Intracranial Pressure-volume Relationship Research Articles

The intracranial pressure-volume relationship following decompressive hinge craniotomy compared to decompressive craniectomy-a human cadaver study.

Decompressive hinge craniotomy (DHC) is an alternative treatment option to decompressive craniectomy (DC) for elevated intracranial pressure (ICP). The aim of this study was to characterize the difference in pressure-volume relationship between DHC and DC. We compared the intracranial pressure-volume relationship in a human cadaver model following either DHC, DC, or fixing of the bone plate by titanium clamps. We inserted an intracranial expandable device in two human cadaver specimens, performed either DHC, DC, or bone plate fixation, and gradually increased the intracranial volume while measuring ICP. Following DHC, we also performed CT-scans at pre-defined intervals. Before ICP exceeded a threshold of 20mmHg, a fixed bone plate tolerated an increase of 130ml of intracranial volume, while DHC and DC allowed an increase of 190ml and 290ml, respectively. CT-derived calculations following DHC determined that the increase in intracranial volume at ICP 22mmHg was 65ml, the maximal increase of intracranial volume was 84ml, the maximal bone displacement was 21mm, and the bone plate volume to be 82ml. Manual stress test of the hinged bone plate did not allow misalignment or intracranial displacement of the bone plate. DHC increases the intracranial volume by up to 84ml and allows for approximately 60ml increase of intracranial volume before ICP exceeds 20mmHg. This indicates, when comparing with results from previous studies of herniation volumes, that DHC will be sufficient in many patients with head injury or cerebral infarction with treatment refractory intracranial hypertension.

Intracranial Pressure and the Role of the Vagus Nerve: A Hypothesis

There is reason to believe that the vagus nerve carries sensory afferent messages from the intracranial cavity as it does from the other body cavities. Considering the arachnoid granulations as a secretory apparatus instead of an organ transporting cerebrospinal fluid, a simple model can be built. Assuming that the arachnoid granulations produce nitric oxide in accordance with changes in the intracranial pressure, the jugular foramen with the vagus nerve lying just subendothelially is where this message would be received. Other chemical substances from the granulations or other intracranial tissues could of course also act as messengers. This would mean that the brain stem could adjust to changes in intracranial pressure with small changes in cerebral venous resistance. The general idea is that intracranial pressure is a passive function of the intracranial pressure-volume relationship. But the hypothesis suggests that the vagus nerve constantly mediates changes in intracranial pressure to the brain stem that can rapidly adjust cerebral venous resistance. This control is totally intracranial and easily overridden by considerable changes in absorption of spinal fluid or intracranial calamities. This article looks for clues in support of the idea that the vagus nerve mediates intracranial pressure changes to the brain stem.

Evaluation of an acute focal epidural mass model to characterize the intracranial pressure-volume relationship in healthy Beagles

To characterize the intracranial pressure-volume relationship (ICPVR) in dogs by use of an acute frontal-parietal mass lesion model. 7 healthy adult female Beagles. Dogs were anesthetized with isoflurane to achieve a surgical plane of anesthesia. A fiberoptic intracranial pressure (ICP) monitor was inserted to a depth of 1 cm in the parenchyma of the right frontal-parietal region of the brain. A Foley balloon-tipped catheter was placed in the epidural space of the left frontal-parietal area through a separate 1-cm burr hole. Baseline measurements were obtained with the balloon deflated. The balloon was then inflated incrementally with 0.5 mL of 0.9% NaCl solution every 10 minutes until ICP exceeded mean arterial blood pressure. Nonlinear regression analysis with 2-factor and 3-factor exponential equations was used to characterize the ICPVR. The mean baseline ICP was 11 mm Hg, with a 95% confidence interval of 2 to 20 mm Hg. The ICPVR was well characterized by 2-factor or 3-factor exponential equations for all dogs (R² > 0.93). Balloon volumes of > 1. 2 mL were associated with ICP > 20 mm Hg. Characterization of the ICPVR may provide clinically useful information regarding the safety of obtaining CSF from the atlanto-occipital space or implantation of brachytherapy catheters and for determining the need for decompressive craniectomy in dogs with acute intracranial disease. High ICP should be suspected in dogs that have an acute frontal-parietal mass lesion estimated to exceed 2% of the brain volume.

A whole-body mathematical model for intracranial pressure dynamics.

Most attempts to study intracranial pressure using lumped-parameter models have adopted the classical "Kellie-Monro Doctrine," which considers the intracranial space to be a closed system that is confined within the nearly-rigid skull, conserves mass, and has equal inflow and outflow. The present work revokes this Doctrine and develops a mathematical model for the dynamics of intracranial pressures, volumes, and flows that embeds the intracranial system in extensive whole-body physiology. The new model consistently introduces compartments representing the tissues and vasculature of the extradural portions of the body, including both the thoracic region and the lower extremities. In addition to vascular connections, a spinal-subarachnoid cerebrospinal fluid (CSF) compartment bridges intracranial and extracranial physiology allowing explict buffering of intracranial pressure fluctuations by the spinal theca. The model contains cerebrovascular autoregulation, regulation of systemic vascular pressures by the sympathetic nervous system, regulation of CSF production in the choroid plexus, a lymphatic system, colloid osmotic pressure effects, and realistic descriptions of cardiac output. To validate the model in situations involving normal physiology, the model's response to a realistic pulsatile cardiac output is examined. A well-known experimentally-derived intracranial pressure-volume relationship is recovered by using the model to simulate CSF infusion tests, and the effect on cerebral blood flow of a change in body position is also examined. Cardiac arrest and hemorrhagic shock are simulated to demonstrate the predictive capabilities of the model in pathological conditions.

A sudden arterial blood pressure decrease is compensated by an increase in intracranial blood volume.

A sudden decrease in arterial blood pressure (ABP) will cause the intracranial blood volume (IBV) to rise, despite the fact that arterial cerebral blood flow decreases. The aim of this study was to test the hypothesis that the increase in IBV is caused by a relative decrease of intracranial venous outflow. In 10 healthy volunteers we studied cerebral autoregulation (CA) by causing an ABP drop with bilaterally deflating leg cuffs. Blood flow velocities (BFV) in the middle cerebral artery and the straight sinus were monitored continuously with transcranial Doppler ultrasound, and the ABP with a non-invasive photoplethysmographic method. After transforming all variables in relative changes, the arterio-venous BFV difference was calculated. Allowing for diameter changes of the intracranial vessels of up to 10 %, and assuming a resting averaged cerebral blood flow of 55 to 60 ml per 100 g brain tissue per minute, an IBV increase of 9 to 10 ml could be calculated. In intact CA, a steep decrease of ABP results in an increase of intracranial blood volume. The transformation of our IBV data by means of the human intracranial pressure-volume relationship results in an excellent agreement with previously reported ICP increases of 10 mmHg. The increase in intracranial blood volume might be of clinical relevance in orthostatic dysregulation by increasing the ischemic tolerance of the brain before cerebral autoregulation becomes effective.

Interaction among autoregulation, CO2 reactivity, and intracranial pressure: a mathematical model.

The relationships among cerebral blood flow, cerebral blood volume, intracranial pressure (ICP), and the action of cerebrovascular regulatory mechanisms (autoregulation and CO2 reactivity) were investigated by means of a mathematical model. The model incorporates the cerebrospinal fluid (CSF) circulation, the intracranial pressure-volume relationship, and cerebral hemodynamics. The latter is based on the following main assumptions: the middle cerebral arteries behave passively following transmural pressure changes; the pial arterial circulation includes two segments (large and small pial arteries) subject to different autoregulation mechanisms; and the venous cerebrovascular bed behaves as a Starling resistor. A new aspect of the model exists in the description of CO2 reactivity in the pial arterial circulation and in the analysis of its nonlinear interaction with autoregulation. Simulation results, obtained at constant ICP using various combinations of mean arterial pressure and CO2 pressure, substantially support data on cerebral blood flow and velocity reported in the physiological literature concerning both the separate effects of CO2 and autoregulation and their nonlinear interaction. Simulations performed in dynamic conditions with varying ICP underline the existence of a significant correlation between ICP dynamics and cerebral hemodynamics in response to CO2 changes. This correlation may significantly increase in pathological subjects with poor intracranial compliance and reduced CSF outflow. In perspective, the model can be used to study ICP and blood velocity time patterns in neurosurgical patients in order to gain a deeper insight into the pathophysiological mechanisms leading to intracranial hypertension and secondary brain damage.

Impact of Cerebral Perfusion Pressure and Autoregulation on Intracranial Dynamics: A Modeling Study

The aim of this work was to study the impact of acute cerebral perfusion pressure (CPP) changes and autoregulation on cerebral hemodynamics, intracranial pressure (ICP), and estimation of the pressure-volume index (PVI) and the possible involvement of these factors in the development of secondary brain damage. The study was performed by using a mathematical model of intracranial hemodynamics and cerebrospinal fluid (CSF) dynamics. The model includes the biomechanics of proximal and distal arterial intracranial vessels, cerebral veins, and CSF circulation, the intracranial pressure-volume relationship, and the action of autoregulation mechanisms on proximal and distal vessels. In the case of normal intracranial dynamics, lowering mean systemic arterial pressure (SAP) in the range of 100 to 60 mm Hg causes only a mild ICP increase (+1-2 mm Hg). In contrast, in the case of severe impairment of intracranial dynamics (reductions in CSF outflow and storage capacity), even a modest mean SAP decrease (from 100 to 90 mm Hg) may induce a transient abrupt ICP rise (+30-40 mm Hg), because of the presence of a vicious cycle among CPP, cerebral blood volume, and ICP. In the case of intact autoregulation, PVI shows a mild positive correlation with SAP in the central autoregulation range and a strongly negative correlation below the autoregulation lower limit. In the case of impaired autoregulation, PVI exhibits higher values than in the regulated case, with a mild negative correlation with SAP. The present study emphasizes the relevant role of CPP changes, elicited by acute arterial hypotension, in intracranial dynamics. To achieve intracranial stability, CPP should be maintained above 80 to 90 mm Hg. PVI is significantly affected by the active response of cerebral vessels. Hence, it may provide misleading information on craniospinal capacity if it is considered as an autonomous index: rather, it should always be considered together with information on CPP and the status of autoregulation.

A non-linear haemodynamic model for the arterial pulsatile component of the intracranial pulse wave.

An indication that pressure pulses in cerebral arteries may play a role in the configuration of intracranial pressure pulsations is given by the observation that vasospasm of cerebral arteries narrows the amplitude of the intracranial pressure wave. The present work develops a mathematical model for the transmission of arterial pressure pulses across the compliant arterial wall to the surrounding intracranial space. Compliance of both the arterial segment and the intracranial space are considered. So as to retain accuracy at higher values of the mean intracranial pressure, a physiological range in which pulse transmission is enhanced due to lower pressure gradients but intracranial compliance is not necessarily decreased, a logistic fit is used to model the intracranial pressure-volume relationship. A sequence of approximations (with error bounds) is obtained for the induced intracranial pressure pulse amplitude as a function of arterial pulse amplitude, mean transmural pressure, and mean intracranial pressure. It is found that at higher mean intracranial pressures, where the usual exponential assumption for the intracranial pressure-volume curve loses validity, the amplitude of the transmitted arterial pressure pulse depends non-linearly on the mean intracranial pressure.

頭蓋内圧波を利用した収縮期脳血流の測定

As an index for estimation of cerebral vasospasm in ruptured aneurysms, systolic cerebral blood inflow rate (SCBIR) has been derived. The relationship between SCBIR and cortical CBF measured by a thermo-gradient flow meter was analyzed in 4 patients with SAH, and the relationship between them was statistically significant (CBF=0.04×SCBIR+33.7, r=0.7, p<0.05, n=10). SCBIR was reduced in all patients who seemed to have vasospasm as estimated by a reduction in CBF. On day 3, a moderate reduction in SCBIR was found in one patient even when no cortical CBF reduction was present. Shortly thereafter, however, cortical CBF started to decrease. Subsequently, SCBIR increased concomitant with the increase in cortical CBF in all surviving patients except one who eventually died one month after the onset. The total reduction in cortical CBF in the vasospasm period was-29.2±6.3% mean sd), while SCBIR at this time was-52.8±7.2% (mean±sd)(p<0.05).In conclusion: (1) SCBIR can be calculated by the ICP pulse wave and intracranial pressure volume relationship (PVI). (2) Generally, SCBIR was correlated with cortical CBF in the early stage of vasospasm and its recovery. However, the statistical test indicated that SCBIR was more sensitive than cortical CBF to the change in cerebral hemodynamics, especially, in the early phase of vasospasm. Thus, there is a possibility of early detection of cerebral vasospasm by analyzing the ICP pulse wave and pressure volume relationship.

Physiological features of the pressure-volume function of brain elasticity in man.

The intracranial pressure-volume relationship of brain elasticity was examined in 20 patients with suspected disorders of the cerebrospinal fluid (CSF) system. Elasticity measurements were made as the patients were studied with a servo-controlled lumbar infusion technique to measure CSF absorptive capacity. The data were evaluated to determine the relationship between intracranial pressure (ICP) and volume, and between ICP variability and the level of ICP. The results confirm the exponential nature of the pressure-volume elasticity function in patients who are not critically ill. Eight of the 20 patients were shown to have normal CSF absorptive capacities, and there was no difference between their elasticity measurements and those of patients with absorptive defects. In addition, ICP variability was shown to be linearly related to the actual level of ICP. The physiological features of the pressure-volume elasticity function are reviewed. Based on these considerations, the clinical value and significance of elasticity measurements is questioned.