SUBCORTICAL ABNORMALITIES IN PARTIAL EPILEPSY: A STUDY USING T2-RELAXOMETRY AT 3 TESLA
Abstract number :
1.208
Submission category :
Year :
2003
Submission ID :
2230
Source :
www.aesnet.org
Presentation date :
12/6/2003 12:00:00 AM
Published date :
Dec 1, 2003, 06:00 AM
Authors :
Regula S. Briellmann, Gaby S. Pell, Ari Syngeniotis, Steve Fleming, David F. Abbott, L. Anne Mitchell, Graeme D. Jackson Brain Research Institute, Austin and Repatriation Medical Centre, Heidelberg West, Victoria, Australia; Department of Medicine (Neurol
There is increasing evidence that brain abnormalities in focal epilepsy are not restricted to the seizure focus area. T2 relaxometry has been established as a reliable tool for the assessment of MR signal changes, particularly in patients with partial epilepsy associated with hippocampal sclerosis (HS). Here we use T2-relaxometry to investigate abnormalities in the mesial temporal lobe and subcortical nuclei in partial epilepsy.
T2-maps were acquired in 45 patients and 50 controls. Nineteen patients had HS, 14 had malformations of cortical development (MCD), and 12 had no obvious abnormalities on anatomical MR (normal MR). Ten coronal slices with eight images per location (CPMG, TE 28ms - 231ms, TR 5000ms) were acquired on a 3T GE LX Horizon scanner. T2 maps were generated using a proprietary GE software package (Functool[reg]). Nine bilateral regions of interest (ROI) were measured (hippocampus, anterior temporal lobe, amygdala, frontal and parietal white matter, caudate, putamen, pallidum, thalamus). All findings were expressed as percentage of control values (100/(mean control T2-measurement) x (individual patient T2-measurement). Level of significance was set at 1%.
In controls, there was no difference between corresponding right and left-hemispheric ROI, and there was no gender difference. T2-relaxometry values were increased in the ipsilateral hippocampus in all three patient groups (HS 121%[plusmn]7, MCD 106%[plusmn]8, normal MR 105%[plusmn]6). Only patients with normal MR had a contralateral hippocampal signal increase as well (103%[plusmn]7). HS patients also showed signal increase in the amygdala (104% [plusmn]6) and anterior temporal lobe (105%[plusmn]6), but in none of the other assessed regions. Patients with MCD also showed signal increase in the anterior temporal lobe (104%[plusmn]5), caudate (106%[plusmn]10) pallidum (112%[plusmn]12), and a trend for signal increase in further four ROI (amygdala, parietal lobe white matter, thalamus, putamen). Patients with normal MR also showed signal increase in the putamen (106%[plusmn]7) and a trend for it in the caudate. The AI was different in patients with HS (-.16 [plusmn].04 p[lt]0.0001) compared to controls (.00[plusmn].04), but in none of the other regions.
Abnormalities in the mesial temporal structures were found not only in HS patients, but also in patients with MCD or normal MR. Therefore, refractory focal epilepsy is commonly associated with signal change in the mesial temporal structures. Subcortical nuclei showed signal increase in patients with MCD and to a lesser degree in patients normal MR, but not in HS. This implies that the nature of the associated MR abnormality influences the degree of involvement of subcortical structures. Patients with HS may have a more localised disease process, compared to patients with MCD or normal MR.
[Supported by: National Health and Medical Research Council, Neurosciences Victoria, and Brain Imaging Research Foundation, Australia]