Cerebral vasodilatation causing acute intracranial hypertension: A method for noninvasive assessment

Deep spontaneous vasodilatatory events are frequently recorded in various c erebral diseases, causing dramatic increases (A-waves) in intracranial pres sure (ICP) and subsequently provoking ischemic brain insults. The relations hip between fluctuations in CBF, ICP, and arterial blood pressure (ABP) is influenced by properties of cerebrovascular control mechanisms and the cere brospinal pressure-volume compensation. The goal of this study was to const ruct 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 deri ved from the ABP waveform using a linear signal transformation. The transfo rmation was modified during the simulation by a relationship between ABP an d 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 w as verified by comparison of simulated and directly measured ICP during A-w aves recorded in seven of the patients. In all simulations, plateau elevati ons of ICP were well replicated. The mean absolute error between real and s imulated 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 simu lated increase in ICP was R = 0.98; P <.001. Similarly, correlation between real and simulated Increase in pulse amplitude of ICP was highly significa nt (R = 0.94; P <.001). The mathematical model of the relationship between ABP, flow velocity, and ICP is of potential clinical use for the noninvasiv e detection of A-waves in patients in whom invasive ICP assessment is not c onducted.