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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.

Seventy patients with cerebral ischemia (21 with transient ischemic attack and 49 with stroke) were studied with short-latency median nerve somatosensory evoked potentials to characterize the evoked potentials in all ischemic patients and to investigate their efficacy for prognosis in stroke. Within 72 hours of symptom onset, all 70 patients received a scaled neurologic function score, with a maximum of 50 points. Somatosensory evoked potential abnormalities were found in 10% (2/19), 42% (15/36), and 93% (14/15) of all patients with initial neurologic examinations who had normal (50 points), mild-moderate (30-49 points), and severe deficits (less than or equal to 29 points), respectively. Thirty-seven of the 49 stroke patients were available for a follow-up neurologic assessment. Eight-nine percent (8/9) of the stroke patients with poor outcome had somatosensory evoked potential abnormalities; 82% (9/11) of the stroke patients with severe neurologic deficits at onset had poor outcome. Results demonstrate that somatosensory evoked potential abnormalities are common in patients with cerebral ischemia but that somatosensory evoked potential findings are not significantly better than a detailed neurologic examination in predicting outcome from stroke.

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 …

A group of 11 patients with a variety of lesions affecting the 3rd ventricle have been treated using a direct transcallosal interfornicial approach to the region. In 3 patients, no attendant hydrocephalus was present. In an effort to minimize potential cortical injury related to the approach, we studied the venous anatomy in the region of the coronal suture. Based on this study, appropriate flap placement and interhemispheric entry points were defined. Although no lasting, clinically apparent morbidity was observed in any of the 11 cases, we performed more sophisticated studies of the interhemispheric transfer of somesthetic and perceptual motor tasks, as well as psychometric testing related to parameters of intelligence and memory, 3 to 8 months postoperatively in 6 cases. The results and clinical material indicate that this surgical technique is a safe, feasible alternative in the management of a wide spectrum of pathological lesions within this region. A transcallosal, interfornicial approach offers excellent visualization of the entire 3rd ventricle without the dependence on hydrocephalus or an extensive extra-axial mass to enhance the exposure. With proper planning and technique. it may be accomplished with a minimum of physiological consequence.

Norepinephrine has been shown to improve signal-to-noise ratios of sensory systems, including that of the auditory system. Yohimbine has been observed to cause a selective increase of cerebral norepinephrine. It was administered in one dose to sensorineurally impaired subjects with the object of improving their speech hearing in noise. Speech intelligibility was measured by the adaptive procedure. Mild, significant improvement was noted in one of the hearing components, "attenuation," and an adverse effect was shown on "distortion," owing to noise. Auditory brainstem response was improved significantly. The objective of temporarily improving intelligibility in noise was not attained.

A 6-year follow-up of patients harboring microprolactinomas suggests that few patients (3 of 27) demonstrate significant growth of their tumor during this time. The major hazard for such patients who are not treated seems to be their risk for the development of premature osteoporosis in the face of sustained hyperprolactinemia. The risks of this complication may exceed the risks of early surgical intervention in selected patients. This short term risk of tumor growth (about 10%) must be weighed in the decision about therapeutic endeavors.