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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.

Objectives: To determine the relative magnitudes of neuron-specific enolase (NSE) levels after complex partial status epilepticus (SE), absence SE, generalized convulsive SE, and subclinical generalized convulsive SE (frequently referred to as acute symptomatic myoclonic status epilepticus).Background: NSE is a marker of acute brain injury and blood–brain barrier dysfunction, which is elevated in SE.Methods: Serum NSE levels were drawn in 31 patients 1, 2, 3, and 7 days after SE. Patients were classified as acute symptomatic or remote symptomatic, and the duration and outcome of SE were determined and correlated with the peak NSE level.Results: NSE was elevated significantly in all four subtypes of SE, but NSE levels were highest in complex partial and subclinical SE. The mean peak NSE level for the complex partial SE group was 23.88 ng/mL (n = 12), 21.5 ng/mL for absence SE (n = 1), 14.10 ng/mL for the generalized convulsive SE group (n = 12), and 37.83 ng/mL for the subclinical SE group (n = 6), all of which was significantly higher than normal control subjects (5.02 ng/mL). Outcome was significantly different between the three groups (p = 0.0007), and was significantly worse for subclinical SE (p = 0.0005, subclinical versus generalized convulsive SE).Conclusion: Serum NSE levels were highest in complex partial and subclinical generalized convulsive SE. The extremely high levels of NSE in subclinical SE reflect the severity of the acute neurologic insults and poor outcome common to subclinical SE. High NSE levels in complex partial SE reflects the long duration of SE in this subgroup, and potential for brain injury.

Reply from the Authors: We welcome the comments of Schmitt and Bandtlow. In review, we reported the first prospective study of serum neuron-specific enolase (s-NSE), a marker of acute neuronal injury after stroke and anoxia, in status epilepticus (SE). Our specific aim was to determine if s-NSE is elevated after SE, and if so, was it correlated with outcome and duration. The results of this pilot study were highly significant. s-NSE was elevated even in those without an acute neurologic insult (remote symptomatic SE). Further, for the 19 patients s-NSE was highly correlated with the 1-week Glasgow Outcome Score (GOS) and the duration of SE. Schmitt and Bandtlow assert that CSF NSE is the more promising marker of brain injury, and cite their own unpublished data. They suggest that s-NSE is more variable than CSF NSE, but multiple studies in animals and humans have shown s-NSE to be a highly specific marker in stroke and anoxic-coma. [2-4] Roine et al. [3] have pointed out "... the relatively high specificity of the serum test and the good correlation between serum and CSF levels of NSE suggest that it may be useful as a routinely available substitute for CSF measurements.'' We have collected CSF and serum samples in 10 patients in SE, and found CSF NSE to be …

Two patients with radiologically confirmed total agenesis of the corpus callosum, and free of gross focal hemispheric pathology, received a battery of lateralized and free-field language and perceptual-motor tests. These tasks allowed a comparison of (1) agenic findings with previous results from surgical commissurotomy patients, and (2) the inter- and intrahemispheric performance for each agenic subject. In general, the results indicate that the two agenic patients do not demonstrate the marked deficits of cross-integration reported after commissurotomy. However, there was an upper limit to their integrative capacity for visual, and to an even greater extent, for fine motor and kinesthetically mediated performance. The tasks that proved particularly difficult appeared to have common factors which may be related to functional capabilities of the ipsilateral motor pathways and anterior commissure.

Pattern-shift visual evoked potentials (VEPs) were recorded in 17 patients with myotonic dystrophy. Abnormalities of latency or amplitude were found in 10 patients (59%) with no obvious retinal or other significant ocular abnormality. All patients had a visual acuity of 20/30 or better. Since most patients had bilateral VEP abnormalities, localization of the disturbance was not certain.