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Metabolic changes in early poststatus epilepticus measured by MR spectroscopy in rats
There is little experimental in vivo data on how differences in seizure duration in experimental status epilepticus influence metabolic injury. This is of interest given that in humans, status duration is a factor that influences the probability of subsequent development of epilepsy. This question i...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4635243/ https://www.ncbi.nlm.nih.gov/pubmed/26104287 http://dx.doi.org/10.1038/jcbfm.2015.145 |
Sumario: | There is little experimental in vivo data on how differences in seizure duration in experimental status epilepticus influence metabolic injury. This is of interest given that in humans, status duration is a factor that influences the probability of subsequent development of epilepsy. This question is studied using 7-T magnetic resonance (MR) spectroscopy, T2 relaxometry in the incremented kainate rodent model of temporal lobe epilepsy, using two durations of status epilepticus, 1.5 and 3 hours. Histologic evaluation was performed in a subset of animals. Three days after status, single-voxel (8 mm(3)) point resolved spectroscopy (PRESS) MR spectroscopic measurements were acquired at 7 T to assess the cerebral metabolites measured as a ratio to total creatine (tCr). The status injury resulted in decreased N-acetylaspartate NAA/tCr, increased myo-inositol/tCr and glutamine/tCr, increased T2, and significant declines in NeuN-stained neuronal counts in both status groups. Regressions were identified in the status groups that provide evidence for neuronal injury and astrocytic reaction after status in both the short and long status duration groups. The long status group displays changes in glutathione/tCr that are not identified in the short status group, this difference possibly representing a maturation of injury and antioxidant response that occurs in synchrony with glutamatergic injury and glial activation. |
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