Baseline Intracranial Pressure Research Articles

Characterization of Interdependency Between Intracranial Pressure and Heart Variability Signals: A Causal Spectral Measure and a Generalized Synchronization Measure

Causal coherence and generalized synchronization (GS) index were extracted from beat-to-beat mean intracranial pressure (ICP) and intervals between consecutive normal sinus heart beats (RR interval) that were recorded from 12 patients undergoing normal pressure hydrocephalus diagnosis. Data were organized into two groups including an ICP B-Wave group and a baseline control group. Maximal classic coherence (CC) between ICP and RR interval within [0.04, 0.15] Hz was found to be significantly greater than zero for both B-Wave and control groups with B-Wave CC greater than that of the baseline group. Causal coherence analysis further revealed that feedforward coherence due to RR interval's effect on ICP always exists for both B-Wave and baseline ICP state and no significant difference exists between two groups. On the other hand, feedback coherence from ICP to RR interval was enhanced during the occurrence of B-Wave. This finding regarding the enhanced directional, from ICP to RR interval, coupling between ICP and RR interval was also confirmed by a modified GS measure.

Seizures Lead to Elevation of Intracranial Pressure in Children Undergoing Invasive EEG Monitoring

To study the effects of intracranial subdural grid electrode placement and seizures on intracranial pressure (ICP) in children undergoing invasive EEG monitoring. Sixteen children with pharmacoresistant epilepsy who underwent two-stage epilepsy surgery with subdural grid placement were included in the study. The ICP was recorded at baseline and with each seizure prospectively. A variety of seizure parameters including type of seizure, length of seizure, extent of seizure spread, and number of subdural grid electrodes inserted were analyzed retrospectively and correlated with the change in ICP. A total of 48 seizures in 16 children were studied. The mean baseline ICP correlated positively with age of the child. Generalized tonic-clonic seizures were associated with the highest rise in ICP. Similarly, ICP rise was associated with seizures involving more electrodes indicating a larger area of brain participating in the seizure. Seizures in general and generalized tonic-clonic seizures, in particular, increase ICP temporarily in patients who are undergoing invasive EEG monitoring with subdural grids.

THE INFLUENCE OF INTRA-ABDOMINAL HYPERTENSION ON THE CENTRAL NERVOUS SYSTEM: CURRENT INSIGHTS AND CLINICAL RECOMMENDATIONS, IS IT ALL IN THE HEAD?

Introduction: Intra-abdominal hypertension (IAH) and abdominal compartment syndrome are a common occurrence in ICU patients. The deleterious effects of IAH on organ function are well known and increasingly appreciated in recent years, especially where renal and respiratory function are concerned.Methods: This review will focus on the available literature from the last years. A Medline and PubMed search was performed in order to find an answer to the question “What is the impact of increased IAP on neurologic function in the critically ill?”Results: The amount of data on the influence of IAH on the central nervous system is more scarce, but several animal and human studies have demonstrated a clear correlation between intra-abdominal pressure (IAP) and intracranial pressure (ICP). This correlation is probably due to transmission of the increased IAP to the thorax leading to increased intrathoracic, pleural pressure and central venous pressure, decreased venous return from the brain and increased ICP. This hypothesis is supported by the observation that the increase in ICP is abolished when a sternotomy and pleuropericardotomy are performed, and by the fact that abdominal decompression has produced good results in treating refractory intracranial hypertension (ICH) in patients with both IAH and ICH.Conclusions: A close relationship between IAP and ICP has been observed in several animal and human studies. The clinical impact of this association is dependent on the baseline ICP and the compensatory reserve of the patient. Some studies have reported good results in treating refractory ICH by abdominal decompression in patients with concomitant IAH. Monitoring of IAP and ICP in risk patients is essential.

Craniosacral Therapy: The Effects of Cranial Manipulation on Intracranial Pressure and Cranial Bone Movement

Quasi-experimental design. To determine if physical manipulation of the cranial vault sutures will result in changes of the intracranial pressure (ICP) along with movement at the coronal suture. Craniosacral therapy is used to treat conditions ranging from headache pain to developmental disabilities. However, the biological premise for this technique has been theorized but not substantiated in the literature. Thirteen adult New Zealand white rabbits (oryctolagus cuniculus) were anesthetized and microplates were attached on either side of the coronal suture. Epidural ICP measurements were made using a NeuroMonitor transducer. Distractive loads of 5, 10, 15, and 20 g (simulating a craniosacral frontal lift technique) were applied sequentially across the coronal suture. Baseline and distraction radiographs and ICP were obtained. One animal underwent additional distractive loads between 100 and 10,000 g. Plate separation was measured using a digital caliper from the radiographs. Two-way analysis of variance was used to assess significant differences in ICP and suture movement. No significant differences were noted between baseline and distraction suture separation (F = 0.045; P>.05) and between baseline and distraction ICP (F = 0.279; P>.05) at any load. In the single animal that underwent additional distractive forces, movement across the coronal suture was not seen until the 500-g force, which produced 0.30 mm of separation but no corresponding ICP changes. Low loads of force, similar to those used clinically when performing a craniosacral frontal lift technique, resulted in no significant changes in coronal suture movement or ICP in rabbits. These results suggest that a different biological basis for craniosacral therapy should be explored.

Combined Transfer Function Analysis and Modelling of Cerebral Autoregulation

The clinical importance of cerebral autoregulation has resulted in a significant body of literature that attempts both to model the underlying physiological processes and to estimate the mathematical relationships between clinically measurable variables, the most common of which are Arterial Blood Pressure and Cerebral Blood Flow Velocity. These approaches have, however, rarely been used together to interpret clinical data. A simple model of cerebral autoregulation is thus proposed here, based on a flow dependent feedback mechanism with gain and time constant that adjusts arterial compliance. Analysis of this model shows that it closely approximates a second order system for typical values of physiological parameters. The model parameters can be optimally estimated from available experimental data for the Impulse Response (IR), yielding physiologically reasonable values, although there is one free parameter that must be fixed. The effects of changes in feedback gain and time constant are found to be significant on the predicted IR and can thus be estimated robustly from experimental data. The effects of elevated baseline Intracranial Pressure (ICP) are found to be exactly equivalent to a reduced feedback gain, although the solution is much less sensitive to the former effect. A transfer function approach can be used to estimate autoregulation status clinically using a physiologically-based model, thus providing greater insight into the processes that govern cerebral autoregulation.

The Effect of Etomidate on Intracranial Pressure and Systemic Blood Pressure in Pediatric Patients with Severe Traumatic Brain Injury

To evaluate the effects of single-dose etomidate in pediatric patients with intracranial hypertension after severe traumatic brain injury. Patients admitted to the pediatric intensive care unit with severe traumatic brain injury were enrolled with the informed consent of their guardians. The experimental intervention was a single dose of etomidate 0.3 mg/kg intravenously. This dosage was administered only when enrolled patients had acute elevations of intracranial pressure (ICP) to over 20 mm Hg for over 5 minutes. ICP and mean arterial pressure (MAP) were monitored continuously. ICP and MAP values for 6 consecutive 5-minute intervals after etomidate administration were averaged for all patients and compared with baseline. Eight patients were enrolled. Mean ICP after etomidate administration was significantly lower than baseline ICP for each 5-minute interval (P < 0.05). The mean MAP for all patients increased from baseline during the first 5-minute interval, but this change was not statistically significant. No patient's MAP decreased below baseline at any time point. In pediatric patients with severe traumatic brain injury, single-dose etomidate administration resulted in statistically significant reductions in ICP and improvement in cerebral perfusion pressure without significantly altering MAP.

Resistance to CSF outflow depends upon duration of symptoms in patients with Normal Pressure Hydrocephalus

Background Cerebrospinal Fluid (CSF) pressure-volume compensatory parameters may change over time under pathological and normal circumstances. Normal ageing may affect CSF compensation: the resistance to CSF outflow increases and the formation of CSF decreases with age. In acute hydrocephalus after subarachnoid haemorrhage, baseline intracranial pressure (ICP) and resistance to CSF outflow acutely increase but they may return towards baseline over the next few weeks. Idiopathic Normal Pressure Hydrocephalus (iNPH) awaits longitudinal studies. Is NPH always the late (compensated) stage of acute hydrocephalus? Are the CSF compensatory parameters invariant in time (counting from the onset of clinical symptoms) or do they change with time?

Effects of pressure- and volume-controlled inverse ratio ventilation on haemodynamic variables, intracranial pressure and cerebral perfusion pressure in rabbits: a model of subarachnoid haemorrhage under isoflurane anaesthesia.

An inverse I : E ratio (inspiratory time > expiratory time) may have benefits in patients suffering trauma who requiring lung ventilation. However, this application may be deleterious if there is concomitant head injury. We aimed to determine the physiological effects of pressure- and volume-controlled modes of inverse ratio (I : E = 2 : 1) ventilation of the lungs, while maintaining normocapnia, in a rabbit model of raised intracranial pressure (ICP). New Zealand White rabbits were anaesthetized with isoflurane and a tracheostomy was performed. Subarachnoid haemorrhage was simulated in two groups by injecting blood into the cisterna magna. Groups 1 and 2 (n = 6, each), controls, were compared with Groups 3 and 4 (n = 6, each) with the simulated subarachnoid haemorrhage. Each ventilation mode was used with an I : E ratio of 2 : 1 for 30 min. Mean arterial pressure (MAP), ICP, cerebral perfusion pressure (CPP), mean airway pressure (P(AW)) and arterial blood-gas status were measured. Both modes increased mean P(AW) (P < 0.02). This increase was greater with the volume-controlled mode (P < 0.02). The baseline value averaged 5.8 +/- 0.4 and 5.6 +/- 0.3 mmHg in Groups 3 and 4, respectively, and increased to 7.8 +/- 0.3 and 10.8 +/- 0.4 mmHg. Inducing subarachnoid haemorrhage increased ICP and MAP (P < 0.02). Baseline ICPs were 10.3 +/- 0.5 and 10.3 +/- 0.4 mmHg in Groups 1 and 2, respectively, whereas they were 25.4 +/- 1.2 and 25.8 +/- 0.8 mmHg in Groups 3 and 4. However, ICP, MAP and CPP did not differ significantly according to the mode. An already raised ICP was altered by the application of induced mean PAW increases as a consequence of inverse ratio ventilation of the lungs with normocapnia.

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 Pressure Changes during Rapid Sequence Intubation: A Swine Model

Controversy and speculation exist regarding intracranial pressure (ICP) changes produced by various combinations of rapid sequence intubation (RSI) agents. In this pilot study, we sought to develop a swine model to investigate these changes in classic RSI. Eight adult swine were instrumented with arterial and intracranial pressure monitors. Four different versions of rapid sequence intubation were then performed sequentially in each animal in a crossover trial design: regimen 1, thiopental; regimen 2, thiopental and succinylcholine; regimen 3, lidocaine, thiopental, and succinylcholine; and regimen 4, pancuronium, lidocaine, thiopental, and succinylcholine. ICP and hemodynamic parameters were recorded and compared. Trials were excluded from analysis if baseline ICP measurements were unstable or if intubation was difficult. Peak changes in ICP were noted at 2 to 3 minutes after administration of induction agents. Mean values for peak changes in ICP were as follows: regimen 1 (n = 5), 3.6 mm Hg (95% confidence interval [CI], 1.0-6.2 mm Hg); regimen 2 (n = 9), 13.6 mm Hg (95% CI, 9.6-17.6 mm Hg); regimen 3 (n = 2), 16.0 mm Hg (95% CI, -34.8-66.8 mm Hg); and regimen 4 (n = 3), 12.0 mm Hg (95% CI, -8.3-32.3 mm Hg). The model is effective. It enables investigators to examine the aggregate ICP effects of combinations of RSI medications. RSI regimens with paralysis produced threefold increases in peak ICP change compared with the sedation-only regimen. Pretreatment agents did not affect ICP changes. Future investigations can examine other agents and add experimental manipulation of ICP to simulate head injury physiology. Additional parameters including cerebral metabolism and/or oxygenation may also be explored.

Relationship between valve opening pressure, body position, and intracranial pressure in normal pressure hydrocephalus: paradigm for selection of programmable valve pressure setting.

There is little scientific basis for guidance in selecting the optimal valve for the treatment of normal pressure hydrocephalus. The aim of this study was to determine the programmable valve opening pressure setting that would result in a slight reduction in intracranial pressure (ICP) after a ventriculoperitoneal shunt is implanted. We also assessed whether shunt-induced ICP could be predicted on the basis of a simple hydrodynamic equation. In this prospective study of 11 patients with normal pressure hydrocephalus, ICP was measured before and after implantation of a shunt incorporating a programmable valve without an antisiphon device. Pressure measurements, including intraperitoneal pressure, were recorded at body angles ranging from 0 to 55 degrees and at valve settings ranging from 30 to 200 mm H(2)O. Measured ICP values were compared with values computed using a simple hydrodynamic equation. Even at a valve setting greater than the mean baseline ICP (200 mm H(2)O), the supine ICP was significantly lower than the baseline value (baseline ICP, 164 +/- 64 mm H(2)O; postoperative ICP, 125 +/- 69 mm H(2)O, P = 0.04). Valve pressure did not equate 1:1 with the measured postoperative ICP. Comprehensive ICP measurements at upright body positions demonstrated a stepwise reduction in ICP rather than a precipitous decline as a result of so-called siphoning. This study indicates that very high valve opening pressure settings may be optimal for the initial treatment of normal pressure hydrocephalus. The relationship between ICP and opening pressure valves is linear but not predicted by simple hydrodynamics.

Slight elevation of baseline intracranial pressure after fluid infusion into CSF space in patients with hydrocephalus

Objective: To investigate the elevation of resting cerebrospinal fluid (CSF) pressure recorded after a CSF infusion test in patients with hydrocephalus.Material and methods: Fifty patients (30 men and 20 women, mean age 68 ± 13 years) with ventriculomegaly and clinical symptoms of normal pressure hydrocephalus have been studied. Lumbar (56%) or intraventricular (44%) computerized infusion studies were performed to investigate the hydrodynamics of CSF. After infusion, the fall in ICP was recorded until a steady-state level was achieved and the difference between pre- and post-infusion resting ICP was calculated (ΔICP).Results: A positive difference (>2 mm Hg) between post- and pre-infusion resting ICP was identified in 31 infusion tests (62%). The mean value of the difference was 6.7 with an SD of 3.5 mm Hg. The patients who demonstrated this phenomenon had a greater elastance coefficient (p>0.05); ΔICP was positively correlated with age (R=0.27; p=0.03), with the size of the brain's ventricles (R=0.63, p=0.03) and inversely with the severity of clinical impairment (Stein-Langfitt score R=–0.61, p=0.02; normal pressure hydrocephalus score: R=0.54; p<0.05). ΔICP was independent of the site of infusion (lumbar or ventricular).Conclusion: In patients with a 'stiffer' brain, ICP returns to the resting level after the infusion test at a slightly higher level than before the test. The magnitude of this increase is greater when ventricles are more dilated and clinical symptoms are less severe.

811 Relationship between Valve Opening Pressure, Body Position, and Intracranial Pressure in Normal-pressure Hydrocephalus: Paradigm for Selection of Programmable Valve Pressure Setting

INTRODUCTION: There is little scientific basis for guidance in selecting the optimal valve for the treatment of normal-pressure hydrocephalus (NPH). The aim of this study was to determine the programmable valve opening pressure (OPV) setting that would result in a slight reduction in intracranial pressure (ICP) after a ventriculoperitoneal (VP) shunt. We also assessed whether shunt-induced ICP changes could be predicted on the basis of a simple hydrodynamic equation. METHODS: In this prospective study of 11 patients with NPH, ICP was measured before and after implantation of a shunt incorporating a programmable valve without an antisiphon device. Pressure measurements, including intraperitoneal pressure (IPP), and shunt hydrostatic column lengths (HC) were recorded at body angles ranging from 0 to 55 degrees and at valve settings ranging from 30 to 200 mm H2O. Measured ICP values were compared with values computed using a simple hydrodynamic equation (ICPPredicted = OPV − HC + IPP). RESULTS: Even at the highest OPV setting of 200 mm H2O, which exceeded the mean baseline ICP (164 ± 64 mm H2O), there was a significant reduction in the postoperative ICP in the supine position (125 ± 69 mm H2O, P = 0.04). The OPV did not equal the measured postoperative ICP. Linear regression revealed a nonunity slope (0.39) and a nonzero y intercept (47 mm H2O versus measured IPPSupine of 69 ± 23 mm H2O). A precipitous decline of ICP at upright body positions, predicted by so-called siphoning, was not seen. Instead, postural ICP profile nearly paralleled that of the baseline measurements. CONCLUSION: This study indicates that very high OPV settings may be optimal for the initial treatment of NPH. The relationship between ICP and OPV is linear but not predicted by simple hydrodynamics. In NPH, VP shunts seem to lower ICP in a “physiological” manner without significant siphoning.

Initial head computed tomographic scan characteristics have a linear relationship with initial intracranial pressure after trauma.

Despite current recommendations by the Brain Trauma Foundation regarding the placement of intracranial pressure (ICP) monitoring devices, advances in computed tomographic (CT) scan technology have led to the suggestion that increased ICP may be predicted by findings on admission head CT scan and that patients without such findings do not require such monitoring. A linear relationship exists between characteristics of admission head CT scan and initial ICP level, allowing for selective placement of ICP monitoring devices. From 1997 to 2001, a retrospective review of patients admitted with a Glasgow Coma Scale (GCS) score < 8 and head CT scan who underwent ventriculostomy placement at our institution, was conducted. Patients undergoing craniotomy with evacuation of mass lesions before ventriculostomy placement were excluded. Age, sex, mechanism of injury, anoxia, osmotic treatment, presence of drugs/alcohol, initial mean arterial pressure, initial GCS score, and initial ICP were recorded. Initial head CT scans were reviewed independently by two neuroradiologists who were blinded to ICP measurements, neurosurgical treatment, patient outcome, and each other's interpretation. Initial CT scans were evaluated and scored on a 1 (normal) to 3 (abnormal) scale with respect to ventricle size, basilar cistern size, sulci size, degree of transfalcine herniation, and gray/white matter differentiation. Initial ICP readings and CT scan findings were compared to determine whether a significant linear relationship existed between the above CT scan findings and ICPs. Logistic and univariate linear regression were used to compare averaged radiologist score versus dichotomized ICP at baseline. Initial head CT scan characteristics show a linear relationship to baseline ICPs. These findings are associative, but are not uniformly predictive. Therefore, the current Brain Trauma Foundation recommendation of ICP monitoring in those patients presenting with a GCS score < 8 with an abnormal CT scan or a normal CT scan with age > 40 years, systolic blood pressure < 90 mm Hg, or exhibiting posturing should be followed.

Desflurane Increases Intracranial Pressure More and Sevoflurane Less Than Isoflurane in Pigs Subjected to Intracranial Hypertension

Desflurane and sevoflurane may have advantages over isoflurane in neuroanesthesia, but this is still under debate. A porcine model with experimental intracranial hypertension was used for paired comparison of desflurane, sevoflurane, and isoflurane with respect to the effects on cerebral blood flow (CBF), cerebrovascular resistance (CVR), and intracranial pressure (ICP). The agents, given in sequence to each of six pigs, were compared at 0.5 and 1.0 minimal alveolar concentrations (MAC) and three mean arterial blood pressure (MAP) levels (50, 70, and 90 mm Hg) at normocapnia and one MAP level (70 mm Hg) at hypocapnia. MAC for each agent had been previously determined in a standardized manner for comparison reliability. CBF was measured with Xe. MAP was lowered by inflation of a balloon catheter in the inferior caval vein and raised by inflation of a balloon catheter in the descending aorta. ICP was measured intraparenchymally. Two Fogarty catheters positioned extradurally were inflated to a baseline ICP of 20 to 22 mm Hg at 0.2 MAC of each agent. CBF and ICP with the three agents at normocapnia and MAP 70 and 90 mm Hg at both 0.5 and 1.0 MAC were as follows (P < 0.05): desflurane > isoflurane > sevoflurane. None of the agents abolished CO2 reactivity. High-dose desflurane resulted in a higher CBF at hypocapnia than corresponding doses of sevoflurane or isoflurane, but there were no significant differences between the agents in ICP at hypocapnia. The present study showed that desflurane increased ICP more and sevoflurane less than isoflurane during normoventilation, but the differences disappeared with hyperventilation.

A model for studies of intracranial volume pressure dynamics in traumatic brain injury.

The present study was undertaken to establish an experimental trauma model where it was possible to alter intracranial pressure (ICP) dynamics without raising intracranial pressure to abnormal levels and monitor metabolic disturbances with microdialysis. Thirty rats were intubated and mechanically ventilated before and after trauma. ICP was measured in the left ventricle. A weight-drop technique (21 g from 35 cm) with a brain compression of 1.5 mm was used to produce the injury. Intracranial compensatory volume was decreased 20 or 60 microL by placement of rubber film between the dura mater and bone. A bolus injection technique was used for the pressure volume response. ICP remained within normal limits for 2 h after trauma irrespective of the reduction in compensatory intracranial volume. Pressure-volume index decreased from 0.0825 +/- 0.009 to 0.0779 +/- 0.011 mL in the sham trauma and from 0.0871 +/- 0.018 to 0.0748 +/- 0.017 mL in the trauma groups (p < 0.015) when the intracranial volume was reduced by 60 microL. Intracranial compliance was not affected significantly. The present study shows that it is possible to vary ICP dynamics in a traumatic brain injury model without causing pathological increases in baseline ICP. This model may be used to study the effects of secondary insults (i.e., hypotension, hypoxia, hypercarbia, and hyperthermia) on the injured brain when ICP is normal but intracranial compensatory volume is impaired.

Effects of pressure- and volume-controlled inverse ratio ventilation on haemodynamic variables, intracranial pressure and cerebral perfusion pressure in rabbits: a model of subarachnoid haemorrhage under isoflurane anaesthesia

Background and objective: An inverse I:E ratio (inspiratory time > expiratory time) may have benefits in patients suffering trauma who requiring lung ventilation. However, this application may be deleterious if there is concomitant head injury. We aimed to determine the physiological effects of pressure- and volume-controlled modes of inverse ratio (I:E = 2:1) ventilation of the lungs, while maintaining normocapnia, in a rabbit model of raised intracranial pressure (ICP). Methods: New Zealand White rabbits were anaesthetized with isoflurane and a tracheostomy was performed. Subarachnoid haemorrhage was simulated in two groups by injecting blood into the cisterna magna. Groups 1 and 2 (n =6, each), controls, were compared with Groups 3 and 4 (n =6, each) with the simulated subarachnoid haemorrhage. Each ventilation mode was used with an I:E ratio of 2:1 for 30 min. Mean arterial pressure (MAP), ICP, cerebral perfusion pressure (CPP), mean airway pressure (PAW) and arterial blood-gas status were measured. Results: Both modes increased mean PAW (P < 0.02). This increase was greater with the volume-controlled mode (P < 0.02). The baseline value averaged 5.8 ± 0.4 and 5.6 ± 0.3 mmHg in Groups 3 and 4, respectively, and increased to 7.8 ± 0.3 and 10.8 ± 0.4 mmHg. Inducing subarachnoid haemorrhage increased ICP and MAP (P < 0.02). Baseline ICPs were 10.3 ± 0.5 and 10.3 ± 0.4 mmHg in Groups 1 and 2, respectively, whereas they were 25.4 ± 1.2 and 25.8 ± 0.8 mmHg in Groups 3 and 4. However, ICP, MAP and CPP did not differ significantly according to the mode. Conclusions: An already raised ICP was altered by the application of induced mean PAW increases as a consequence of inverse ratio ventilation of the lungs with normocapnia.

Metabolic suppressive therapy as a treatment for intracranial hypertension--why it works and when it fails.

Thirty years after its first description metabolic suppressive therapy is still controversial in patients with intractable intracranial hypertension. In this study high dose propofol was used to induce metabolic suppression. The effects on intracranial pressure (ICP) and the cerebral metabolic rates for oxygen and glucose (CMRO2 and CMRGlc) are reported. A total of 28 studies were performed on 14 head injured patients. A Xenon133 cerebral blood flow (CBF) and a CO2-reactivity (CO2R) test were performed prior to induction of metabolic suppression. The following parameters were continuously monitored: EEG, etCO2, SjvO2, ICP, MAP and bilateral MCA flow velocity (VMCA). PCO2 was obtained before and during propofol-induced EEG burst-suppression in arterial and jugular-venous blood. CMRO2, CMRGlc and Metabolic Ratio (MR = CMRO2/CMRGlc) were calculated. MR < 0.6 was defined as relative hyperglycolysis. ICP decreased by 24.1 +/- 29.0% during burst-suppression. Arterial, jugular-venous and etCO2 also decreased. Multiple regression analysis revealed that CO2 was the strongest predictor for ICP. Lower baseline ICP and normal CO2 reactivity were predictors for normal metabolic suppression reactivity. In studies with normal metabolic ratio, ICP reduction was associated with a reduction in CMRO2. In studies with hyperglycolysis, ICP reduction was poor but CMRGlc decreased significantly. In conclusion, intact CO2R, normal or only moderately elevated ICP and normal MR are predictive of ICP reduction with high dose propofol after head injury.

Enigma of raised intracranial pressure in patients with complex craniosynostosis: The role of abnormal intracranial venous drainage. Taylor WJ, Hayward RD, Lasjaunias P, Britto JA, Thompson DNP, Jones BM, Evans RD. J Neurosurg 2001;94:377–385.

Raised intracranial pressure (ICP) may complicate all forms of craniosynostosis. Several factors have been associated with increased ICP in patients with craniosynostosis, including craniocerebral dysproportion, hydrocephalus, the secondary effects of respiratory obstruction, and venous hypertension. In rare, but well-recognized instances, raised ICP can cause papilledema leading to secondary optic atrophy, reduced visual field and visual acuity, and even blindness. In this study, the authors investigated whether patterns of intracranial venous drainage in children with complex craniosynostosis associated with raised ICP were abnormal and, thus, could support the theory that venous hypertension is a major contributor to raised ICP in these patients, putting them at risk for impaired visual function. The authors analyzed the anatomy of intracranial venous drainage as demonstrated on 24 angiography studies from 23 patients, all of whom had either a craniosynostosis-related syndrome (18 patients) or a nonsyndromic multisutural synostosis (five patients). Twenty-one patients had evidence of raised ICP one to six weeks before undergoing angiography. Of the two remaining patients whose ICP monitoring was normal immediately before angiography, each had undergone two previous cranial vault expansion procedures. In 18 angiography studies, a 51% to 99% stenosis or no flow at all could be observed in the sigmoid-jugular sinus complex either bilaterally (11 patients) or unilaterally (seven patients). In 11 of these patients a florid collateral circulation through the stylomastoid emissary venous plexus was also seen. Comparison of two angiography studies performed in one patient with Crouzon syndrome demonstrated a progression of the abnormal venous anatomy. There was no obvious correlation between each patient’s baseline ICP and the degree of abnormality of their venous anatomy. The authors assert that in children with complex forms of craniosynostosis in whom other factors, such as hydrocephalus, are absent, abnormalities of venous drainage that particularly affect the sigmoid-jugular sinus complex produce a state of venous hypertension, which in turn, is responsible for the majority of cases of raised ICP. The incidence of these changes is unknown, but an analysis of the ages of the children in this study indicated that the period of particular vulnerability to the effects of venous hypertension lasts until the affected child is approximately six years old. After that age the collateral venous drainage through the stylomastoid plexus will likely become sufficient to allow ICP to normalize.—Nancy J. Newman

The effects of rigid collar placement on intracranial and cerebral perfusion pressures.

Rigid collars are routinely used to immobilise the cervical spine during early management of trauma victims until spinal injury is excluded. Spinal injuries commonly coexist in patients with severe head injury, and there is still uncertainty as to whether application of a rigid collar may adversely affect intracranial pressure. The aim of this study was to examine this effect by applying rigid collars to patients with traumatic head injury. The results showed a significant rise from the baseline intracranial pressure when the collars were applied (mean rise = 4.6 mmHg, p < 0.0001). The mean rise in intracranial pressure was greater in those patients with a baseline intracranial pressure > 15 mmHg compared to those with a baseline intracranial pressure < 15 mmHg (p < 0.05). Since there was no significant change in cardiorespiratory parameters during this time, venous compression in the neck seems a likely explanation for the effect observed. These findings suggest that in head-injured patients, rigid collars should be removed as soon as cervical spine injury has been excluded or, if this is delayed, an alternative method of spinal stabilisation considered.