Subject(s)
Cell Transformation, Neoplastic/genetics , Leukemia, Myeloid/genetics , Acute Disease , Female , Gene Rearrangement , Genes, abl/genetics , Genes, bcl-2/genetics , Humans , Leukemia, Myeloid/etiology , Male , Middle Aged , Myelodysplastic Syndromes/complications , Myelodysplastic Syndromes/geneticsABSTRACT
Neuron-specific enolase (NSE) is a marker of brain injury after acute neurologic insults. We report changes in serum NSE (s-NSE) in 25 patients (15 with epilepsy and 10 patients with nonepileptic events) during continuous inpatient video/EEG monitoring. s-NSE was significantly increased as compared with baseline and normal controls after the first ictal event in the epileptic group, especially in patients with secondarily generalized tonic-clonic seizures (p = 0.01), but s-NSE was not increased in patients with nonepileptic events. These preliminary data indicate that s-NSE may be increased after complex partial seizures--and generalized tonic-clonic seizures (GTCS).
Subject(s)
Brain/physiopathology , Electroencephalography , Epilepsy/enzymology , Hospitalization , Phosphopyruvate Hydratase/blood , Adult , Blood-Brain Barrier/physiology , Electroencephalography/methods , Epilepsy/diagnosis , Epilepsy, Complex Partial/diagnosis , Epilepsy, Complex Partial/enzymology , Epilepsy, Tonic-Clonic/diagnosis , Epilepsy, Tonic-Clonic/enzymology , Female , Humans , Male , Middle Aged , Monitoring, Physiologic , Psychophysiologic Disorders/diagnosis , Psychophysiologic Disorders/enzymology , Videotape RecordingABSTRACT
Neuron-specific enolase (NSE) is a sensitive marker of brain injury after stroke, global ischemia, and coma. We report changes in serum NSE (s-NSE) in 19 patients who sustained status epilepticus. s-NSE peaked within 24 to 48 hours after status epilepticus. The mean peak s-NSE level for the entire group was elevated compared with the levels for normal controls (24.87 ng/ml versus 5.36 ng/ml, p = 0.0001) and for epileptic controls (24.87 ng/ml versus 4.61 ng/ml, p = 0.0001). The mean peak s-NSE level for the 11 subjects without an acute neurologic insult (15.44 ng/ml) was also significantly increased compared with levels for normal and epileptic controls. Further, s-NSE was significantly correlated with outcome and duration. We conclude that s-NSE is a promising in vivo marker of brain injury in status epilepticus and warrants further study in larger populations.
