Temporal Lobe Epilepsy, Stroke, and Traumatic Brain Injury: Mechanisms of Hyperpolarized, Depolarized, and Flow-Through Ion Channels Utilized as Tri-Coordinate Biomarkers of Electrophysiologic Dysfunction

Abstract

The brain is an integrated network of multiple variables that when compromised create a diseased state. The neuropathology of temporal lobe epilepsy (TLE), stroke, and traumatic brain injury (TBI) demonstrate both similarity and complexity that reflects this integrated variability; TLE with its live human tissue resection provides opportunity for translational science to demonstrate scale equivalent experimentation between the macroscopic world of clinical disease and the microscopic world of basic science. The extended value of this research is that the neuroinflammatory abnormalities that occur throughout astrocytes with hippocampal sclerosis and damaged or even reversed signaling pathways (inhibition to excitation such as with gaba-aminobutyric acid) are similar to those seen in post-stroke and TBI models. In evaluation of the epilepsy population this interconnectedness of pathology warrants further evaluation with collaborative efforts. This review summarizes patterns that could shift experimentation closer to the macro level of humanity, but still represent the micro world of genetics, epigenetics, and neuro-injury across etiologies of physiologic dysfunction such as TLE, stroke, and TBI with evaluation of cell function using electrophysiology. In conclusion we demonstrate the plausibility of electrophysiologic voltage and current measurement of brain tissue by patch clamp analysis to specify actual electrophysiologic function for comparison to electroencephalography in order to aid neurologic evaluation. Finally, we discuss the opportunity with multiscale modeling to display integration of the hyperpolarization cyclic-nucleotide gated channel, the depolarized calcium channels, and sodium-potassium-chloride-one/potassium-chloride-two co-transporter channels as potential mechanisms utilized as tri-coordinate biomarkers with these three forms of neurologic disease at a molecular scale of electrophysiologic pathology.

Intranasal Delivery of Nanoformulations: A Potential Way of Treatment for Neurological Disorders

“…Epilepsy is a disorder of the CNS characterized by periodic loss of consciousness with or without epileptic seizures associated with abnormal electrical activity in the brain [33,34]. Epileptic seizures can result from almost any insult that perturbs brain function: for example, traumatic brain injury or stroke, infectious diseases such as neurocysticercosis, autoimmune diseases, and genetic mutations [35]. Currently, more than 500 genes associated with epilepsy have been identified.…”

Circular RNA cZNF292 silence alleviates OGD/R-induced injury through up-regulation of miR-22 in rat neural stem cells (NSCs)

“…Despite advances in technology, the incidence of cerebral palsy caused by perinatal hypoxic is still higher than 2 per 11,000 newborns [2]. The exhaustion of brain cell energy production, the reduction of tissue glucose metabolism as well as the occurrence and development of cell damage are closely related to HIE [3,4]. Since the time and reason of brain damage caused by HIE are difficult to determine, there are no signals and methods for the effective treatment of HIE currently.…”

(–)-Epigallocatechin-3-Gallate Protects Against Lithium-Pilocarpine-Induced Epilepsy by Inhibiting the Toll-Like Receptor 4 (TLR4)/Nuclear Factor-κB (NF-κB) Signaling Pathway

“…Temporal lobe epilepsy (TLE) is the most common type of intractable epilepsy in humans, and is often accompanied by cognitive impairment. The behavioral and pathological features of the lithium-pilocarpine-induced epilepsy rat model are similar to those in humans caused by an inciting injury, such as hypoxia, status epilepticus (SE), traumatic brain injury, stroke, tumor, or febrile seizures, followed by spontaneous recurrent seizures (SRSs) after a period of silence [ 6 ]. The process leading from the initial injury to the subsequent SRSs is called epileptogenesis [ 7 ].…”