Effect of Carbamazepine and Oxcarbazepine on Serum Neuron-specific Enolase and S100B in Focal Seizures

Effect of Carbamazepine and Oxcarbazepine on Serum Neuron-specific Enolase and S100B in Focal Seizures

Effect of Carbamazepine and Oxcarbazepine on Serum Neuron-specific Enolase and S100B in Focal Seizures

The present study has been planned to assess the level of serum neuron-specific enolase (NSE) in focal seizures and its changes after antiepileptic therapy.

Epileptic seizures can cause neuronal cell death, enhanced neurogenesis, axonal sprouting, dendritic changes, and reactive gliosis. Histopathological analyses have suggested that the initial insult and recurrent seizures contribute to the neuronal damage. Activation of mesial temporal structures is more likely to cause damage than that of other areas of brain; therefore, one of the consequences of prolonged seizures is selective neuronal loss in the hippocampus. The excitotoxic damage is considered the most important mechanism of injury but there is also evidence that programmed cell death contributes to neuronal damage. Various biomarkers of brain damage have been studied in the context of epilepsy and brain damage but most widely investigated biochemical biomarker is neuron-specific enolase (NSE). NSE is γγ-isoenzyme of enolase involved in glycolysis pathway. NSE originates predominantly from the cytoplasm of neurons and neuroendocrine cells. Neuronal damage and impairment of blood brain barrier integrity can be detected by the release of NSE into cerebrospinal fluid (CSF) and eventually into blood. NSE is therefore regarded as a marker of neuronal damage and prognosis in various disorders associated with cell damage in the central or peripheral nervous system. CSF and serum NSE levels obtained within first 48 hours were found to be elevated and correlated well with the duration of epilepsy and outcome of patients. Some studies have shown elevated NSE levels in temporal lobe epilepsy, after single tonic-clonic seizures, and status epilepticus. Literature review reveals that there is lack of data on serum NSE in focal seizures and there is no study on the effect of antiepileptic drugs on the level of serum NSE. So the present study has been planned to assess the level of serum NSE in focal seizures and its changes after antiepileptic therapy.

Twenty five (25) healthy individuals of same age group will serve as the control group. Control subjects will be evaluated at baseline only.

Twenty five (25) patients recruited in this group will receive Tab. Carbamazepine. Carbamazepine will be started with a dose of 200 mg/day for one week and then increased to 400 mg/day for one week and then 600mg/day for next two weeks.

Twenty five (25) patients recruited in this group will receive Tab. Oxcarbazepine. Oxcarbazepine will be started with 10mg/kg daily dose for one week followed by 15mg/kg daily for next one week and then will be increased to 20mg/kg for next two weeks.

Carbamazepine will be started with a dose of 200 mg/day for one week and then increased to 400 mg/day for one week and then 600mg/day for next two weeks.

Oxcarbazepine will be started with 10mg/kg daily dose for one week followed by 15mg/kg daily for next one week and then will be increased to 20mg/kg for next two weeks.

The scale was developed at the Chalfont Centre for Epilepsy based on the Chalfont Seizure Severity Scale. It can be used to measure the severity of the seizures and to evaluate anti-epileptic agents during clinical trials.

Quality of Life in Epilepsy Inventory (QOLIE-31) contains seven multi-item scales that tap the following health concepts: emotional well-being, social functioning, energy/fatigue, cognitive functioning, seizure worry, medication effects, and overall quality of life. A QOLIE31 overall score is obtained using a weighted average of the multi-item scale scores.

Inclusion Criteria: All patients with the clinical diagnosis of localization related epilepsy/focal seizure (International League Against Epilepsy 2010) with a history of an episode of seizure within 48 hours of presentation Treatment naïve patients or patients who had not taken any treatment for at least 3 weeks before inclusion. Exclusion Criteria: History of any recent traumatic brain injury, cerebral ischemia/transient ischemic attack/stroke Patients with neuroendocrinal tumours History of any invasive neurosurgical /non-invasive neuropsychiatric procedure. Patients who are already under treatment for the presenting conditions. Medication history of psychoactive or central nervous system depressant drugs Pregnant and nursing women

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