Both experimental and clinical studies have established that status epilepticus (SE) induces neuronal injury. Whether brief recurrent seizures damage the brain is controversial. The markers of brain damage, neuron-specific enolase (NSE) and S-100b protein (S-100b) have been used to assess the primary injury as well as to predict outcome after various brain-damaging conditions. The levels of NSE may increase after SE, but the question whether a single tonic-clonic or complex partial seizure induces elevation of NSE and S-100b is still open. Cerebrospinal fluid (CSF) tau protein measurements have been suggested for the diagnosis of Alzheimer’s disease, and total tau (T-tau) may also be a marker of axonal damage and neuronal degeneration. CSF tau levels have not been previously measured after epileptic seizures. Electroconvulsive therapy (ECT) is the most effective treatment for patients with severe depression. An adequate generalized epileptic seizure is necessary for a therap! eutic response; therefore, possibility of neuronal loss or dysfunction in some patients still raises concerns. At present, studies using biomarkers in patients treated with ECT are scant.
The levels of NSE, S-100b and tau were measured in different patient groups with seizures. Patients with newly onset seizures, patients with refractory epilepsy, and patients with generalized tonic-clonic seizures with various etiologies were included in the study,. Serum and CSF samples were collected shortly after seizures. Serial serum samples of NSE and S-100b were obtained also from patients treated with ECT.
CSF NSE or S-100b concentrations were not increased in patients with single uncomplicated newly onset seizures. On the other hand, serial serum measurements of both NSE and S-100b levels showed elevations in patients with refractory temporal lobe epilepsy (TLE), whereas in extratemporal epilepsies (XTLE) the changes were not significant. CSF tau levels after seizures were not increased in patients with idiopathic or probably symptomatic (cryptogenic) epilepsy, and abnormal CSF tau levels were only found in patients with either acute or remote symptomatic seizures. Serial serum measurements of NSE or S-100b did not show significant changes in patients treated with ECT. However, a transient elevation of S-100b after ECT in four out of ten patients was observed, and high S-100b levels at 2 h and 6 h after ECT correlated with the treatment response.
Our results imply that single uncomplicated seizures do not increase the levels of these biomarkers indicating absence of seizure-induced neuronal injury. In TLE, increased levels of NSE and S-100b suggest that in refractory TLE with repeated seizures the sensitivity to damage is different, and the damage induced by recurrent brief seizures over the years contribute to the progression of the disorder. S-100b has a dual role as a marker of either glial damage or glial activation. Our results of S-100b levels after ECT do not indicate neuronal injury but rather demonstrate glial activation induced by ECT. The activation could be neurotrophic in nature and the antidepressant effect of ECT may be mediated by this glial activation.
