Acute Changes In Intracranial Pressure Research Articles

Prevention of postoperative stroke in pediatric moyamoya patients: a standardized perioperative care protocol.

Perioperative stroke is a major complication of revascularization surgery in patients with moyamoya. Vomiting is common after neurosurgical procedures and may result in acute changes in intracranial pressure and cerebral blood flow. The authors instituted a standardized perioperative nausea and vomiting protocol for children with moyamoya undergoing indirect bypass surgery at their institution and analyzed its association with perioperative stroke. They hypothesized that instituting a standardized perioperative nausea and vomiting protocol would be associated with reduction in the number of perioperative strokes in children with moyamoya undergoing indirect bypass surgery. The authors retrospectively reviewed consecutive cases of children and young adults with moyamoya who underwent indirect bypass surgery before and after implementation of a new perioperative nausea and vomiting protocol at a single institution. They compared the rate of strokes in the perioperative period (postoperative days 0 and 1) in the 31 months following implementation to 31 months prior to implementation using Fisher's exact test. The median ages pre- and postimplementation were 8.5 (IQR 4-12) years and 8.3 (IQR 5-15) years, respectively. There were no significant differences between the cohorts in disease severity or other potentially confounding factors. In the 31 months prior to initiation of the perioperative nausea and vomiting protocol, there were 5 strokes in 137 surgically treated hemispheres (3.6%). After initiation of the protocol, there were no strokes in 114 surgically treated hemispheres (p = 0.065). Instituting a standardized perioperative nausea and vomiting protocol was associated with reduction in perioperative strokes in children with moyamoya treated with indirect bypass surgery.

Abstract TMP21: Association Of A Perioperative Nausea And Vomiting Treatment Protocol With Reduction In Perioperative Strokes In Children And Young Adults With Moyamoya

Introduction: Perioperative stroke is a major complication of revascularization surgery in patients with moyamoya. Vomiting is common after neurosurgical procedures and may result in acute changes in intracranial pressure and cerebral blood flow. We instituted a standardized perioperative nausea and vomiting protocol for children and young adults with moyamoya undergoing indirect bypass surgery at our institution. Hypothesis: Instituting a standardized perioperative nausea and vomiting protocol will be associated with reduction in the number of perioperative strokes in children with moyamoya undergoing indirect bypass surgery. Methods: We retrospectively reviewed consecutive cases of children and young adults with moyamoya who underwent indirect bypass surgery before and after implementation of a new perioperative nausea and vomiting protocol. We compared the rate of strokes in the perioperative period (post-operative day 0 and 1) in the 41 months following implementation (155 surgically treated hemispheres) to 155 surgically treated hemispheres (over 30 months) prior to implementation using Fisher’s Exact test. Results: The mean age prior to implementation was 8.7 years (SD 5.5 years) and 9.9 years (SD 6.2 years) post implementation which was not significantly different (p=0.17). In the 30 months prior to initiation of the perioperative nausea and vomiting protocol there were 5 strokes in 155 surgically treated hemispheres (3.2%). After initiation of the protocol, there were no strokes in 155 surgically treated hemispheres (p = 0.03). Conclusions: Instituting a standardized perioperative nausea and vomiting protocol was associated with reduction in perioperative strokes in children with moyamoya treated with indirect bypass surgery.

Effects of Acute Intracranial Pressure Changes on Optic Nerve Head Morphology in Humans and Pig Model

ABSTRACT Purpose The lamina cribrosa (LC) is a layer of fenestrated connective tissue tethered to the posterior sclera across the scleral canal in the optic nerve head (ONH). It is located at the interface of intracranial and intraocular compartments and is exposed to intraocular pressure (IOP) anteriorly and intracranial pressure (ICP) or Cerebrospinal fluid (CSF) pressure (CSFP) posteriorly. We hypothesize that the pressure difference across LC will determine LC position and meridional diameter of scleral canal (also called Bruch’s membrane opening diameter; BMOD). Methods We enrolled 19 human subjects undergoing a medically necessary lumbar puncture (LP) to lower CSFP and 6 anesthetized pigs, whose ICP was increased in 5 mm Hg increments using a lumbar catheter. We imaged ONH using optical coherence tomography and measured IOP and CSFP/ICP at baseline and after each intervention. Radial tomographic ONH scans were analyzed by two independent graders using ImageJ, an open-source software. The following ONH morphological parameters were obtained: BMOD, anterior LC depth and retinal thickness. We modeled effects of acute CSFP/ICP changes on ONH morphological parameters using ANOVA (human study) and generalized linear model (pig study). Results For 19 human subjects, CSFP ranged from 5 to 42 mm Hg before LP and 2 to 19.4 mm Hg after LP. For the six pigs, baseline ICP ranged from 1.5 to 9 mm Hg and maximum stable ICP ranged from 18 to 40 mm Hg. Our models showed that acute CSFP/ICP changes had no significant effect on ONH morphological parameters in both humans and pigs. Conclusion We conclude that ONH does not show measurable morphological changes in response to acute changes of CSFP/ICP. Proposed mechanisms include compensatory and opposing changes in IOP and CSFP/ICP and nonlinear or nonmonotonic effects of IOP and CSFP/ICP across LC.

The Effects of Acute Intracranial Pressure Changes on the Episcleral Venous Pressure, Retinal Vein Diameter and Intraocular Pressure in a Pig Model

ABSTRACT Purpose Orbital veins such as the retinal veins and episcleral veins drain into the cavernous sinus, an intracranial venous structure. We studied the effects of acute intracranial pressure (ICP) elevation on episcleral venous pressure, intraocular pressure and retinal vein diameter in an established non-survival pig model. Methods In six adult female domestic pigs, we increased ICP in 5 mm Hg increments using saline infusion through a lumbar drain. We measured ICP (using parenchymal pressure monitor), intraocular pressure (using pneumatonometer), episcleral venous pressure (using venomanometer), retinal vein diameter (using OCT images) and arterial blood pressure at each stable ICP increment. The average baseline ICP was 5.4 mm Hg (range 1.5–9 mm Hg) and the maximum stable ICP ranged from 18 to 40 mm Hg. Linear mixed models with random intercepts were used to evaluate the effect of acute ICP increase on outcome variables. Results With acute ICP elevation, we found loss of retinal venous pulsation and increased episcleral venous pressure, intraocular pressure and retinal vein pressure in all animals. Specifically, acute ICP increase was significantly associated with episcleral venous pressure (β = 0.31; 95% CI 0.14–0.48, p < .001), intraocular pressure (β = 0.37, 95%CI 0.24–0.50; p < .001) and retinal vein diameter (β = 11.29, 95%CI 1.57–21.00; p = .03) after controlling for the effects of arterial blood pressure. Conclusion We believe that the ophthalmic effects of acute ICP elevation are mediated by increased intracranial venous pressure producing upstream pressure changes within the orbital and retinal veins. These results offer exciting possibilities for the development of non-invasive ophthalmic biomarkers to estimate acute ICP elevations following significant neuro-trauma.

Quantitative Association Between Peripapillary Bruch's Membrane Shape and Intracranial Pressure.

PurposeThe purpose of this study was to determine if there is a quantitative relationship between chronic intracranial pressure (ICP) and peripapillary Bruch's membrane (pp-BM) shape and to determine whether change in pp-BM shape can be detected within 1 hour after ICP lowering by lumbar puncture (LP).MethodsIn this study, 30° nasal-temporal optical coherence tomography B-scans were obtained within 1 hour before and after LP in 39 eyes from 20 patients (age = 23–86 years, 75% female, ICP [opening pressure] = 10–55 cm H2O). A total of 16 semi-landmarks defined pp-BM on each image. Geometric morphometric analysis identified principal components of shape in the image set. Generalized estimating equation models, accounting for within-subject correlation, were used to identify principal components that were associated with chronic ICP (comparing pre-LP images between eyes) and/or acute ICP changes (comparing pre- and post-LP images within eyes). The pp-BM width and anterior pp-BM location were calculated directly from each image and were studied in the same manner.ResultsPrincipal component 1 scalar variable on pre-LP images was associated with ICP (P < 0.0005). Principal component 4 magnitude changed within eyes after LP (P = 0.003). For both principal components 1 and 4, lower ICP corresponded with a more posterior position of pp-BM. Chronic ICP was associated with both pp-BM width (6.81 μm/cm H2O; P = 0.002) and more anterior location of temporal and nasal pp-BM margins (3.41, 3.49 μm/cm H2O; P < 0.0005, 0.002).ConclusionsThis study demonstrates a quantitative association between pp-BM shape and chronic ICP level. Changes in pp-BM shape are detectable within 1 hour of lowering ICP. pp-BM shape may be a useful marker for chronic ICP level and acute ICP changes. Further study is needed to determine how pp-BM shape changes relate to clinical markers of papilledema.

Optical coherence tomography of the optic nerve head detects acute changes in intracranial pressure

We aimed to determine if there are measurable objective changes in the optic nerve head (ONH) immediately after cerebrospinal fluid (CSF) drainage in a prospective case-series of five patients undergoing a clinically indicated lumbar puncture (LP) for diagnosis of idiopathic intracranial hypertension. A Cirrus high-definition optical coherence tomography machine (Carl Zeiss Meditec, Dublin, CA, USA) was used to acquire images in the lateral decubitus position. Optic disc cube and high-definition line raster scans centered on the ONH were obtained immediately before and after draining CSF, while the patient maintained the lateral decubitus position. Measured parameters included retinal nerve fiber layer (RNFL) thickness, peripapillary retinal pigment epithelium/Bruch’s membrane (RPE/BM) angulation, transverse neural canal diameter (NCD) and the highest vertical point of the internal limiting membrane from the transverse diameter (papillary height). The mean (±standard deviation) opening and closing CSF pressures were 34.3±11.8 and 11.6±3.3cmH2O, respectively. Mean RNFL thickness (pre LP: 196±105μm; post LP: 164±77μm, p=0.1) and transverse NCD (pre LP: 1985±559μm; post LP: 1590±228μm, p=2.0) decreased in all subjects, but with non-significant trends. The RPE/BM angle (mean change: 5.8±2.0degrees, p=0.003) decreased in all subjects. A decrease in papillary height was seen in three of five subjects (mean: pre LP: 976±275μm; post LP: 938±300μm, p=0.9). Our results show a measurable, objective change in the ONH after acute lowering of the lumbar CSF pressure, suggesting a direct link between the lumbar subarachnoid space and ONH regions, and its potential as a non-invasive method for monitoring intracranial pressures.

Intracranial pressure modulates distortion product otoacoustic emissions: a proof-of-principle study.

There is an important need to develop a noninvasive method for assessing intracranial pressure (ICP). We report a novel approach for monitoring ICP using cochlear-derived distortion product otoacoustic emissions (DPOAEs), which are affected by ICP. We hypothesized that changes in ICP may be reflected by altered DPOAE responses via an associated change in perilymphatic pressure. We measured the ICP and DPOAEs (magnitude and phase angle) during opening and closing in 20 patients undergoing lumbar puncture. We collected data on 18 patients and grouped them based on small (<4 mm Hg), medium (5-11 mm Hg), or large (≥15 mm Hg) ICP changes. A permutation test was applied in each group to determine whether changes in DPOAEs differed from zero when ICP changed. We report significant changes in the DPOAE magnitudes and angles, respectively, for the group with the largest ICP changes and no changes for the group with the smallest changes; the group with medium changes had variable DPOAE changes. We report, for the first time, systematic changes in DPOAE magnitudes and phase in response to acute ICP changes. Future studies are warranted to further develop this new approach. DPOAE, distortion product otoacoustic emissionICP, intracranial pressureIIH, idiopathic intracranial hypertensionLP, lumbar punctureTBI, traumatic brain injury.

Editorial: Patient-specific intracranial pressure

The accompanying article by Lazaridis et al. describes in detail a study challenging the conventional wisdom of traditional intracranial pressure (ICP) monitoring in the setting of traumatic brain injury (TBI).3 A number of recent studies have failed to show that controlling or reducing ICP below an absolute threshold results in improvement in neurological outcome or mortality rate. Prior reports have challenged the dogma of ICP monitoring as well.1,2 Still, most centers continue to treat posttraumatic brain swelling with control of the absolute ICP to values below 20 or 25 mm Hg, a practice that dates back more than 2 decades, with no supporting Level I evidence. In an age of increased capability for sophisticated monitoring of physiological parameters and neurochemical changes, traditional ICP monitoring continues to play a key role in the management of TBI, despite the mounting evidence questioning its value. Changes in the way we practice require good evidence for an alternative strategy. It is refreshing, therefore, to see a study such as this one in our literature. Rather than proposing the use of additional, expensive, and untested measures, Dr. Lazaridis’ group has proposed an analysis of currently collected physiological parameters that instead takes into account variations in arterial blood pressure to arrive at an index of cerebrovascular reactivity. This approach is rooted in the observation that patients seem to fare better when ICP changes happen slowly and cerebrovascular reactivity remains normal. It has long been observed that patients with chronic increases in ICP (for example, due to slow-growing tumors, pseudotumor, and hydrocephalus) are often minimally symptomatic. The difference between such patients and those with more acute changes in ICP (such as those due to acute epidural hematomas) probably has to do with the lack of cerebrovascular compensation in the latter group. This study attempts to quantify this cerebrovascular reactivity in the setting of TBI, and to examine whether this index has a prognostic significance. This is an elegant study, and appears to provide a way forward in terms of more “personalized” physiological monitoring. Using measures we already collect in our intensive care units, it allows clinicians to derive more meaningful parameters in real time. These parameters do appear to have prognostic value, as these authors show. The more difficult question to ask is whether correcting abnormalities in the derived measures would make a difference in outcome. It is possible that measures such as “ICP dose” and pressure reactivity index (PRx) are mere markers of a bad outcome and cannot be changed with intervention. Only further work looking at how these calculated ICP parameters correlate with other biomarkers and therapeutic interventions will resolve this important issue. The calculated ICP parameters could also help us address why certain patients deteriorate when their abnormally high ICP is reduced too rapidly. It is well known that certain patients with long-standing intracranial hypertension actually get worse when their ICP is normalized. Once again, cerebrovascular reactivity changes are suspected in these situations. Physiological parameters such as ICP dose may help guide therapy in these situations, and prevent neurological sequelae. The authors of this study are helping usher in a new age of physiological monitoring in the neurocritical care unit—one that goes well beyond traditional cardiopulmonary measures and absolute ICPs. Additional studies will further outline the utility, implications, and limitations of these cerebrovascular measures. My only regret is that the software that they have created is available only as a commercial product. Scientific progress and iterative improvements are always more robust when tools such as these are shared with other academic units. (http://thejns.org/doi/abs/10.3171/2013.10.JNS132024)

Intracranial Pressure and Optic Nerve Sheath Diameter as Cephalic Venous Pressure Increases in Swine

Nontraumatic, nonhydrocephalic increases in intracranial pressure (ICP) are often difficult to diagnose and may underlie spaceflight-related visual changes. This study looked at the utility of a porcine animal model of increasing cephalic venous pressure to mimic acute changes in ICP and optic nerve sheath diameter (ONSD) from cephalic venous fluid shifts observed during spaceflight. Anesthetized juvenile piglets were assigned to groups of either naïve (N = 10) or elevated superior vena cava pressure (SVCP; N = 20). To elevate SVCP, a 6F custom latex balloon catheter was inserted and inflated to achieve SVCP of 20 and 40 mmHg for 1 h at each pressure. In both groups, serial measurements of ICP, internal jugular pressure (IJP), and external jugular pressure (EJP) were made hourly for 3 h, and ONSD of the right eye was measured hourly by ultrasound (US). There was a significant linear correlation between IJP and ICP (slope: 0.9614 +/- 0.0038, r = 0.9683). With increasing SVCP, resulting ONSD was also well correlated with the ICP (slope: 0.0958 +/- 0.0061, r = 0.7841). The receiver operating characteristic curve for ONSD in diagnosing elevated ICP had an area under the curve of 0.9632 with a sensitivity and specificity of 92% and 91%, respectively, for a cutoff of 5.45 mm. Increases in SVCP result in ICP changes that are well correlated with alteration in ONSD. These changes are consistent with observed ONSD changes monitored during spaceflight.

Continuous Electroencephalography in Neuroscience ICU Setting as a Potential Modality of Detecting Intracranial Pressure Changes (P06.263)

Objective: To describe the clinical correlation and concomitant benefits of dual monitoring in two cases where clinical changes related to elevated intracranial pressure (ICP) were also associated with acute changes in the continuous electroencephalogram (cEEG). Background Multimodal neurologic monitoring is one of the significant advances of neurocritical care. ICP monitoring and cEEG are among the widely used modalities in the neuroscience intensive care unit. We describe two cases where cEEG was predictive of acute ICP changes. Design/Methods: Observational; case series. Results: We describe two patients who had elevated ICP suspected on the basis of clinical history, examination, tachypnea –bradypnea and bradycardia-tachycardia. One patient had a medulloblastoma. The second patient had a complex Dandy-Walker cyst with associated hydrocephalus. Suspected ICP elevation was confirmed with ventriculostomy placement and ICP measurements that occurred within minutes after the change in clinical exam. During these events continuous cEEG had been in progress and demonstrated broad significant attenuation in the background rhythm and amplitude (greater than 50% change) as well as changes in the character of the background rhythm. These changes resolved when the elevated ICP was treated. Conclusions: Correlation between sudden changes in ICP and cEEG has not been previously reported in the literature. We suggest that cEEG may be useful as a non-invasive correlate to ICP monitoring. Disclosure: Dr. Hornik has nothing to disclose. Dr. Vitorovic has nothing to disclose. Dr. Singh has nothing to disclose. Dr. Schneck has nothing to disclose. Dr. Baldwin has nothing to disclose. Dr. Morales-Vidal has nothing to disclose.

Sonography for Determining the Optic Nerve Sheath Diameter With Increasing Intracranial Pressure in a Porcine Model

This study investigated whether it is feasible to use sonography to monitor changes in the optic nerve sheath diameter in a porcine model. A fiber-optic intracranial pressure transducer was surgically placed through the frontal sinus directly into the brain parenchyma of adult Yorkshire pigs (n = 5). A second bolt was placed on the contralateral side for intraparenchymal fluid infusion. Optic nerve sheath diameter measurements were acquired by each of 2 ultrasound operators around the leading edge of the nerve, 3 to 5 mm distal from the origin of the optic nerve. To induce a change in diameter, intracranial pressure was manipulated by injecting normal saline into the intraparenchymal infusion catheter located in the symmetric contralateral position as the pressure-monitoring probe. Data from 1 pig were unusable because of a cerebrospinal fluid leak into the sinus and orbital fissure. Saline aliquots of 1 to 10 mL were able to generate intracranial pressures typically starting from 10 to 15 mm Hg and increasing to 75 to 90 mm Hg, which eventually evoked a Cushing response. Fluid injection was controlled to increase pressures by 60 mm Hg over a 15- to 20-minute period. Regression analysis of all animals showed that the optic nerve sheath diameter increased by 0.0034 mm/mm Hg of intracranial pressure; however, this slope ranged from 0.0025 to 0.0046, depending on the animal measured. There was no discernible effect of the ultrasound operator on the slope; however, measurements made by 1 operator were consistently higher than the others by about 8% of the overall diameter range. These results suggest that the use of the optic nerve sheath diameter to noninvasively confirm acute changes in intracranial pressure over 1 hour is feasible in a porcine model. We recommend that this method be validated in humans using direct intracranial pressure measurement where possible to confirm it as a screening tool for acute and chronically increased diameters secondary to elevated pressure in clinical settings.

Pseudomeningocele induced transient loss of consciousness in Marfan syndrome

Anterior and posterior meningoceles are the severest clinical expression of dural ectasia in patients with Marfan syndrome. Meningoceles and pseudomeningoceles have been reported from either asymptomatic, to causing headache, back pain, leg pain, radiculopathy, constipation and/or urinary symptoms. This article includes a case report of a 31-year-old woman, who presented with recurrent transient loss of consciousness thought to be secondary to acute changes in intracranial pressure transmitted from a pseudomeningocele.

Acute changes in intracranial pressure and pressure-volume index after forebrain ischemia in normoglycemic and hyperglycemic rats.

Hyperglycemia enhances the deleterious effect of global cerebral ischemia. One possible explanation is that increased anaerobic glycolysis leads to exaggeration of intracellular acidosis and increased postischemic edema. To examine the importance of this edema on postischemic cerebral perfusion dynamics, we measured acute changes in intracranial pressure (ICP), specific gravity, and the pressure-volume index (PVI) after forebrain ischemia in normoglycemic and hyperglycemic rats. Rats underwent 15 minutes of forebrain ischemia and 90 minutes of reperfusion. ICP and mean arterial pressure were continuously monitored. Before ischemia, rats received either saline or glucose intravenously. Ninety minutes after ischemia, the specific gravity of the neocortex was measured. In a second experiment, the PVI was measured at 20 and 60 minutes after ischemia. Preischemic ICP (mean+/-SD) was 7 +/- 1 mm Hg in both groups. A peak ICP (approximately 11 mm Hg) occurred within 15 to 20 minutes after ischemia in both groups. Between 25 and 80 minutes after ischemia, ICP was significantly but only slightly greater in hyperglycemic than in normoglycemic rats. Cerebral perfusion pressure was similar between groups and remained greater than 100 mm Hg. Specific gravity was also similar for both groups but was less than normal values. The PVI in hyperglycemic rats was lower than in normoglycemic rats, indicating reduced compliance. These findings indicate that hyperglycemia-augmented intraischemic tissue acidosis does not contribute to worsened outcome by means of compromised cerebral perfusion pressure during the early stages of recovery. Nevertheless, evidence was found for decreased cerebral compliance, indicating an effect of hyperglycemia on intracranial volume compartments other than cortical parenchyma.

A Mathematical Model Of Intracranial PressureAnd Cerebral Hemodynamics ResponseTo CO2 Changes

Alterations in blood CO] tension (paco) are frequently used in neurosurgical Intensive Care Units to manage patients with severe brain diseases and to test the status of mechanisms regulating cerebral blood flow. In this work, the complex relationships between Pacc>2> cerebral blood volume, cerebral blood flow and intracranial pressure (ICP) are investigated by means of an original mathematical model. The model incorporates the intracranial compliance, the cerebrospinal fluid production and reabsorption processes, the collapse of the terminal cerebral veins, and the active response of large and small cerebral arteries to perfusion pressure changes (autoregulation) and to changes inpaCO; (chemical regulation). Two different kinds of simulations have been performed to validate the model and to test its possible clinical usefulness. In a first stage, ICP was maintained constant to mimic experiments with the open skull and the ccrebrovascular response to changes in systemic arterial pressure and in Paco^ was reproduced. The results of the model show that agreement with the experimental curves of various authors is quite good. In the second stage, conditions occurring with a closed skull were simulated. These are characterized by acute changes in ICP, induced by active changes in cerebral blood volume. In these conditions, the model was used to reproduce the time pattern of ICP and blood flow velocity at the level of the middle cerebral artery observed in patients during alterations in systemic arterial pressure and Paco^A comparison between simulation results and real tracings is presented and discussed. The model may represent a valid tool to interpret the complex relationships between cerebral hemodynamic quantities in neurosurgical Intensive Care Units. Transactions on Biomedicine and Health vol 4, © 1997 WIT Press, www.witpress.com, ISSN 1743-3525