A case of Creutzfeldt-Jakob disease (CJD) is reported in a 28-year-old woman who had received a cadaveric dural graft 19 months earlier after resection of a cholesteatoma. The circumstances of the case point to the graft as the most likely source of the disease. Cadaveric dura should be added to the list of materials that may transmit CJD, and it must be very carefully screened if it is used at all for grafting. Autologous tissue should be considered whenever possible.

Object The authors describe the artificial neural network (ANN) as an innovative and powerful modeling tool that can be increasingly applied to develop predictive models in neurosurgery. They aimed to demonstrate the utility of an ANN in predicting survival following traumatic brain injury and compare its predictive ability with that of regression models and clinicians. Methods The authors designed an ANN to predict in-hospital survival following traumatic brain injury. The model was generated with 11 clinical inputs and a single output. Using a subset of the National Trauma Database, the authors “trained” the model to predict outcome by providing the model with patients for whom 11 clinical inputs were paired with known outcomes, which allowed the ANN to “learn” the relevant relationships that predict outcome. The model was tested against actual outcomes in a novel subset of 100 patients derived from the same database. For comparison with traditional forms of modeling, 2 regression models were developed using the same training set and were evaluated on the same testing set. Lastly, the authors used the same 100-patient testing set to evaluate 5 neurosurgery residents and 4 neurosurgery staff physicians on their ability to predict survival on the basis of the same 11 data points that were provided to the ANN. The ANN was compared with the clinicians and the regression models in terms of accuracy, sensitivity, specificity, and discrimination. Results Compared with regression models, the ANN was more accurate (p < 0.001), more sensitive (p < 0.001), as specific (p = 0.260), and more discriminating (p < 0.001). There was no difference between the neurosurgery residents and staff physicians, and all clinicians were pooled to compare with the 5 best neural networks. The ANNs were more accurate (p < 0.0001), more sensitive (p < 0.0001), as specific (p = 0.743), and more discriminating (p < 0.0001) than the clinicians. Conclusions When given the same limited clinical information, the ANN significantly outperformed regression models and clinicians on multiple performance measures. While this paradigm certainly does not adequately reflect a real clinical scenario, this form of modeling could ultimately serve as a useful clinical decision support tool. As the model evolves to include more complex clinical variables, the performance gap over clinicians and logistic regression models will persist or, ideally, further increase.

Background and Purpose-Local Ca 2ϩ release events (Ca 2ϩ sparks) caused by the opening of ryanodine-sensitive Ca

Abstract-Cerebral vasospasm following aneurysmal subarachnoid hemorrhage (SAH) has devastating consequences.Oxyhemoglobin (oxyhb) has been implicated in SAH-induced cerebral vasospasm as it causes cerebral artery constriction and increases tyrosine kinase activity. Voltage-dependent, Ca 2ϩ -selective and K ϩ -selective ion channels play an important role in the regulation of cerebral artery diameter and represent potential targets of oxyhb. Here we provide novel evidence that oxyhb selectively decreases 4-aminopyridine sensitive, voltage-dependent K ϩ channel (K v ) currents by Ϸ30% in myocytes isolated from rabbit cerebral arteries but did not directly alter the activity of voltage-dependent Ca 2ϩ channels or large conductance Ca 2ϩ -activated (BK) channels. A combination of tyrosine kinase inhibitors (tyrphostin AG1478, tyrphostin A23, tyrphostin A25, genistein) abolished both oxyhb-induced suppression of K v channel currents and oxyhb-induced constriction of isolated cerebral arteries. The K v channel blocker 4-aminopyridine also inhibited oxyhb-induced cerebral artery constriction. The observed oxyhb-induced decrease in K v channel activity could represent either channel block, or a decrease in K v channel density on the plasma membrane. To explore whether oxyhb altered trafficking of K v channels to the plasma membrane, we used an antibody generated against an extracellular epitope of K v 1.5 channels. In the presence of oxyhb, staining of K v 1.5 on the plasma membrane surface was markedly reduced. Furthermore, oxyhb caused a loss of spatial distinction between staining with K v 1.5 and the general anti-phosphotyrosine antibody PY-102. We propose that oxyhb-induced suppression of K v currents occurs via a mechanism involving enhanced tyrosine kinase activity and channel endocytosis. This novel mechanism may contribute to oxyhb-induced cerebral artery constriction following SAH.