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Neuron‐Specific Enolase, a Marker of Acute Neuronal Injury, is Increased in Complex Partial Status Epilepticus
Author(s) -
DeGiorgio Christopher M.,
Gott Peggy S.,
Rabinowicz Adrian L.,
Heck Christi N.,
Smith Thomas D.,
Correale Jorge D.
Publication year - 1996
Publication title -
epilepsia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.687
H-Index - 191
eISSN - 1528-1167
pISSN - 0013-9580
DOI - 10.1111/j.1528-1157.1996.tb00623.x
Subject(s) - enolase , status epilepticus , emergency department , medicine , anesthesia , psychology , epilepsy , neuroscience , psychiatry , immunohistochemistry
Summary:Purpose: To determine whether complex partial status epilepticus (CPSE) causes brain injury in humans. Serum neuron‐specific enolase (s‐NSE) is an accepted marker of acute brain injury, and increases in s‐NSE have been correlated with the duration and outcome of generalized convulsive status epilepticus. s‐NSE levels in CPSE are unknown. Increase in s‐NSE in CPSE would provide new information about the degree of brain injury in CPSE and would help confirm that CPSE is a medical emergency. Methods: This was a pilot prospective study of serial levels of s‐NSE and outcome in CPSE. Eight patients with confirmed CPSE and no acute neurologic deficit were identified prospectively. Results were compared with those of normal and epileptic control groups, and outcome was assessed at hospital discharge or at 7 days with the Glasgow Oucome Scale (GOS). Results: The mean peak s‐NSE was 21.81 ng/ml, which for the 8 patients with CPSE was four times higher than that of normal controls (mean s‐NSE = 5.36 SD = 1.66, p = 0.0003) and epileptic controls (mean s‐NSE = 4.61 SD = 1.74, p. = 0.001). Conclusion: The increase in s‐NSE provides new evidence that CPSE causes brain injury in humans.