Cerebrospinal Compensatory Reserve Research Articles

Relationship between the shape of intracranial pressure pulse waveform and computed tomography characteristics in patients after traumatic brain injury

BackgroundMidline shift and mass lesions may occur with traumatic brain injury (TBI) and are associated with higher mortality and morbidity. The shape of intracranial pressure (ICP) pulse waveform reflects the state of cerebrospinal pressure–volume compensation which may be disturbed by brain injury. We aimed to investigate the link between ICP pulse shape and pathological computed tomography (CT) features.MethodsICP recordings and CT scans from 130 TBI patients from the CENTER-TBI high-resolution sub-study were analyzed retrospectively. Midline shift, lesion volume, Marshall and Rotterdam scores were assessed in the first CT scan after admission and compared with indices derived from the first 24 h of ICP recording: mean ICP, pulse amplitude of ICP (AmpICP) and pulse shape index (PSI). A neural network model was applied to automatically group ICP pulses into four classes ranging from 1 (normal) to 4 (pathological), with PSI calculated as the weighted sum of class numbers. The relationship between each metric and CT measures was assessed using Mann–Whitney U test (groups with midline shift > 5 mm or lesions > 25 cm3 present/absent) and the Spearman correlation coefficient. Performance of ICP-derived metrics in identifying patients with pathological CT findings was assessed using the area under the receiver operating characteristic curve (AUC).ResultsPSI was significantly higher in patients with mass lesions (with lesions: 2.4 [1.9–3.1] vs. 1.8 [1.1–2.3] in those without; p << 0.001) and those with midline shift (2.5 [1.9–3.4] vs. 1.8 [1.2–2.4]; p < 0.001), whereas mean ICP and AmpICP were comparable. PSI was significantly correlated with the extent of midline shift, total lesion volume and the Marshall and Rotterdam scores. PSI showed AUCs > 0.7 in classification of patients as presenting pathological CT features compared to AUCs ≤ 0.6 for mean ICP and AmpICP.ConclusionsICP pulse shape reflects the reduction in cerebrospinal compensatory reserve related to space-occupying lesions despite comparable mean ICP and AmpICP levels. Future validation of PSI is necessary to explore its association with volume imbalance in the intracranial space and a potential complementary role to the existing monitoring strategies.

Intracranial pressure waveform characteristics in idiopathic normal pressure hydrocephalus and late-onset idiopathic aqueductal stenosis

BackgroundIdiopathic normal pressure hydrocephalus (iNPH) and late-onset idiopathic aqueductal stenosis (LIAS) are two forms of chronic adult hydrocephalus of different aetiology. We analysed overnight intracranial pressure (ICP) monitoring to elucidate ICP waveform changes characteristic for iNPH and LIAS to better understand pathophysiological processes of both diseases.Methods 98 patients with iNPH and 14 patients with LIAS from two neurosurgical centres were included. All patients underwent diagnostic overnight computerised ICP monitoring with calculation of mean ICP, ICP heartbeat related pulse wave amplitude calculated in the frequency domain (AMP) and the time domain (MWA), index of cerebrospinal compensatory reserve (RAP) and power of slow vasogenic waves (SLOW).ResultsICP was higher in LIAS than iNPH patients (9.3 ± 3.0 mmHg versus 5.4 ± 4.2 mmHg, p = 0.001). AMP and MWA were higher in iNPH versus LIAS (2.36 ± 0.91 mmHg versus 1.81 ± 0.59 mmHg for AMP, p = 0.012; 6.0 ± 2.0 mmHg versus 4.9 ± 1.2 mmHg for MWA, p = 0.049). RAP and SLOW indicated impaired reserve capacity and compliance in both diseases, but did not differ between groups. INPH patients were older than LIAS patients (77 ± 6 years versus 54 ± 14 years, p < 0.001).ConclusionsICP is higher in LIAS than in iNPH patients, likely due to the chronically obstructed CSF flow through the aqueduct, but still in a range considered normal. Interestingly, AMP/MWA was higher in iNPH patients, suggesting a possible role of high ICP pulse pressure amplitudes in iNPH pathophysiology. Cerebrospinal reserve capacity and intracranial compliance is impaired in both groups and the pressure-volume relationship might be shifted towards lower ICP values in iNPH. The physiological influence of age on ICP and AMP/MWA requires further research.

Influence of mild-moderate hypocapnia on intracranial pressure slow waves activity in TBI

BackgroundIn traumatic brain injury (TBI) the patterns of intracranial pressure (ICP) waveforms may reflect pathological processes that ultimately lead to unfavorable outcome. In particular, ICP slow waves (sw) (0.005–0.05 Hz) magnitude and complexity have been shown to have positive association with favorable outcome. Mild-moderate hypocapnia is currently used for short periods to treat critical elevations in ICP. Our goals were to assess changes in the ICP sw activity occurring following sudden onset of mild-moderate hypocapnia and to examine the relationship between changes in ICP sw activity and other physiological variables during the hypocapnic challenge.MethodsICP, arterial blood pressure (ABP), and bilateral middle cerebral artery blood flow velocity (FV), were prospectively collected in 29 adult severe TBI patients requiring ICP monitoring and mechanical ventilation in whom a minute volume ventilation increase (15–20% increase in respiratory minute volume) was performed as part of a clinical CO2-reactivity test. The time series were first treated using FFT filter (pass-band set to 0.005–0.05 Hz). Power spectral density analysis was performed. We calculated the following: mean value, standard deviation, variance and coefficient of variation in the time domain; total power and frequency centroid in the frequency domain; cerebrospinal compliance (Ci) and compensatory reserve index (RAP).ResultsHypocapnia led to a decrease in power and increase in frequency centroid and entropy of slow waves in ICP and FV (not ABP). In a multiple linear regression model, RAP at the baseline was the strongest predictor for the decrease in the power of ICP slow waves (p < 0.001).ConclusionIn severe TBI patients, a sudden mild-moderate hypocapnia induces a decrease in mean ICP and FV, but also in slow waves power of both signals. At the same time, it increases their higher frequency content and their morphological complexity. The difference in power of the ICP slow waves between the baseline and the hypocapnia period depends on the baseline cerebrospinal compensatory reserve as measured by RAP.

Observations on the Cerebral Effects of Refractory Intracranial Hypertension After Severe Traumatic Brain Injury

BackgroundRaised intracranial pressure (ICP) is a prominent cause of morbidity and mortality after severe traumatic brain injury (TBI). However, in the clinical setting, little is known about the cerebral physiological response to severe and prolonged increases in ICP.MethodsThirty-three severe TBI patients from a single center who developed severe refractory intracranial hypertension (ICP > 40 mm Hg for longer than 1 h) with ICP, arterial blood pressure, and brain tissue oxygenation (PBTO2) monitoring (subcohort, n = 9) were selected for retrospective review. Secondary parameters reflecting autoregulation (including pressure reactivity index—PRx, which was available in 24 cases), cerebrospinal compensatory reserve (RAP), and ICP pulse amplitude were calculated.ResultsPRx deteriorated from 0.06 ± 0.26 a.u. at baseline levels of ICP to 0.57 ± 0.24 a.u. (p < 0.0001) at high levels of ICP (> 50 mm Hg). In 4 cases, PRx was impaired (> 0.25 a.u.) before ICP was raised above 25 mm Hg. Concurrently, PBTO2 decreased from 27.3 ± 7.32 mm Hg at baseline ICP to 12.68 ± 7.09 mm Hg at high levels of ICP (p < 0.001). The pulse amplitude of the ICP waveform increased with increasing ICP but showed an ‘upper breakpoint’—whereby further increases in ICP lead to decreases in pulse amplitude—in 6 out of the 33 patients.DiscussionSevere intracranial hypertension after TBI leads to decreased brain oxygenation, impaired pressure reactivity, and changes in the pulse amplitude of ICP. Impaired pressure reactivity may denote increased risk of developing refractory intracranial hypertension in some patients.

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.

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.

Slow vasogenic fluctuations of intracranial pressure and cerebral near infrared spectroscopy—an observational study

Increased slow-wave activity in intracranial pressure (ICP) signifies an exhausted cerebrospinal compensatory reserve across a range of conditions. In this study, we attempted to describe synchronisation between slow waves of ICP and of near-infrared spectroscopy (NIRS) variables during controlled elevation of ICP. Nineteen patients presenting with symptomatic hydrocephalus underwent a Computerised Infusion Test. NIRS-derived indices, ICP and arterial blood pressure (ABP) were recorded simultaneously. ICP increased from 9.3 (6.0) mmHg to a 17.1 (8.9) mmHg during infusion. Slow waves in ICP were accompanied by concurrent waves in each NIRS variable (including deoxygenated haemoglobin (Hb) and oxygenated haemoglobin (HbO2)) with a mean coherence of >0.7 and no significant phase shift. In the same bandwidth (0.3-1.8 min(-1)), ABP fluctuations occurred with a coherence of 0.77 and phase lead of 40° with respect to ICP. The power of ICP slow waves increased significantly during infusion plateau with a corresponding increase in power of Hb waves. Slow fluctuations in cerebral oximetry as detected by NIRS coincide with and are implicated in the origin of ICP slow waves and increases during periods of exhausted cerebrospinal compensatory reserve. NIRS may be used as a non-invasive marker of increased ICP slow waves (and therefore reduced CSF compensatory reserve).

Cerebrospinal compensation of pulsating cerebral blood volume in hydrocephalus

Objective: The aim of the study was to develop a computational method for the assessment of brain pressure compensation of cerebrospinal arterial blood inflow. The method was verified using clinical recordings performed during infusion studies in a group of patients diagnosed with hydrocephalus.Materials and methods: We studied 27 patients suspected of having normal pressure hydrocephalus. The infusion test was used to measure the resistance to cerebrospinal fluid outflow, and the elastance coefficient was performed together with recording of the blood flow velocity in the middle cerebral artery. From the blood flow velocity waveform, the pulsatile pattern of increasing cerebral blood volume during one heart cycle was evaluated as a time integral of the arterial blood flow velocity minus the mean arterial blood flow. Cerebrospinal 'compliance index' (Ci) was calculated as the amplitude of change in blood volume divided by the amplitude of intracranial pressure pulse waveform.Results: Compliance index Ci decreased during the infusion test, proportionally inverse to the rise in intracranial pressure controlled by the external infusion of saline (R=−0·76; p<0·005). A relative change in compliance (from baseline to the plateau phase of the study) was positively associated with greater brain elasticity (R=0·61; p<0·005) and poorer compensatory reserve at the phase of infusion (R=0·51; p=0·009)Conclusion: Ci decreases during the infusion study and seems to well replicate the relative changes in cerebrospinal compensatory reserve in hydrocephalus.

INDEX OF CEREBROSPINAL COMPENSATORY RESERVE IN HYDROCEPHALUS

An index of cerebrospinal compensatory reserve (RAP) has been introduced as a potential descriptor of neurological deterioration after head trauma. It is numerically computed as a linear correlation coefficient between the mean intracranial pressure and the pulse amplitude of the pressure waveform. We explore how RAP varies with different forms of physiological or nonphysiological intracranial volume loads in adult hydrocephalus, with and without a functioning cerebrospinal fluid (CSF) shunt. A database of intracranial pressure recordings during CSF infusion studies and overnight monitoring in hydrocephalic patients was reviewed for clinical comparison of homogeneous subgroups of patients with hypothetical differences of pressure-volume compensatory reserve. The database includes 980 patients of mixed etiology: idiopathic normal pressure hydrocephalus (NPH), 47%; postsubarachnoid hemorrhage NPH, 12%; noncommunicating hydrocephalus, 22%; others, 19%. All CSF compensatory parameters were calculated by using intracranial pressure waveforms. In NPH, RAP correlated strongly with the resistance to CSF outflow (r(s) = 0.35; P = 0.045), but weakly correlated with ventriculomegaly (r(s) = 0.13; P = 0.41). In idiopathic nonshunted NPH patients, RAP did not correlate significantly with elasticity calculated from the CSF infusion test (r(s) = 0.11; P = 0.21). During infusion studies, RAP increased in comparison to values recorded at baseline (from a median of 0.45-0.86, P = 0.14 * 10(-8)), indicating a narrowing of the volume-pressure compensatory reserve. During B-waves associated with the REM (rapid eye movement) phase of sleep, RAP increased from a median of 0.53 to 0.89; P = 1.2 * 10(-5). After shunting, RAP decreased (median before shunting, 0.59; median after shunting, 0.34; P = 0.0001). RAP also showed the ability to reflect the functional state of the shunt (patent shunt median, 0.36; blocked shunt median, 0.84; P = 0.0002). RAP appears to characterize pressure-volume compensatory reserve in patients with hydrocephalus.

O.039 Index of cerebrospinal compensatory reserve in hydrocephalus

Hydrocephalus (HC) caused by blockade of ventricular cerebrospinal fluid (CSF) pathways is denoted non-communicating HC. One issue not previously addressed is how the prevalence of cardiovascular disease compares between patients with non-communicating HC and the general population.We examined whether the prevalence of cardiovascular disease (arterial hypertension, angina pectoris, cardiac infarction, and diabetes) differed between cases with non-communicating HC and a general control population, represented by participants of the North-Trøndelag Health 3 Survey (The HUNT3 Survey). A second control group consisted of patients with communicating hydrocephalus (idiopathic normal pressure hydrocephalus, iNPH).The study included 50 cases with non-communicating HC (53.4 + 10.5 years), and two control cohorts: 35,413 participants of the HUNT3 Survey (52.8 + 9.6 years), and 176 iNPH patients (61.2 + 8.3 years). All individuals were aged 35–70 years. Among the non-communicating HC patients, the results showed increased prevalence for arterial hypertension (males), cardiac infarction (females), and diabetes (females), as compared with the HUNT3 control group with significant odds ratio estimates. However, the prevalence of cardiovascular disease did not significantly differ between patients with non-communicating HC or iNPH. In patients with either non-communicating HC or iNPH and elevated pulsatile intracranial pressure (ICP) during overnight monitoring, the prevalence of diabetes was increased.This study showed significantly increased prevalence of cardiovascular disease in non-communicating HC, indicating an association between cardiovascular disease and the development of non-communicating HC. Further, diabetes was associated with abnormal pulsatile ICP in both non-communicating HC and iNPH patients.

Wavelet assessment of cerebrospinal compensatory reserve and cerebrovascular reactivity

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 = 1×10−4 (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.

Predicting the response of intracranial pressure to moderate hyperventilation

Hyperventilation may cause brain ischaemia after traumatic brain injury. However, moderate reductions in PaCO(2) are still an option in the management of raised intracranial pressure (ICP) under some circumstances. Being able to predict the ICP-response to such an intervention would be advantageous. We investigated the ability of pre-hyperventilation ICP and cerebrospinal compensatory reserve to predict the reduction in ICP achievable with moderate hyperventilation in head injured patients. Thirty head injured patients requiring sedation and mechanical ventilation were investigated. ICP was monitored via an intraparenchymal probe and intracranial cerebrospinal compensatory reserve was assessed using an index (R(ap)) based on the relationship between mean ICP and its pulse amplitude. Measurements were made at a constant level of PaCO(2) during a 20-minute baseline period. The patients were then subjected to an acute decrease in PaCO(2) of approximately 1 kPa and, after an equilibration period of 10 minutes, measurements were again made at a constant level of PaCO(2) for a further 20 minutes. A multiple linear regression model, incorporating baseline PaCO(2), ICP, and R(ap) was used to identify the relevant predictors of ICP reduction. Baseline ICP and R(ap) were both significant predictors of ICP-reduction (p=0.02 and 0.001 respectively) with R(ap) being the more powerful parameter. A model based on cerebrospinal compensatory reserve and ICP can predict the achievable ICP-reduction and may potentially be used to optimise patient selection and intensity of hyperventilation.

Intracranial hypertension: what additional information can be derived from ICP waveform after head injury?

Although intracranial hypertension is one of the important prognostic factors after head injury, increased intracranial pressure (ICP) may also be observed in patients with favourable outcome. We have studied whether the value of ICP monitoring can be augmented by indices describing cerebrovascular pressure-reactivity and pressure-volume compensatory reserve derived from ICP and arterial blood pressure (ABP) waveforms. 96 patients with intracranial hypertension were studied retrospectively: 57 with fatal outcome and 39 with favourable outcome. ABP and ICP waveforms were recorded. Indices of cerebrovascular reactivity (PRx) and cerebrospinal compensatory reserve (RAP) were calculated as moving correlation coefficients between slow waves of ABP and ICP, and between slow waves of ICP pulse amplitude and mean ICP, respectively. The magnitude of 'slow waves' was derived using ICP low-pass spectral filtration. The most significant difference was found in the magnitude of slow waves that was persistently higher in patients with a favourable outcome (p<0.00004). In patients who died ICP was significantly higher (p<0.0001) and cerebrovascular pressure-reactivity (described by PRx) was compromised (p<0.024). In the same patients, pressure-volume compensatory reserve showed a gradual deterioration over time with a sudden drop of RAP when ICP started to rise, suggesting an overlapping disruption of the vasomotor response. Indices derived from ICP waveform analysis can be helpful for the interpretation of progressive intracranial hypertension in patients after brain trauma.

Testing of cerebrospinal compensatory reserve in shunted and non-shunted patients: a guide to interpretation based on an observational study.

To design a computerised infusion test to compensate for the disadvantages of Katzman's lumbar infusion method: inadequate accuracy of estimation of the resistance to cerebrospinal fluid outflow and poor predictive value in normal pressure hydrocephalus. Accuracy was improved by intracranial pressure signal processing and model analysis for measurement of cerebrospinal compensatory variable. These include the CSF outflow resistance, brain compliance, pressure-volume index, estimated sagittal sinus pressure, CSF formation rate, and other variables. Infusion may be made into the lumbar space, ventricles, or, when assessing shunt function in vivo, the shunt chamber. The computerised test has been used for five years in a multicentre study in 350 hydrocephalic patients of various ages, aetiologies, and states of cerebrospinal compensation. The principles of using the test to characterise different types of CSF circulatory disorders in patients presenting with ventricular dilatation, including brain atrophy and normal and high pressure hydrocephalus, are presented and illustrated. Previous studies showed a positive correlation between cerebrospinal compensatory variables and the results of shunting, but such a prediction remains difficult in idiopathic normal pressure hydrocephalus, particularly in elderly patients. The technique is helpful in the assessment of shunt malfunction, including posture-related overdrainage, over-drainage related to the nocturnal B wave activity, and proximal or distal shunt obstruction. The appendix presents an introduction of the mathematical modelling of CSF pressure volume-compensation included in computerised infusion test software.

Cerebrospinal compensation in hydrocephalic children.

One hundred and fifteen cases of hydrocephalus in children were analysed. Cerebrospinal compensatory reserve was assessed by a computerized, constant rate, lumbar infusion test. Head circumference and ventricular size were measured and a psychometric examination carried out. A classification of hydrocephalus based on resting cerebrospinal fluid pressure (CSFP) and resistance to cerebrospinal fluid outflow (RCSF) was introduced. Parameters of compensatory reserve were compared in atrophy (low CSFP, low RCSF), normal-pressure hydrocephalus (low CSFP, increased RCSF), non-communicating hydrocephalus (high CSFP, low RCSF) and acute hydrocephalus (high CSFP and increased RCSF). Significant differences were found between the factors describing compensatory ability in these groups. Sixty-two patients could be classified on the basis of resting CSFP and RCSF. Differentiation between the types of hydrocephalus was shown to be more accurate when all variables measured during the pressure-volume test were considered. The patterns of the time courses of CSFP during rate infusion tests in the different types of hydrocephalus are presented.