Intracranial Pressure Pulse Amplitude Research Articles

Univariate comparison of performance of different cerebrovascular reactivity indices for outcome association in adult TBI: a CENTER-TBI study

BackgroundMonitoring cerebrovascular reactivity in adult traumatic brain injury (TBI) has been linked to global patient outcome. Three intra-cranial pressure (ICP)-derived indices have been described. It is unknown which index is superior for outcome association in TBI outside previous single-center evaluations. The goal of this study is to evaluate indices for 6- to 12-month outcome association using uniform data harvested in multiple centers.MethodsUsing the prospectively collected data from the Collaborative European NeuroTrauma Effectiveness Research in TBI (CENTER-TBI) study, the following indices of cerebrovascular reactivity were derived: PRx (correlation between ICP and mean arterial pressure (MAP)), PAx (correlation between pulse amplitude of ICP (AMP) and MAP), and RAC (correlation between AMP and cerebral perfusion pressure (CPP)). Univariate logistic regression models were created to assess the association between vascular reactivity indices with global dichotomized outcome at 6 to 12 months, as assessed by Glasgow Outcome Score–Extended (GOSE). Models were compared via area under the receiver operating curve (AUC) and Delong’s test.ResultsTwo separate patient groups from this cohort were assessed: the total population with available data (n = 204) and only those without decompressive craniectomy (n = 159), with identical results. PRx, PAx, and RAC perform similar in outcome association for both dichotomized outcomes, alive/dead and favorable/unfavorable, with RAC trending towards higher AUC values. There were statistically higher mean values for the index, % time above threshold, and hourly dose above threshold for each of PRx, PAx, and RAC in those patients with poor outcomes.ConclusionsPRx, PAx, and RAC appear similar in their associations with 6- to 12-month outcome in moderate/severe adult TBI, with RAC showing tendency to achieve stronger associations. Further work is required to determine the role for each of these cerebrovascular indices in monitoring of TBI patients.

A Precision Medicine Approach to Cerebral Edema and Intracranial Hypertension after Severe Traumatic Brain Injury: Quo Vadis?

Standard clinical protocols for treating cerebral edema and intracranial hypertension after severe TBI have remained remarkably similar over decades. Cerebral edema and intracranial hypertension are treated interchangeably when in fact intracranial pressure (ICP) is a proxy for cerebral edema but also other processes such as extent of mass lesions, hydrocephalus, or cerebral blood volume. A complex interplay of multiple molecular mechanisms results in cerebral edema after severe TBI, and these are not measured or targeted by current clinically available tools. Addressing these underpinnings may be key to preventing or treating cerebral edema and improving outcome after severe TBI. This review begins by outlining basic principles underlying the relationship between edema and ICP including the Monro-Kellie doctrine and concepts of intracranial compliance/elastance. There is a subsequent brief discussion of current guidelines for ICP monitoring/management. We then focus most of the review on an evolving precision medicine approach towards cerebral edema and intracranial hypertension after TBI. Personalization of invasive neuromonitoring parameters including ICP waveform analysis, pulse amplitude, pressure reactivity, and longitudinal trajectories are presented. This is followed by a discussion of cerebral edema subtypes (continuum of ionic/cytotoxic/vasogenic edema and progressive secondary hemorrhage). Mechanisms of potential molecular contributors to cerebral edema after TBI are reviewed. For each target, we present findings from preclinical models, and evaluate their clinical utility as biomarkers and therapeutic targets for cerebral edema reduction. This selection represents promising candidates with evidence from different research groups, overlap/inter-relatedness with other pathways, and clinical/translational potential. We outline an evolving precision medicine and translational approach towards cerebral edema and intracranial hypertension after severe TBI.

Validation of Pressure Reactivity and Pulse Amplitude Indices against the Lower Limit of Autoregulation, Part I: Experimental Intracranial Hypertension.

The purpose of this study was to provide validation of intracranial pressure (ICP) derived continuous indices of cerebrovascular reactivity against the lower limit of autoregulation (LLA). Utilizing an intracranial hypertension model within white New Zealand rabbits, ICP, transcranial Doppler (TCD), laser Doppler flowmetry (LDF), and arterial blood pressure were recorded. Data were retrospectively analyzed in a cohort of 12 rabbits with adequate signals for interrogating the LLA. We derived continuous indices of cerebrovascular reactivity: PRx (correlation between ICP and mean arterial pressure [MAP]), PAx (correlation between pulse amplitude of ICP [AMP] and MAP), and Lx (correlation between LDF-based cerebral blood flow [CBF] and cerebral perfusion pressure [CPP]). LLA was derived via piecewise linear regression of CPP versus LDF or CPP versus systolic flow velocity (FVs) plots. We then produced error bar plots for PRx, PAx, and Lx against 2.5 mm Hg bins of CPP, to display the relationship between these indices and the LLA. We compared the CPP values at clinically relevant thresholds of PRx and PAx, to the CPP defined at the LLA. Receiver operating curve (ROC) analysis was performed for each index across the LLA using 2.5 mm Hg bins for CPP. The mean LLA was 51.5 ± 8.2 mm Hg. PRx and PAx error bar plots demonstrate that each index correlates with the LLA, becoming progressively more positive below the LLA. Similarly, CPP values at clinically relevant thresholds of PRx and PAx were not statistically different from the CPP derived at the LLA. Finally, ROC analysis indicated that PRx and PAx predicted the LAA, with areas under the curve (AUCs) of 0.795 (95% confidence interval [CI]: 0.731-0.857, p < 0.0001) and 0.703 (95% CI: 0.631-0.775, p < 0.0001), respectively. Both PRx and PAx generally agree with LLA within this experimental model of intracranial hypertension. Further analysis of clinically used indices of autoregulation across the LLA within pure arterial hypotension models is required.

Impaired cerebral compensatory reserve is associated with admission imaging characteristics of diffuse insult in traumatic brain injury

BackgroundContinuous assessment of cerebral compensatory reserve is possible using the moving correlation between pulse amplitude of intra-cranial pressure (AMP) and intra-cranial pressure (ICP), called RAP. Little is known about the behavior and associations of this index in adult traumatic brain injury (TBI). The goal of this study is to evaluate the association between admission cerebral imaging findings and RAP over the course of the acute intensive care unit stay.MethodsWe retrospectively reviewed 358 adult TBI patients admitted to the Addenbrooke’s Hospital, University of Cambridge, from March 2005 to December 2016. Only non-craniectomy patients were studied. Using archived high frequency physiologic signals, RAP was derived and analyzed over the first 48 h and first 10 days of recording in each patient, using grand mean, percentage of time above various thresholds, and integrated area under the curve (AUC) of RAP over time. Associations between these values and admission computed tomography (CT) injury characteristics were evaluated.ResultsThe integrated AUC, based on various thresholds of RAP, was statistically associated with admission CT markers of diffuse TBI and cerebral edema. Admission CT findings of cortical gyral effacement, lateral ventricle compression, diffuse cortical subarachnoid hemorrhage (SAH), thickness of cortical SAH, presence of bilateral contusions, and subcortical diffuse axonal injury (DAI) were all associated with AUC of RAP over time. Joncheere-Terpstra testing indicated a statistically significant increase in mean RAP AUC across ordinal categories of the abovementioned associated CT findings.ConclusionsRAP is associated with cerebral CT injury patterns of diffuse injury and edema, providing some confirmation of its potential measurement of cerebral compensatory reserve in TBI.

Validation of Intracranial Pressure-Derived Cerebrovascular Reactivity Indices against the Lower Limit of Autoregulation, Part II: Experimental Model of Arterial Hypotension.

The aim of this work was to explore the relationship between intracranial pressure (ICP)-derived indices of cerebrovascular reactivity and the lower limit of autoregulation (LLA) during arterial hypotension. We retrospectively reviewed recorded physiological data from piglets that underwent controlled hypotension. Hypotension was induced by inflation of a balloon catheter in the inferior vena cava. ICP, cortical laser Doppler flowmetry (LDF), and arterial blood pressure (ABP) monitoring was conducted. ICP-derived indices were calculated: pressure reactivity index (PRx; correlation between ICP and mean arterial pressure [MAP]); pulse amplitude index (PAx; correlation between pulse amplitude of ICP [AMP] and MAP); and RAC (correlation between AMP and cerebral perfusion pressure [CPP]). LLA was estimated by piece-wise linear regression of CPP versus LDF. We produced error bar plots for PRx, PAx, and RAC against 5-mm Hg bins of CPP, displaying the relationship with the LLA. We compared CPP values at clinically relevant thresholds of PRx, PAx, and RAC to CPP measured at the LLA. Receiver operating curve (ROC) analysis was performed for each index across the LLA using 5-mm Hg bins for CPP. Mean LLA was 36.2 ± 10.5 mm Hg. Error bar plots demonstrated that PRx, PAx, and RAC increased, with CPP decreasing below the LLA. CPP at clinically relevant thresholds for PRx, PAx, and RAC displayed weak associations with the LLA, indicating that thresholds defined in TBI may not apply to a model of arterial hypotension. ROC analysis indicated that PRx, PAx, and RAC predicted the LLA, with AUCs of: 0.806 (95% confidence interval [CI], 0.750-0.863; p < 0.0001), 0.726 (95% CI, 0.664-0.789; p < 0.0001), and 0.710 (95% CI, 0.646-0.775; p < 0.0001), respectively. Three ICP-derived continuous indices of cerebrovascular reactivity, PRx, PAx, and RAC, were validated against the LLA within this experimental model of arterial hypotension, with PRx being superior.

A Description of a New Continuous Physiological Index in Traumatic Brain Injury Using the Correlation between Pulse Amplitude of Intracranial Pressure and Cerebral Perfusion Pressure.

To describe a new continuous index of physiologic measurement in a traumatic brain injury (TBI) population, the moving correlation coefficient between intracranial pressure (ICP) pulse amplitude (AMP) and cerebral perfusion pressure (CPP), which we refer to as RAC. We use patient examples of sustained intracranial hypertension, systemic arterial hypotension, and plateau waves, as well as the retrospective analysis of 358 non-decompressive craniectomy (DC) TBI patients with high-frequency ICP and arterial blood pressure data, to explore the relationships of this new index, RAC, with AMP, ICP, CPP, RAP (correlation coefficient between AMP and ICP), pressure reactivity index (PRx), and pulse amplitude index (PAx). We compared the RAC-CPP relationship to that observed between CPP and both PRx and PAx. RAC displays temporal responsiveness to sustained increased ICP, arterial hypotension, and plateau waves, with positive values found during episodes of high ICP and low CPP. Analysis of AMP versus CPP and AMP versus ICP relationships in data from the entire non-DC cohort show lower breakpoints for AMP/CPP at CPP = 40 mm Hg and upper breakpoints for AMP/ICP at ICP = 50-60 mm Hg. RAC trends to positive values with increasing ICP, particularly with ICP values above the peak in AMP (ICP >50 mm Hg), though its interpretation requires concomitant interpretation of AMP, RAP, and PRx/PAx to determine contributions of compensatory reserve and cerebrovascular responsiveness to the changes observed in RAC. There is a parabolic relationship between RAC versus CPP, with trends toward positive RAC values near (and beyond) limits for low and high CPPs, suggesting that RAC may be used in the determination of optimum CPP. RAC appears to carry information regarding both cerebrovascular responsiveness and cerebral compensatory reserve. This contributes to RAC's uniqueness and complex interpretation. Further prospective, clinical studies of RAC in CPP optimum estimation and outcome prediction in TBI are required.

Assessing Cerebral Hemodynamic Stability After Brain Injury.

Following brain injury, unstable cerebral hemodynamics can be characterized by abnormal rises in intracranial pressure (ICP). This behavior has been quantified by the RAP index: the correlation (R) between ICP pulse amplitude (A) and mean (P). While RAP could be a valuable indicator of autoregulatory processes, its prognostic ability is not well established and its validity has been questioned due to potential errors in measurement. Here, we test (1) whether RAP is a consistent measure of intracranial hemodynamics and (2) whether RAP has prognostic value in predicting hemodynamic instability following brain injury. RAP was tested in seven brain injured patients treated in a surgical intensive care unit. A sample of ICP data was randomly chosen and segmented into 1 hour periods. Hours were then categorized as either stable, which contained no sharp rises in ICP, or unstable, which contained ≥1 sharp rise-where a sharp rise is defined as ICP exceeding a mean slope of 0.15 mmHg/s. Equal numbers of stable and unstable segments were then selected for each patient. RAP was calculated as the Pearson's correlation coefficient between ICP pulse amplitude (AMP) and mean (mICP), determined in 6 second windows, according to established methods. Results showed that (1) average AMP and ICP levels were similar between stable and unstable periods and (2) unstable periods were identified by RAP values exceeding 0.6 with an average positive predictive value of 74%. We conclude that RAP can provide a valid measure of ICP dynamics, is not affected by sensor drift, and can better distinguish periods of instability than ICP or AMP alone.

Mathematical Modelling of CSF Pulsatile Flow in Aqueduct Cerebri.

The phase-contrast MRI technique permits the non-invasive assessment of CSF movements in cerebrospinal fluid cavities of the central nervous system. Of particular interest is pulsatile cerebrospinal fluid (CSF) flow through the aqueduct cerebri. It is allegedly increased in hydrocephalus, having potential diagnostic value, although not all scientific reports contain unequivocally positive conclusions. For the mathematical simulation of CSF flow, we used a computational model of cerebrospinal blood/fluid circulation designed by a former student as his PhD project. With this model, cerebral blood flow and CSF may be simulated in various vessels using a system of non-linear differential equations as time-varying signals. The amplitude of CSF flow seems to be positively related to the amplitude of pulse waveforms of intracranial pressure (ICP) in situations where mean ICP increases, such as during simulated infusion tests and following step increases of resistance to CSF outflow. An additional positive association between the pulse amplitude of ICP and CSF flow can be seen during simulated increases in the amplitude of arterial pulses (without changes in mean arterial pressure, MAP). The opposite effect can be observed during step increases in the resistance of the aqueduct cerebri and with decreasing elasticity of the system, where the CSF flow amplitude and the ICP pulse amplitude are related inversely. Vasodilatation caused by both gradual decreases in MAP and by increases in PaCO2 provokes an elevation in the observed amplitude of pulsatile CSF flow. Preliminary results indicate that the pulsations of CSF flow may carry information about both CSF-circulatory and cerebral vasogenic components. In most cases, the pulsations of CSF flow are positively related to the pulse amplitudes of both arterial pressure and ICP and to a degree of cerebrovascular dilatation.

Correlation of rheoencephalogram and intracranial pressure: results of a rat study**In memory of Emil Pásztor.

Measuring brain electrical impedance (rheoencephalography-REG) is a potential technique for noninvasive, continuous neuro-monitoring. Typically, intracranial pressure (ICP), an invasive monitoring modality, is used in brain monitoring. Our hypothesis was that both modalities would reflect cerebrovascular reactivity. In the present study we compared results of REG to results of ICP measurement. Rats were used under anesthesia (; 36 control and 59 vinpocetine infusions). REG was measured by two bipolar REG amplifiers; time constants (Tc) were 3 and 0.3 s. The vinpocetine injection caused a transient decrease in systemic arterial pressure (SAP) and a simultaneous increase in ICP and REG pulse amplitude. SAP decrease was 25% ± 14%; ICP was 28% ± 16%; REG pulse amplitude increase was 209% ± 17% (Tc 3) and 107% ± 68% (Tc 0.3). ICP increase correlated with REG pulse amplitude increase. Area under the receiver operating characteristic curve was 0.9481 for ICP–REG time constants 3 and 0.9335 for ICP–REG time constants 0.3; both with . The fact that both REG and ICP reflect cerebrovascular reactivity indicates the usefulness of REG as a potential technique for noninvasive, continuous neuro-monitoring. The Tc of REG amplifier requires optimization for continuous monitoring of pressure reactivity index.

Changes in Cerebral Partial Oxygen Pressure and Cerebrovascular Reactivity During Intracranial Pressure Plateau Waves.

Plateau waves in intracranial pressure (ICP) are frequently recorded in neuro intensive care and are not yet fully understood. To further investigate this phenomenon, we analyzed partial pressure of cerebral oxygen (pbtO2) and a moving correlation coefficient between ICP and mean arterial blood pressure (ABP), called PRx, along with the cerebral oxygen reactivity index (ORx), which is a moving correlation coefficient between cerebral perfusion pressure (CPP) and pbtO2 in an observational study. We analyzed 55 plateau waves in 20 patients after severe traumatic brain injury. We calculated ABP, ABP pulse amplitude (ampABP), ICP, CPP, pbtO2, heart rate (HR), ICP pulse amplitude (ampICP), PRx, and ORx, before, during, and after each plateau wave. The analysis of variance with Bonferroni post hoc test was used to compare the differences in the variables before, during, and after the plateau wave. We considered all plateau waves, even in the same patient, independent because they are separated by long intervals. We found increases for ICP and ampICP according to our operational definitions for plateau waves. PRx increased significantly (p=0.00026), CPP (p<0.00001) and pbtO2 (p=0.00007) decreased significantly during the plateau waves. ABP, ampABP, and HR remained unchanged. PRx during the plateau was higher than before the onset of wave in 40 cases (73%) with no differences in baseline parameters for those with negative and positive ΔPRx (difference during and after). ORx showed an increase during and a decrease after the plateau waves, however, not statistically significant. PbtO2 overshoot after the wave occurred in 35 times (64%), the mean difference was 4.9±4.6Hg (mean±SD), and we found no difference in baseline parameters between those who overshoot and those who did not overshoot. Arterial blood pressure remains stable in ICP plateau waves, while cerebral autoregulatory indices show distinct changes, which indicate cerebrovascular reactivity impairment at the top of the wave. PbtO2 decreases during the waves and may show a slight overshoot after normalization. We assume that this might be due to different latencies of the cerebral blood flow and oxygen level control mechanisms. Other factors may include baseline conditions, such as pre-plateau wave cerebrovascular reactivity or pbtO2 levels, which differ between studies.

Alterations of pulsation absorber characteristics in experimental hydrocephalus

Analysis of waveform data in previous studies suggests that the pulsatile movement of CSF may play a role in attenuating strong arterial pulsations entering the cranium, and its effectiveness in attenuating these pulsations may be altered by changes in intracranial pressure (ICP). These findings were obtained in studies performed in canines with normal anatomy of the CSF spaces. How then would pulsation absorbance respond to changes in CSF movement under obstructive conditions such as the development of hydrocephalus? In the present study, chronic obstructive hydrocephalus was induced by the injection of cyanoacrylate gel into the fourth ventricle of canines, and pulsation absorbance was compared before and after hydrocephalus induction. Five animals were evaluated with simultaneous recordings of ICP and arterial blood pressure (ABP) before and at 4 and 12 weeks after fourth ventricle obstruction by cyanoacrylate. To assess how the intracranial system responds to the arterial pulsatile component, ABP and ICP waveforms recorded in a time domain had to be analyzed in a frequency domain. In an earlier study the authors introduced a particular technique that allows characterization of the intracranial system in the frequency domain with sufficient accuracy and efficiency. This same method was used to analyze the relationship between ABP and ICP waveforms recorded during several acute states including hyperventilation as well as CSF withdrawal and infusion under conditions before and after inducing chronic obstructive hydrocephalus. Such a relationship is reflected in terms of a gain, which is a function of frequency. The cardiac pulsation absorbance (CPA) index, which is simply derived from a gain evaluated at the cardiac frequency, was used to quantitatively evaluate the changes in pulsation absorber function associated with the development of hydrocephalus within each of the animals, which did become hydrocephalic. To account for normal and hydrocephalic conditions within the same animal and at multiple time points, statistical analysis was performed by repeated-measures ANOVA. The performance of the pulsation absorber as assessed by CPA significantly deteriorated after the development of chronic hydrocephalus. In these animals the decrement in CPA was far more significant than other anticipated changes including those in ICP, compliance, or ICP pulse amplitude. To the extent that the free CSF movement acts as a buffer of arterial pulsation input to flow in microvessels, alterations in the pulsation absorber may play a pathophysiological role. One measure of alterations in the way the brain deals with pulsatile input-the CPA measurement-changes dramatically with the imposition of hydrocephalus. Results in the present study suggest that CPA may serve as a complementary metric to the conventional static measure of intracranial compliance in other experimental and clinical studies.

Cerebrospinal fluid pulse pressure amplitude during lumbar infusion in idiopathic normal pressure hydrocephalus can predict response to shunting

BackgroundWe have previously seen that idiopathic normal pressure hydrocephalus (iNPH) patients having elevated intracranial pressure (ICP) pulse amplitude consistently respond to shunt surgery. In this study we explored how the cerebrospinal fluid pressure (CSFP) pulse amplitude determined during lumbar infusion testing, correlates with ICP pulse amplitude determined during over-night ICP monitoring and with response to shunt surgery. Our goal was to establish a more reliable screening procedure for selecting iNPH patients for shunt surgery using lumbar intrathecal infusion.MethodsThe study population consisted of all iNPH patients undergoing both diagnostic lumbar infusion testing and continuous over-night ICP monitoring during the period 2002-2007. The severity of iNPH was assessed using our NPH grading scale before surgery and 12 months after shunting. The CSFP pulse was characterized from the amplitude of single pressure waves.ResultsTotally 62 iNPH patients were included, 45 of them underwent shunt surgery, in whom 78% were shunt responders. Among the 45 shunted patients, resistance to CSF outflow (Rout) was elevated (≥ 12 mmHg/ml/min) in 44. The ICP pulse amplitude recorded over-night was elevated (i.e. mean ICP wave amplitude ≥ 4 mmHg) in 68% of patients; 92% of these were shunt responders. In those with elevated overnight ICP pulse amplitude, we found also elevated CSFP pulse amplitude recorded during lumbar infusion testing, both during the opening phase following lumbar puncture and during a standardized period of lumbar infusion (15 ml Ringer over 10 min). The clinical response to shunting after 1 year strongly associated with the over-night ICP pulse amplitude, and also with the pulsatile CSFP during the period of lumbar infusion. Elevated CSFP pulse amplitude during lumbar infusion thus predicted shunt response with sensitivity of 88 and specificity of 60 (positive and negative predictive values of 89 and 60, respectively).ConclusionsIn iNPH patients, shunt response can be anticipated in 9/10 patients with elevated overnight ICP pulse amplitude, while in only 1/10 with low ICP pulse amplitude. Additionally, the CSFP pulse amplitude during lumbar infusion testing was elevated in patients with elevated over-night ICP pulse amplitude. In particular, measurement of CSFP pulse amplitude during a standardized infusion of 15 ml Ringer over 10 min was useful in predicting response to shunt surgery and can be used as a screening procedure for selection of iNPH patients for shunting.

What Shapes Pulse Amplitude of Intracranial Pressure?

The pulsatile component of intracranial pressure (ICP) has been shown to be a predictor of outcome in normal pressure hydrocephalus (NPH) and traumatic brain injury (TBI). Experimental studies have demonstrated that the pulse amplitude of ICP (AMP(ICP)) is dependent on the mean ICP (mICP), and on the pulse amplitude of the cerebral arterial blood volume (AMP(CaBV)), according to the exponential craniospinal compliance curve. In this study, we compared the influence of mICP and AMP(CaBV) on AMP(ICP) in patients with NPH (infusion study) and TBI (spontaneous recording). We retrospectively analyzed 25 NPH and 43 TBI patients with continuous monitoring of ICP and cerebral blood flow velocity (CBFV), as assessed with transcranial doppler. AMP(CaBV) was extracted from the CBFV waveform. The influence of mICP and AMP(CaBV) on AMP(ICP) were determined using partial coefficients a, b, and c of the multiple regression model: AMP(ICP) = a * mICP + b * AMP(CaBV) + c. AMP(ICP) was more dependent on mICP in NPH patients than in TBI patients (partial coefficient a = 0.93 versus -0.03; p < 0.001). On the contrary, AMP(ICP) was more dependent on AMP(CaBV) in patients with TBI than in those with NPH (b = 0.86 versus 0.10; p < 0.001). This study shows that AMP(ICP) depends mostly on changes in mean ICP during cerebrospinal fluid (CSF) infusion studies in patients with NPH, and on changes in cerebral arterial blood volume (AMP(CaBV)) in TBI patients. Further clinical studies will reveal whether AMP(ICP) is a better indicator of clinical severity and outcome than mICP in TBI and NPH patients.

Intracranial pressure pulse amplitude during changes in head elevation: a new parameter for determining optimum cerebral perfusion pressure?

During short-term postural changes, the factors determining the amplitude of intracranial pulse pressure (ICPPA) remain constant, except for cerebrovascular resistance (CVR). Therefore, it may be possible to draw conclusions from the ICPPA onto the cerebrovascular resistance (CVR) and thus the relative change in cerebral perfusion pressure (CPP). Age, sex, disease, Glasgow Coma Scale score, placement of ventricular drain, blood gas analysis, and parameters of airway management were prospectively recorded in 40 patients. The changes in intracranial pressure (ICP), CPP, mean arterial pressure (MAP), and ICPPA at head elevations of 0 degrees, 30 degrees, and 60 degrees were measured and analyzed online. Status of cerebrovascular autoregulation was checked using the pressure-reactivity index (PRx). Altogether 36 subjects fulfilled the study conditions. Three patients had positive PRx indicating disturbed autoregulation and were excluded. Thus, 33 were left for analysis (18 females and 15 males). All of them were sedated and mechanically ventilated with Glasgow Coma scores ranging from 3-8. During change in head elevation from 0 degrees to 60 degrees, we found a significant (p < 0.05) improvement of the ICP, an increase of the ICCPA, a reduction of the MAP, and a decrease in the CPP. Increasing ICPPA was linked to decreasing CPP (0 degrees to 60 degrees, r = -0.42, p < 0.05). Head elevation is an important part of the ICP and CPP therapy in neurointensive care. When searching for the patient-specific optimum upper body position, ICPPA may provide additional information. Providing that the cerebral autoregulation is intact, the lowest ICPPA of a patient corresponds to the individual upper body position with the highest CPP.

Changes in intracranial pulse pressure amplitudes after shunt implantation and adjustment of shunt valve opening pressure in normal pressure hydrocephalus

We have previously reported that the intracranial pulse pressure amplitudes were elevated in idiopathic normal pressure hydrocephalus (NPH) patients responding to shunt surgery. Whether or not shunt implantation or adjustment of the shunt valve opening pressure modifies the intracranial pulse pressure amplitudes in NPH patients remains to be established. This report summarises our observations. Thirteen patients with NPH (idiopathic in nine and secondary in four) are presented in whom continuous intracranial pressure (ICP) monitoring was done before and after shunt implantation. In two, ICP monitoring was also done during adjustment of shunt valve opening pressure. The mean ICP and mean ICP wave amplitude (i.e. pulse pressure amplitudes) were determined in 6-s time windows. After shunt implantation there was a fall in both mean ICP and mean ICP wave amplitude; the reduction in the two ICP parameters correlated significantly. However, mean ICP in the supine position was normal (i.e. <15 mmHg) in 12 of 13 patients before shunt placement, and remained normal after shunting. According to our criteria, the mean ICP wave amplitudes were elevated before shunting in 12 of 13 patients and became "normalised" the day after shunting in nine patients. The reduction in mean ICP wave amplitude after shunt was highly significant at the group level. Moreover, adjustment of shunt valve opening pressure modified the levels of mean ICP wave amplitudes. The present observations in 13 NPH patients indicate that shunt implantation reduces mean ICP wave amplitudes. Moreover, the level of reduction can be tailored by adjustment of the shunt valve opening pressure.

Value of Overnight Monitoring of Intracranial Pressure in Hydrocephalic Children

Objective: Exaggerated nocturnal intracranial pressure (ICP) dynamics are commonly observed in hydrocephalic children with a compromise of CSF compensatory reserve capacity. Successful shunting restores this cerebrospinal reserve. We used ICP overnight monitoring combined with positional maneuvers in complex hydrocephalic children with a suspected shunt malfunction for the assessment of shunt function. Methods: In 32 hydrocephalic children, we performed 65 computerized overnight recordings and 25 positional maneuvers. Baseline ICP was considered abnormal if it exceeded the operating pressure of the shunt by more than 2.5 mm Hg. The maximum ICP (normal = <25 mm Hg), RAP coefficient (the correlation coefficient between pulse amplitude and mean intracranial pressure, which indicates pressure volume compensatory reserve; normal = <0.6), magnitude of slow waves (SLOW) and ICP pulse amplitude (AMP) were calculated for each night. Results: Using baseline ICP, maximum ICP and RAP, 19 recordings were classified as ‘normal’ (group 1), 13 as ‘questionable’ (group 2), and 33 as ‘pathological’ (group 3) indicating shunt dysfunction or active hydrocephalus. ICP, AMP, RAP and SLOW were significantly different between groups and significantly elevated in group 3 compared to group 1. Positional tests identified shunt overdrainage in 5 of 25 occasions. In patients of group 1, who underwent revision, shunts turned out to be functional. All patients of group 3 eventually underwent shunt revision with improvement of symptoms thereafter. Conclusion: Computerized ICP monitoring can benefit the assessment of shunt function, and can accurately characterize the status of CSF compensation in shunted children with a complex presentation.

Clinical testing of CSF circulation

Since shunting is almost a purely mechanical treatment that radically affects pressure-volume compensation, patients' cerebrospinal fluid hydrodynamics compensation should be examined before a shunt is implanted. Apart from an opening pressure and a resistance to cerebrospinal fluid outflow, pulse amplitude of intracranial pressure and the content of vasogenic waves are useful to gauge cerebrospinal fluid dynamics. Infusion studies, although invasive, may help with the decision about surgery. They also provide basic information for further management of shunted patients, when complications, such as shunt blockage, under- and over-drainage, arise.

Association between intracranial, arterial pulse pressure amplitudes and cerebral autoregulation in head injury patients

Objective: To explore whether intracranial pulse pressure amplitudes relate to arterial pulse pressure amplitudes and whether correlations between time-related changes in intracranial and arterial pulse pressure amplitudes associate with indices of cerebral autoregulation.Methods: A total of 257 continuous and simultaneous intracranial pressure (ICP), arterial blood pressure (ABP) and middle cerebral artery (MCA) blood velocity recordings were obtained 1–14 days after ictus in 76 traumatic head injury patients and analysed retrospectively. Clinical outcome was assessed using the Glasgow outcome scale (GOS). Pulse pressure amplitudes of corresponding single ICP and ABP waves were correlated in consecutive 200 wave pairs. Mean ICP, mean ABP and mean ICP wave amplitudes, and mean and systolic MCA blood flow velocities, were computed in consecutive 6 second time windows. The indices of cerebral autoregulation PRx (moving correlation between mean ICP and mean ABP), and Mx and Sx (moving correlation between mean and systolic MCA blood velocity and cerebral perfusion pressure) were calculated over 4 minute periods and averaged over each recording.Results: Intracranial pulse pressure amplitudes were not related to arterial pulse pressure amplitudes (mean of Pearson's correlations coefficients: 0.04). Outcome was related to mean ICP, PRx and Sx (p ≤ 0.04, multiple regression analysis). Correlations between intracranial and arterial pulse pressure amplitudes were weakly related to PRx (Pearson's correlation coefficient: 0.16; p=0.01), but were not related to the indices of cerebral autoregulation Mx (Pearson's correlation coefficient: 0.07) and Sx (Pearson's correlation coefficient: 0.04).Conclusions: In this cohort of pressure recordings, we found no evidence of a correlation between intracranial and arterial blood pressure amplitudes. The correlation appeared not to be related to the state of cerebral autoregulation, although a weak correlation was found with pressure reactivity index PRx.

Association between intracranial pulse pressure levels and brain energy metabolism in a patient with an aneurysmal subarachnoid haemorrhage

This report addresses whether intracranial pulse pressure amplitudes are associated with brain energy metabolism, examined by intracerebral microdialysis. We present a 65-year-old female with an aneurysmal subarachnoid haemorrhage (SAH) from a left posterior communicating artery (PCOM) aneurysm. She underwent simultaneous intracranial pressure (ICP) monitoring and microdialysis (MD) as part of a diagnostic workout because of a lack of clinical improvement after long-term intensive care management. Over a 4-day period, a total of 128 samples of metabolites (glutamate, glycerol, lactate and pyruvate) were gathered, allowing retrospective comparisons with the levels of intracranial pulse pressure amplitudes (the mean ICP wave amplitude). During this 4-day period, mean ICP was normal (<15 mmHg), while mean ICP wave amplitude was high (>/=5 mmHg) in 47% of the recording time. There was a highly significant relationship between the levels of the mean ICP wave amplitude and the levels of glutamate, glycerol and lactate/pyruvate ratio. The levels of metabolites were increased when the mean ICP wave amplitude was >/=5 mmHg as compared with mean ICP wave amplitude levels <5 mmHg. We tentatively suggest that increased mean ICP wave amplitudes indicative of reduced intracranial compliance can be associated with brain ischaemia.

Pulse pressure waveform in hydrocephalus: what it is and what it isn't

Apart from its mean value, the pulse waveform of intracranial pressure (ICP) is an essential element of pressure recording. The authors reviewed their experience with the measurement and interpretation of ICP pulse amplitude by referring to a database of recordings in hydrocephalic patients. The database contained computerized pressure recordings from 2100 infusion studies (either lumbar or intraventricular) or overnight ICP monitoring sessions in patients suffering from hydrocephalus of various types (both communicating and noncommunicating), origins, and stages of management (shunt or no shunt). Amplitude was calculated from ICP waveforms by using a spectral analysis methodology. The appearance of a pulse waveform amplitude is positive evidence of a technically correct recording of ICP and helps to distinguish between postural and vasogenic variations in ICP. Pulse amplitude is significantly correlated with the amplitude of cerebral blood flow velocity (R = 0.4, p = 0.012) as assessed using Doppler ultrasonography. Amplitude is positively correlated with a mean ICP (R = 0.21 in idiopathic normal-pressure hydrocephalus [NPH]; number of cases 131; p < 0.01) and resistance to cerebrospinal fluid outflow (R = 0.22) but does not seem to be correlated with cerebrospinal elasticity, dilation of ventricles, or severity of hydrocephalus (NPH score). Amplitude increases slightly with age (R = 0.39, p < 0.01; number of cases 46). A positive association between pulse amplitude and increased ICP during an infusion study is helpful in distinguishing between hydrocephalus and predominant brain atrophy. A large amplitude is associated with a good outcome after shunting (positive predictive power 0.9), whereas a low amplitude has no predictive power in outcome prognostication (0.5). Pulse amplitude is reduced by a properly functioning shunt. Proper recording, detection, and interpretation of ICP pulse waveforms provide clinically useful information about patients suffering from hydrocephalus.