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

Abstract

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. 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. 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.