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Lidia Głodzik-Sobańska, Agnieszka Słowik, Justyna Kozub, Barbara Sobiecka, Andrzej Urbanik, Andrzej Szczudlik
Med Sci Monit 2004; 10(3): 88-93
Background:Experimental studies have suggested that ischemic stroke causes increment in extracellular level of gamma-aminobutyric acid in response to excessive glutamate concentration and function. The increased GABA concentration is followed by subsequent inhibition of GABA synthesis, thus leading to GABA-ergic dysfunction Enhancing GABA function seems to be a way of neuroprotec- tion after cerebral insult.
Animal models have shown there is overactivity of excitatory neurotransmitters and decreased tone of GABA-ergic system also in the remote neocortical regions. Data concerning changes in brain areas outside the stroke lesion in humans are sparse. These region could be possible targets for therapeutic intervention. Progress in imaging techniques enables separation of a great number of chemical compounds .Our aim was to assess GABA levels outside the ischemic lesion by means of proton magnetic resonance spectroscopy ([sup]1[/sup] H MRS).Material/Methods: The study compared 31 patients with first-ever ischemic stroke and 20 healthy subjects. Single voxel H[sup] 1[/sup] MRS was performed to measure GABA/Cr ratios in structurally normal prefrontal regions, distant from the stroke lesion. The amount of the remaining metabolites (NAA, Cho, mI, Glx) was also estimated. Patients underwent the examination in the acute phase of the disease and 3 months later.Results: Both early after stroke and more than 3 months later, the patients had lower GABA levels. However, during the second examination, this difference was evident only in the frontal cortex ipsilateral to the lesion.Conclusions: These findings suggest that GABA function is decreased outside the infarct. Further studies are needed for confirmation of the results and elucidation of the possible role of GABA alterations in stroke recovery and therapy.