Pressure Autoregulation Research Articles

Dynamic Cerebral Autoregulation Changes during Sub-Maximal Handgrip Maneuver

PurposeWe investigated the effect of handgrip (HG) maneuver on time-varying estimates of dynamic cerebral autoregulation (CA) using the autoregressive moving average technique.MethodsTwelve healthy subjects were recruited to perform HG maneuver during 3 minutes with 30% of maximum contraction force. Cerebral blood flow velocity, end-tidal CO2 pressure (PETCO2), and noninvasive arterial blood pressure (ABP) were continuously recorded during baseline, HG and recovery. Critical closing pressure (CrCP), resistance area-product (RAP), and time-varying autoregulation index (ARI) were obtained.ResultsPETCO2 did not show significant changes during HG maneuver. Whilst ABP increased continuously during the maneuver, to 27% above its baseline value, CBFV raised to a plateau approximately 15% above baseline. This was sustained by a parallel increase in RAP, suggestive of myogenic vasoconstriction, and a reduction in CrCP that could be associated with metabolic vasodilation. The time-varying ARI index dropped at the beginning and end of the maneuver (p<0.005), which could be related to corresponding alert reactions or to different time constants of the myogenic, metabolic and/or neurogenic mechanisms.ConclusionChanges in dynamic CA during HG suggest a complex interplay of regulatory mechanisms during static exercise that should be considered when assessing the determinants of cerebral blood flow and metabolism.

The frequency response of cerebral autoregulation

The frequency-response of pressure autoregulation is not well delineated; therefore, the optimal frequency of arterial blood pressure (ABP) modulation for measuring autoregulation is unknown. We hypothesized that cerebrovascular autoregulation is band-limited and delineated by a cutoff frequency for which ABP variations induce cerebrovascular reactivity. Neonatal swine (n = 8) were anesthetized using constant minute ventilation while positive end-expiratory pressure (PEEP) was modulated between 6 and 0.75 cycles/min (min(-1)). The animals were hemorrhaged until ABP was below the lower limit of autoregulation (LLA), and PEEP modulations were repeated. Vascular reactivity was quantified at each frequency according to the phase lag between ABP and intracranial pressure (ICP) above and below the LLA. Phase differences between ABP and ICP were small for frequencies of >2 min(-1), with no ability to differentiate cerebrovascular reactivity between ABPs above or below the LLA. For frequencies of <2 min(-1), ABP and intracranial pressure (ICP) showed phase shift when measured above LLA and no phase shift when measured below LLA [above vs. below LLA at 1 min(-1): 156° (139-174°) vs. 30° (22-50°); P < 0.001 by two-way ANOVA for both frequency and state of autoregulation]. Data taken above LLA fit a Butterworth high-pass filter model with a cutoff frequency at 1.8 min(-1) (95% confidence interval: 1.5-2.2). Cerebrovascular reactivity occurs for sustained ABP changes lasting 30 s or longer. The ability to distinguish intact and impaired autoregulation was maximized by a 60-s wave (1 min(-1)), which was 100% sensitive and 100% specific in this model.

Towards simulation of germinal matrix hemorrhage as a complication of premature birth

The germinal matrix being an accumulation of immature blood vessels in the premature infant brain is known to be the main cause of the intracranial hemorrhage. To investigate the injuring mechanism to the blood vessels of the germinal matrix, a modeling scenario that consists of three basic steps is proposed. First, the cerebral blood flow that depends on autoregulation, CO2 reactivity, and variations of intracranial pressure is modeled. Second, the chaotic blood vessel network of the germinal matrix is generated, and blood pressures in the vessels of this network are computed dependent on the outcome of the first step. In the third step, the pressures computed on the second step are used in finite element simulations of separate blood vessels of the germinal matrix to detect critical values for vessels impairment.

Posterior reversible encephalopathy syndrome induced after blood transfusion for severe anemia

Posterior reversible encephalopathy syndrome (PRES) is a clinicoradiological syndrome characterized by headache, confusion, seizures, and cortical visual loss, as well as subcortical edema without infarction on neuroimaging. We report a 56-year-old woman who developed typical manifestations of PRES, 6 days after blood transfusion for severe anemia. Acute volume overloads by transfusion may exceed the capacity of autoregulation of perfusion pressure, possibly resulting in vasogenic edema. We propose that it is clinically important to recognize that rapid correction of anemia by blood transfusion may carry the risk of inducing PRES.

Critical Thresholds for Cerebrovascular Reactivity: Fact or Fiction?

To the Editor, We read with interest the recent publication by Sorrentino et al. [1] entitled: ‘‘Critical Thresholds for Cerebrovascular Reactivity after Traumatic Brain Injury’’. The study is based on the hypothesis that bedside real-time calculation of the pressure-reactivity index (PRx) allows a continuous estimation of cerebral pressure autoregulation [1–3]. From measurements of hydrostatic pressure alone the authors define threshold levels for survival as well as favorable outcome in patients with severe traumatic brain lesions. Pressure autoregulation is present in many tissues but it is most pronounced in the brain and the kidney. The main ‘‘physiological purpose’’ of pressure autoregulation is probably to keep intracapillary hydrostatic pressure relatively constant [4]. Changes in precapillary resistance (R) underlying cerebral pressure autoregulation are calculated from cerebral perfusion pressure (CPP) divided by cerebral blood flow (F): R = (Pa ICP)/F [5]. Accordingly, to describe cerebral vasoreactivity it is necessary to assess not only arterial blood pressure (Pa) and intracranial pressure (ICP) but also F. The authors behind the PRx method claim that cerebrovascular pressure reactivity may be estimated by observing the response of ICP to changes in Pa. PRx is in this study determined by calculating the correlation coefficient between 30 consecutive data points resulting from the time averaging of ICP and Pa signals with a width of the moving-average window of 8 s [1]. However, in our opinion it is obvious from the equation above that cerebrovascular resistance cannot be calculated unless cerebral blood flow is also assessed. The method of PRx is based on the assumption that the observed change in Pa is the primary and independent cause of the variations in the other three monitored variables. In the validity study of the PRx method Pa was increased by i.v. vasopressor infusion and F was measured utilizing PET-technique [3]. In this defined, experimental situation it is possible that the increase in Pa is the primary and independent cause of the variations in the other variables. Under clinical conditions this is, however, often not the case. During neurocritical care fluctuations in pain, sedation, stress level, local neuronal excitation, etc., will cause changes in cerebral energy metabolism resulting in variations in precapillary vasoconstriction and cerebral blood flow that are not a function of simultaneously occurring changes in Pa. All these sources of error are neglected when PRx is interpreted as a measure of cerebral pressure autoregulation. As the Cambridge group has also suggested that PRx is correlated to cerebral energy metabolism [6] it seems unlikely that this index might be used for continuous estimation pressure autoregulation as well. In their analyses of prognostic threshold levels the authors use mean values for the entire monitoring period for each parameter: ICP, CPP, and PRx. In the study, the monitoring periods vary between 6 h and 20 days. The authors comment on this fact in the section of limitations. However, in our opinion the consequences are more serious than mentioned by the authors and may invalidate the threshold levels arrived at. In patients with brain trauma mortality is usually caused by an increase in ICP and patients who die within the first few days of admission usually have a high ICP. However, patients who initially may have equally high ICP (in this C.-H. Nordstrom (&) T. H. Nielsen Department of Neurosurgery, Odense University Hospital, Odense, Denmark e-mail: carl-henrik.nordstrom@med.lu.se

Effects of Hypothermia on Cerebral Autoregulatory Vascular Responses in Two Rodent Models of Traumatic Brain Injury

Traumatic brain injury (TBI) can trigger disturbances of cerebral pressure autoregulation that can translate into the generation of secondary insults and increased morbidity/mortality. Few therapies have been developed to attenuate the damaging consequences of disturbed autoregulatory control, although some suggest that hypothermia may exert such protection. Here we reexamine this issue of traumatically induced autoregulatory disturbances and their modulation by hypothermic intervention, examining these phenomena in two different models of TBI. Adult rats were subjected to either impact acceleration injury (IAI) or lateral fluid percussion injury (LFPI) followed by the insertion of cranial windows to assess the pial arteriolar cerebral autoregulatory vascular response to the post-traumatic induction of sequential reductions of arterial blood pressure. The potential for continued pial vasodilation in response to declining blood pressure was directly measured post-injury and compared with that in injured groups subjected to 33° C of hypothermia of 1-2 h duration initiated 1 h post-injury. We observed that the TBI resulted in either impaired or abolished cerebral vascular dilation in response to the sequential declines in blood pressure. Following IAI there was a 50% reduction in the vasculature's ability to dilate in response to the induced hypotension. In contrast, following LFPI, the vascular response to hypotension was abolished both ipsilateral and contralateral to the LFPI. In animals sustaining IAI, the use of 1 h post-traumatic hypothermia preserved vascular dilation in response to declines in blood pressure in contrast to the LFPI in which the use of the same strategy afforded no improvement. However, with LFPI, the use of 2 h of hypothermia provided partial vascular protection. These results clearly illustrate that TBI can alter the cerebral autoregulatory vascular response to sequentially induced hypotensive insult, whereas the use of post-traumatic hypothermia provides benefit. Collectively, these studies also demonstrate that different animal models of TBI can evoke different biological responses to injury.

Continuous Monitoring of Cerebrovascular Reactivity Using Pulse Waveform of Intracranial Pressure

Guidelines for the management of traumatic brain injury (TBI) call for the development of accurate methods for assessment of the relationship between cerebral perfusion pressure (CPP) and cerebral autoregulation and to determine the influence of quantitative indices of pressure autoregulation on outcome. We investigated the relationship between slow fluctuations of arterial blood pressure (ABP) and intracranial pressure (ICP) pulse amplitude (an index called PAx) using a moving correlation technique to reflect the state of cerebral vasoreactivity and compared it to the index of pressure reactivity (PRx) as a moving correlation coefficient between averaged values of ABP and ICP. A retrospective analysis of prospective 327 TBI patients (admitted on neurocritical care unit of a university hospital in the period 2003-2009) with continuous ABP and ICP monitoring. PAx was worse in patients who died compared to those who survived (-0.04 ± 0.15 vs. -0.16 ± 0.15, χ2 = 28, p < 0.001). In contrast to PRx, PAx was able to differentiate between fatal and non-fatal outcome in a group of 120 patients with ICP levels below 15 mmHg (-0.04 ± 0.16 vs. -0.14 ± 0.16, χ2 = 6, p = 0.01). PAx is a new modified index of cerebrovascular reactivity which performs equally well as established PRx in long-term monitoring in severe TBI patients, but importantly is potentially more robust at lower values of ICP. In view of establishing an autoregulation-oriented CPP therapy, continuous determination of PAx is feasible but its value has to be evaluated in a prospective controlled trail.

Impaired cerebrovascular autoregulation and CO2 response are related to changes in systolic pressure after long‐duration spaceflight

Intracranial hypertension has been identified as a risk for long‐duration spaceflight. We monitored changes in cerebral blood flow velocity (CBFV) in response to changes in blood pressure (autoregulation) and CO2 before and after spaceflight (147±49 days) in 5 men and 1 woman to determine if changes in CBFV or cerebrovascular resistance index (CVRi) related to changes in systolic blood pressure (SBP). Autoregulation and CO2 reactivity were measured during a test where two breaths of 10% CO2 were given 4 times during a 5min period. The autoregulatory index of the CVRi response to BP was reduced post‐flight (0.035±0.007 to 0.029±0.005, p&lt;0.05) with a trend to a greater CBFV response to a change in BP (p=0.128). The post‐flight CVRi response to CO2 was significantly reduced (−0.038±0.018 to −0.028±0.012, p&lt;0.05) with a simultaneous reduction in the CBFV response to CO2 (p=0.056). The change in SBP from pre‐ to post‐flight was correlated with the change in CBFV per mmHg change in BP (r=0.66) and the change in CBFV per mmHg change in CO2 (r=0.71). Individuals with elevated post‐flight SBP were more likely to have impairment of autoregulation and of cerebrovascular health as indicated by CO2 reactivity. With short‐flights no impairment was found in non‐syncopal astronauts; it is unknown if sustained intracranial hypertension and/or elevated environmental CO2 contributed to these changes. Funded by Canadian Space Agency.

Computational modelling of the piglet brain to simulate near-infrared spectroscopy and magnetic resonance spectroscopy data collected during oxygen deprivation

We describe a computational model to simulate measurements from near-infrared spectroscopy (NIRS) and magnetic resonance spectroscopy (MRS) in the piglet brain. Piglets are often subjected to anoxic, hypoxic and ischaemic insults, as experimental models for human neonates. The model aims to help interpret measurements and increase understanding of physiological processes occurring during such insults. It is an extension of a previous model of circulation and mitochondrial metabolism. This was developed to predict NIRS measurements in the brains of healthy adults i.e. concentration changes of oxyhaemoglobin and deoxyhaemoglobin and redox state changes of cytochrome c oxidase (CCO). We altered and enhanced the model to apply to the anaesthetized piglet brain. It now includes metabolites measured by 31P-MRS, namely phosphocreatine, inorganic phosphate and adenosine triphosphate (ATP). It also includes simple descriptions of glycolysis, lactate dynamics and the tricarboxylic acid (TCA) cycle. The model is described, and its simulations compared with existing measurements from piglets during anoxia. The NIRS and MRS measurements are predicted well, although this requires a reduction in blood pressure autoregulation. Predictions of the cerebral metabolic rate of oxygen consumption (CMRO2) and lactate concentration, which were not measured, are given. Finally, the model is used to investigate hypotheses regarding changes in CCO redox state during anoxia.

The predominance of metabolic regulation of cerebral blood flow and the lack of "Classic" autoregulation curves in the viable brain

Background:The influence of cerebral perfusion pressure (CPP) on real-time focal cerebral blood flow (fCBF) is not fully understood, in either intact or injured brain. We wanted to evaluate that relationship, and by implication investigate the relative importance of perfusion pressure versus metabolism in the regulation and control of cerebral blood flow. Our hypothesis was that metabolic needs dominated over a physiologic range of blood pressure.Methods:This was an observational study of 23 patients, most of them with closed head injury, three with subarachnoid hemorrhage, one with a gunshot wound to the brain, and one monitored after craniotomy for unruptured aneurysm. Arterial lines, ventriculostomies, and fCBF monitors were placed. CPP (mean arterial pressure – intracranial pressure) and fCBF were measured and recorded to a computer database every minute. The relationship between CPP and fCBF was graphed and correlation coefficients were compared between survivors and non-survivors.Results:Graphs of CPP versus fCBF did not show any linearity over a range of 50–150 mm Hg in patients who survived. In those who died, four of seven showed some indication of linearity. The difference in the correlation coefficients between survivors and non-survivors was statistically significant (P < 0.05), with survivors having essentially no correlation, as expected with autoregulation intact, and non-survivors having a mean correlation of 0.311.Conclusions:In the functioning and viable brain, metabolic regulation of cerebral blood flow (CBF) predominates, leading to the lack of an obvious relationship between perfusion pressure and flow. This predominance of metabolic regulation is robust and preserved over a wide range of brain injury, with pressure autoregulation necessary but not clinically apparent in the metabolically active brain. This robust and constantly varying relationship of pressure and flow shown by our real-time measurements of fCBF has important implications for interpreting clinical measurements of autoregulation. Perhaps most importantly, the development of a correlation between pressure and flow may indicate and be an early warning of deterioration.

Are Optimal Cerebral Perfusion Pressure and Cerebrovascular Autoregulation Related to Long-term Outcome in Patients With Aneurysmal Subarachnoid Hemorrhage?

Continuous assessment of the cerebrovascular autoregulation (CVA) through use of the pressure reactivity index (PRx), a moving linear correlation coefficient between mean arterial blood pressure and intracranial pressure, has been effective in optimizing cerebral perfusion pressure (CPPopt) in traumatic brain injured (TBI) patients. This study investigates the feasibility of measuring CPPopt in patients with aneurysmal subarachnoid hemorrhage (aSAH) by continuously assessing the CVA. Twenty-nine aSAH patients were enrolled, and data from CVA status, CPPopt, and periods when CPP was below, within, or above CPPopt were computed daily. Outcome was assessed at 6 months with the Glasgow Outcome Scale. Mann-Whitney U test was used to analyze differences in the duration of impaired CVA and duration of CPP below CPPopt in patients with good and poor outcomes. Multivariable logistic regression analysis was used to identify independent predictors of outcome. CVA monitoring data were available for all 29 patients with a total monitoring time of 2757 h. The duration of impaired CVA was 36.5% (interquartile range: 24.6 to 49.8) of the total monitoring time in 15 patients with good outcome and 71.6% of the total monitoring time (51.2 to 80.0) in 14 patients with poor outcome (Mann-Whitney U test 3.295, P=0.0010). PRx-based CPPopt could be identified in 26 patients (89.6%) with a total monitoring time of 2691 h. The duration of CPP below the CPPopt range was 28.0% (interquartile range: 18.0 to 47.0) of the total monitoring time in patients with good outcome and 76.0% (48.5 to 82.5) in patients with poor outcome (Mann-Whitney U test 2.779, P=0.0054). Glasgow Coma Scale score and duration of impaired CVA were independently associated with 6-month outcome (Glasgow Coma Scale score odds ratio: 1.95, 95% confidence interval: 1.01-3.75; duration of impaired CVA odds ratio: 0.88, 95% confidence interval: 0.78-0.99). The assessment of CVA and CPPopt is feasible in aSAH patients and may provide important information regarding long-term outcome. A PRx above the 0.2 threshold and a CPP below the CPPopt range are associated with worse outcome.

Are Features of the Metabolic Syndrome Associated with Macular Thickness in Individuals without Diabetes Mellitus?

Background: Maculopathy is a common feature at diagnosis of type 2 diabetes. However, it is not known whether macular thickening, a potential preclinical sign of macular oedema, occurs in individuals with risk factors for diabetes. Purposes: To examine whether macular thickness is increased in individuals with features of the metabolic syndrome, namely waist circumference, blood pressure, and fasting levels of triglycerides, HDL-cholesterol and glucose in non-diabetic individuals. Methods: 50 non-diabetic Caucasian individuals were recruited (25 males, age range: 26-78 years, BMI range: 20-46 kg/m2). Macular thickness, divided into fovea and the inner and outer temporal, nasal, superior and inferior quadrants, was assessed by Optical Coherence Tomography. Additional assessments included: arterial blood pressure, fasting glucose and lipid profile (including triglycerides and HDL-cholesterol), BMI and waist circumference. Features of the metabolic syndrome were collectively entered into a forced regression model to examine their relationship with thickness in the macular subdivisions. Results: Fovea thickness was within the normal range for all participants. Features of the metabolic syndrome were not collectively associated with macular thickness. However, mean arterial blood pressure (MAP) was independently associated with macular thickness in all regions (standardized beta>0.381, p<0.05) except for the outer nasal quadrant (standardized beta=0.346, p=0.071) and a vascular fovea region (standardized beta=0.105, p=0.591). Conclusions: MAP, independent of other features of the metabolic syndrome, is associated with thickness in the inner and outer quadrants of the macular. Further research is needed to fully elucidate this relationship. However, potential explanations include altered pressure autoregulation (pressure or metabolic induced) and microvascular rarefaction.

Multimodality Monitoring for Cerebral Perfusion Pressure Optimization in Comatose Patients With Intracerebral Hemorrhage

Limited data exist to recommend specific cerebral perfusion pressure (CPP) targets in patients with intracerebral hemorrhage. We sought to determine the feasibility of brain multimodality monitoring for optimizing CPP and potentially reducing secondary brain injury after intracerebral hemorrhage. We retrospectively analyzed brain multimodality monitoring data targeted at perihematomal brain tissue in 18 comatose intracerebral hemorrhage patients (median monitoring, 164 hours). Physiological measures were averaged over 1-hour intervals corresponding to each microdialysis sample. Metabolic crisis was defined as a lactate/pyruvate ratio >40 with a brain glucose concentration <0.7 mmol/L. Brain tissue hypoxia (BTH) was defined as P(bt)O(2) <15 mm Hg. Pressure reactivity index and oxygen reactivity index were calculated. Median age was 59 years, median Glasgow Coma Scale score was 6, and median intracerebral hemorrhage volume was 37.5 mL. The risk of BTH, and to a lesser extent metabolic crisis, increased with lower CPP values. Multivariable analyses showed that CPP <80 mm Hg was associated with a greater risk of BTH (odds ratio, 1.5; 95% confidence interval, 1.1-2.1; P=0.01) compared to CPP >100 mm Hg as a reference range. Six patients died (33%). Survivors had significantly higher CPP and P(bt)O(2) and lower ICP values starting on postbleed day 4, whereas lactate/pyruvate ratio and pressure reactivity index values were persistently lower, indicating preservation of aerobic metabolism and pressure autoregulation. P(bt)O(2) monitoring can be used to identify CPP targets for optimal brain tissue oxygenation. In patients who do not undergo multimodality monitoring, maintaining CPP >80 mm Hg may reduce the risk of BTH.

Pulsatile Intracranial Pressure and Cerebral Autoregulation After Traumatic Brain Injury

Strong correlation between mean intracranial pressure (ICP) and its pulse wave amplitude (AMP) has been demonstrated in different clinical scenarios. We investigated the relationship between invasive mean arterial blood pressure (ABP) and AMP to explore its potential role as a descriptor of cerebrovascular pressure reactivity after traumatic brain injury (TBI). We retrospectively analyzed data of patients suffering from TBI with brain monitoring. Transcranial Doppler blood flow velocity, ABP, ICP were recorded digitally. Cerebral perfusion pressure (CPP) and AMP were derived. A new index-pressure-amplitude index (PAx)-was calculated as the Pearson correlation between (averaged over 10s intervals) ABP and AMP with a 5min long moving average window. The previously introduced transcranial Doppler-based autoregulation index Mx was evaluated in a similar way, as the moving correlation between blood flow velocity and CPP. The clinical outcome was assessed after 6months using the Glasgow outcome score. 293 patients were studied. The mean PAx was -0.09 (standard deviation 0.21). This negative value indicates that, on average, an increase in ABP causes a decrease in AMP and vice versa. PAx correlated strong with Mx (R (2)=0.46, P<0.0002). PAx also correlated with age (R (2)=0.18, P<0.05). PAx was found to have as good predictive outcome value (area under curve 0.71, P<0.001) as Mx (area under curve 0.69, P<0.001). We demonstrated significant correlation between the known cerebral autoregulation index Mx and PAx. This new index of cerebrovascular pressure reactivity using ICP pulse wave information showed to have a strong association with outcome in TBI patients.

Rapid Assessment of Cerebral Autoregulation by Near-Infrared Spectroscopy and a Single Dose of Phenylephrine

Rapid bedside determination of cerebral blood pressure autoregulation (AR) may improve clinical utility. We tested the hypothesis that cerebral Hb oxygenation (HbDiff) and cerebral Hb volume (HbTotal) measured by near-infrared spectroscopy (NIRS) would correlate with cerebral blood flow (CBF) after single dose phenylephrine (PE). Critically ill patients requiring artificial ventilation and arterial lines were eligible. During rapid blood pressure rise induced by i.v. PE bolus, ΔHbDiff and ΔHbTotal were calculated by subtracting values at baseline (normotension) from values at peak blood pressure elevation (hypertension). With the aid of NIRS and bolus injection of indocyanine green, relative measures of CBF, called blood flow index (BFI), were determined during normotension and during hypertension. BFI during hypertension was expressed as percentage from BFI during normotension (BFI%). Autoregulation indices (ARIs) were calculated by dividing BFI%, ΔHbDiff, and ΔHbTotal by the concomitant change in blood pressure. In 24 patients (11 newborns and 13 children), significant correlations between BFI% and ΔHbDiff (or ΔHbTotal) were found. In addition, the associations between Hb-based ARI and BFI%-based ARI were significant with correlation coefficients of 0.73 (or 0.72). Rapid determination of dynamic AR with the aid of cerebral Hb signals and PE bolus seems to be reliable.

The Role of Ocular Blood Flow in the Pathogenesis of Glaucomatous Damage

Ocular blood flow (OBF) is on average lower in glaucoma patients than in healthy controls. This reduction is more pronounced in normal-tension than in high-tension glaucoma and more distinct in cases with progressing damage as compared to those with stable disease. Besides a secondary component caused by atrophy, there is an important primary component of OBF reduction, which also has a predictive value. The fact that hypoxia-related factors are upregulated in eyes of glaucoma patients indicates oxygen depletion. It is, however, not constant hypoxia, but rather the fluctuation of oxygen supply that leads to tissue damage, likely because of oxidative stress. Low perfusion pressure and disturbed autoregulation are the major causes of insufficient and fluctuating oxygen supply, and both systemic hypotension and disturbed autoregulation are often consequences of the primary vascular dysregulation syndrome. The observed splinter hemorrhages in these patients are a consequence of a local breakdown of the blood–brain or blood–retinal barrier. The often associated vein occlusions can be a consequence of a local vein dysregulation.

Favorable Outcome in Traumatic Brain Injury Patients With Impaired Cerebral Pressure Autoregulation When Treated at Low Cerebral Perfusion Pressure Levels

Cerebral pressure autoregulation (CPA) is defined as the ability of the brain vasculature to maintain a constant blood flow over a range of different systemic blood pressures by means of contraction and dilatation. To study CPA in relation to physiological parameters, treatment, and outcome in a series of traumatic brain injury patients. In this prospective observational study, 44 male and 14 female patients (age, 15-72 years; mean, 38.7 years; Glasgow Coma Scale score, 4-13; median, 7) were analyzed. Patients were divided into groups on the basis of status of CPA (more pressure active vs more pressure passive) and level of cerebral perfusion pressure (CPP; low vs high CPP). The proportions of favorable outcome in the groups were assessed. Differences in physiological variables in the different groups were analyzed. Patients with more impaired CPA treated at CPP levels below median had a significantly higher proportion of favorable outcome compared with patients with more impaired CPA treated at CPP levels above median. No significant difference in outcome was seen between patients with more intact CPA when divided by level of CPP. In patients with more impaired CPA, CPP<50 mm Hg and CPP<60 mm Hg were associated with favorable outcome, whereas CPP>70 mm Hg and CPP>80 mm Hg were associated with unfavorable outcome. In patients with more intact CPA, no difference in physiological variables was seen between patients with favorable and unfavorable outcomes. Our results support that in traumatic brain injury patients with impaired CPA, CPP should not be elevated.

Simulated annealing-based particle swarm optimisation with adaptive jump strategy for modelling of dynamic cerebral pressure autoregulation mechanism

This paper proposes a new particle swarm optimisation (PSO) algorithm based on simulated annealing (SA) with adaptive jump strategy to alleviate some of the limitations of the standard PSO algorithm. In this algorithm, swarm particles jump into the space to find new solutions. The jump radius is selected adaptively based on the particle velocity and its distance from the global best position. The designed algorithm has been tested on benchmark optimisation functions and on known autoregressive exogenous (ARX) model design problem. The results are superior as compared to the existing PSO methods. Finally, the designed algorithm has been applied for the analysis of the dynamic cerebral autoregulation mechanism.

Regulation of Cerebral Blood Flow

The control of cerebral blood flow is complex, and only beginning to be elucidated. Studies have identified three key regulatory paradigms. The first is cerebral pressure autoregulation, which maintains a constant flow in the face of changing cerebral perfusion pressure. Flow-metabolism coupling refers to the brains ability to vary blood flow to match metabolic activity. An extensive arborization of perivascular nerves also serves to modulate cerebral blood flow, so-called neurogenic regulation. Central to these three paradigms are two cell types: endothelium and astrocytes. The endothelium produces several vasoactive factors that are germane to the regulation of cerebral blood flow: nitric oxide, endothelium-dependent hyperpolarization factor, the eicosanoids, and the endothelins. Astrocytic foot processes directly abut the blood vessels, and play a key role in regulation of cerebral blood flow. Lastly, new research has been investigating cell-cell communication at the microvascular level. Several lines of evidence point to the ability of the larger proximal vessels to coordinate vasomotor responses downstream.

Hemodynamic Studies of Intracranial Dural Arteriovenous Fistulas Using Arterial Spin-Labeling MR Imaging

Arterial spin-labeling (ASL) magnetic resonance imaging (MRI) enables non-invasive acquisition of the brain perfusion information in cerebrovascular disease. We investigated hemodynamic changes in intracranial dural arteriovenous fistulas (DAVFs) using ASL-MRI. ASL-MRI by a Q2TIPS sequence on a 3.0-Tesla MRI was performed for three patients with Cognard's IIa+b type of DAVFs before and after treatment. Perfusion images obtained by ASL-MRI (ASL images) before treatment were visually compared with those by single-photon emission computed tomography images (SPECT images). Increasing rates of temporal changes of regional perfusion values in ASL images (ASL values) before and after treatment were also calculated. In all three patients, ASL images before treatment demonstrated high perfusion in regions around the shunting areas, where normal or low perfusion were detected on SPECT images; thus, ASL images might have demonstrated the abundant arterial shunting flow via the fistulas. On days eight to 20 after treatment, ASL values around the shunt areas remained the same or decreased, and those in the regions other than the shunt areas increased in all three patients. This might have been due to a combination of the following: a decrease in shunt flow volume, an amelioration of venous congestion, and a sustained an upward shift in the autoregulation of the brain perfusion pressure. All regional ASL values decreased on days 112 and 120 after treatment in two patients, which possibly reflects a reduction in the upward shift in autoregulation. ASL-MRI might be useful for identifying the hemodynamic behavior of DAVFs before and after treatment.