Pathophysiological changes in cerebrovascular distensibility in patients undergoing chronic shunt therapy.

OBJECT: Patients undergoing long-term shunt therapy following shunt malfunction often present with acute neurological deterioration, high intracranial pressure (ICP), and yet small or slit ventricles. It is believed that low brain compliance prevents ventricle enlargement in such cases. To elucidate the underlying pathophysiology, the authors estimated compliance as a function of cerebrovascular distensibility in 45 patients undergoing chronic shunt therapy. METHODS: The ICP and pressure-volume index (PVI) were measured at end-tidal CO2 of 30 mm Hg (PVI30) and 40 mm Hg (PVI40). The ventricle volume was dichotomized as slit/small/normal or dilated based on the frontooccipital horn ratio. In 18 patients PVI30 was normal (18.4 +/- 4 ml), whereas in 27 patients it was significantly elevated (45.5 +/- 14 ml). Clinical symptoms or ventricle size at presentation did not correlate with the PVI30. The ICP and PVI at end-tidal CO2 of 40 mm Hg were significantly higher than those at end-tidal CO2 of 30 mm Hg (p < 0.001 and < 0.02, respectively) suggesting an increased cerebrovascular distensibility. CONCLUSIONS: The authors did not observe a low compliance in patients undergoing chronic shunt therapy who, at shunt malfunction, presented with a slit/small/normal ventricle; however, analysis of the findings strongly indicated that an increased cerebrovascular distensibility was present in these patients. This may explain the high ICP and acute clinical deterioration following shunt malfunction in such cases.

Immune reactions associated with silicone-based ventriculo-peritoneal shunt malfunctions in children.

The implantation of ventriculo-peritoneal (VP) shunting systems is the most commonly performed neurological procedure in children with hydrocephalus. Although the overall complication risk is low, the cumulative risk of shunt failure is high and unfortunately results in a high prevalence of revision surgeries. In this study, we explored the concept that some pediatric patients may develop an immune response to either the proteins attached to the silicone implant surface or to the biomaterial itself, and that this reaction may contribute to VP shunt failure in some individuals. The data displays that the sterile shunt malfunction group had a higher rate of protein deposition and increased levels of autoantibodies to the extracted surface proteins as compared to individuals with functioning shunting systems. The precise nature of the shunt-bound proteins that serve as antigens in this experiment have not yet been determined. The data also indicated that some individuals develop antibodies to polymeric substances that cross-react with partially polymerized acrylamide. The detection of significant amounts of shunt-bound protein, antibody responses to these proteins and to polymeric substances suggest that an immunological response to these proteins may play a role in the mechanism behind sterile shunt malfunctions.