Investigation of tryptophan-kynurenin pathway metabolite levels in epilepsy patients

Epilepsy is a neurological disorder caused by abnormal electrical activity of brain cells. This causes the temporary emission of uncontrolled electrical signals in the brain. Epilepsy is the second most common neurological disorder after headache in outpatient admissions. The prevalence of epilepsy in the world is estimated to be approximately 1%. According to this estimate, 700,000 people in Turkey have epilepsy. It is estimated that approximately 65 million people in the world have epilepsy. Although the pathogenesis of epilepsy is not yet known, various factors are thought to play a role in the occurrence of seizures. Factors such as neurotransmitters, electrolytes, enzymes, hypoglycemia, asphyxia cause different effects on neurons and cause neurons in the CNS to acquire epileptogenic pacemaker properties. Although disruption of inhibitory and excitatory balance plays an important role in the pathogenesis of epilepsy, the pathophysiology of epilepsy is still not fully elucidated. The first evidence for the role of quinurenins in the brain was presented in 1978 by Lapin, who reported contractions following intracerebroventricular injection of quinolinic acid into rats. Shortly thereafter, it was shown that iontophoretic administration of quinolinic acid stimulated rat cortical neurons and that intracerebral injection of quinolinic acid caused excitotoxic lesions in the rat brain. Subsequent studies have reported altered KP metabolites in animal models of epilepsy and in human epilepsy. Therefore, it is important to consider the role of quinurenine pathway mechanisms in epilepsy, a condition characterized by an imbalance in excitation and inhibition. Furthermore, the kynurenine pathway is induced by inflammatory cytokines and is part of the inflammatory response, which is increasingly recognized to play a role in epilepsy and epileptogenesis. Based on these findings, we suggest that quinurenins may play an important role in the pathogenesis of epilepsy, considering both the neuromodulatory properties of quinurenine metabolites and the common role of inflammatory exacerbations and oxidant damage in epilepsy pathogenesis and activation of the quinurenine pathway. Therefore, our aim in this study was to investigate a group of patients who were admitted to the Neurology Outpatient Clinic of Selçuk University Faculty of Medicine Hospital with a diagnosis of epilepsy and who presented to the same outpatient clinic with complaints such as headache, weakness, dizziness and were found to have no chronic disease, The aim of this study was to measure serum tryptophan, quinurenine, 3-hydroxyquinurenine, 3-hydroxyquinurenine, 3-hydroxyanthranilic acid, quinolinic acid and quinurenic acid levels in blood samples taken from individuals for routine biochemistry tests.