Abstracts

MAGNETOENCEPHALOGRAPHY-GUIDED MR SPECTROSCOPY SHOW AREAS OF METABOLITE ABNORMALITIES IN FRONTAL LOBE EPILEPSY

Abstract number : 1.095
Submission category :
Year : 2005
Submission ID : 5147
Source : www.aesnet.org
Presentation date : 12/3/2005 12:00:00 AM
Published date : Dec 2, 2005, 06:00 AM

Authors :
1Jerry J. Shih, and 2Michael P. Weisend

Magnetoencephalography (MEG) can detect interictal spike foci. We have previously shown in patients with temporal lobe epilepsy that these spike foci indicate areas of neuronal cell loss or dysfunction as demonstrated by proton magnetic resonance spectroscopy (MRS). We report our experience using MEG to guide proton MRS to areas of neuronal loss or dysfunction in frontal lobe epilepsy (FLE). Proton MRS examination of frontal lobe regions with focal MEG spiking activity will show evidence of neuronal loss and dysfunction. Twenty-five consecutive patients undergoing testing at a tertiary epilepsy center and meeting criteria for frontal lobe epilepsy were studied. Criteria included seizure semiology consistent with FLE, MRI documenting absence of structural lesions outside frontal lobe, and concordant EEG findings. We used a 122-channel biomagnetometer to record spontaneous magnetic fields. We source-modeled with a realistic head model using multiple-dipole spatio-temporal algorithm (Picker, Ltd). Spikes were identified by off-line visual analysis. A 3.375 cm3 voxel encompassing the centroid of spikes in the frontal lobe is examined with 1H-MRS. The homologous contralateral region is also examined with 1H-MRS. A paired T-Test is used to assess for metabolite differences between the MEG spike zone and contralateral homologous region. Eighteen of 25 patients had lower NAA/(Cho+Cr) ratios in the MEG spike zone compared to the contralateral homologous region. NAA/(Cho+Cr) ratio was 0.88 [plusmn] 0.23 for MEG spike zones and 1.07 [plusmn] 0.26 for the contralateral homologous region (p=0.02). We demonstrate multi-modal MEG and 1H-MRS identifies areas of significant neuronal loss or dysfunction in frontal lobe epilepsy. (Supported by NCRR 3 M01; RR 00997-25S3 and NCRR P20; RR15636-01. We are grateful for the support of the UNM GCRC.)