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Valproate (VPA) interferes with mitochondrial metabolism causing hyperammonemia, thereby shifting the balance reaction of glutamine (Gln)/glutamate (Glu) toward Gln. In this study we wanted to determine whether metabolic changes could be reproduced in VPA-treated patients with epilepsy and whether the results differed from those known in chronic hepatic encephalopathy (CHE). Seven patients with epilepsy pretreated with VPA and seven healthy volunteers were investigated on a 3T-scanner. We performed proton magnetic resonance spectroscopy (1H-MRS) using a short echo time point-resolved spectroscopy (PRESS) in the parietal and occipital lobe, respectively. Spectral analysis was performed by LCModel, allowing a separation of Glu and Gln at 3T. Absolute values of myo-Inositol (mI), choline (Cho), creatine (Cr), N-acetyl-aspartate (NAA), glutamine (Gln), glutamate (Glu), and the sum of Gln and Glu (Glx) were calculated. In the parietal lobe, mI was significantly decreased in the patients’ group compared to the healthy volunteers. After separation of the signals of Gln and Glu, a significant increase of Gln was observed in the parietal lobe in the patients’ group. No significant differences in the occipital spectra could be observed between the groups. In VPA-treated patients the alteration of the Glu/Gln ratio differs from that in patients with CHE, where Glx is markedly increased because of an increase in Gln. The expected shift from the biochemical balance reaction of Gln/Glu induced by VPA could be reproduced for the parietal lobe. Significantly reduced mI in the parietal lobe of VPA-treated patients most likely reflects an osmolytic compensation for high Gln. [ABSTRACT FROM AUTHOR]

Purpose: Exercise reduces cognitive deficits in traumatic brain injury (TBI), but early post-trauma exercise is often discouraged due to potential harm. The purpose was to evaluate the interaction between pre- and post-injury physical exercise on cognition, neuronal survival and inflammation., Methods: Rats were either sham-operated and kept sedentary (Sham) or subjected to controlled cortical impact injury and then distributed into sedentary (Tbi), pre-injury exercise (Pre-Tbi), post-injury exercise with early (24 hours, Tbi-early) or late (6 days, Tbi-late) onset, and a combination of pre- and post-injury exercise with early (Pre-Tbi-early) or late (Pre-Tbi-late) onset. Object recognition memory, hippocampal volume, neuronal survival (NeuN + ) in the hippocampus and perirhinal cortex, and microglial activity (Iba-1) in the hippocampus were evaluated., Results: All exercise conditions, except TBI-early, attenuated the significant memory impairment at 24-hour retention caused by TBI. Additionally, Pre-TBI-early treatment led to memory improvement at 3-hour retention. Pre-TBI reduced neuronal death and microglial activation in the hippocampus. TBI-late, but not TBI-early, mitigated hippocampal volume loss, loss of mature neurons in the hippocampus, and inflammation. Combining pre-injury and early-onset exercise reduced memory deficits but did not affect neuronal death or microglial activation. Combining pre-injury and late-onset exercise had a similar memory-enhancing effect than late post-injury treatment alone, albeit with reduced effects on neuronal density and neuroinflammation., Conclusions: Pre-TBI physical exercise reduces the necessary onset delay of post-TBI exercise to obtain cognitive benefits, yet the exact mechanisms underlying this reduction require further research., Competing Interests: Declaration of Conflicting InterestsThe author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Purpose: Valproate (VPA) interferes with mitochondrial metabolism causing hyperammonemia, thereby shifting the balance reaction of glutamine (Gln)/glutamate (Glu) toward Gln. In this study we wanted to determine whether metabolic changes could be reproduced in VPA-treated patients with epilepsy and whether the results differed from those known in chronic hepatic encephalopathy (CHE)., Methods: Seven patients with epilepsy pretreated with VPA and seven healthy volunteers were investigated on a 3T-scanner. We performed proton magnetic resonance spectroscopy ((1)H-MRS) using a short echo time point-resolved spectroscopy (PRESS) in the parietal and occipital lobe, respectively. Spectral analysis was performed by LCModel, allowing a separation of Glu and Gln at 3T. Absolute values of myo-Inositol (mI), choline (Cho), creatine (Cr), N-acetyl-aspartate (NAA), glutamine (Gln), glutamate (Glu), and the sum of Gln and Glu (Glx) were calculated., Results: In the parietal lobe, mI was significantly decreased in the patients' group compared to the healthy volunteers. After separation of the signals of Gln and Glu, a significant increase of Gln was observed in the parietal lobe in the patients' group. No significant differences in the occipital spectra could be observed between the groups., Discussion: In VPA-treated patients the alteration of the Glu/Gln ratio differs from that in patients with CHE, where Glx is markedly increased because of an increase in Gln. The expected shift from the biochemical balance reaction of Gln/Glu induced by VPA could be reproduced for the parietal lobe. Significantly reduced mI in the parietal lobe of VPA-treated patients most likely reflects an osmolytic compensation for high Gln.