Cerebral vasodilatation causing acute intracranial hypertension: a method for noninvasive assessment.

Deep spontaneous vasodilatatory events are frequently recorded in various cerebral diseases, causing dramatic increases (A-waves) in intracranial pressure (ICP) and subsequently provoking ischemic brain insults. The relationship between fluctuations in CBF, ICP, and arterial blood pressure (ABP) is influenced by properties of cerebrovascular control mechanisms and the cerebrospinal pressure-volume compensation. The goal of this study was to construct a mathematical model of this relationship and to assess its ability to predict the occurrence and time course of A-waves. A group of 17 severely head-injured patients were included in the study. In our model ICP was derived from the ABP waveform using a linear signal transformation. The transformation was modified during the simulation by a relationship between ABP and flow velocity, i.e., by the characterization of the cerebrovascular bed. In this way the ICP could be calculated from the ABP waveform. This model was verified by comparison of simulated and directly measured ICP during A-waves recorded in seven of the patients. In all simulations, plateau elevations of ICP were well replicated. The mean absolute error between real and simulated ICP was 8.3 +/- 5.4 mm Hg at the baseline and 7.9 +/- 4.3 mm Hg at the top of plateau waves. The correlation coefficient between real and simulated increase in ICP was R = 0.98; P < .001. Similarly, correlation between real and simulated increase in pulse amplitude of ICP was highly significant (R = 0.94; P < .001). The mathematical model of the relationship between ABP, flow velocity, and ICP is of potential clinical use for the noninvasive detection of A-waves in patients in whom invasive ICP assessment is not conducted.