When laterality of the seizure focus was taken into account, no differences were found among both patients with MTLE and patients with FLE, with exception for the Trail Making Test part B (TMT-B) in which patients with RMTLE performed significantly worse than patients with LMTLE.Seizure frequency was higher for FLE.
Although significant differences between the output and compression ratio of the NAL-NL2 and the APDB fitting formula existed, no differences in bimodal auditory performance were observed.
Silencing Nwd1 in mice using an adeno-associated virus (AAV) profoundly suppressed neuronal hyperexcitability and the occurrence of acute seizures, which may have been caused by reducing GluN2B-containing NMDA receptor-dependent glutamatergic synaptic transmission.
In conclusion, the over-expression of 5-HT6 receptor and activated Jab-1/p-c-Jun plays an important role in pilocarpine-induced seizures and learning-memory impairment.
Previously, we showed that the overexpression of <i>ORAI</i><i>1</i> calcium channel in neurons of murine brain led to spontaneous occurrence of seizure-like events in aged animals of transgenic line FVB/NJ-Tg(ORAI1)Ibd (Nencki Institute of Experimental Biology).
In contrast to tPA and uPAR genes, the expression of which returned to the basal level 6 hr following seizures, urokinase and plasminogen activator inhibitor-1 gene expression showed a delayed activation only at 3 days after seizures.
When administered at seizure onset, PCH, and SCP were both effective at terminating seizure activity against all NAs, with ED<sub>50</sub> values for SCP generally being lower.
These data suggested that overexpression of P-gp and CYP3A during seizures and treated with CBZ may be regulated by PXR or NF-κB p65 activity and expression, which revealed a mechanism underlying the development of DRE.
This review focuses on the most well-characterized of these models, the FAST (seizure-prone) and SLOW (seizure-resistant) rat strains, which were derived by selective breeding for differential amygdala electrical kindling rates.
Our results showed that serine racemase (SR), a key enzyme in regulating the L-to-D-serine conversion, was significantly up-regulated in hippocampal astrocytes in rats and patients who experienced seizure, in comparison with control rats and patients.
Up-regulation of miR-223 alleviated convulsion attack and improved learning and memory ability, while inhibiting pathological injury of hippocampal neurons and inflammatory injury in FS rats.
We established that oral CBD attenuated the time-dependent increase in seizure burden and improved TLE-associated motor comorbidities of epileptic rats in the RISE-SRS model without affecting gait.
This paper introduces; 1) the theoretical development of methodology, 2) the effect of GSR biofeedback in reducing seizure frequency in drug resistant epilepsy, 3) insights into the neural mechanisms of effective GSR biofeedback through neuromodulatory autonomic control and 3) future prospects of this approach as a therapeutic tool instantiated as an Autonomic Cognitive Rehabituation Training (ACRT).
Status epilepticus (a prolonged seizure activity, SE) differently affects vasogenic edema formation and dystrophin-aquaporin 4 (AQP4) expressions between the rat hippocampus and the piriform cortex (PC).
These data demonstrate that Acot7, a fatty acid metabolic enzyme highly enriched in neurons, regulates both brain-specific metabolic processes related to seizure susceptibility and the whole body response to dietary lipid.
Downregulation of miR-125a-5p was found in hippocampus of PTZ-induced epilepsy rats. miR-125a-5p overexpression attenuated seizure and decreased inflammatory factor level in hippocampus of PTZ-induced rats. miR-125a-5p alleviated epileptic seizure and inflammation of PTZ-induced by suppressing its target gene, CAMK4.
To evaluate the underlying mechanism, we profiled and compared eight cytokines (IL [interleukin]-1<i>β</i>, IL-6, IL-8, IL-10, IFN-<i>γ</i> [interferon-<i>γ</i> ], MCP-1 [monocyte chemoattractant protein-1], MIP-1<i>β</i> [macrophage inflammatory protein-1<i>β</i>], and TNF-<i>α</i> [tumor necrosis factor-<i>α</i>]) in the cerebrospinal fluid (CSF) of 33 neonates with seizures who had no other well-known causes of seizures and 13 control patients (rotavirus-induced gastroenteritis but without seizures).
Mutations in the gene triosephosphate isomerase (TPI) lead to a severe multisystem condition that is characterized by hemolytic anemia, a weakened immune system, and significant neurologic symptoms such as seizures, distal neuropathy, and intellectual disability.No effective therapy is available.