Methods
Collectively, group of 143 patients (n = 143) were included in this study and subsequently divided into two groups consisting of individuals after singular generalized tonic-clonic seizures (n = 50) and patients with chronic epilepsy (n = 93). The samples from patients with acute epilepsy were collected 1-3 hours and 72 h after seizure, and a single collection was performed from patients with chronic epilepsy. These samples were compared to the control group (n = 48) using ELISA.
Objective
Epilepsy is a chronic neurological disorder characterized by the periodic and unpredictable occurrence of seizures. The serum level of brain-derived neurotrophic factor (BDNF) has been suggested to be a potential biomarker that could detect differences in epilepsy patients. Although there is considerable neurobiological evidence linking BDNF to epilepsy, only a small number of studies investigated the relationship between BDNF serum levels and epilepsy, and these studies obtained inconsistent
Results
In the present study, we observed a significant decrease of BDNF serum levels in patients after generalized tonic-clonic seizures compared to the control group. Furthermore, the observed decrease of BDNF levels in this group was sustained at 1 and 72 h after seizure insult. We did not show the relationship between BDNF levels and age, etiology of epilepsy and the duration of illness. Significance: Our results and the findings of previous studies indicate that the serum BDNF level significantly decreases after seizures and should be considered when measuring BDNF in patients with chronic epilepsy. It might be also influenced by neurodegenerative processes, which may be involved in the etiopathogenesis of particular epilepsy syndromes.
Significance
Our results and the findings of previous studies indicate that the serum BDNF level significantly decreases after seizures and should be considered when measuring BDNF in patients with chronic epilepsy. It might be also influenced by neurodegenerative processes, which may be involved in the etiopathogenesis of particular epilepsy syndromes.