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Query: UMLS:C0268318 (ICP)
 10,007 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The involvement of the cholinergic basal forebrain in the control of ICP and the cerebrovascular bed was investigated by simultaneous measurement of CBF, BP, ICP and ETCO2 in rats and cats. Single unit spikes were also continuously recorded during ICP changes in the dorsomedial hypothalamic nucleus (DMH) of cats. Glutamate or acetylcholine (Ach) microinjection into the magnocellular basal nucleus (nucleus basalis Meynert: NBM, substantia innominata: SI) of rats or the DMH of cats caused persistent increases in ICP associated with slightly decreased BP. Microinjection of Ach into the NBM or the DMH also induced consistent increases in CBF in the cerebral cortex. Spike activities in DMH neurons increased before and during spontaneous ICP elevation. The firing rate of the DMH neurons increased in phase with the plateau wave-like ICP variations elicited by microinjection of Ach into the cholinoceptive pontine area or the contralateral DMH. Glutamate- or Ach-induced increases in ICP resulted from an increased CBV in response to a reduced cerebral vasoconstrictor tone. Activity within the cholinergic basal forebrain, as well as the central noradrenergic system, contribute to ICP changes and may be the intrinsic neuronal origin of the plateau waves occurring in some pathological conditions.
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PMID:Control of ICP and the cerebrovascular bed by the cholinergic basal forebrain. 977 11

In the past several years, improvements in technology have advanced the monitoring capabilities for patients with TBI. The primary goal of monitoring the patient with TBI is to prevent secondary insults to the brain, primarily cerebral ischemia. Cerebral ischemia may occur early and without clinical correlation and portends a poor outcome. Measurement of ICP is the cornerstone of monitoring in the patient with TBI. Monitoring of ICP provides a measurement of CPP and a rough estimation of CBF. However, with alterations in pressure autoregulation, measurement of CPP does not always allow for determination of CBF. To circumvent this problem, direct measurements of CBF can be performed using clearance techniques (133Xe, N2O, Xe-CT) or invasive monitoring techniques (LDF, TDF, NIRS). Although direct and quantitative, clearance techniques do not allow for continuous monitoring. Invasive CBF monitoring techniques are new, and artifactual results can be problematic. The techniques of jugular venous saturation monitoring and TCD are well established and are powerful adjuncts to ICP monitoring. They allow the clinician to monitor cerebral oxygen extraction and blood flow velocity, respectively, for any given CPP. Use of TCD may predict posttraumatic vasospasm before clinical sequelae. Jugular venous saturation monitoring may detect clinically occult episodes of cerebral ischemia and increased oxygen extraction. Jugular venous saturation monitoring optimizes the use of hyperventilation in the treatment of intracranial hypertension. Although PET and SPECT scanning allow direct measurement of CMRO2, these techniques have limited application currently. Similarly, microdialysis is in its infancy but has demonstrated great promise for metabolic monitoring. EEG and SEP are excellent adjuncts to the monitoring arsenal and provide immediate information on current brain function. With improvements in electronic telemetry, functional monitoring by EEG or SEP may become an important part of routine monitoring in TBI.
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PMID:Monitoring in traumatic brain injury. 1008 12

The rat endovascular filament model has been utilized to study subarachnoid hemorrhage (SAH). Because the severity of the hemorrhage with this model has proven difficult to modulate, we attempted to vary the hemorrhage by modifying filament size, and compared this model to the blood injection method with regards to acute physiological responses and hemorrhage size. SAH was achieved using either a 3-0 or 4-0 filament, or by injecting 0.3 cc of autologous blood into the cisterna magna. Peak ICP elevations were lowest in the 4-0 filament group. CBF decreased acutely and rose from its nadir in all three models with the injection model demonstrating the earliest recovery. In the injection group, mean arterial blood pressure rose acutely and remained elevated, whereas in the 3-0 group, MABP rose transiently and in the 4-0 group it did not rise significantly. Histologically, there was less subarachnoid blood in the 4-0 group vs. the injection or 3-0 groups and a different distribution of blood in the two experimental models. Varying filament size provides a method to modulate the severity of SAH in the filament model. In addition, the rat endovascular filament and blood injection models produce different distribution of blood and physiological responses.
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PMID:Experimental models of subarachnoid hemorrhage in the rat: a refinement of the endovascular filament model. 1072 Jun 81

Chronic prophylactic hyperventilation therapy should be avoided during the first 5 days after severe TBI and particularly during the first 24 h. CBF measurements in patients with severe TBI demonstrate that blood flow early after injury is low and strongly suggest that in the first few hours after injury the absolute values approach those consistent with ischemia. These findings are corroborated by AVdO2 and SjO2 and brain tissue O2 measurements. Hyperventilation will reduce CBF values even further, but will not consistently cause a reduction of ICP and may cause loss of autoregulation. The cerebral vascular response to hypocapnia is reduced in those with the most severe injuries (subdural hematomas and diffuse contusions), and there is substantial local variability in perfusion. While the CBF level at which irreversible ischemia occurs has not been clearly established, ischemic cell change has been demonstrated in 90% of those who die following TBI, and there is PET evidence that such damage is likely to occur when CBF drops below 15-20 cc/100 g/min. A prospective randomized clinical trial has determined that outcomes are worse when TBI patients are treated with chronic prophylactic hyperventilation therapy. Within the standard, guideline, and options, specific paCO2 thresholds have been described that are different for each of the three parameters. These individual thresholds were selected based on the preponderance of literature supporting those thresholds in the contexts of the statements which included them. With the exception of the threshold included for the standard in this guideline, it is emphasized that the paCO2 threshold is not as important as the general concept of hyperventilation. The preponderance of the physiologic literature concludes that hyperventilation during the first few days following severe traumatic brain injury, whatever the threshold, is potentially deleterious in that it can promote cerebral ischemia.
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PMID:The Brain Trauma Foundation. The American Association of Neurological Surgeons. The Joint Section on Neurotrauma and Critical Care. Hyperventilation. 1093 94

We used steady-state susceptibility contrast MRI to evaluate the regional cerebral blood volume (rCBV) response to hypocapnia in anesthetised rats. The rCBV was determined in the dorsoparietal neocortex, the corpus striatum, the cerebellum, as well as blood volume in extracerebral tissue (group 1). In addition, we used laser-Doppler flow (LDF) measurements in the left dorsoparietal neocortex (group 2), to correlate changes in CBV and in cerebral blood flow. Baseline values, expressed as a percentage of blood volume in each voxel, were higher in the brain regions than in extracerebral tissue. Hypocapnia (P(a)CO(2) approximately 25 mmHg) resulted in a significant decrease in CBV in the cerebellum (-17 +/- 9%), in the corpus striatum (-15 +/- 6%) and in the neocortex (-12 +/- 7%), compared to the normocapnic CBV values (group 1). These changes were in good agreement with the values obtained using alternative techniques. No significant changes in blood volume were found in extracerebral tissue. The CBV changes were reversed during the recovery period. In the left dorsoparietal neocortex, the reduction in LDF (group 2) induced by hypocapnia (-21 +/- 8%) was in accordance with the values predicted by the Poiseuille's law. We conclude that rCBV changes during CO(2) manipulation can be accurately measured by susceptibility contrast MRI. Abbreviations used: ANOVA analysis of variance CBF cerebral blood flow CBV cerebral blood volume CPMG Carr-Purcell-Meiboom-Gill FiO(2) fractional inspired oxygen ICP intracranial pressure LDF laser-Doppler flow MABP mean arterial blood pressure MRI magnetic resonance imaging MTT mean transit time PaCO(2) arterial partial pressure of carbon dioxide PaO(2) arterial partial pressure of oxygen PET positron emission tomography rCBV regional cerebral blood volume SPECT single-photon emission computed tomography
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PMID:Regional cerebral blood volume response to hypocapnia using susceptibility contrast MRI. 1111 61

Intracerebral contusions can lead to regional ischemia caused by extensive release of excitotoxic aminoacids leading to increased cytotoxic brain edema and raised intracranial pressure. rCBF measurements might provide further information about the risk of ischemia within and around contusions. Therefore, the aim of the presented study was to compare the intra- and perilesional rCBF of hemorrhagic, non-hemorrhagic and mixed intracerebral contusions. In 44 patients, 60 stable Xenon-enhanced CT CBF-studies were performed (EtCO2 30 +/- 4 mmHg SD), initially 29 hours (39 studies) and subsequent 95 hours after injury (21 studies). All lesions were classified according to localization and lesion type using CT/MRI scans. The rCBF was calculated within and 1-cm adjacent to each lesion in CT-isodens brain. The rCBF within all contusions (n = 100) of 29 +/- 11 ml/100 g/min was significantly lower (p < 0.0001, Mann-Whitney U) compared to perilesional rCBF of 44 +/- 12 ml/100 g/min and intra/perilesional correlation was 0.4 (p < 0.0005). Hemorrhagic contusions showed an intra/perilesional rCBF of 31 +/- 11/44 +/- 13 ml/100 g/min (p < 0.005), non-hemorrhagic contusions 35 +/- 13/46 +/- 10 ml/100 g/min (p < 0.01). rCBF in mixed contusions (25 +/- 9/44 +/- 12 ml/100 g/min, p < 0.0001) was significantly lower compared to hemorrhagic and non-hemorrhagic contusions (p < 0.02). Intracontusional rCBF is significantly reduced to 29 +/- 11 ml/100 g/min but reduced below ischemic levels of 18 ml/100 g/min in only 16% of all contusions. Perilesional CBF in CT normal appearing brain closed to contusions is not critically reduced. Further differentiation of contusions demonstrates significantly lower rCBF in mixed contusions (defined by both hyper- and hypodense areas in the CT-scan) compared to hemorrhagic and non-hemorrhagic contusions. Mixed contusions may evolve from hemorrhagic contusions with secondary increased perilesional cytotoxic brain edema leading to reduced cerebral blood flow and altered brain metabolism. Therefore, the treatment of ICP might be individually modified by the measurement of intra- and pericontusional cerebral blood.
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PMID:rCBF in hemorrhagic, non-hemorrhagic and mixed contusions after severe head injury and its effect on perilesional cerebral blood flow. 1145 9

Glucose (Gluc) is the main energy source for the brain. After severe head-injury energy demand is massively increased and supply is often decreased. In pilot microdialysis studies, many patients with severe head-injury had undetectable glucose concentrations, probably reflecting changes in metabolism and/or reduced supply. We therefore investigated whether patients with low ECF glucose (criterion: < 50 microM for > or = 5 hrs), LOWgluc, differ from patients with higher glucose levels (NORMALgluc) We also tested the interrelationships between other parameters such as lactate, glutamate, K+, brain O2 and CO2, ICP, CPP, and CBF in these two groups. We found that patients with low ECF glucose, LOWgluc, have significantly lower lactate concentrations than patients with "normal" glucose, NORMALgluc, levels do. Spearman correlations between glucose and most other parameters were similar in both patient groups. However, glutamate correlated positively with glucose, lactate, brain CO2 and negatively with brain O2 in the NORMALgluc patient group, whereas glutamate did not significantly correlate with any of these parameters in the LOWgluc group. There was also no correlation between outcome and the dialysate glucose. The results indicate that low ECF glucose is almost always present in severe head-injury. Moreover, the lack of correlation between low glucose and outcome, however, suggests that other energy substrates, such as lactate, are important after TBI.
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PMID:Low extracellular (ECF) glucose affects the neurochemical profile in severe head-injured patients. 1145 59

Neuroscientists continue the search for the "magic bullet" that will prevent the deleterious effects of primary and secondary brain injury. Indirect measurement of the effects of primary and secondary brain injury through the study of ICP- or CPP-directed management, CBF monitoring, Sjo2 monitoring, and TCD monitoring has led to improved care of persons with brain injury. Although the findings from brain injury research using microsensor and microdialysis technology are only preliminary and extensive research is still needed, these technologies have dramatically expanded knowledge about brain injury at the cellular level. Extended neuromonitoring is poised to enter a new and exciting phase because of the growth in knowledge regarding the cellular events associated with brain injury. The recent approval of NeuroTrend by the FDA will further promote this growth. Applications of the technology have already expanded to include uses beyond the management of traumatic brain injury. Microsensor and microdialysis technology is being used intraoperatively to determine "safe" temporary clipping times for aneurysm surgery and is also being used within the critical care setting to improve the monitoring and management of subarachnoid hemorrhage patients who are experiencing vasospasm. The ultimate application of this new technology is to improve long-term outcomes for patients with brain injury through the reduction of secondary brain injury. If that goal is to be accomplished, then it will be important for nurses caring for patients with brain injury to become immersed in this exciting new phase in brain injury monitoring. Nurses must obtain a comprehensive knowledge base of brain injury pathophysiology and how extended neuromonitoring can lead to improved outcomes. Technical proficiency will also be important to ensure that treatment and research conclusions are based on accurate data. Finally and perhaps most importantly, it will be critical for nurses to participate in and develop research studies that explore the impact of interventions, especially nursing care activities, on the injured brain if these exciting new advances are to be translated into tangible benefits for brain-injured patients.
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PMID:Microsensor and microdialysis technology. Advanced techniques in the management of severe head injury. 1185 47

The brain of neurosurgical patients are exposed to various manipulations in the ICU or during surgery. Under such conditions brain O2 balance may become negative and as a result brain vitality and function will deteriorate. In order to evaluate brain vitality in real time it is important to measure more than one parameter. The multiparametric monitoring system used in our previous study to monitor comatose patients (Mayevsky et al., Brain Res. 740: 268-274, 1996) was changed into a "simplified" tissue spectroscope for real time monitoring of brain O2 balance. Mitochondrial function was evaluated by monitoring the NADH redox state by surface fluorometry. Microcirculatory blood flow was assessed by laser Doppler flowmetry. The combined optical probe was located on the surface of the brain during various neurosurgical procedures and the responses were recorded and presented in real time to the surgeon. A total of 32 patients were monitored during various procedures. The results could be summarized as follows: 1. Hypercapnia led to 3 different types of responses. In two patients the 'stealing' like event was recorded. In the other 7 patients the responses to high CO2 was not detectable. In the last group of 6 patients a clear CBF elevation was recorded with variable response of mitochondrial NADH. 2. Our monitoring device was able to evaluate the efficacy of the STA-MCA anastomosis during aneurysm surgery. 3. A significant correlation was recorded between CBF and NADH redox state during changes in blood pressure, papaverine injection, spontaneous drop in blood supply to the brain or during releasing of high ICP levels. We conclude that in order to evaluate the metabolic state of the brain during neurosurgical procedures it is necessary to monitor both CBF and mitochondrial NADH by using the tissue spectroscope.
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PMID:The evaluation of brain CBF and mitochondrial function by a fiber optic tissue spectroscope in neurosurgical patients. 1216 49

The 'Cushing Response' is a significant phenomenon associated with elevated ICP. The purpose of our study was to examine the effects of the intracranial hypertension level and duration on the cerebral tissue physiology, using a Multiprobe assembly (MPA). The parameters monitored simultaneously included ICP, CBF, mitochondrial NADH redox state, extracellular K+ and H+ levels, DC potential and ECoG, calculated CPP and blood pressure. Two groups of rats were used. In one group, ICP was elevated to 50-60 mmHg for 13-15 min and, in the second group, ICP was elevated to 20 mmHg for 30 min. The results show that ICP of 50-60 mmHg led to CPP reduction below the lower limits of autoregulation. However, ICP of 20 mmHg, even for a prolonged period of time is completely tolerated. Additionally, we found that the 'Cushing Response', developed in the moderate treatment (ICP = 20 mmHg) is beneficial, assuring high CBF levels under intracranial hypertension. Furthermore, CBF and CPP monitoring, apparently, are not sufficient for autoregulation assessment; more parameters are needed.
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PMID:Effects of elevated ICP on brain function: can the multiparametric monitoring system detect the 'Cushing Response'? 1256 25


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