Literature DB >> 15668431

Whole-brain T2 mapping demonstrates occult abnormalities in focal epilepsy.

F J Rugg-Gunn1, P A Boulby, M R Symms, G J Barker, J S Duncan.   

Abstract

OBJECTIVES: To examine the cerebral structure of 14 patients with partial seizures and acquired lesions, 20 patients with malformations of cortical development (MCDs), and 45 patients with partial seizures and normal conventional MRI using whole-brain T2 mapping and statistical parametric mapping (SPM).
METHODS: T2 maps were calculated, and individual patients were compared with a group of 30 control subjects using SPM.
RESULTS: T2 mapping and objective voxel-by-voxel statistical comparison identified regions of increased T2 signal in all 14 patients with acquired nonprogressive cerebral lesions and partial seizures. In all of these, the areas of increased T2 signal concurred with abnormalities identified on visual inspection of conventional MRI. In 18 of 20 patients with MCDs, SPM detected regions of increased T2 signal, all of which corresponded to abnormalities identified on visual inspection of conventional MRI. In addition, in both groups, there were areas that were normal on conventional imaging, which demonstrated abnormal T2 signal. Voxel-by-voxel statistical analysis identified increased T2 signal in 23 of the 45 patients with cryptogenic focal epilepsy. In 20 of these, the areas of increased T2 signal concurred with epileptiform EEG abnormality and clinical seizure semiology. Group analysis of MRI-negative patients with electroclinical seizure onset localizing to the left and right temporal and left and right frontal regions revealed increased T2 signal within the white matter of each respective lobe.
CONCLUSIONS: T2 mapping analyzed using statistical parametric mapping was sensitive in patients with malformations of cortical development and acquired cerebral damage. Increased T2 signal in individual and grouped MRI-negative patients suggests that minor structural abnormalities exist in occult epileptogenic cerebral lesions.

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Year:  2005        PMID: 15668431     DOI: 10.1212/01.WNL.0000149642.93493.F4

Source DB:  PubMed          Journal:  Neurology        ISSN: 0028-3878            Impact factor:   9.910


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