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Because of its sensitivity to metabolic and ionic disturbances related to ischemia, the EEG can be a potentially useful tool for acute stroke detection and for monitoring affected tissue. However, the clinical use of the EEG in detecting stroke is determined in part by how accurately the spatial information is characterized. The purpose of the current study was to determine the effects of spatial undersampling on the distribution and interpretation of the stroke-related topographic EEG. Using a 128-channel sensor montage, EEG was recorded from six stroke patients acutely (between 8 and 36 hours) after symptom onset. The EEG was submitted to a spectral analysis and was compared with patient symptoms and MRI and computed tomographic findings. To determine loss of spatial and clinical information resulting from spatial undersampling, the average-referenced data from the original 128-channel recording montage were subsampled into 64-, 32-, and 19-channel arrays. Furthermore, the analytical findings were compared with a board-certified electroencephalographer's review of the raw EEG using a conventional clinical montage. As predicted, the results showed that accurate description of stroke-related topographic EEG changes is dependent on adequate spatial sampling density. Accurate description of the spatial distribution of the stroke-related EEG was achieved only with the 64- and 128-channel EEG. As the recording density decreases to 32 channels, the distribution of the scalp EEG spectra is distorted, potentially resulting in mislocalization of the affected region. Results of the clinical review by an expert electroencephalographer corroborated the quantitative analyses, and the results also demonstrated the shortcomings of the conventional 10-20 recording density for capturing focal EEG abnormalities in several cases. The EEG provides useful information about the localization of acute cerebral ischemia, but recording densities of 64 channels or higher are required for accurate spatial characterization of focal stroke-related EEG changes.

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BACKGROUND: Diagnosis of ventriculoperitoneal (VP) shunt pathology remains a dilemma in patients with nonspecific constitutional signs and symptoms. Eosinophilia has been described in association with shunt infection and malfunction. Our purpose was to further define the relationship of eosinophilia and shunt pathology and to determine other predictors of VP shunt infection and malfunction. METHODS: Records of all patients admitted with a suspected VP shunt infection or malfunction were reviewed. The following data were abstracted: age; reason for and age at initial shunt placement; number of revisions; date of last revision; history of fever or vomiting; ventricular fluid cell count; differential and culture; complete blood count and differential; need for shunt revision or replacement; and use of antibiotics. After exclusion of patients admitted for initial shunt placement, the remainder were divided into three groups: those with shunt infection; those with shunt malfunction; and those without documented infection or malfunction. RESULTS: Of 12 patients with shunt infection and 69 with shunt malfunction, 2 and 11, respectively, had eosinophilia defined as > or =5%. The presence of eosinophilia had a 96% positive predictive value for shunt pathology and raised the pretest probability of pathology from 84% to a post test probability of 96%. The combination of fever history and ventricular fluid neutrophils >10% had a 99% specificity for shunt infection, had a 93 and 95% positive and negative predictive value, respectively, and raised the pretest probability of infection from 12% to a posttest probability of 92%. CONCLUSIONS: In patients suspected of having a VP shunt malfunction, the presence of > or =5% eosinophils in the ventricular fluid indicates shunt pathology. The combination of fever and ventricular fluid neutrophils > 10% is predictive of shunt infection.

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OBJECTIVE: To describe the development and implementation of a pediatric critical care nurse practitioner role in a tertiary academic pediatric intensive care unit. DATA SOURCES: Selected relevant articles from the literature. DATA EXTRACTION/SYNTHESIS: Over the past two decades, the role of critical care nurse practitioners in neonatal and adult settings has developed. More recently, the role has emerged in the setting of pediatric critical care. Literature to date focuses on implementation of the nurse practitioner role in neonatal and adult critical care units, with limited publications on the role in the pediatric critical care arena. In addition, information on the practice of critical care nurse practitioners in tertiary care centers is lacking. We therefore, sought to describe the design, implementation, scope of practice, and outcomes to date of a pediatric nurse practitioner program in our pediatric critical care unit. CONCLUSIONS: A pediatric critical care nurse practitioner role can be implemented successfully in a tertiary center's pediatric intensive care unit. However, before integration of the pediatric critical care nurse practitioner into the health care team, definition of entry level requirements and the overall role with respect to scope of practice, daily operations, and professional practice is essential. Future endeavors should include evaluation of the impact of the pediatric critical care nurse practitioner on patient outcomes in the tertiary care center.

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BACKGROUND: The Accreditation Council for Graduate Medical Education is embarking on the major task of a paradigm shift in graduate education in the direction of competency-based medical education and evaluation of outcomes. The Objective Structured Clinical Examination (OSCE), a measure of clinical competence that focuses on outcomes via observable behaviors, is gaining national recognition. OBJECTIVE: To review the pediatric literature relevant to the OSCE. METHOD: A MEDLINE search from the date of the original report of the OSCE (1975) to the present was performed. All English-language studies regarding the use of the OSCE in pediatric education published in the United States and Great Britain were reviewed. MAIN OUTCOME MEASURES: Reliability and validity of the OSCE were examined. Use of standardized pediatric patients was discussed. RESULTS: A greater number of stations and similarity between tasks at different stations increased the reliability of the OSCE. A greater number of stations increased sampling of material and content validity. Correlation between the OSCE and precertification examinations ranged between 0.59 and 0.71, with P< or =.01. Correlation between the OSCE and monthly clinical evaluations was much lower (0.39-0.57), but still statistically significant at P< or =.05. Gaps between expected and actual performance were documented. Overall, the experience of being a standardized patient was viewed as positive by children and their parents. CONCLUSIONS: With appropriate attention to design, acceptable reliability and validity can be achieved for the OSCE. Significant correlations between the OSCE and precertification examinations as well as monthly clinical evaluations were found, the former being stronger than the latter. We conclude that the combination of the OSCE, standardized board examinations, and direct observation in the clinical setting has the potential to become the "gold standard" for measuring physician competence.

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BACKGROUND: Leukocyte filters have been used in cardiopulmonary bypass circuits to decrease potentially deleterious consequences of white blood cell product release in adults undergoing cardiac operations. Studies in animal models have also demonstrated benefits of white blood cell depletion during cardiopulmonary bypass. We sought to examine the efficacy of a leukocyte filter placed in the bypass circuit of infants undergoing operation for correction of congenital heart disease. METHODS: We conducted a retrospective study of infants undergoing correction of congenital heart defects (all had left-to-right shunts) between July 1993 and May 1994. Six infants (group I) had a Leukoguard-3 leukocyte filter (Pall Biomedical Products) placed in the arterial limb of the bypass circuit, and 6 infants (group II) had no filter. We analyzed for differences between groups in intraoperative variables (total pump time, aortic cross-clamp time, deep hypothermic cardiac arrest time, and time for rewarming), postoperative clinical variables (fever in the first 24 hours, days of mechanical ventilation, length of intensive care unit stay, and total hospital stay) and laboratory variables (change in white blood cell and platelet counts preoperatively to postoperatively, and arterial oxygen tension/inspired oxygen fraction ratio). RESULTS: Comparisons between groups were made using Student's t test or chi 2 where appropriate, and results were considered significant at p less than 0.05. No differences between groups were seen in the demographic data or in any of the intraoperative variables. Fever was the only parameter (clinical or laboratory) showing statistical significance between the groups, affecting 1/6 patients in group I and 5/6 patients in group II (chi 2 = 5.33; p < 0.05). CONCLUSIONS: Although these data suggest that the leukocyte filter offers little clinical benefit, a prospective, randomized study should be undertaken to further elucidate the efficacy of leukocyte depletion for infants undergoing cardiopulmonary bypass for correction of congenital heart disease.

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An alcoholic patient presented with profound hyponatremia of uncertain etiology. Despite partial correction of hyponatremia within 24 hours, central pontine myelinolysis (CPM) ensued and the patient subsequently died. The optimal rate of correction of severe, symptomatic hyponatremia has not yet been elucidated.

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We evaluated the cardiac response to dynamic exercise in a group of otherwise healthy insulin-dependent older children and adolescents and in a nondiabetic control group by postexercise echocardiography. Both groups had similar left ventricular function at rest. After exercise we found abnormalities in the indicators of systolic function, fractional shortening (0.37 vs. 0.43) and rate-corrected velocity of circumferential fiber shortening (2.80 vs. 3.35 circumferences/s). In addition, we found an association of flattened interventricular septal motion with finger contractures in the diabetic subjects. Echocardiographic abnormalities in asymptomatic young diabetic adolescents can be elucidated by postexercise echocardiography. Postexercise echocardiography is a noninvasive procedure that can easily be done in the adolescent population and is useful for evaluating subclinical cardiomyopathy.

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Regional effects of electrical stimulation of the cerebellar surface were quantitatively analyzed. Computer controlled stimulus sequences were delivered to ventrolateral thalamus and evoked responses recorded from ipsilateral sensorimotor cortex in the cat. Threshold and excitability profiles were produced with an on-line computer, and their modification by cerebellar stimulation was determined. The results of electrical stimulation of the cerebellar surface were: (1) depressed excitability from paramedian lobule and lobulus simplex; (2) uniquely elevated thresholds from paramedian lobule; and (3) a profound and long-lasting depression of excitability following termination of lobulus simplex stimulation. In comparison with our anticonvulsant drug studies, these data suggest that cerebellar surface stimulation has a far greater capacity to control excitability and threshold responsiveness of thalamocortical systems. Cerebellar electrode placement and temporal pattern of stimulation appear to be important factors in the production of antiepileptic effects.

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Sodium valproate and ethosuximide are anticonvulsants employed in the treatment of petit mal epilepsy; both drugs are considered to be thalamically active. Valproate and ethosuximide both decreased the average evoked response following the second of two stimuli delivered to the ventrolateral thalamus at stimulus frequencies in the region of 3 Hz. Ethosuximide, but not valproate, enhanced the average evoked response at high stimulus frequencies an action shared with several convulsant treatments having different modes of action. The clinical effects of valproate and ethosuximide can be related to this differential modulation of thalamocortical excitability.

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Comparative effects of anticonvulsant drugs on the thalamocortical system were analyzed quantitatively. Paired stimuli were delivered to the ventrolateral thalamus with evoked responses recorded from the ipsilateral sensorimotor cortex in the cat. Threshold and excitability profiles were developed with an on-line computer. Effects of phenytoin and diazepam were generally similar, with depression of excitability and slight elevation of thresholds. Ethosuximide produced a pronounced pair-interval dependent effect of unchanged or increased excitability and lowered threshold at shorter intervals, with depressed excitability and raised threshold at longer intervals. These data demonstrate a marked difference in effect of the petit mal and grand mal agents tested and suggest a basis for the effectiveness of ethosuximide in controlling 3-per-second repetitive activity.

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Epilepsy typifies instability in a complex control system. We have previously identified parameters of the thalamocortical motor system of the cat which correlate with epileptiform activity and are controlled by common anticonvulsants. This study is concerned with the control of such parameters by cerebellar stimulation, potencially promoting stability within the motor system. Under computer control, stimuli were delivered to both ventrolateral thalamus and cerebellar cortex, with multichannel recording of evoked responses obtained from sensorimotor cortex. Cortical evoked responses were plotted as an excitability curve (mean response amplitude as a function of pulse interval) or a family of threshold curves (mean response amplitude as a function of stimulus amplitude at various fixed intervals). The present study reveals that cerebellar epidural stimulation can reduce both the height and duration of the excitability curve, as well as increase the response threshold and reduce the saturation level of the threshold curve. The degree and direction of these parameter changes are dependent on the frequency, polarity, and amplitude of cerebellar stimulation, with the amount of parameter change exceeding that achieved by monotoxic doses of anticonvulsants. These data suggest that control of parameters related to excitability and threshold in the thalamocortical motor system may be the means by which cerebellar stimulation accomplishes control of clinical seizures.

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The mechanisms of petit mal epilepsy remain a mystery despite successful therapy. Previous workers have proposed that paroxysmal activity of cortical inhibitory systems plays a role in absence seizures. In this study, we have compared the effects of bicuculline, a potent convulsive agent and GABA antagonist, with ethosuximide, a drug used to treat petit mal epilepsy, on the thalamocortical motor system of the cat. Under chloralose anesthesia, sequential pairs of pulses were delivered to ventrolateral thalamus (VL) varying either pulse amplitude or interval. The evoked responses were recorded from sensorimotor cortex, analyzed on-line by computer, and plotted as an excitability curve (mean response amplitude as a function of pulse interval), or a family of threshold curves (mean response amplitude as a function of stimulus amplitude at various fixed intervals). Administration of each drug resulted in increased thalamocortical excitability and decreased threshold to stimulation for short pulse-pair intervals, with diminished duration of the excitability curve. Increased alertness was produced by both drugs. Studies with grand mal anticonvulsants demonstrated entirely different effects. Because GABA is thought to be the primary inhibitory transmitter in VL and cerebral cortex, bicuculline would be expected to result in disinhibition. The similarity of the data for ethosuximide suggests that ethosuximide also suppresses inhibition in the thalamocortical motor system and adds further to the accumulating evidence of the role of inhibitory system in petit mal epilepsy.

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A patient with a small infarct located posteriorly in the internal capsule had 9 years of weakness of the contralateral face, arm, and leg. At necropsy, it was found that degeneration of the corticospinal tract was almost complete in the midbrain and medullary pyramid. This case supports the increasing evidence that the human pyramidal tract is located in the third quarter of the posterior limb of the internal capsule.

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