Peggy S. Gott

Hippocampal pyramidal cell loss in human status epilepticus

Summary: A pilot case‐control quantitative study of the hippocampus in patients with severe status epilepticus was performed to identify specific patterns of pyramidal cell loss. Pyramidal cell densities from five patients who died following status epilepticus were compared with five normal controls and five controls matched for age, hypoxialischemia, previous epilepsy, and alcohol abuse. Neuronal densities were greatest in the normal control group and least in patients with status epilepticus. Significant reductions were identified in Sommers sector (prosubiculum and CA1) as well as in CA3 when compared to normal controls.

Transcallosal, interfornicial approaches for lesions affecting the third ventricle: surgical considerations and consequences

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.

Serum neuron-specific enolase in the major subtypes of status epilepticus

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.

The frequently low cobalamin levels in dementia usually signify treatable metabolic, neurologic and electrophysiologic abnormalities

Abstract: Cobalamin levels are frequently low in patients with dementia, but it is unclear if they represent definable deficiency and what the mechanisms are. Therefore, patients being evaluated for dementia who had low cobalamin levels but no obvious evidence of deficiency were studied hematologically, neurologically and with metabolic tests and were re‐evaluated after cobalamin treatment. Abnormalities suggestive of or diagnostic for deficiency were documented in most of the 16 demented and nondemented patients. Metabolic results: 50% of patients tested had abnormal deoxyuridine suppression and 44% had increased serum methylmalonic acid and/or homocysteine levels; these test results correlated with each other. Neurologic results: 73% of patients had clinical abnormalities, primarily mild neuropathies, not attributable to other causes, 75% had electroencephalographic abnormalities, 77% had abnormal visual evoked potentials and 33% had abnormal somatosensory potentials. Metabolic and neurologic dysfunction were present together or absent together in all but 2 cases. Cobalamin therapy improved 50–100% of the various types of abnormalities, although it did not improve cognitive function in the 13 demented patients. Food‐cobalamin malabsorption was found in 60% of the patients. Despite the absence of megaloblastic anemia and rarity of traditional malabsorption of free cobalamin, low cobalamin levels in demented patients frequently represent mild cobalamin deficiency and are often associated with food‐cobalamin malabsorption. Perhaps most importantly, this is accompanied not only by metabolic changes but by evidence of mild neurologic dysfunction. Their frequent reversibility by cobalamin confirms that these defects indeed arise from cobalamin deficiency. Although the long‐standing dementia does not improve, treating such patients with cobalamin has other concrete benefits.

Neuron-specific enolase, a marker of acute neuronal injury, is increased in complex partial status epilepticus.

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.

Serum neuron‐specific enolase in human status epilepticus

Article abstract—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.

Natural History of Microprolactinomas: Six-Year Follow-up

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.

Predictive value of P300 event-related potentials compared with EEG and somatosensory evoked potentials in non-traumatic coma

Developments in ethical decision making are increasing demand for more accurate predictions of outcome in coma. New neurophysiologic tests are needed to improve the ability to predict awakening as well as poor outcome. We have recently reported that the P300 event‐related potential (P300) correlates with awakening and depth of nontraumatic coma. In this companion study, the predictive value of the P300 was compared with median nerve somatosensory evoked potentials (SEP) and EEG in 20 patients in non‐traumatic coma. We also evaluated the predictive value of a simplified grading scale for both the EEG and SEP (the USC SEP scale and USC EEG scale). The resence of a P300 was significantly associated with higher Glasgow coma scores (GCS) and awakening. Severe abnormalities of the somatosensory evoked potentials significantly correlated with the absence of awakening and a low GCS. Moderate abnormalities of the SEP were significantly associated with awakening and higher GCS scores. the EEG was significantly associated with GCS score and severe abnormalities of the EEG were predictive of the absence of awakening and very low GCS scores. The data indicates that the P300 and SEP are more effective than the EEG in predicting awakening, and that the SEP and EEG are more effective than the P300 in predicting poor outcome. We conclude that, in addition to EEG and SEP, the P300 should be considered in the prognostic evaluation of patients in nontraumatic coma. Further, simplified scales for the EEG and SEP are predictive of depth of coma and outcome.

Bromocriptine treatment of prolactin-secreting tumors: surgical implications.

Ten of 19 patients with Stage III-IV prolactin-secreting tumors experienced significant reduction in the size of the tumor when treated with therapeutic doses of bromocriptine. Those tumors that responded favorably to preoperative pharmacological manipulation were found to have an improved surgical cure rate. These preliminary data suggest that a preoperative effort to reduce the size of large prolactin-secreting tumors may result in significant improvement of our surgical ventures.

Voluntary control of two lateralized conscious states: validation by electrical and behavioral studies.

A subject is described who can voluntarily select and hold either of two qualitatively different states of consciousness. Evidence is presented which confirmed differential left or right hemisphere dominance in each state. Asymmetries of EEG alpha and task performance scores indicated a state-dependent shift in functional lateralization. Evoked response studies showed directional changes in rate of interhemispheric transmission correlated with state-related hemisphere dominance. These findings demonstrated that capability for voluntary endogenous control of cerebral dominance under natural conditions.