Elevated serum neuron-specific enolase in patients with temporal lobe epilepsy: A video–EEG study

• Published in: Epilepsy research 2008-10, Vol.81 (2), p.155-160
• Main Authors: Palmio, Johanna, Keränen, Tapani, Alapirtti, Tiina, Hulkkonen, Janne, Mäkinen, Riikka, Holm, Päivi, Suhonen, Jaana, Peltola, Jukka
• Format: Article
• Language: English
• Subjects: Adult; Anticonvulsants. Antiepileptics. Antiparkinson agents; Biological and medical sciences; Brain damage; Electroencephalography; Epilepsy, Temporal Lobe - blood; Epilepsy, Temporal Lobe - physiopathology; Extratemporal lobe epilepsy; Female; Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy; Humans; Immunoassay; Male; Medical sciences; Middle Aged; Nervous system (semeiology, syndromes); Neurology; Neuron-specific enolase; Neuropharmacology; Pharmacology. Drug treatments; Phosphopyruvate Hydratase - blood; S-100 protein; S100 Proteins - blood; Statistics, Nonparametric; Temporal lobe epilepsy; Time Factors; Video Recording - methods; Video–EEG monitoring; Young Adult
• ISSN: 0920-1211; 1872-6844
• DOI: 10.1016/j.eplepsyres.2008.05.006

Summary Established markers of brain damage, neuron-specific enolase (NSE) and S-100b protein (S-100), may increase after status epilepticus, but whether a single tonic-clonic or complex partial seizure induces elevation of these markers is not known. Furthermore, it is unclear whether the risk of seizure-related neuronal damage in temporal lobe epilepsy (TLE) differs from that in extratemporal lobe epilepsies (XTLE). The aim of this study was to analyze NSE and S-100 in patients with TLE and XTLE after acute seizures. The levels of NSE and S-100 were measured in serum before (0 h) and at 3, 6, 12, and 24 h after acute seizures in 31 patients during inpatient video–EEG monitoring. The patients were categorized into the TLE and the XTLE group based on video–EEG recordings and MRI findings. Fifteen patients had TLE and 16 XTLE. Index seizures were mainly complex partial seizures ( n = 21). In TLE mean ± S.D. values for NSE levels (μg/L) were 8.36 ± 2.64 (0 h), 11.35 ± 3.84 (3 h), 13.48 ± 4.49 (6 h), 12.95 ± 5.46 (12 h) and 10.33 ± 3.13 (24 h) ( p = 0.006, ANOVA). In XTLE the changes were not significant ( p = 0.3). There was less increase in the levels of S-100 in TLE ( p = 0.05) and no significant change in XTLE ( p = 0.4). The levels of markers of neuronal damage were increased in patients with TLE, not only after tonic-clonic but also after complex partial seizures. These data suggest that TLE may be associated with brain damage.