Changes In Cerebral Blood Velocity Research Articles

Continuous monitoring methods of cerebral compliance and compensatory reserve: a scoping review of human literature.

Continuous monitoring of cerebrospinal compliance (CC)/ cerebrospinal compensatory reserve (CCR) is crucial for timely interventions and preventing more substantial deterioration in the context of acute neural injury, as it enables the early detection of abnormalities in intracranial pressure (ICP). However, to date, the literature on continuous CC/CCR monitoring is scattered and occasionally challenging to consolidate. 
Approach: 
We subsequently conducted a systematic scoping review of the human literature to highlight the available continuous CC/CCR monitoring methods.
Main Results:
This systematic review incorporated a total number of 76 studies, covering diverse patient types and focusing on three primary continuous CC or CCR monitoring metrics and methods - Moving Pearson's correlation between ICP pulse amplitude waveform (AMP) and ICP, referred to as RAP, the Spiegelberg Compliance Monitor, changes in cerebral blood velocity (CBV) with respect to the alternation of ICP measured through Transcranial Doppler (TCD), changes in centroid metric, high frequency centroid (HFC) or higher harmonics centroid (HHC), and the P2/P1 ratio which are the distinct peaks of ICP pulse wave (ICPW). The majority of the studies in this review encompassed RAP metric analysis (n=43), followed by Spiegelberg Compliance Monitor (n=11), TCD studies (n=9), studies on the HFC/HHC (n=5), and studies on the P2/P1 ratio studies (n=6). These studies predominantly involved acute traumatic neural injury (i.e. Traumatic Brain Injury (TBI)) patients and those with hydrocephalus. RAP is the most extensively studied of the five focused methods and exhibits diverse applications. However, most papers lack clarification on its clinical applicability, a circumstance that is similarly observed for the other methods.
Significance: Future directions involve exploring RAP patterns and identifying characteristics and artifacts, investigating neuroimaging correlations with continuous CC/CCR and integrating machine learning, holding promise for simplifying CC/CCR determination. These approaches should aim to enhance the precision and accuracy of the metric, making it applicable in clinical practice.&#xD.

Rapid Changes in Cerebrovascular Compliance During Vasovagal Syncope

Background: The rapid reduction in arterial blood pressure (ABP) during vasovagal syncope (VVS) is associated with a characteristic decline in diastolic cerebral blood velocity (CBV) and maintained systolic CBV as measured by transcranial Doppler. This increased pulsatility was originally considered to be indicative of a “dysfunctional” increase in cerebrovascular resistance (CVR). Conversely, it may be due to increased cerebrovascular compliance (Ci) that partially attenuates the cerebral effects of rapid hypotension. We tested the hypothesis that Ci supports CBV during pre-syncope in VVS. Method: Finger ABP and right middle cerebral artery blood velocity (MCAv) were recorded from 15 otherwise healthy patients (n = 11 female, 40 ± 16 years, 24.9 ± 4.0 kg/m2) at rest and during head-up tilt (80°, 5 to 28 min). Individual ABP and CBV waveforms of every second heartbeat during VVS were input into a modified Windkessel model to calculate Ci and CVR. MCAv pulsatility was determined as pulse amplitude (systolic MCAv-diastolic MCAv) and Pulsatility Index (Pi; pulse amplitude/mean MCAv). Linear mixed models assessed the contribution of Ci to changes in CBV and Pi. Within-subject mediation analysis investigated the possibility of Ci mediating the relation between blood pressure (i.e., mean ABP and pulse pressure, PP) and cerebrovascular pulsatility. Results: Diastolic and systolic ABP decreased progressively during presyncope, resulting in a nadir reduction of mean ABP of Δ24 ± 9 mmHg at end-tilt (all p ≤ 0.04 vs mid-tilt). Mean MCAv decreased by 22 ± 12% prior to end-tilt (p < 0.01 vs mid-tilt). CVR decreased progressively for 10s prior to end-tilt (p ≤ 0.04 vs mid-tilt). Pi increased significantly, with peak increases occurring at 4 s prior to end-tilt (77 ± 50%, p < 0.01 vs mid-tilt). The increase in Ci (307 ± 223%, p < 0.01 vs mid-tilt) significantly contributed to changes in MCAv (χ2 =10.6, p < 0.01) and Pi (χ2 = 4.9, p = 0.03). Correlations of PP and ABP with Pi were not significant. However, PP was related to MCAv pulse amplitude (total effect: b = 1.57) and Ci ( b = -0.01, both p < 0.01). Ci partially mediated (indirect effect: b = -0.78, p < 0.01) the direct relation between PP and MCAv pulse amplitude ( b = 0.79, p = 0.01). Conclusion: These data provide evidence that Ci attenuates the fall in CBV under conditions of falling PP. Cerebrovascular regulation in VVS appears to be functioning as in healthy populations. However, this regulation is not suffcient to preserve flow in the presence of such extreme and rapid reductions in ABP. USRI — Western University, Natural Sciences and Engineering Research Council of Canada (NSERC, Grant No. RGPIN-2018-06255). This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Abstract 17121: Elevated Aortic Stiffness and Impairments in Cerebrovascular Regulation in Cancer Survivorship

Background: Approximately 46% of cancer survivors report cognitive impairments across many types of cancer, which has been associated with anti-cancer therapy and often results in reduced quality of life. Pre-clinical studies suggest that predictors of cognitive decline may involve vascular dysfunction. We aimed to characterize local (cerebrovascular reactivity and cerebral autoregulation) and global (aortic arch stiffness) vascular regulation in cancer survivorship. Methods: Cerebral autoregulation was determined using Mx, a moving 10s-windowed correlation between finger plethysmography-derived blood pressure and cerebral blood velocity of the middle cerebral artery. Higher Mx values represent pressure-passive cerebral blood flow, indicating poor cerebral autoregulation. In addition, cerebral blood velocity, blood pressure, and end-tidal CO 2 were collected during a rebreathing task. MAP was used to calculate an index of cerebrovascular conductance (CVCi). Cerebrovascular reactivity was calculated as the change in cerebral blood velocity or CVCi over the change in end-tidal CO 2 . Aortic arch stiffness, as pulse wave velocity (aaPWV), was calculated from ultrasound scans of the aortic valve and the descending aorta. Differences between groups were assessed with Mann-Whitney tests. Results: Eleven women were recruited (5 controls and 6 cancer survivors who had received treatment). Cancer types included melanoma, lymphoma, and breast cancer. Age and resting MAP were similar between groups. Mx values were higher in cancer survivors (-0.13 ± 0.14 vs. 0.14 ± 0.11, p < 0.05). Cerebrovascular reactivity, both absolute (2.8 ± 1.1 vs. 1.6 ± 0.8, p = 0.05) and as CVCi (16.8 ± 2.4 vs. 2.3 ± 9.4, p < 0.05), were lower in cancer survivors. aaPWV was higher in cancer survivors (2.7 ± 0.8 vs. 3.8 ± 0.6, p < 0.05). Across the entire study sample, aaPWV trended towards an association only with absolute cerebrovascular reactivity (Spearman r = -0.6, p = 0.054). Conclusion: Aortic stiffness was elevated and both cerebrovascular regulatory functions were impaired in cancer survivors compared to healthy controls. Present findings highlight the importance of monitoring cerebral and global vascular function in cancer survivors at high-risk for cognitive decline.

NEUROVASCULAR COUPLING AND CEREBROVASCULAR HAEMODYNAIMCS ARE MODIFIED BY EXERCISE TRAINING STATUS AT DIFFERENT STAGES OF MATURATION DURING YOUTH.

Neurovascular coupling (NVC) is mediated via nitric oxide signalling, which is independently influenced by sex hormones and exercise training. Whether exercise training differentially modifies NVC pre- vs. post-puberty, where levels of circulating sex hormones will differ greatly within- and between-sexes, remains to be determined. Therefore, we investigated the influence of exercise training-status on resting intra-cranial haemodynamics and NVC at different stages of maturation. Posterior and middle cerebral artery velocities (PCAv and MCAv) and pulsatility index (PCAPI and MCAPI) were assessed via trans-cranial Doppler ultrasound at rest and during visual NVC stimuli. N=121 exercise-trained (males: n=32, females: n=32) and untrained (males: n=28, females: n=29) participants were characterised as pre- (males: n=33, females: n=29) or post- (males: n=27, females: n=32) peak height velocity (PHV). Exercise-trained youth demonstrated higher resting MCAv (P=0.010). Maturity- and training-status did not affect the ∆PCAv and ∆MCAv during NVC. However, pre-PHV untrained males (19.4±13.5 vs. 6.8±6.0%; P≤0.001) and females (19.3±10.8 vs. 6.4±7.1%; P≤0.001) had a higher ∆PCAPI during NVC than post-PHV untrained counterparts, while the ∆PCAPI was similar in pre- and post-PHV trained youth. Pre-PHV untrained males (19.4±13.5 vs. 7.9±6.0%; P≤0.001) and females (19.3±10.8 vs 11.1±7.3%; P=0.016) also had a larger ∆PCAPI than their pre-PHV trained counterparts during NVC, but the ∆PCAPI was similar in trained and untrained post-PHV youth. Collectively, our data indicate that exercise training elevates regional cerebral blood velocities during youth, but training-mediated adaptations in NVC are only attainable during early stages of adolescence. Therefore, childhood provides a unique opportunity for exercise-mediated adaptations in NVC.

Application of transcranial Doppler in cerebrovascular diseases.

Transcranial Doppler (TCD) is a rapid and non-invasive diagnostic technique that can provide real-time measurements of the relative changes in cerebral blood velocity (CBV). Therefore, TCD is a useful tool in the diagnosis and treatment of clinical cerebrovascular diseases (CVDs). In this review, the basic principles of TCD and its application in CVD were outlined. Specifically, TCD could be applied to evaluate occlusive CVD, assess collateral circulation in patients with ischemic stroke, and monitor cerebral vascular occlusion before and after thrombolysis as well as cerebral vasospasm (VSP) and microembolization signals after aneurysmal subarachnoid hemorrhage (SAH). Moreover, TCD could predict short-term stroke and transient cerebral ischemia in patients with anterior circulation occlusion treated with endovascular therapy and in patients with anterior circulation vascular occlusion. Additionally, TCD not only could monitor blood velocity signals during carotid endarterectomy (CEA) or carotid artery stenting (CAS) but also allowed earlier intervention through early recognition of sickle cell disease (SCD). Presently, TCD is a useful prognostic tool to guide the treatment of CVD. On the one hand, TCD is more commonly applied in clinical research, and on the other hand, TCD has an increasing role in the management of patients. Collectively, we review the principles and clinical application of TCD and propose some new research applications for TCD.

Directional sensitivity of dynamic cerebral autoregulation in squat-stand maneuvers.

Dynamic cerebral autoregulation (CA), the transient response of cerebral blood flow (CBF) to rapid changes in arterial blood pressure (BP), is usually modeled as a linear mechanism. We tested the hypothesis that dynamic CA can display nonlinear behavior resulting from differential efficiency dependent on the direction of BP changes. Cerebral blood velocity (CBV) (transcranial Doppler), heart rate (HR) (three-lead ECG), continuous BP (Finometer), and end-tidal CO2 (capnograph) were measured in 10 healthy young subjects during 15 squat-stand maneuvers (SSM) with a frequency of 0.05 Hz. The protocol was repeated with a median (interquartile range) of 44 (35-64) days apart. Dynamic CA was assessed with the autoregulation index (ARI) obtained from CBV step responses estimated with an autoregressive moving-average model. Mean BP, HR, and CBV were different (all P < 0.001) between squat and stand, regardless of visits. ARI showed a strong interaction ( P < 0.001) of SSM with the progression of transients; in general, the mean ARI was higher for the squat phase compared with standing. The changes in ARI were partially explained by concomitant changes in CBV ( P = 0.023) and pulse pressure ( P < 0.001), but there was no evidence that ARI differed between visits ( P = 0.277). These results demonstrate that dynamic CA is dependent on the direction of BP change, but further work is needed to confirm if this finding can be generalized to other physiological conditions and also to assess its dependency on age, sex and pathology.

Does gradual change in head positioning affect cerebrovascular physiology?

We studied cerebral blood velocity (CBV), and associated hemodynamic parameters during gradual changes in head positioning in a nonstroke group. CBV (transcranial Doppler ultrasound), beat‐to‐beat blood pressure (BP, Finometer), and end‐tidal carbon dioxide (ETCO 2, capnography) were recorded between lying flat (0°) and sitting up (30°) head positions, in 18 volunteers (10 female, mean age, 57 ± 16 years), at two visits (12 ± 8 days). A significant reduction was found between 5‐min FLAT (0°) and 5‐min SIT (30°) positions in CBV (visit 1: 4.5 ± 3.3%, P = 0.006; visit 2: 4.1 ± 3.5%, P = 0.003), critical closing pressure (CrCP; visit 1: 15.5 ± 14.0%, P = 0.0002; visit 2: 14.1 ± 7.8%, P = 0.009) and BP (visit 1: 8.3 ± 7.4%, P = 0.001; visit 2: 11.0 ± 11.3%, P < 0.001). For 5 min segments of data, the autoregulation index and other hemodynamic parameters did not show differences either due to head position or visit. For 30 sec time intervals, significant differences were observed in the following: (BP, P < 0.001; dominant hemisphere (DH) CBV, P < 0.005; nondominant hemisphere (NDH) CBV, P < 0.005; DH CrCP, P < 0.001; NDH CrCP, P < 0.001; DH resistance area product (RAP), P = 0.002; NDH RAP, P = 0.033). Significant static changes in BP, CBV and CrCP, and large transient changes in key hemodynamic parameters occur during 0° to 30°, and vice versa, with reproducible results. Further studies are needed following acute ischemic stroke to determine if a similar responses is present.

Blunted cerebral vascular responsiveness to hypercapnia in obese individuals.

What is the central question of this study? Is there a difference in the cerebral vascular response to rebreathing-induced hypercapnia between obese and lean individuals? What is the main finding and its importance? The main finding is that obese individuals have an attenuated increase in cerebral vascular conductance during hypercapnia relative to lean individuals. This finding suggests cerebral vascular dysfunction in this population, which might contribute to the greater prevalence of cerebral vascular and neurocognitive disease in this population. Obesity increases the risk of cardiovascular disease by >45%. Furthermore, obesity is a contributory factor to cognitive impairment and Alzheimer's disease. The mechanisms accounting for this increased disease risk have not been clarified. This study tested the hypothesis that the total range of change (a) in cerebral blood velocity (CBV) and cerebral vascular conductance (CVCI) and the maximal (y0) CBV and CVCI achieved during rebreathing-induced hypercapnia would be attenuated in obese individuals. Sixteen lean and 15 obese individuals participated. The magnitude of rebreathing-induced hypercapnia was similar between groups (lean, ∆15±3mmHg versus obese, ∆15±2mmHg; P=0.82). The total range of change in CBV during rebreathing (a; expressed as a percentage) was similar between groups (lean, 91±24% versus obese, 76±19%, P=0.07), whereas the total range of change in CVCI during rebreathing (a; expressed as a percentage) was attenuated in the obese individuals (lean, 71±20% versus obese, 51±15%, P<0.01). Likewise, the maximal increase in CBV during rebreathing (y0; expressed as a percentage) was similar between groups (lean, 189±22% versus obese, 179±20%, P=0.20), whereas the maximal increase in CVCI during rebreathing (y0; expressed as a percentage) was attenuated in the obese individuals (lean, 172±19% versus obese, 155±17 %, P=0.01). These data indicate that the cerebral vascular response to rebreathing-induced hypercapnia is attenuated in obese individuals. This impairment might be a factor contributing to the elevated cerebral vascular and neurocognitive disease risk in this population.

Neurovascular coupling response is maintained despite exposure to repetitive sub-concussive head trauma over the course of one contact-sport season

ObjectiveTo examine how head-impact exposures affect the elevation in cerebral blood velocity (CBV) in the posterior cerebral artery (PCA) during visual tasks.DesignProspective Cohort.SettingLaboratory.ParticipantsTo date: 40 male contact-sport athletes (19.4±1.2 years) and 3 cross-country athletes (20.0±1.0 years) have completed testing (non-contact controls).InterventionTranscranial Doppler ultrasound indexed PCA CBV during visual tasks. Participants closed their eyes (20-seconds), and when prompted, opened them and completed a visual task (40-seconds). Testing occurred prior-to and upon-completion-of the competitive athletic season. Raw traces from each trial were averaged to enhance the signal-to-noise ratio of outcome measurements. Independent variable tested was time (2).OutcomeEyes-closed CBV (cm/s), peak elevation in CBV (cm/s), relative change in CBV (%) and total activation during the first 30 seconds of the task (indexed via area under the curve-AUC). Head-impact exposure was characterised in a subset of contact-sport athletes (n=29) using the xPatch (X2 Biosystems).Main resultsRM-ANOVA indicated the contact-sport season had no effects on any outcome metrics: Eyes-closed CBV (p=0.181), peak CBV (p=0.117),% CBV elevation (p=0.252) and AUC (p=0.366), despite experiencing cumulative peak linear accelerations of 8147.2±6215.5g, and cumulative peak rotational accelerations of 34.5×106± 59.0×106rad/?s2.ConclusionsThe results from this study suggest neurovascular coupling metrics are maintained throughout a contact-sport season. This indicates nutrient delivery is maintained for neurocognitive challenges despite possible impairments in cerebrovasculature’s ability to buffer blood pressure challenges associated elevations in rotational accelerations experienced during a contact-sport season.Competing interestsNone.

A history of multiple concussions does not alter the transcranial doppler-based assessment of the neurovascular coupling response

ObjectiveTo determine how a history of 3+ concussions alters elevations in cerebral blood velocity (CBV) in the posterior cerebral artery (PCA) during visual tasks.DesignRetrospective Cohort.SettingLaboratory.Participants136 male contact-sport athletes (19.1±1.4 years, 66 football, 70 hockey) were recruited; 39 presented with 0 previous concussions, 16 with 3+ previous concussions; exclusion criteria included history of concussion within 6 months.InterventionTranscranial Doppler ultrasound indexed PCA-CBV during a series of visual tasks. Participants closed their eyes (20-seconds) and, when prompted, opened their eyes to complete a visual task (40-seconds). Testing occurred prior to the start of their athletic season. The visual trial raw traces were averaged together to enhance the signal-to-noise ratio of outcome measurements. The independent variable tested was concussion history.OutcomesEyes-closed CBV (cm/s), peak elevation in CBV after eyes-open (cm/s), relative change in CBV (%), and total activation during the first 30 seconds of the task (indexed via area under the curve-AUC)Main resultsIndependent samples T-Tests indicated there were no effects of concussion history on any outcome: Eyes-closed CBV (p=0.950), peak CBV (p=0.903), % CBV elevation (p=0.593), and AUC (p=0.718).ConclusionsA history of multiple concussions does not alter the cerebrovasculature’s ability to maintain nutrient delivery required for visual challenges in cortical areas supplied by the PCA. This is an important finding; despite the long-term neurocognitive deficits associated with a history of concussions, the transcranial Doppler assessment of neurovascular coupling appears intact for this population of younger adult contact-sport athletes.Competing interestsNone.

Learning and assessment with images: A view of cognitive load through the lens of cerebral blood flow

AbstractUnderstanding the relationship between cognitive processing and learner performance on tasks using digital media has become increasingly important as the transition towards online learning programs increases. Determining the impact of implementation of instructional resources is often limited to performance outcomes and comparisons to the status quo. This study measured changes in cerebral blood velocity (CBV) of the right middle cerebral artery during visual learning tasks using static images. Transcranial Doppler ultrasonography was used to compare the changes in CBV during learning of individuals with high and low spatial ability. Our results show that there is a slight increase from baseline values of CBV in individuals with high spatial ability during the learning task for the present study. In contrast, individuals with low spatial ability experience a decrement from baseline during the learning task. These results suggest spatial ability mitigates cognitive load and potentially has an impact on learner performance on visual learning tasks.

Reproducing the Hemoglobin Saturation Profile, a Marker of the Blood Oxygenation Level Dependent (BOLD) fMRI Effect, at the Microscopic Level.

The advent of functional MRI in the mid-1990s has catalyzed progress pertaining to scientific discoveries in neuroscience. With the prospect of elucidating the physiological aspect of the Blood Oxygenation Level Dependent (BOLD) effect we present a computational capillary-tissue system capable of mapping venous hemoglobin saturation— a marker of the BOLD hemodynamic response. Free and facilitated diffusion and convection for hemoglobin and oxygen are considered in the radial and axial directions. Hemoglobin reaction kinetics are governed by the oxyhemoglobin dissociation curve. Brain activation, mimicked by dynamic transitions in cerebral blood velocity (CBv) and oxidative metabolism (CMRO2), is simulated by normalized changes in m = (ΔCBv/CBv)/(ΔCMRO2/CMRO2) of values 2, 3 and 4. Venous hemoglobin saturation profiles and peak oxygenation results, for m = 2, based upon a 50% and a 25% increase in CBv and CMRO2, respectively, lie within physiological limits exhibiting excellent correlation with the BOLD signal, for short-duration stimuli. Our analysis suggests basal CBv and CMRO2 values of 0.6 mm/s and 200 μmol/100g/min. Coupled CBv and CMRO2 responses, for m = 3 and m = 4, overestimate peak hemoglobin saturation, confirming the system’s responsiveness to changes in hematocrit, CBv and CMRO2. Finally, factoring in neurovascular effects, we show that no initial dip will be observed unless there is a time delay in the onset of increased CBv relative to CMRO2.

Brain Blood Flow and Velocity

Because transcranial Doppler sonography (TCD) is unable to measure arterial diameter, it remains unproven whether the changes in cerebral blood velocity it measures are representative of changes in cerebral blood flow (CBF). Our study was designed to compare velocity changes with flow changes measured by two magnetic resonance imaging (MRI) techniques, perfusion MRI and arterial spin labeling (ASL), using flavanol-rich cocoa to induce CBF changes in healthy volunteers. We enrolled 20 healthy volunteers aged 62 to 80 years (mean, 73 years). Each was studied at baseline and after drinking standardized servings of cocoa for 7 to 14 days. Changes in middle cerebral artery (MCA) flow by TCD were significantly correlated with changes in perfusion assessed by gadolinium-enhanced MRI (r = 0.63; P < .03). Measurements with ASL showed a stronger correlation with borderline significance. Changes in flow velocity in the MCA associated with drinking cocoa were highly correlated with changes in CBF measured by the two MRI techniques using the tracer gadolinium and ASL. These results validate Doppler measurements of CBF velocity as representative assessments of CBF.

Study on Yangxue Qingnao granule in treating chronic cerebrovascular insufficiency

To observe the therapeutic effect of Yangxue Qingnao granule (YXQNG) in treating chronic cerebrovascular insufficiency (CCI) and its possible mechanism. Eighty-three patients with CCI were randomly divided into YXQNG and nimodipine (ND) groups, the score of vertigo and the change in cerebral blood velocity before and after treatment were observed. And in the animal experiment, the authors adopted bilateral ligation of cervical carotid communis artery to establish CCI rat models in order to observe the effect of YXQNG and ND on incubation period of vertigo in rats and on memory performance. After clinical treatment, the vertigo score of YXQNG group was 2.34, and that of the ND group was 4.18, the comparison between the two groups showed that the difference was significant (P < 0.05). After treatment, the middle cerebral artery mean velocity (MCA Vm) of YXQNG group was 64.78 cm/s, vertebral artery mean velocity (VA Vm) was 29.78 cm/s, while that of ND group was 60.34 cm/s and 23.23 cm/s respectively, the comparison between these two groups showing statistical significance and the difference being obvious (P < 0.05). Experimental study showed that the rats in the model group after 12 weeks learning and memory were markedly lowered, the vertigo incubation period significantly lengthened, and compared with that of the model group, learning and memory of the YXQNG group was markedly improved and vertigo incubation period shortened, with the difference from that of the ND group insignificant, P > 0.05. YXQNG could effectively improve CCI patients' vertigo and other clinical symptoms and increase the cerebral blood flow, lessen the vertigo incubation of model group rats, elevate model group rats' memory performance.

Electrodermal activity in patients with neurally mediated syncope.

Electrodermal activity (EDA) increases during arousal, emotional stimuli or thermoregulatory sweating and is sometimes apparent in unfiltered ECG recordings. We hypothesized that changes in EDA precede any change in blood pressure (BP) or cerebral blood velocity (CBV) observed at syncope. Data from 70 patients referred for recurrent syncope were retrospectively analyzed. 400Hz continuous waveforms were recorded of BP (Finapres), CBV (transcranial Doppler), expired CO(2) (PCO(2)) and ECG at rest and during 80 degrees head-up tilt (HUT). Two independent investigators determined the onset and termination of EDA in relation to syncope using the raw and a low pass filtered ECG trace. Of the 53 patients who experienced syncope during HUT, 33 (62 %) increased EDA 257 +/- 357s prior to syncope that continued for 75 +/- 73s following syncope. Seven patients (13%) had EDA only after syncope for 208 +/- 213s. In 13 patients (25 %), EDA was not detectable. In most cases, EDA preceded any change in BP, PCO(2) or CBV and persisted past the hemodynamic recovery following syncope. Although variable, EDA may be an objective correlate to the clinical observation that patients' symptoms precede any measurable change in cerebral perfusion. The actual relationship between EDA and symptoms of presyncope requires further investigation.

Middle cerebral artery blood velocity depends on cardiac output during exercise with a large muscle mass.

We tested the hypothesis that pharmacological reduction of the increase in cardiac output during dynamic exercise with a large muscle mass would influence the cerebral blood velocity/perfusion. We studied the relationship between changes in cerebral blood velocity (transcranial Doppler), rectus femoris blood oxygenation (near-infrared spectroscopy) and systemic blood flow (cardiac output from model flow analysis of the arterial pressure wave) as induced by dynamic exercise of large (cycling) vs. small muscle groups (rhythmic handgrip) before and after cardioselective beta 1 adrenergic blockade (0.15 mg kg-1 metoprolol i.v.). During rhythmic handgrip, the increments in systemic haemodynamic variables as in middle cerebral artery mean blood velocity were not influenced significantly by metoprolol. In contrast, during cycling (e.g. 113 W), metoprolol reduced the increase in cardiac output (222 +/- 13 vs. 260 +/- 16%), heart rate (114 +/- 3 vs. 135 +/- 7 beats min-1) and mean arterial pressure (103 +/- 3 vs. 112 +/- 4 mmHg), and the increase in cerebral artery mean blood velocity also became lower (from 59 +/- 3 to 66 +/- 3 vs. 60 +/- 2 to 72 +/- 3 cm s-1; P < 0.05). Likewise, during cycling with metoprolol, oxyhaemoglobin in the rectus femoris muscle became reduced (compared to rest: -4.8 +/- 1.8 vs. 1.2 +/- 1.7 mumol L-1, P < 0.05). Neither during rhythmic handgrip nor during cycling was the arterial carbon dioxide tension affected significantly by metoprolol. The results suggest that as for the muscle blood flow, the cerebral circulation is also affected by a reduced cardiac output during exercise with a large muscle mass.

Cerebrovascular and cardiovascular measurements during neurally mediated syncope induced by head-up tilt.

This study examines changes in systemic hemodynamics and in cerebral blood velocity that occur during neurally mediated syncope (NMS) to determine whether cerebral autoregulation is intact or impaired in patients with recurrent NMS. Beat-to-beat recordings of heart rate, blood pressure (volume clamp photoplethysmography), stroke volume (impedance cardiography), and right middle cerebral artery blood velocity (transcranial Doppler sonography) were performed at rest and during 80 degrees head-up tilt. Twelve patients with NMS and 10 healthy control subjects were studied. Baseline values and the initial response to head-up tilt of control subjects and patients with NMS were similar. The mean latency to onset of syncope was 11.8 +/- 11.1 minutes. At syncope, heart rate, systolic and diastolic blood pressure, and diastolic cerebral blood velocity decreased significantly, whereas systolic cerebral blood velocity did not change. Calculated cerebrovascular resistance was significantly reduced from 1.85 +/- 0.60 to 1.32 +/- 0.27 mm Hg/cm per second, whereas the pulsatility index increased from 0.92 +/- 0.16 to 1.52 +/- 0.21. We never observed a change in cerebral blood velocity before the rapid decline in blood pressure, nor did we observe any significant change in respiratory pattern. The decrease in cerebrovascular resistance during NMS indicates that the integrity of cerebrovascular autoregulation is maintained even when syncope is imminent. The selective loss of diastolic flow during syncope and the increase in pulsatility index are likely caused by collapse of downstream vessels as diastolic blood pressure decreases below the critical closing pressure of cerebral vessels.

Changes in cerebral blood velocity after intravenous diazepam

Cerebral blood velocity (CBV) was measured with transcranial Doppler in 6 normal right-handed male volunteers before and for 50 min after an intravenous injection of 0.1 mg/kg of diazepam and normal saline during 2 separate visits to the laboratory. Blood pressure, pulse rate, end tidal levels of carbon dioxide and mood changes were quantified before and after the injections. Diazepam injection was associated with significant increases in fatigue and sleepiness. There were no significant changes in end tidal carbon dioxide, respiration, pulse rate, and blood pressure after the injection. Postdiazepam CBV was significantly lower following diazepam compared to CBV following placebo.

Effect of Pneumothorax-lnduced Systemic Blood Pressure Alterations on the Cerebral Circulation in Newborn Dogs

Pneumothorax has been associated with intraventricular hemorrhage in premature infants, although the mechanism for this relationship is not clear. Because alterations in cerebral blood flow are believed to be important in the pathogenesis of intraventricular hemorrhage, the effect of induced pneumothorax and subsequent evacuation on the cerebral circulation in 16 newborn dogs was evaluated. Continuous Doppler ultrasound was used to monitor changes in cerebral blood velocity. Pneumothorax was induced by slow infusion (5 cc/kg/min) or rapid infusion (5 to 10 seconds) of air to reduce mean arterial blood pressure to half of base-line levels. Both methods of pneumothorax induction resulted in significant elevations of central venous pressure and intrapleural pressure, whereas mean arterial blood pressure and cerebral blood velocity decreased significantly. In each group, the pneumothorax was evacuated either by slow withdrawal of air (10 cc/kg/min) or as rapidly as possible. Rapid evacuation of air resulted in an immediate increase in mean arterial blood pressure and cerebral blood velocity to supranormal levels. Slow evacuation led to a more gradual normalization of mean arterial blood pressure and cerebral blood velocity. It is suggested that the precipitous increases in mean arterial blood pressure and cerebral blood velocity following rapid evacuation of a tension pneumothorax may account for the observed association between pneumothorax and intraventricular hemorrhage in premature infants.

Regional cerebral blood flow, cerebral blood velocity, and pulsatility index in newborn dogs.

A technique employing a Doppler ultrasound probe to measure cerebral blood velocity was used to study the cerebral circulation continuously in 30 newborn mongrel dogs. Utilizing a transfontanelle approach, the probe was maintained in fixed position throughout a given experiment. In 20 animals, changes in systolic, diastolic, and mean cerebral blood velocity during hypo- and hypercarbia were directly correlated (P less than 0.01) with changes in regional cerebral blood flow (rCBF) determined in 12 regions of the brain by the [14C]iodoantipyrine autoradiography technique. In an additional 10 dogs, multiple determinations of systolic, diastolic, and mean blood velocity were made over a wide range of PaCO2 values and found to be directly related to the PaCO2 (P less than 0.001). These data suggest that changes in cerebral blood velocity are closely related to changes in cerebral blood flow. We also calculated the pulsatility index (PI) from the peak systolic and end diastolic velocities and found a poor, but direct (r = 0.28, P less than 0.05) relationship between the PI and PaCO2 rather than the indirect relationship, which has been suggested in published clinical studies. We conclude that the Doppler technique may be valuable in monitoring dynamic events of the neonatal cerebral circulation if a constant probe position is maintained. Our results suggest, however, that the PI is not a reliable index of cerebral vascular resistance.