Observational (n=29)
Absolute Event Rate: 0.51% vs 0.26%
p-value: p=1x10(-4)
A novel wavelet transfer model characterizing ABP and ICP fluctuations can effectively differentiate cerebral hemodynamic states and predict outcomes in patients with cerebral lesions.
Higher low-frequency gain may aid outcome stratification in cerebral lesions; leaves open prospective validation of this wavelet model before clinical adoption.
We introduce a wavelet transfer model to relate spontaneous arterial blood pressure (ABP) fluctuations to intracranial pressure (ICP) fluctuations. We employ a complex continuous wavelet transform to develop a consistent mathematical framework capable of parametrizing both cerebral compensatory reserve and cerebrovascular reactivity. The frequency-dependent gain and phase of the wavelet transfer function are introduced because of the non-stationary character of the ICP and ABP time series. The gain characterizes the dampening of spontaneous ABP fluctuations and is interpreted as a novel measure of cerebrospinal compensatory reserve. For a group of 12 patients who died as a result of cerebral lesions (Glasgow Outcome Scale (GOS) = 1) the average gain in the low-frequency (0.02- 0.07 Hz) range was 0.51 +/- 0.13 and significantly exceeded that of 17 patients with GOS = 2 having an average gain of 0.26 +/- 0.11 with p = 1x10(-4) (Kruskal-Wallis test). A time-averaged synchronization index (which may vary from 0 to 1) defined in terms of the wavelet transfer function phase yields information about the stability of the phase difference of the ABP and ICP signals and is used as a cerebrovascular reactivity index. A low value of synchronization index reflects a normally reactive vascular bed, while a high value indicates pathological entrainment of ABP and ICP fluctuations. Such entrainment is strongly pronounced in patients with fatal outcome (for this group the low-frequency synchronization index was 0.69 +/- 0.17). The gain and synchronization parameters define a cerebral hemodynamic state space (CHS) in which the patients with GOS = 1 are to large extent partitioned away from those with GOS = 2. The concept of CHS elucidates the interplay of vascular and compensatory mechanisms.
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Kolodziej et al. (2007) conducted an observational in Cerebral lesions (n=29). Fatal outcome (GOS = 1) vs. GOS = 2 was evaluated on Average gain in the low-frequency (0.02- 0.07 Hz) range (p=1x10(-4)).
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