Abstracts

Rationale: Malformations of cortical development (MCD) is an important cause of epilepsy and the elucidation of pathophysiological basis may help to understand of human epileptogenesis. Some previous studies with MRS have demonstrated abnormal metabolites, indicating dysfuntions of neuronal nature in the cortex beyond the visible lesions. To the moment, there are no studies with phosphorus magnetic resonance spectroscopy (31P-MRS) in MCD. The purpose of this study is to evaluate phospholipids metabolism in patients with malformations of cortical development (MCD). Methods: We have performed phosphorus magnetic resonance spectroscopy (31P-MRS) at high field in eight patients with MCD and in eight healthy volunteers. Pulse acquire sequence was applied with decoupling and a matrix of 6 slices, 7 columns and 8 lines with each voxel size of 25 x 25 x 20 mm. Individual voxels were selected in the focal lesions and in the contralateral normal appearing parenchyma (CNAP) of patients and in right and left cerebral hemispheres of controls (Figure 1). The amplitude values of each metabolite divided by the sum of all metabolites were obtained. The following metabolite peaks were identified: PE - phosphoril-etanolamine, PC - phosphoril-coline, Pi - inorganic phosphate, GPE - glicero-phosphoril-etanolamine, GPC - glicero-phosphoril-coline, PCr - phosphocreatine, g-, a- and b-ATP - adenosine triphosphate. We also calculated the total ATP, phosphodiesthers - PDE and phosphomonoesthers - PME. Results: The PCr values were significantly higher in the lesions (0.1980 0.0150) compared with control subjects (0.1789 0.0203), p=0.03 (Table 1). We found a significant reduction in patients of GPC (0.1144 0.0254 in lesions, 0.1186 0.0158 in NACP, 0.1373 0.0134 in controls, p=0.007 and 0.005, respectively) and PDE (0.1872 0.0309 in lesions, 0.1942 0.0164 in NACP, 0.2166 0.021, p=0.01 and 0.01, respectively). In the other hand, there was significantly increase of PME in lesions (0.1788 0.0216) compared to controls (0.1612 0.0194), p=0.05 and also a significantly increase of PE in NACP of patients (0.1357 0.0199) compared to controls (0.1166 0.0165), p= 0.02. Conclusions: In excitable tissues, the PCr acts as an energy buffer. Increased energy consumption can lead to an observable decrease in PCr levels. Our hypothesis is that MCD present higher levels of PCr because they are less metabolically active. Moreover, we found significant reduction of GPC and PDE in patients compared to controls and significant increase in PE and PME in patients versus controls. This finding could indicate a deregulation in the membrane synthesis in MCD. To our knowledge, this is the first work that demonstrates this pattern of metabolic abnormality in MCD with an in vivo study.