Abstracts

The Correlation between Neuroimaging and Neuropathologic Findings in Rasmussen Encephalitis.

Abstract number : 2.205
Submission category :
Year : 2001
Submission ID : 2323
Source : www.aesnet.org
Presentation date : 12/1/2001 12:00:00 AM
Published date : Dec 1, 2001, 06:00 AM

Authors :
S. Kim, MD, Dept of Neurology(Child), Medical College of Georgia, Augusta, GA; Y.D. Park, MD, Dept of Neurology(Child), Medical College of Georgia, Augusta, GA; R. Hessler, MD, Dept of Pathology, Medical College of Georgia, Augusta, GA; J.J. Pillai, MD, D

RATIONALE: Rasmussen encephalitis (RE) is considered a focal, unilateral, progressive neurologic disorder that causes intractable seizures, cognitive deterioration, and contralateral neurologic deficits. The aim of this study was to investigate the correlates of serial MRIs and neuropathological findings in RE patients.
METHODS: We prospectively obtained serial brain MRI scans in 4 patients who had clinically and pathologically proven RE (mean age = 12 years: range 3 [ndash] 22 years). All subjects were unresponsive to conventional antiepileptics and had undergone brain biopsy (3) and functional hemispherectomy (4). Three to six (mean = 4) MRI scans were performed during clinical treatments. The neuropathologic interpretation focused on the phase of the disease. Histologic findings were characterized as active inflammation , grade 1 (A1: few microglial nodules/scant perivascular infiltrates), grade 2 (A2: easily identified nodules, thicker perivascular infiltrates), grade 3 (A3: confluent microglial nodules, thick perivascular infiltrates); resolving inflammation grade 1 (R1: A1 plus hypertrophic reactive gliosis (HG)), grade 2 (R2: A2 plus HG) , grade 3 (R3: A3 plus HG); chronic scar (C: gliosis, no residual inflammation) and no significant changes (N).
RESULTS: Neuropathologic findings in areas displaying high signal intensity on T2WI included only the C & R phases, but the active (A) phase abnormalities were noted in tissue obtained from the margin of the high signal intensity. Atrophic areas on T1WI showed all stages but predominantly C & R phases. Patients with shorter duration (less than 6 mos) of epilepsia partialis continua (EPC) demonstrated A1-3 and normal findings, while patients with longer duration ( longer than 1 year) of EPC showed C&R phases.
CONCLUSIONS: The margin of the MRI abnormality might be the ideal site for biopsy rather than the central regions of T2 signal abnormality on MRI. The most active inflammation is present in areas demonstrating subtle T2-weighted signal abnormalities.