Tada, H.
AU  - Tanabe, Y.
AU  - Yamanouchi, H.
AU  - Fujimoto, S.
AU  - Kato, M.
AU  - Kawatani, M.
AU  - Sudo, A.
AU  - Ozawa, H.
AU  - Okanishi, T.
AU  - Ishitobi, M.
AU  - Maegaki, Y.
AU  - Koyasu, Y.
TI  - Diffusion MRI abnormalities after prolonged febrile seizures with encephalopathy
AID  - 10.1212/01.wnl.0000210487.36667.a5
DP  - 2006 May 09
TA  - Neurology
PG  - 1304--1309
VI  - 66
IP  - 9
4099  - http://n.neurology.org/content/66/9/1304.short
4100  - http://n.neurology.org/content/66/9/1304.full
SO  - Neurology2006 May 09; 66
AB  - Background: Patients with encephalopathy heralded by a prolonged seizure as the initial symptom often have abnormal subcortical white matter on diffusion-weighted MRI (DWI). Objective: To determine if these patients share other common features. Methods: Patients with encephalopathy heralded by a prolonged seizure and followed by the identification of abnormal subcortical white matter on MRI were collected retrospectively. Their clinical, laboratory, and radiologic data were reviewed. Results: Seventeen patients were identified, ages 10 months to 4 years. All had a prolonged febrile seizure (longer than 1 hour in 12 patients) as their initial symptom. Subsequent seizures, most often in clusters of complex partial seizures, were seen 4 to 6 days after the initial seizure in 16 patients. Outcome ranged from almost normal to severe mental retardation. MRI performed within 2 days of presentation showed no abnormality. Subcortical white matter lesions were observed on DWI between 3 and 9 days in all 17 patients. T2-weighted images showed linear high intensity of subcortical U fibers in 13 patients. The lesions were predominantly frontal or frontoparietal in location with sparing of the perirolandic region. The diffusion abnormality disappeared between days 9 and 25, and cerebral atrophy was detected later than 2 weeks. Three patients having only frontal lesions had relatively good clinical outcome. Conclusions: Although the pathophysiologic mechanism remains unknown, these patients seem to have a distinctive encephalopathy syndrome. MRI is helpful in establishing the diagnosis of this encephalopathy.