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Relationship between Increased Intracranial Pressure and Mastoid Effusion.

ABSTRACT: OBJECTIVE:This study aimed to assess the relationship between increased intracranial pressure (ICP) and mastoid effusions (ME). METHODS:Between January 2015 and October 2018, patients who underwent intracranial surgery and had ICP monitoring catheters placed were enrolled. ICP was recorded hourly for at least 3 days. ME was determined by the emergence of opacification in mastoid air cells on follow-up brain imaging. C-reactive protein (CRP) levels, presence of endotracheal tube (ETT) and nasogastric tube (NGT), duration of intensive care unit (ICU) stay, duration of mechanical ventilator application, diagnosis, surgical modalities, and presence of sinusitis were recorded. Each factor's effect on the occurrence of ME was analyzed by binary logistic regression analyses. To analyze the independent effects of ICP as a predictor of ME a multivariable logistic regression analysis was performed. RESULTS:Total of 61 (53%) out of 115 patients had ME. Among the patients who had unilateral brain lesions, 94% of subject (43/50) revealed the ipsilateral development of ME. ME developed at a mean of 11.1±6.2 days. The variables including mean ICP, peak ICP, age, trauma, CRP, ICU stays, application of mechanical ventilators and presence of ETT and NGT showed statistically significant difference between ME groups and non-ME groups in univariate analysis. Sex and the occurrence of sinusitis did not differ between two groups. Adding the ICP variables significantly improved the prediction of ME in multivariable logistic regression analysis. CONCLUSION:While multiple factors affect ME, this study demonstrates that ICP and ME are probably related. Further studies are needed to determine the mechanistic relationship between ICP and middle ear pressure.

SUBMITTER: Jung H

PROVIDER: S-EPMC7477151 | biostudies-literature | 2020 Sep

REPOSITORIES: biostudies-literature

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Relationship between Increased Intracranial Pressure and Mastoid Effusion.

Jung Hoonkyo H Jang Kyoung Min KM Ko Myeong Jin MJ Choi Hyun Ho HH Nam Taek Kyun TK Kwon Jeong-Taik JT Park Yong-Sook YS

Journal of Korean Neurosurgical Society 20200901 5

<h4>Objective</h4>This study aimed to assess the relationship between increased intracranial pressure (ICP) and mastoid effusions (ME).<h4>Methods</h4>Between January 2015 and October 2018, patients who underwent intracranial surgery and had ICP monitoring catheters placed were enrolled. ICP was recorded hourly for at least 3 days. ME was determined by the emergence of opacification in mastoid air cells on follow-up brain imaging. C-reactive protein (CRP) levels, presence of endotracheal tube (E ...[more]

PMID: 32883058

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Project description:BackgroundRepeated invasive intracranial pressure (ICP) monitoring is desirable because many neurosurgical pathologies are associated with elevated ICP. On the other hand, it could become a risk for children to repeat sedation, anesthesia, or radiation exposure. As a non-invasive method, measurements of optic nerve sheath diameter (ONSD) has been revealed to accurately predict increased ICP. However, no studies have indicated a relationship among age, brain, and ventricular parameters in normal children, nor a prediction of increased ICP with artificial intelligence.Methods and findingsThis study enrolled 400 normal children for control and 75 children with signs of increased ICP between 2009 and 2019. Measurements of the parameters including ONSD on CT were obtained. A supervised machine learning was applied to predict suspected increased ICP based on CT measurements. A linear correlation was shown between ln(age) and mean ONSD (mONSD) in normal children, revealing mONSD = 0.36ln(age)+2.26 (R2 = 0.60). This study revealed a linear correlation of mONSD measured on CT with ln(age) and the width of the brain, not the width of the ventricles in 400 normal children based on the univariate analyses. Additionally, the multivariate analyses revealed minimum bicaudate nuclei distance was also associated with mONSD. The results of the group comparison between control and suspected increased ICP revealed a statistical significance in mONSD and the width of the ventricles. The study indicated that supervised machine learning application could be applied to predict suspected increased ICP in children, with an accuracy of 94% for training, 91% for test.ConclusionsThis study clarified three issues regarding ONSD and ICP. Mean ONSD measured on CT was correlated with ln(age) and the width of the brain, not the width of the ventricles in 400 normal children based on the univariate analyses. The multivariate analyses revealed minimum bicaudate nuclei distance was also associated with mONSD. Mean ONSD and the width of ventricles were statistically significant in children with signs of elevated ICP. Finally, the study showed that machine learning could be used to predict children with suspected increased ICP.

Project description:Functional and molecular changes associated with pathophysiological conditions are relatively easily detected based on tissue samples collected from patients. Population specific cellular responses to disease might remain undiscovered in samples taken from organs formed by a multitude of cell types. This is particularly apparent in the human cerebral cortex composed of a yet undefined number of neuron types with a potentially different involvement in disease processes. We combined cellular electrophysiology, anatomy and single cell digital PCR in human neurons identified in situ for the first time to assess mRNA expression and corresponding functional changes in response to edema and increased intracranial pressure. In single pyramidal cells, mRNA copy numbers of AQP1, AQP3, HMOX1, KCNN4, SCN3B and SOD2 increased, while CACNA1B, CRH decreased in edema. In addition, single pyramidal cells increased the copy number of AQP1, HTR5A and KCNS1 mRNAs in response to increased intracranial pressure. In contrast to pyramidal cells, AQP1, HMOX1and KCNN4 remained unchanged in single cell digital PCR performed on fast spiking cells in edema. Corroborating single cell digital PCR results, pharmacological and immunohistochemical results also suggested the presence of KCNN4 encoding the α-subunit of KCa3.1 channels in edema on pyramidal cells, but not on interneurons. We measured the frequency of spontaneous EPSPs on pyramidal cells in both pathophysiological conditions and on fast spiking interneurons in edema and found a significant decrease in each case, which was accompanied by an increase in input resistances on both cell types and by a drop in dendritic spine density on pyramidal cells consistent with a loss of excitatory synapses. Our results identify anatomical and/or physiological changes in human pyramidal and fast spiking cells in edema and increased intracranial pressure revealing cell type specific quantitative changes in gene expression. Some of the edema/increased intracranial pressure modulated and single human pyramidal cell verified gene products identified here might be considered as novel pharmacological targets in cell type specific neuroprotection.

Project description:In the search for optimal monitoring and predictive tools in neurocritical care, the relationship of the pulsatile component of intracranial pressure (ICP) and the pressure itself has long been of great interest. Higher pressure often correlates with a higher pulsatile response to the heartbeat, interpreted as a type of compliance curve. Various mathematical approaches have been used, but regardless of the formula used, it is implicitly assumed that a reproducible curve exists. The authors investigated the stability of the correlation between static and pulsatile ICPs in patients with subarachnoid hemorrhage (SAH) who were observed for several hours by using data sets large enough to allow such calculations to be made.The ICP recordings were obtained in 39 patients with SAH and were parsed into 6-second time windows (1,998,944 windows in 197 recordings). The ICP parameters were computed for each window as follows: static ICP was defined as the mean ICP, and pulsatile ICP was characterized by mean ICP wave amplitude, rise time, and rise time coefficient.The mean ICP and ICP wave amplitudes were simultaneously high or low (the expected correlation) in only approximately 60% of observations. Furthermore, static and pulsatile ICP correlated well only over short intervals; the degree of correlation weakened over periods of hours and was inconsistent across patients and within individual patients over time. Decorrelation originated with abrupt shifting and gradual drifting of mean ICP and ICP wave amplitude over several hours.The relationship between the static and pulsatile components of ICPs changes over time. It evolves, even in individual patients, over a number of hours. This can be one reason the observation of high pulsatile ICP (indicative of reduced intracranial compliance) despite normal mean ICP that is seen in some patients with SAH. The meaning and potential clinical usefulness of such changes in the curves is uncertain, but it implies that clinical events result not only from moving further out on a compliance curve; in practice, the curve, and the biological system that underlies the curve, may itself change.

Project description: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.

Project description:Brain tissue oxygen (PbtO2) monitoring in traumatic brain injury (TBI) has demonstrated strong associations with global outcome. Additionally, PbtO2 signals have been used to derive indices thought to be associated with cerebrovascular reactivity in TBI. However, their true relationship to slow-wave vasogenic fluctuations associated with cerebral autoregulation remains unclear. The goal of this study was to investigate the relationship between slow-wave fluctuations of intracranial pressure (ICP), mean arterial pressure (MAP) and PbtO2 over time. Using the Collaborative European NeuroTrauma Effectiveness Research in Traumatic Brain Injury (CENTER-TBI) high resolution ICU sub-study cohort, we evaluated those patients with recorded high-frequency digital intra-parenchymal ICP and PbtO2 monitoring data of a minimum of 6 h in duration. Digital physiologic signals were processed for ICP, MAP, and PbtO2 slow-waves using a moving average filter to decimate the high-frequency signal. The first 5 days of recording were analyzed. The relationship between ICP, MAP and PbtO2 slow-waves over time were assessed using autoregressive integrative moving average (ARIMA) and vector autoregressive integrative moving average (VARIMA) modelling, as well as Granger causality testing. A total of 47 patients were included. The ARIMA structure of ICP and MAP were similar in time, where PbtO2 displayed different optimal structure. VARIMA modelling and IRF plots confirmed the strong directional relationship between MAP and ICP, demonstrating an ICP response to MAP impulse. PbtO2 slow-waves, however, failed to demonstrate a definite response to ICP and MAP slow-wave impulses. These results raise questions as to the utility of PbtO2 in the derivation of cerebrovascular reactivity measures in TBI. There is a reproducible relationship between slow-wave fluctuations of ICP and MAP, as demonstrated across various time-series analytic techniques. PbtO2 does not appear to reliably respond in time to slow-wave fluctuations in MAP, as demonstrated on various VARIMA models across all patients. These findings suggest that PbtO2 should not be utilized in the derivation of cerebrovascular reactivity metrics in TBI, as it does not appear to be responsive to changes in MAP in the slow-waves. These findings corroborate previous results regarding PbtO2 based cerebrovascular reactivity indices.

Dataset Information

Relationship between Increased Intracranial Pressure and Mastoid Effusion.

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Relationship between Increased Intracranial Pressure and Mastoid Effusion.

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