Can Epilepsy cause Brain damage? Before getting to this let’s know about Epilepsy. Billions of nerve cells, commonly known as neurons, make up the brains. Electrical activity is used by these neurons to communicate and deliver signals. According to WHO, Epilepsy affects almost 50 million individuals worldwide, making it one of the most common neurological diseases. Epilepsy, a disorder marked by recurrent seizures, is a complicated disease that affects people of all ages, with a special affinity for children and the elderly. In addition to seizures, many patients suffer cognitive and psychological issues as a result of the seizures and their treatment. Epilepsy has a broad array of etiologies, both idiopathic and acquired, and treatment responses. Despite the availability of several therapies for recurrent seizures, such as drugs, diets, immunotherapy, surgery, and neuromodulatory devices, a significant percentage of patients continue to experience the consequences of uncontrolled seizures, which include societal stigma and death. GABA is inhibitory neurotransmitter in Brain. It has 2 classes of receptors GABAA receptors that are ligand-operated ion channels and the G-protein-coupled metabotropic GABAB receptors. Epileptic seizures are caused by disruption of GABAergic transmission caused by genetic mutations or the usage of GABA receptor antagonists, whereas antiepileptic medicines boost GABAergic transmission. Subsets of hippocampal GABA neurons are lost in animal epilepsy models and tissue from patients with temporal lobe epilepsy. Electrophysiological and neurochemical investigations, on the other hand, show a compensatory increase in GABAergic transmission at specific synapses. Furthermore, neurodegeneration-induced loss of GABAA receptors is followed by significantly changed expression of receptor subunits in the dentate gyrus and other areas of the hippocampus formation, indicating altered GABAA receptor physiology and pharmacology. Seizure induction, enhancement of endogenous protective systems, and resistance to antiepileptic medication therapy may all be affected by these pathways. Other research suggests that GABAB receptors have a function in absence seizures. Presynaptic GABAB receptors inhibit the release of neurotransmitters. There may be anticonvulsant or proconvulsant effects depending on whether this activity is performed in GABAergic or glutamatergic neurons.
Isolated brief seizures are unlikely to damage neurons, while severe and repeated seizures (i.e. status epilepticus) almost surely do.Neuronal death has been postulated as an intrinsic aspect of acquired epileptogenesis because status epilepticus destroys neurons while simultaneously causing persistent epilepsy. Several studies, particularly in the developing brain, have suggested that neuronal death is not required for acquired epileptogenesis; however, proving the absence of neuronal death is difficult, if not impossible, and more recent studies have cast doubt on this theory. Far beyond standard notions of necrosis and apoptosis, novel methods of cell death include autophagy, phagoptosis, necroptosis, and pyroptosis. The classic explanation for why neuronal death is required for epilepsy is based on the repetition of development hypothesis, in which axonal sprouting and synaptic circuit reconfiguration are induced by a loss of synaptic input from dying neurons. The neuronal death pathway hypothesis, which says that epilepsy is caused or aided by biochemical mechanisms generating planned neurodegeneration, rather than by neuronal death per se. If true, necroptosis or pyroptosis is thought to be the source of neuronal death pathway reprogramming.
Though there are many anti-epileptic drugs in the market and in severe scenario surgeries are done yet it is necessary to know to what extent epilepsy causes brain damage.