Systemic evidence of acute seizure-associated elevation in serum neuronal injury biomarker in patients with temporal lobe epilepsy

Abstract

Background: Patients with drug refractory temporal lobe epilepsy frequently accumulate cognitive impairment over time, suggesting loss of neurons induced by seizures. Our objective was to determine whether there is a temporal association between changes in serum levels of neural injury markers and electroencephalographic (EEG) evidence of seizures and interictal spikes. Methods: We measured serum levels of neuron-specific enolase (NSE), a neuronal injury marker, relative to levels of S100β, a marker of glial injury, at 6 AM, 9 AM, noon, 3 PM, and 6 PM over the course of several days in 7 epilepsy patients undergoing continuous video-EEG monitoring and in 4 healthy controls. Results: All epilepsy patients exhibited significant deviations in NSE levels through time, and 4 of the epilepsy patients exhibited large sample entropy values and large signal variation metrics for NSE relative to S100β. Controls did not exhibit such changes. Correlation analysis revealed that NSE levels were significantly elevated after seizures. There was also a highly significant relationship between increased EEG spike frequency and an increase in serum NSE levels measured 24 h later. Conclusions: The detection of large but transient post-ictal increases in NSE suggests that even self-limited seizures may cause an injury to neurons that underlies cognitive decline in some patients. While this study used a small patient population, the pilot findings suggest that post-ictal assessment of serum NSE may serve as a biomarker for measuring the efficacy of future acute neuroprotective strategies in epilepsy patients.

Serum neuron-specific enolase, magnetic resonance imaging, and electrophysiology for predicting neurodevelopmental outcomes of neonates with hypoxic-ischemic encephalopathy: a prospective study

“…Elevated NSE levels have been reported after stroke, brain injury, cardiac surgery, cardiopulmonary arrest, and perinatal asphyxia [ 46 – 48 ]. Kunda et al [ 49 ] showed that important increases in NSE levels could be observed after seizures in patients with temporal lobe epilepsy, suggesting neuronal damage, but the cause-to-effect relationship could not be established. Lee et al [ 50 ] suggested that NSE levels could be used for the differential diagnosis of seizures over syncope.…”

Role of neuron specific enolase as a biomarker in Parkinson’s disease

“…It is also increased in malignant pheochromocytoma [92,93], Guillain-Barré syndrome [94], Creutzfeldt-Jakob disease [95][96][97], carcinoid tumors [98], dysgerminomas [99,100], immature teratomas [101,102], Merkel cell tumor [103], melanoma [104], seminoma [105], renal cell carcinoma [106]. Among neurological diseases, increased NSE is associated with intracerebral hemorrhage [70,71], ischemic stroke [72][73][74][75][76], seizures [107,108], TBI [70,71,77], and comatose patients after cardiopulmonary resuscitation for cardiac arrest [109][110][111][112][113], newborns with perinatal hypoxic-ischemic encephalopathy [114][115][116], acute spinal cord injury [62,[117][118][119].…”

Serum biomarkers of cerebral cellular stress after self-limiting tonic clonic seizures: An exploratory study

“…Previous studies demonstrated elevations of serum neuron specific enolase (NSE) and protein S100 after some but not all seizures [2,3]. These markers are expressed in other tissues and are even used as tumor markers of these [4].…”