I Savic1, A Lekvall, D Greitz, G Helms. 1. Department of Neurology, Huddinge University Hospital, Stockholm, Sweden. ivanka.savic-berglund@neuro.ki.se
Abstract
PURPOSE: Neuropsychological studies suggest frontal lobe dysfunctions in patients with juvenile myoclonic epilepsy (JME). In this study we investigated whether an underlying mechanism could be a regional neuronal damage not visible with structural magnetic resonance (MR), but detectable with magnetic resonance spectroscopy (MRS). METHODS: The study included 15 patients with JME and 10 matched healthy controls. Quantitative single voxel MRS was conducted at 1.5 Tesla by using a STEAM sequence (TR/TE/TM = 6,000/30/13.7 ms). The voxels were placed over the right cerebellum, right thalamus, and the prefrontal and occipital cortex. The quantitation included fitting of transmitter gain, and correction for partial volume of cerebrovascular fluid. LC-Model was used for estimation of the absolute concentrations of total N-acetyl aspartate (NAA), cholines, total creatine, and myoinositol. RESULTS: Patients with JME had significantly reduced prefrontal concentrations of NAA in relation to controls (9.1 +/- 1.0 vs. 10.2 +/- 0.8 mM; p = 0.031 after Bonferroni correction). The other regions showed normal NAA values, as did the other metabolites. CONCLUSIONS: The observed reduction in NAA levels suggests a prefrontal neuronal lesion in patients with JME.
PURPOSE: Neuropsychological studies suggest frontal lobe dysfunctions in patients with juvenile myoclonic epilepsy (JME). In this study we investigated whether an underlying mechanism could be a regional neuronal damage not visible with structural magnetic resonance (MR), but detectable with magnetic resonance spectroscopy (MRS). METHODS: The study included 15 patients with JME and 10 matched healthy controls. Quantitative single voxel MRS was conducted at 1.5 Tesla by using a STEAM sequence (TR/TE/TM = 6,000/30/13.7 ms). The voxels were placed over the right cerebellum, right thalamus, and the prefrontal and occipital cortex. The quantitation included fitting of transmitter gain, and correction for partial volume of cerebrovascular fluid. LC-Model was used for estimation of the absolute concentrations of total N-acetyl aspartate (NAA), cholines, total creatine, and myoinositol. RESULTS:Patients with JME had significantly reduced prefrontal concentrations of NAA in relation to controls (9.1 +/- 1.0 vs. 10.2 +/- 0.8 mM; p = 0.031 after Bonferroni correction). The other regions showed normal NAA values, as did the other metabolites. CONCLUSIONS: The observed reduction in NAA levels suggests a prefrontal neuronal lesion in patients with JME.
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