Critical closing pressure during experimental intracranial hypertension: comparison of three calculation methods.

Objectives: The critical closing pressure (CrCP) defines arterial blood pressure below which cerebral arteries collapse. It represents a clinically relevant parameter for the estimation of cerebrovascular tone. Although there are few methods to assess CrCP, there is no consensus which of them estimates this parameter most accurately. The aim of present retrospective, experimental study was to compare three methods of CrCP estimation: conventional Aaslid's formula and methods based on the cerebrovascular impedance: the established continuous flow forward (CFF) and a new pulsatile flow forward (PFF) model.Methods: The effects of the following physiological manoeuvres on the CrCP were studied in New Zealand white rabbits: lumbar infusion of Hartmann's solution to induce mild intracranial hypertension, sympathetic blockade to induce arterial hypotension, and modulation of respiratory tidal volume to induce hypocapnia or hypercapnia.Results: During intracranial hypertension, all CrCP estimates were significantly higher than at baseline, decreased with decreasing ABP and increased with gradual hypocapnia. During hypercapnia, all CrCP estimates were significantly decreased but only in the case of CrCPA the negative, non-physiological values were observed (16% of the cases). The Bland-Altman analysis revealed that a good agreement between each impedance method and Aaslid's method deteriorated significantly in the low range of the average numerical value of the estimates.Discussion: Our results confirm the limited usage of Aaslid's formula for the calculation of CrCP. Although both impedance methods seem to be equivalent, the fact that PFF model better describes cerebrovascular hemodynamic allows the recommendation of this model for the calculation of CrCP.

Increased ICP and Its Cerebral Haemodynamic Sequelae.

OBJECTIVES: Increased intracranial pressure (ICP) is a pathological feature of many neurological diseases; however, the local and systemic sequelae of raised ICP are incompletely understood. Using an experimental paradigm, we aimed to describe the cerebrovascular consequences of acute increases in ICP. MATERIALS AND METHODS: We assessed cerebral haemodynamics [mean arterial blood pressure (MAP), ICP, laser Doppler flowmetry (LDF), basilar artery Doppler flow velocity (Fv) and estimated vascular wall tension (WT)] in 27 basilar artery-dependent rabbits during experimental (artificial lumbar CSF infusion) intracranial hypertension. WT was estimated as the difference between critical closing pressure and ICP. RESULTS: From baseline (~9 mmHg) to moderate increases in ICP (~41 mmHg), cortical LDF decreased (from 100 to 39.1%, p < 0.001), while mean global Fv was unchanged (from 47 to 45 cm/s, p = 0.38). In addition, MAP increased (from 88.8 to 94.2 mmHg, p < 0.01 and WT decreased (from 19.3 to 9.8 mmHg, p < 0.001). From moderate to high ICP (~75 mmHg), both global Fv and cortical LDF decreased (Fv, from 45 to 31.3 cm/s, p < 0.001; LDF, from 39.1 to 13.3%, p < 0.001) while MAP increased further (94.2 to 114.5 mmHg, p < 0.001) and estimated WT was unchanged (from 9.7 to 9.6 mmHg, p = 0.35). CONCLUSION: In this analysis, we demonstrate a cortical vulnerability to increases in ICP and two ICP-dependent cerebro-protective mechanisms: with moderate increases in ICP, WT decreases and MAP increases to buffer cerebral perfusion, while with severe increases of ICP, an increased MAP predominates.

Critical Closing Pressure During a Controlled Increase in Intracranial Pressure.

OBJECTIVES: The objectives were to compare three methods of estimating critical closing pressure (CrCP) in a scenario of a controlled increase in intracranial pressure (ICP) induced during an infusion test in patients with suspected normal pressure hydrocephalus (NPH). METHODS: We retrospectively analyzed data from 37 NPH patients who underwent infusion tests. Computer recordings of directly measured intracranial pressure (ICP), arterial blood pressure (ABP) and transcranial Doppler cerebral blood flow velocity (CBFV) were used. The CrCP was calculated using three methods: first harmonics ratio of the pulse waveforms of ABP and CBFV (CrCPA) and two methods based on a model of cerebrovascular impedance, as a function of cerebral perfusion pressure (CrCPinv), and as a function of ABP (CrCPninv). RESULTS: There is good agreement among the three methods of CrCP calculation, with correlation coefficients being greater than 0.8 (p < 0.0001). For the CrCPA method, negative values were found for about 20% of all results. Negative values of CrCP were not observed in estimators based on cerebrovascular impedance. During the controlled rise of ICP, all three estimators of CrCP increased significantly (p < 0.05). The strongest correlation between ICP and CrCP was found for CrCPinv (median R = 0.41). CONCLUSION: Invasive CrCP is most sensitive to variations in ICP and can be used as an indicator of the status of the cerebrovascular system during infusion tests.

Effect of Mild Hypocapnia on Critical Closing Pressure and Other Mechanoelastic Parameters of the Cerebrospinal System.

OBJECTIVE: Brain arterial critical closing pressure (CrCP) has been studied in several diseases such as traumatic brain injury (TBI), subarachnoid haemorrhage, hydrocephalus, and in various physiological scenarios: intracranial hypertension, decreased cerebral perfusion pressure, hypercapnia, etc. Little or nothing so far has been demonstrated to characterise change in CrCP during mild hypocapnia. METHOD: We retrospectively analysed recordings of intracranial pressure (ICP), arterial blood pressure (ABP) and blood flow velocity from 27 severe TBI patients (mean 39.5 ± 3.4 years, 6 women) in whom a ventilation increase (20% increase in respiratory minute volume) was performed over 50 min as part of a standard clinical CO2 reactivity test. CrCP was calculated using the Windkessel model of cerebral arterial flow. Arteriolar wall tension (WT) was calculated as a difference between CrCP and ICP. The compartmental compliances arterial (C a ) and cerebrospinal fluid space (C i ) were also evaluated. RESULTS: During hypocapnia, ICP decreased from 17±6.8 to 13.2±6.6 mmHg (p < 0.000001). Wall tension increased from 14.5 ± 9.9 to 21.7±9.1 mmHg (p < 0.0002). CrCP, being a sum of WT + ICP, changed significantly from 31.5 ± 11.9 mmHg to 34.9±11.1 mmHg (p < 0.002), and the closing margin (ABP-CrCP) remained constant at an average value of 60 mmHg. C a decreased significantly during hypocapnia by 30% (p < 0.00001) and C i increased by 26% (p < 0.003). CONCLUSION: During hypocapnia in TBI patients, ICP decreases and WT increases. CrCP increases slightly as the rise in wall tension outweighs the decrease in ICP. The closing margin remained unchanged, suggesting that the risk of hypocapnia-induced ischemia might not be increased.

Critical Closing Pressure During Controlled Increase in Intracranial Pressure-Comparison of Three Methods.

GOAL: Critical closing pressure (CrCP) is the arterial blood pressure (ABP) threshold, below which small arterial vessels collapse and cerebral blood flow ceases. Here, we aim to compare three methods for CrCP estimation in scenario of a controlled increase in intracranial pressure (ICP), induced by infusion tests performed in patients with suspected normal pressure hydrocephalus (NPH). METHODS: Computer recordings of directly-measured ICP, ABP, and transcranial Doppler cerebral blood flow velocity (CBFV), from 37 NPH patients undergoing infusion tests, were retrospectively analyzed. The CrCP was calculated with three methods: one with the first harmonics ratio of the pulse waveforms of ABP and CBFV (CrCPA) and two methods based on a model of cerebrovascular impedance, as functions of both cerebral perfusion pressure (CrCPinv), and of ABP (CrCPninv). CONCLUSION: All methods give similar results in response to ICP changes. In the case of individual CrCP measurements for each patient, CrCPA may provide negative, nonphysiological values. Invasive critical closing pressure is most sensitive to variations in ICP and CPP and can be used as an indicator of the cerebrospinal and the cerebrovascular system status during infusion tests.

Cerebral haemodynamics during experimental intracranial hypertension.

Intracranial hypertension is a common final pathway in many acute neurological conditions. However, the cerebral haemodynamic response to acute intracranial hypertension is poorly understood. We assessed cerebral haemodynamics (arterial blood pressure, intracranial pressure, laser Doppler flowmetry, basilar artery Doppler flow velocity, and vascular wall tension) in 27 basilar artery-dependent rabbits during experimental (artificial CSF infusion) intracranial hypertension. From baseline (∼9 mmHg; SE 1.5) to moderate intracranial pressure (∼41 mmHg; SE 2.2), mean flow velocity remained unchanged (47 to 45 cm/s; p = 0.38), arterial blood pressure increased (88.8 to 94.2 mmHg; p < 0.01), whereas laser Doppler flowmetry and wall tension decreased (laser Doppler flowmetry 100 to 39.1% p < 0.001; wall tension 19.3 to 9.8 mmHg, p < 0.001). From moderate to high intracranial pressure (∼75 mmHg; SE 3.7), both mean flow velocity and laser Doppler flowmetry decreased (45 to 31.3 cm/s p < 0.001, laser Doppler flowmetry 39.1 to 13.3%, p < 0.001), arterial blood pressure increased still further (94.2 to 114.5 mmHg; p < 0.001), while wall tension was unchanged (9.7 to 9.6 mmHg; p = 0.35).This animal model of acute intracranial hypertension demonstrated two intracranial pressure-dependent cerebroprotective mechanisms: with moderate increases in intracranial pressure, wall tension decreased, and arterial blood pressure increased, while with severe increases in intracranial pressure, an arterial blood pressure increase predominated. Clinical monitoring of such phenomena could help individualise the management of neurocritical patients.

The Ontogeny of Cerebrovascular Pressure Autoregulation in Premature Infants.

Our objective was to quantify cerebrovascular autoregulation as a function of gestational age (GA) and across the phases of the cardiac cycle. One hundred eighty-six premature infants, with a GA range of 23-33 weeks, were monitored using umbilical artery catheters and transcranial Doppler insonation of middle cerebral artery flow velocity (FV) for 1-h sessions over the first week of life. Autoregulation was quantified as a moving correlation coefficient between systolic arterial blood pressure (ABP) and systolic FV (Sx); mean ABP and mean FV (Mx); diastolic ABP and diastolic FV (Dx). Autoregulation was compared across GAs for each aspect of the cardiac cycle. Systolic FV was pressure-passive in infants with the lowest GA, and Sx decreased with increased GA (r = -0.3; p < 0.001). By contrast, Dx was elevated in all subjects, and showed minimal change with increased GA (r = -0.06; p = 0.05). Multivariate analysis confirmed that GA (p < 0.001) and the "closing margin" (p < 0.01) were associated with Sx. Premature infants have low and almost always pressure-passive diastolic cerebral blood FV. Conversely, the regulation of systolic cerebral blood FV by autoregulation was manifested in this cohort at a GA of between 23 and 33 weeks.

The Diastolic Closing Margin Is Associated with Intraventricular Hemorrhage in Premature Infants.

Premature infants are at an increased risk of intraventricular hemorrhage (IVH). The roles of hypotension and hyperemia are still debated. Critical closing pressure (CrCP) is the arterial blood pressure (ABP) at which cerebral blood flow (CBF) ceases. When diastolic ABP is equal to CrCP, CBF occurs only during systole. The difference between diastolic ABP and CrCP is the diastolic closing margin (DCM). We hypothesized that a low DCM was associated with IVH. One hundred eighty-six premature infants, with a gestational age (GA) range of 23-33 weeks, were monitored with umbilical artery catheters and transcranial Doppler insonation of middle cerebral artery flow velocity for 1-h sessions over the first week of life. CrCP was calculated linearly and using an impedance model. A multivariate generalized linear regression model was used to determine associations with severe IVH (grades 3-4). An elevated DCM by either method was associated with IVH (p < 0.0001 for the linear method; p < 0.001 for the impedance model). Lower 5-min Apgar scores, elevated mean CBF velocity, and lower mean ABP were also associated with IVH (p < 0.0001). Elevated DCM, not low DCM, was associated with severe IVH in this cohort.

Monitoring Cerebral Autoregulation After Subarachnoid Hemorrhage.

INTRODUCTION: Delayed cerebral ischemia (DCI) is a major contributor to morbidity and mortality after subarachnoid hemorrhage (SAH). Data challenge vasospasm being the sole cause of ischemia and suggest other factors. We tested the hypothesis that early autoregulatory failure might predict DCI. METHODS: This is a prospective observational study of cerebral autoregulation following SAH in which the primary end point was DCI at 21 days. Cox proportional hazards and multivariate models were used and the benefit of using multiple indices was analyzed. RESULTS: Ninety-eight patients were included in the study. There was an increased risk of DCI with early dysautoregulation (odds ratio [OR]: 7.46, 95% confidence interval [CI]: 3.03-18.40 and OR: 4.52, 95 % CI: 1.84-11.07 for the transcranial Doppler index of autoregulation [Sxa] and near-infrared spectroscopy index of autoregulation [TOxa], respectively), but not vasospasm (OR: 1.36, 95 % CI: 0.56-3.33). Sxa and TOxa remained independent predictors of DCI in the multivariate model (OR: 12.66, 95 % CI: 2.97-54.07 and OR: 5.34, 95 % CI: 1.25-22.84 for Sxa and TOxa, respectively). There was good agreement between different indices. All 13 patients with impaired autoregulation in all three methods developed DCI. CONCLUSIONS: Disturbed autoregulation in the first 5 days after SAH is predictive of DCI. Although colinearities exist between the methods assessed, multimodal monitoring of cerebral autoregulation can aid the prediction of DCI.

Cerebral Critical Closing Pressure During Infusion Tests.

We studied possible correlations between cerebral hemodynamic indices based on critical closing pressure (CrCP) and cerebrospinal fluid (CSF) compensatory dynamics, as assessed during lumbar infusion tests. Our data consisted of 34 patients with normal-pressure hydrocephalus who undertook an infusion test, in conjunction with simultaneous transcranial Doppler ultrasonography (TCD) monitoring of blood flow velocity (FV). CrCP was calculated from the monitored signals of ICP, arterial blood pressure (ABP), and FV, whereas vascular wall tension (WT) was estimated as CrCP - ICP. The closing margin (CM) expresses the difference between ABP and CrCP. ICP increased during infusion from 6.67 ± 4.61 to 24.98 ± 10.49 mmHg (mean ± SD; p < 0.001), resulting in CrCP rising by 22.93 % (p < 0.001), with WT decreasing by 11.33 % (p = 0.005) owing to vasodilatation. CM showed a tendency to decrease, albeit not significantly (p = 0.070), because of rising ABP (9.12 %; p = 0.005), and was significantly different from zero for the whole duration of the tests (52.78 ± 22.82 mmHg; p < 0.001). CM at baseline correlated inversely with brain elasticity (R = -0.358; p = 0.038). Neither CrCP nor WT correlated with CSF compensatory parameters. Overall, CrCP increases and WT decreases during infusion tests, whereas CM at baseline pressure may act as a characterizing indicator of the cerebrospinal compensatory reserve.

Derangement of Cerebral Blood Flow Autoregulation During Intracranial Pressure Plateau Waves as Detected by Time and Frequency-Based Methods.

Plateau waves are sudden elevations of intracranial pressure (ICP) above 40 mmHg, lasting at least 5 min, and are associated with cerebral vasodilatation. We studied the performance of several parameters for cerebral autoregulation assessment during 30 plateau waves of 24 patients with traumatic brain injury. Continuous signals were collected for ICP, arterial blood pressure (ABP) and transcranial Doppler flow velocity (FV). Parameters both in the time domain (autoregulation index, ARI and mean flow index, Mx) and the frequency domain (transfer function gain, phase and coherence) were analysed. The role of different inputs, using either ABP or cerebral perfusion pressure (CPP) as input, was also tested.Autoregulation deteriorated from baseline to plateau, which could be demonstrated by a significant decrease in both ARI between ABP and FV (p = 0.013) and ARI between CPP and FV (p = 0.014). There was also a significant increase in Mx between CPP and FV (p = 0.004), but not in Mx between ABP and FV (p = 0.472). From the baseline to plateau, there was a significant increase in coherence between the ABP and FV at the very low frequency (p = 0.004). The transfer function phase and gain, on the other hand, revealed inconsistent performance.

The Ontogeny of Cerebrovascular Critical Closing Pressure.

Premature infants are at risk of vascular neurological insults. Hypotension and hypertension are considered injurious, but neither condition is defined with consensus. Critical closing pressure (CrCP) is the arterial blood pressure (ABP) at which cerebral blood flow ceases. CrCP may serve to define subject-specific low or high ABP. Our objective was to quantify CrCP as a function of gestational age (GA). One hundred eighty-six premature infants with a GA range of 23-33 weeks, were monitored with umbilical artery catheters and transcranial Doppler insonation of middle cerebral artery flow velocity (FV) for 1-h sessions over the first week of life. CrCP was calculated using an impedance model derivation with Doppler-based estimations of cerebrovascular resistance and compliance. CrCP increased significantly with GA (r = 0.47; slope = 1.4 mmHg/week gestation), an association that persisted with multivariate analysis (p < 0.001). Higher diastolic ABP and higher GA were associated with increased CrCP (p <0.001 for both). CrCP increases significantly at the end of the second and beginning of the third trimester. The low CrCP observed in premature infants may explain their ability to tolerate low ABP without global cerebral infarct or hemorrhage.

Measurement of Intraspinal Pressure After Spinal Cord Injury: Technical Note from the Injured Spinal Cord Pressure Evaluation Study.

Intracranial pressure (ICP) is routinely measured in patients with severe traumatic brain injury (TBI). We describe a novel technique that allowed us to monitor intraspinal pressure (ISP) at the injury site in 14 patients who had severe acute traumatic spinal cord injury (TSCI), analogous to monitoring ICP after brain injury. A Codman probe was inserted subdurally to measure the pressure of the injured spinal cord compressed against the surrounding dura. Our key finding is that it is feasible and safe to monitor ISP for up to a week in patients after TSCI, starting within 72 h of the injury. With practice, probe insertion and calibration take less than 10 min. The ISP signal characteristics after TSCI were similar to the ICP signal characteristics recorded after TBI. Importantly, there were no associated complications. Future studies are required to determine whether reducing ISP improves neurological outcome after severe TSCI.

Waveform Analysis of Intraspinal Pressure After Traumatic Spinal Cord Injury: An Observational Study (O-64).

Following a traumatic brain injury (TBI), intracranial pressure (ICP) increases, often resulting in secondary brain insults. After a spinal cord injury, here the cord may be swollen, leading to a local increase in intraspinal pressure (ISP). We hypothesised that waveform analysis methodology similar to that used for ICP after TBI may be applicable for the monitoring of patients with spinal cord injury.An initial cohort of 10 patients with spinal cord injury, as presented by the first author at a meeting in Cambridge in May 2012, were included in this observational study. The whole group (18 patients) was recently presented in the context of clinically oriented findings (Werndle et al., Crit Care Med, 42(3):646-655, 2014, PMID: 24231762). Mean pressure, pulse and respiratory waveform were analysed along slow vasogenic waves.Slow, respiratory and pulse components of ISP were characterised in the time and frequency domains. Mean ISP was 22.5 ± 5.1, mean pulse amplitude 1.57 ± 0.97, mean respiratory amplitude 0.65 ± 0.45 and mean magnitude of slow waves (a 20-s to 3-min period) was 3.97 ± 3.1 (all in millimetres of mercury). With increasing mean ISP, the pulse amplitude increased in all cases. This suggests that the ISP signal is of a similar character to ICP recorded after TBI. Therefore, the methods of ICP analysis can be helpful in ISP analysis.

Elevated Diastolic Closing Margin Is Associated with Intraventricular Hemorrhage in Premature Infants.

OBJECTIVE: To determine whether the diastolic closing margin (DCM), defined as diastolic blood pressure minus critical closing pressure, is associated with the development of early severe intraventricular hemorrhage (IVH). STUDY DESIGN: A reanalysis of prospectively collected data was conducted. Premature infants (gestational age 23-31 weeks) receiving mechanical ventilation (n = 185) had ∼1-hour continuous recordings of umbilical arterial blood pressure, middle cerebral artery cerebral blood flow velocity, and PaCO2 during the first week of life. Models using multivariate generalized linear regression and purposeful selection were used to determine associations with severe IVH. RESULTS: Severe IVH (grades 3-4) was observed in 14.6% of the infants. Irrespective of the model used, Apgar score at 5 minutes and DCM were significantly associated with severe IVH. A clinically relevant 5-mm Hg increase in DCM was associated with a 1.83- to 1.89-fold increased odds of developing severe IVH. CONCLUSION: Elevated DCM was associated with severe IVH, consistent with previous animal data showing that IVH is associated with hyperperfusion. Measurement of DCM may be more useful than blood pressure in defining cerebral perfusion in premature infants.

Prospective Study on Noninvasive Assessment of Intracranial Pressure in Traumatic Brain-Injured Patients: Comparison of Four Methods.

Elevation of intracranial pressure (ICP) may occur in many diseases, and therefore the ability to measure it noninvasively would be useful. Flow velocity signals from transcranial Doppler (TCD) have been used to estimate ICP; however, the relative accuracy of these methods is unclear. This study aimed to compare four previously described TCD-based methods with directly measured ICP in a prospective cohort of traumatic brain-injured patients. Noninvasive ICP (nICP) was obtained using the following methods: 1) a mathematical "black-box" model based on interaction between TCD and arterial blood pressure (nICP_BB); 2) based on diastolic flow velocity (nICP_FVd); 3) based on critical closing pressure (nICP_CrCP); and 4) based on TCD-derived pulsatility index (nICP_PI). In time domain, for recordings including spontaneous changes in ICP greater than 7 mm Hg, nICP_PI showed the best correlation with measured ICP (R = 0.61). Considering every TCD recording as an independent event, nICP_BB generally showed to be the best estimator of measured ICP (R = 0.39; p < 0.05; 95% confidence interval [CI] = 9.94 mm Hg; area under the curve [AUC] = 0.66; p < 0.05). For nICP_FVd, although it presented similar correlation coefficient to nICP_BB and marginally better AUC (0.70; p < 0.05), it demonstrated a greater 95% CI for prediction of ICP (14.62 mm Hg). nICP_CrCP presented a moderate correlation coefficient (R = 0.35; p < 0.05) and similar 95% CI to nICP_BB (9.19 mm Hg), but failed to distinguish between normal and raised ICP (AUC = 0.64; p > 0.05). nICP_PI was not related to measured ICP using any of the above statistical indicators. We also introduced a new estimator (nICP_Av) based on the average of three methods (nICP_BB, nICP_FVd, and nICP_CrCP), which overall presented improved statistical indicators (R = 0.47; p < 0.05; 95% CI = 9.17 mm Hg; AUC = 0.73; p < 0.05). nICP_PI appeared to reflect changes in ICP in time most accurately. nICP_BB was the best estimator for ICP "as a number." nICP_Av demonstrated to improve the accuracy of measured ICP estimation.

Intraspinal pressure and spinal cord perfusion pressure after spinal cord injury: an observational study.

OBJECT: In contrast to intracranial pressure (ICP) in traumatic brain injury (TBI), intraspinal pressure (ISP) after traumatic spinal cord injury (TSCI) has not received the same attention in terms of waveform analysis. Based on a recently introduced technique for continuous monitoring of ISP, here the morphological characteristics of ISP are observationally described. It was hypothesized that the waveform analysis method used to assess ICP could be similarly applied to ISP. METHODS: Data included continuous recordings of ISP and arterial blood pressure (ABP) in 18 patients with severe TSCI. RESULTS: The morphology of the ISP pulse waveform resembled the ICP waveform shape and was composed of 3 peaks representing percussion, tidal, and dicrotic waves. Spectral analysis demonstrated the presence of slow, respiratory, and pulse waves at different frequencies. The pulse amplitude of ISP was proportional to the mean ISP, suggesting a similar exponential pressure-volume relationship as in the intracerebral space. The interaction between the slow waves of ISP and ABP is capable of characterizing the spinal autoregulatory capacity. CONCLUSIONS: This preliminary observational study confirms morphological and spectral similarities between ISP in TSCI and ICP. Therefore, the known methods used for ICP waveform analysis could be transferred to ISP analysis and, upon verification, potentially used for monitoring TSCI patients.

Cerebral critical closing pressure in hydrocephalus patients undertaking infusion tests.

OBJECTIVES: Links between cerebrospinal fluid (CSF) compensation and cerebral blood flow (CBF) have been studied in many clinical scenarios. In hydrocephalus, disturbed CSF circulation seems to be a primary problem, having been linked to CBF disturbances, particularly in white matter close to surface of dilated ventricles. We studied possible correlations between cerebral haemodynamic indices using transcranial Doppler (TCD) ultrasonography and CSF compensatory dynamics assessed during infusion tests. METHODS: We analysed clinical data from infusion tests performed in 34 patients suspected to suffer from normal pressure hydrocephalus, with signals including intracranial pressure (ICP), arterial blood pressure (ABP) and TCD blood flow velocity (FV). Cerebrospinal fluid compensatory parameters (including elasticity) were calculated according to a hydrodynamic model of the CSF circulation. Critical closing pressure (CrCP) was calculated with the cerebrovascular impedance methodology, while wall tension (WT) was estimated as CrCP-ICP. Closing margin (CM) was expressed as the difference between ABP and CrCP. RESULTS: Intracranial pressure increased during infusion from 6.7 ± 4.6 to 25.0 ± 10.5 mmHg (mean ± SD; P < 0.001), resulting in CrCP rising by 22.9% (P < 0.001) and WT decreasing by 11.3% (P = 0.005). Closing margin showed a tendency to decrease, albeit not significantly (P = 0.070) due to rising ABP (9.1%; P = 0.005). Closing margin at baseline ICP was inversely correlated to brain elasticity (R = (0.358; P = 0.038), while being significantly different from zero for the whole duration of the tests (52.8 ± 22.8 mmHg; P < 0.001). Neither CrCP nor WT was correlated with CSF compensatory parameters. DISCUSSION: Critical closing pressure increases and WT decreases during infusion tests. Closing margin at baseline pressure may act as an indicator of the cerebrospinal compensatory reserve.

Ontogeny of cerebrovascular critical closing pressure.

BACKGROUND: Premature infants are at risk of vascular neurologic insults. Hypotension and hypertension are considered injurious, but neither condition is defined with consensus. Cerebrovascular critical closing pressure (CrCP) is the arterial blood pressure (ABP) at which cerebral blood flow (CBF) ceases. CrCP may serve to define subject-specific low or high ABP. Our objective was to determine the ontogeny of CrCP. METHODS: Premature infants (n = 179) with gestational age (GA) from 23-31 wk had recordings of ABP and middle cerebral artery flow velocity twice daily for 3 d and then daily for the duration of the first week of life. All infants received mechanical ventilation. CrCP was calculated using an impedance-model derivation with Doppler-based estimations of cerebrovascular resistance and compliance. The association between GA and CrCP was determined in a multivariate analysis. RESULTS: The median (interquartile range) CrCP for the cohort was 22 mm Hg (19-25 mm Hg). CrCP increased significantly with GA (r = 0.6; slope = 1.4 mm Hg/wk gestation), an association that persisted with multivariate analysis (P < 0.0001). CONCLUSION: CrCP increased significantly from 23 to 31 wk gestation. The low CrCP observed in very premature infants may explain their ability to tolerate low ABP without global cerebral infarct or hemorrhage.

Expansion duroplasty improves intraspinal pressure, spinal cord perfusion pressure, and vascular pressure reactivity index in patients with traumatic spinal cord injury: injured spinal cord pressure evaluation study.

We recently showed that, after traumatic spinal cord injury (TSCI), laminectomy does not improve intraspinal pressure (ISP), spinal cord perfusion pressure (SCPP), or the vascular pressure reactivity index (sPRx) at the injury site sufficiently because of dural compression. This is an open label, prospective trial comparing combined bony and dural decompression versus laminectomy. Twenty-one patients with acute severe TSCI had re-alignment of the fracture and surgical fixation; 11 had laminectomy alone (laminectomy group) and 10 had laminectomy and duroplasty (laminectomy+duroplasty group). Primary outcomes were magnetic resonance imaging evidence of spinal cord decompression (increase in intradural space, cerebrospinal fluid around the injured cord) and spinal cord physiology (ISP, SCPP, sPRx). The laminectomy and laminectomy+duroplasty groups were well matched. Compared with the laminectomy group, the laminectomy+duroplasty group had greater increase in intradural space at the injury site and more effective decompression of the injured cord. In the laminectomy+duroplasty group, ISP was lower, SCPP higher, and sPRx lower, (i.e., improved vascular pressure reactivity), compared with the laminectomy group. Laminectomy+duroplasty caused cerebrospinal fluid leak that settled with lumbar drain in one patient and pseudomeningocele that resolved completely in five patients. We conclude that, after TSCI, laminectomy+duroplasty improves spinal cord radiological and physiological parameters more effectively than laminectomy alone.