Systems analysis of cerebrovascular pressure transmission: an observational study in head-injured patients

Piper, Ian; Miller, J. D.; Dearden, N. M.; Leggate, James; Robertson, I. S.

doi:10.3171/jns.1990.73.6.0871

Cited by 96 publications

(63 citation statements)

References 21 publications

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“…2 There are two concepts regarding the origin of the lumbar cerebrospinal¯uid pulse wave (L-CSFPW): that it arises from pulsation of the spinal cord. 3,4 and that it is due to pulsation of the brain which is transmitted through the subarachnoid space of the spine.…”

Section: Introductionmentioning

confidence: 99%

Lumbar cerebrospinal fluid pulse wave rising from pulsations of both the spinal cord and the brain in humans

1997

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There are two theories regarding the origin of the lumbar cerebrospinal¯uid pulse wave (L-CSFPW): that it arises from the arteries supplying the spinal cord, and that it is due to the pulsations of the brain transmitted through the subarachnoid space of the spine.We investigated L-CSFPW of 11 myelopathic patients with a complete (®ve patients, CBgroup) or an incomplete spinal block (six, ICB-group) on myelography to determine the origin of L-CSFPW. Since arterial pressure amplitude (APA), the energy source of L-CSFPW, is not the same between individuals or between before and after operation, not only L-CSFPW itself but also the transfer function between the arterial pressure wave and the L-CSFPW calculated by the system analysis method was analyzed to eliminate the in¯uence of hemodynamic uctuations. In the system analysis, the arterial pressure wave, L-CSFPW and transfer function were decomposed into ®ve harmonic waves (HW).In the CB group, L-CSFPW was observed to be 0.72 mmHg on average (range, 0.25 ± 1.00) in spite of blocking pulsations of the brain, showing that there was a contribution to L-CSFPW unrelated to the brain, that is, the spinal cord. In the CB group, however, the preoperative transfer function value of HW1 (mean, 0.056; range, 0.012 ± 0.170) was lower than that in the ICB group (mean, 0.137; range, 0.061 ± 0.236) (P50.05), indicating that the brain pulsation also contributed to L-CSFPW.In the ICB group, there was signi®cant reduction of HW1 (P50.01) and HW2 (P50.05) transfer function after posterior decompression surgery in spite of improvement in the subarachnoid space narrowing: preoperative HW1, mean, 0.137, range, 0.061 ± 0.236; postoperative HW1, mean, 0.065, range, 0.021 ± 0.153; preoperative HW2, mean, 0.092, range, 0.011 ± 0.148; postoperative HW2, mean, 0.044, range, 0.030 ± 0.066. It has been reported that the spinal cord blood¯ow is decreased 20% or more by laminectomy, therefore, L-CSFPW measurement may be sensitive enough to detect a 20% or higher decrease in this ow. This suggests that L-CSFPW could possibly be used clinically as a non-invasive method of monitoring the spinal cord blood¯ow. For broad clinical application of CSFPW, however, further studies are needed, especially on the direct relationship between CSFPW and spinal cord blood¯ow itself.

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Section: Introductionmentioning

confidence: 99%

Lumbar cerebrospinal fluid pulse wave rising from pulsations of both the spinal cord and the brain in humans

1997

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“…Slow waves of ABP, lasting from 20 seconds to 3 minutes, are almost always present in patients receiving mechanical ventilation and are of sufficient magnitude to provoke a vasomotor response. 1,20,23,24,27 Taking advantage of this fact, cerebrovascular pressure reactivity can be determined continuously without manipulation of ABP by monitoring the response of ICP to such changes in mean ABP.…”

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confidence: 99%

“…7,24 Some authors have suggested that cerebrovascular pressure reactivity could be derived from the characteristic pulse waveform from ABP, 26,27 although this has never been demonstrated to work in clinical practice. Perhaps changes in ABP are too fast (a fraction of a second) to mobilize an active vasoregulatory response.…”

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confidence: 99%

Continuous monitoring of cerebrovascular pressure reactivity in patients with head injury

Zweifel

Lavinio

Steiner

et al. 2008

FOC

191

112

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Object Cerebrovascular pressure reactivity is the ability of cerebral vessels to respond to changes in transmural pressure. A cerebrovascular pressure reactivity index (PRx) can be determined as the moving correlation coefficient between mean intracranial pressure (ICP) and mean arterial blood pressure. Methods The authors analyzed a database consisting of 398 patients with head injuries who underwent continuous monitoring of cerebrovascular pressure reactivity. In 298 patients, the PRx was compared with a transcranial Doppler ultrasonography assessment of cerebrovascular autoregulation (the mean index [Mx]), in 17 patients with the PET–assessed static rate of autoregulation, and in 22 patients with the cerebral metabolic rate for O2. Patient outcome was assessed 6 months after injury. Results There was a positive and significant association between the PRx and Mx (R2 = 0.36, p < 0.001) and with the static rate of autoregulation (R2 = 0.31, p = 0.02). A PRx > 0.35 was associated with a high mortality rate (> 50%). The PRx showed significant deterioration in refractory intracranial hypertension, was correlated with outcome, and was able to differentiate patients with good outcome, moderate disability, severe disability, and death. The graph of PRx compared with cerebral perfusion pressure (CPP) indicated a U–shaped curve, suggesting that too low and too high CPP was associated with a disturbance in pressure reactivity. Such an optimal CPP was confirmed in individual cases and a greater difference between current and optimal CPP was associated with worse outcome (for patients who, on average, were treated below optimal CPP [R2 = 0.53, p < 0.001] and for patients whose mean CPP was above optimal CPP [R2 = −0.40, p < 0.05]). Following decompressive craniectomy, pressure reactivity initially worsened (median −0.03 [interquartile range −0.13 to 0.06] to 0.14 [interquartile range 0.12–0.22]; p < 0.01) and improved in the later postoperative course. After therapeutic hypothermia, in 17 (70.8%) of 24 patients in whom rewarming exceeded the brain temperature threshold of 37°C, ICP remained stable, but the average PRx increased to 0.32 (p < 0.0001), indicating significant derangement in cerebrovascular reactivity. Conclusions The PRx is a secondary index derived from changes in ICP and arterial blood pressure and can be used as a surrogate marker of cerebrovascular impairment. In view of an autoregulation–guided CPP therapy, a continuous determination of a PRx is feasible, but its value has to be evaluated in a prospective controlled trial.

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“…Decreases in ABP were observed at the beginning of plateau waves [37], and A waves [38]. Moreover, system analysis [39] suggested that a change in the transfer function that relates ABP to ICP may precede elevations. Several other investigators have also attempted to make predictions using wavelet decomposition of the ICP signal [40][41][42].…”

Section: Predicting Intracranial Hypertensionmentioning

confidence: 99%

Real-Time Analysis of Intracranial Pressure Waveform Morphology

Scalzo¹,

Hamilton²,

Hu³

2012

Advanced Topics in Neurological Disorders

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Systems analysis of cerebrovascular pressure transmission: an observational study in head-injured patients

Cited by 96 publications

References 21 publications

Lumbar cerebrospinal fluid pulse wave rising from pulsations of both the spinal cord and the brain in humans

Lumbar cerebrospinal fluid pulse wave rising from pulsations of both the spinal cord and the brain in humans

Continuous monitoring of cerebrovascular pressure reactivity in patients with head injury

Real-Time Analysis of Intracranial Pressure Waveform Morphology

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