What is the molecular mechanism behind inflammation in epilepsy?4 answersIn epilepsy, inflammation plays a significant role in the pathogenesis of the disease by contributing to neuronal hyperexcitability, seizure generation, and neurological comorbidities. The inflammatory molecules in the epileptogenic area activate intracellular signaling pathways in neurons, glia, and the blood-brain barrier, leading to alterations in synaptic transmission and plasticity. These molecules induce rapid posttranslational changes in ion channels and regulate gene expression, showcasing a neuromodulatory role distinct from their immune functions. Various inflammatory markers like pro-inflammatory cytokines (IL-6, IL-17, TNF-α, TGF-β) are involved in neuroimmunoinflammation, disrupting the blood-brain barrier and promoting CNS inflammation, potentially contributing to epileptogenesis and drug resistance. The inflammatory mediators, released by microglia, astrocytes, neurons, and endothelial cells, interact with cognate receptors, leading to pathophysiologic effects that contribute to inflammation, providing potential targets for anti-inflammatory therapies.
Bis modulating neuropathic pain?4 answersBis-quaternary ammonium compounds have shown promise in treating neuropathic pain. Neuropathic pain, resulting from nervous system damage, involves complex mechanisms encompassing both peripheral and central factors. Studies have linked neuropathic pain to nerve degeneration and altered myelin protein expression, suggesting a potential correlation between pain and nerve morphology. Additionally, neurostimulation techniques, including Transcranial Direct Current Stimulation (tDCS), have demonstrated neuromodulating effects on neuropathic pain, with varying efficacy across different causes of neuropathic pain. Overall, the modulation of peripheral GABA-B receptors has been proposed as a strategy to promote nerve regeneration and alleviate neuropathic pain, indicating a multifaceted approach to addressing this challenging condition.
What are the differences between ECT and magnetic seizure therapy?4 answersECT and magnetic seizure therapy (MST) are both convulsive therapies used to treat depression. Both treatments have been found to be effective in improving depressive symptoms, with similar response rates and remission rates. However, there are some differences between the two therapies. MST has been shown to have fewer cognitive side effects compared to ECT. MST has also been found to result in shorter recovery times for consciousness, spontaneous breathing, and orientation compared to ECT. In terms of cognitive effects, MST has been found to have no significant effects on global cognitive status, attention, language, and executive functions. On the other hand, ECT has been found to have significant improvements in only one cognitive inhibition task. Overall, while both ECT and MST are effective in treating depression, MST may have advantages in terms of cognitive side effects and recovery times.
What modulate Ion channel activity?5 answersIon channel activity is modulated by various factors including auxiliary subunits specific to the channel type. Other mechanisms that regulate ion channel activity include ions, binding proteins, nucleotides, phosphorylation, the redox state, and channel subunit composition. Additionally, proteolysis, or the breakdown of proteins, has been identified as a novel and widespread mechanism for altering ion channel activity. Furthermore, the membrane potential and intracellular signal transduction pathways can be controlled by voltage-gated and ligand-gated ion channels on immune cells. Overall, ion channel activity is regulated by a complex interplay of various factors and mechanisms.
What are the mechanisms by which neuronal oscillation can be modulated?5 answersNeuronal oscillations can be modulated through various mechanisms. One mechanism is through brain stimulation, where external stimulation is delivered to specific phases of oscillatory cycles in neural circuits. Another mechanism is the use of square-wave stimuli, which can modulate the firing times of neural oscillators and achieve desynchronization of firing patterns. Additionally, dynamic interaction through coherent oscillations is likely involved in integrating and selecting information in distributed networks, allowing for flexible and context-dependent binding and the efficient routing of signals. Furthermore, studies have shown that neuronal oscillations can be driven using transcranial electrical current stimulation, leading to changes in visual perception and indicating the causal role of oscillations in brain function. Finally, network mechanisms involving electrical and inhibitory synapses can switch individual neurons or groups of neurons between different network oscillations.
What are the mechanisms of epileptogenesis in human and animals?3 answersEpileptogenesis, the process by which a previously healthy brain develops a tendency toward recurrent seizures, involves various mechanisms in both humans and animals. These mechanisms include inflammation, neurogenesis, migration of neurons, neural reorganization, and neuroplasticity. Neuroinflammation, neurodegeneration, and epigenetic modifications also play a role in epileptogenesis. In patients with focal seizure origin, such as temporal lobe epilepsy, hippocampal sclerosis is a common finding, which involves segmental neuronal cell loss and astrogliosis. Hyperactivation of the mTORC1 pathway due to gene mutations is associated with malformation of cortical development and epilepsy. Epigenetic changes, specifically DNA hypermethylation, have been implicated in the conversion of a non-epileptic brain to an epileptic brain, and targeting these changes may offer therapeutic interventions.