1H-MAGNETIC RESONANCE SPECTROSCOPY IN THE ASSESSMENT OF EPILEPTIC MALFORMATIONS OF CORTICAL DEVELOPMENT
Abstract number :
3.197
Submission category :
5. Neuro Imaging
Year :
2012
Submission ID :
15576
Source :
www.aesnet.org
Presentation date :
11/30/2012 12:00:00 AM
Published date :
Sep 6, 2012, 12:16 PM
Authors :
J. G. Burneo, S. Nikolova, R. Bartha,
Rationale: Malformations of cortical development (MCDs) are disturbances in brain formation that arise from abnormalities affecting the processes of cortical development and involve cells that under normal circumstances would participate in formation of the cerebral cortex. Medically-intractable Epilepsy has been increasingly associated with MCDs. Proton (1H) MR spectroscopy (MRS) may have the potential to detect abnormalities in patients with MCDs. MRS can measure N-acetylaspartate (NAA), a marker of functional neuronal integrity, as well as creatine and phosphocreatine (Cr), choline (Cho), glutamate (Glu) and myo-inositol (Myo). The purpose of this study is to evaluate the metabolic profile of MCDs using 1H MRS. Methods: Data were acquired on a 3.0T Siemens Magnetom Tim Trio MRI, using a 12 channel head RF coil. Water suppressed spectroscopy data were acquired using PRESS (point resolved spectroscopy), from a 1.5x1.2x1.2 cm3 voxel centered on the cortex containing the malformation in each patient (repetition time (TR)/Echo time (TE) = 3200/35 ms), and in similar cortical regions in controls. Metabolite levels were measured from spectra using the fitMAN (v1.7) software, and were normalized to Cr. 1H-MRS data were obtained for seven controls and five patients (two with cortical dysplasia and three with polymicrogyria) and compared using a t-test. Results: Figure 1 shows pooled metabolite ratios in patients (red) and controls (blue). There was a significant decrease in NAA/Cr (p<0.05) and a significant increase in Glu/Cr (p<0.05) in patients compared to controls. Additional patients will be recruited to validate these results. Evidence of neuronal dysfunction in patients with MCD may have relevance for the mechanisms of seizure generation in these forms of epilepsy. Conclusions: This preliminary study demonstrates some metabolite differences between patients with MCDs and control subjects, although the small sample size did not allow specific analysis of each group of malformations. Further recruitment is necessary as there may be some particular findings pertaining to each different type of MCDs.
Neuroimaging