• M L Daley, C W Leffler, M Czosnyka, and J D Pickard.
• Department of Electrical and Computer Engineering, The University of Memphis, Memphis, TN, USA. mdaley@memphis.edu
• Acta Neurochir. Suppl. 2005 Jan 1;95:327-32.

ObjectiveTo test the validity of the hypothesis that active vasodilatation and vasoconstriction underlie the occurrence of intracranial pressure (ICP) plateau waves by evaluating corresponding changes of cerebrovascular pressure transmission of arterial blood pressure (ABP) to ICP.MethodsDigitized recordings of ICP and ABP sampled at 30 Hz were obtained from nine patients with traumatic brain injury. For each 16.5 s recording interval mean values of ICP, ABP, cerebral perfusion pressure (CPP), and the corresponding highest modal frequency (HMF) of cerebrovascular pressure transmission were calculated.ResultsMean ICP and HMF significantly increased (P < 0.003) and mean CPP decreased significantly (P < 0.00036) at onset of the wave. Conversely at termination, mean ICP and HMF significantly decreased (P < 0.026) and mean CPP significantly increased (P < 0.028). In addition, the strong negative correlations between mean ICP and mean CPP (r = -0.87) and mean HMF and CPP (r = -0.87) were demonstrated.ConclusionThe findings that HMF increased at onset and decreased at the termination of plateau wave support the validity of the vasodilatatory/constriction cascade model that postulates active vasodilation at the onset and active vasoconstriction of the cerebrovascular bed at the termination of a plateau wave.

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