Index Of Dynamic Cerebral Autoregulation Research Articles

Association Between Cerebral Autoregulation and Long-Term Outcome in Patients With Acute Ischemic Stroke.

Dynamic cerebral autoregulation (CA) is known to be impaired in patients with acute ischemic stroke (AIS), but whether or not dynamic CA can predict long-term outcomes is unclear. This prospective study included 103 patients with AIS between September 2017 and April 2019. We measured the middle cerebral artery blood flow velocity and blood pressure within 7 days of AIS onset using a transcranial Doppler and Finometer, respectively. We conducted transfer function analysis to calculate dynamic CA indices (phase and gain), with lower phase and higher gain parameters reflecting less efficient CA. We followed up all patients after 3 and 12 months. Patients with 12-month modified Rankin Scale scores of <2 and ≥2 were defined as having favorable and unfavorable outcomes, respectively. We then analyzed the predictors of unfavorable outcomes after 3 and 12 months using logistic regression. The ipsilesional phase parameter was significantly lower in patients with unfavorable outcomes than in those with favorable outcomes. Multiple logistic regression analysis revealed that the ipsilesional phase parameter and the National Institutes of Health Stroke Scale score were nonmodifiable predictors of short-term and long-term outcomes. Moreover, in receiver operating characteristic analysis, the area under the curve of the ipsilesional phase parameter was 0.646 (95% confidence interval: 0.513-0.779, P =0.044). Notably, the optimal cut-off value was 20.33 degrees (sensitivity: 63%, specificity: 70%). Dynamic CA is an independent predictor of outcomes at 3 and 12 months in patients with AIS.

IMPAIRED CEREBRAL AUTOREGULATION IN PATIENTS WITH ADVANCED LIVER FAILURE: AN UNDER-RECOGNIZED PHENOMENON

IMPAIRED CEREBRAL AUTOREGULATION IN PATIENTS WITH ADVANCED LIVER FAILURE: AN UNDER-RECOGNIZED PHENOMENON

Cerebral perfusion pressure and autoregulation in eclampsia—a case control study

Dynamic cerebral autoregulation and cerebral perfusion pressure are altered in pregnancies complicated by preeclampsia compared with normotensive pregnancies, but the connections of dynamic cerebral autoregulation, cerebral perfusion pressure, and cerebral complications in preeclampsia remain unclear. This study aimed to assess dynamic cerebral autoregulation and cerebral perfusion pressure after delivery in women with eclampsia, in women with preeclampsia both with and without severe features, and in normotensive women. This was a prospective case control study at a large referral hospital in Cape Town, South Africa. The recruitment of participants was done at diagnosis (cases) or at admission for delivery (controls). Transcranial Doppler examinations with continuous noninvasive blood pressure measurements and end-tidal CO2 monitoring were conducted for cases and controls after delivery. Cerebral perfusion pressure and dynamic cerebral autoregulation index were calculated, and values were compared among groups. We included 16 women with eclampsia, 18 women with preeclampsia with severe features, 32 women with preeclampsia without severe features, and 21 normotensive women with uncomplicated pregnancies. Dynamic cerebral autoregulation was depressed in pregnant women with eclampsia; (autoregulation index, 3.9; interquartile range, 3.1-5.2) compared with all other groups (those with preeclampsia with severe features, autoregulation index, 5.6 [interquartile range, 4.4-6.8]; those with preeclampsia without severe features, autoregulation index, 6.8 [interquartile range, 5.1-7.4]; and normotensive controls, autoregulation index, 7.1 [interquartile range, 6.1-7.9]). Pregnant women with eclampsia had increased cerebral perfusion pressure (109.5 mm Hg; interquartile range, 91.2-130.9) compared with those with preeclampsia without severe features and those with normal blood pressure (84 mm Hg [interquartile range, 73.0-122.0] and 80.0 mm Hg [interquartile range, 67.5-92.0], respectively); furthermore, there was no difference in cerebral perfusion pressure between pregnant women with eclampsia and pregnant women with preeclampsia with severe features (109.5 mm Hg [interquartile range, 91.2-130.9] vs 96.5 mm Hg [interquartile range, 75.8-110.5]). Cerebral perfusion pressure and dynamic cerebral autoregulation are altered in eclampsia and may be important in the pathophysiological pathway and constitute a therapeutic target in the prevention of cerebral complications in preeclampsia.

Exposure to rotational acceleration over the course of one athletic season is related to impairments in an index of dynamic cerebral autoregulation

ObjectiveTo examine the relationship between cerebral autoregulation changes and impact exposuresthroughout a season of contact sports (hockey or football).DesignProspective Cohort.SettingLaboratory.Participants40 male contact sport athletes (19.4±1.2 years); to date, 3 cross-country athletes (20.0±1.0 years) have completed testing (non-contact controls).InterventionParticipants completed testing prior to the start of their athletic seasons (T1), and again after the conclusion of each season (T2). Blood pressure (BP) oscillations were driven by stand-squat manoeuvres at 0.05 and 0.10 Hz. BP and cerebral blood velocity (CBV) in the middle cerebral artery were indexed non-invasively using finger photoplethysmography and transcranial Doppler ultrasound, respectively. RM-ANOVA independent variables included time (2) and frequency (2).Outcome measuresPoint-estimates ofcoherence(correlation),phase(synchronisation), andgain(amplitude buffer) transfer function analysis metrics were calculated. Biomechanical data on head-impact exposure was estimated in a subset of contact-sport athletes (n=29) using the xPatch (X2 Biosystems), affixed to the right mastoid.ResultsSignificant frequency-time interaction forgainin contact-sport athletes (p=0.048) but not controls (p=0.213). Simple effects analysis revealed a time effect at 0.10 Hz (p&lt;0.001), wherebygainincreased at T2 (95% CI: 0.070–0.229%/%). The ΔgainT2-T1at 0.10 Hz was correlated withestimated cumulativerotational acceleration exposure (r=0.462, p=0.015).ConclusionsThese findings suggest cumulative exposure to the rotational component of sustained head-impactsduring participation in a season of contact-sport (hockey or football) impairs the ability of the cerebrovasculature to buffer BP challenges experienced during everyday activities.Competing interestsNone.

Acute effect of coffee drinking on dynamic cerebral autoregulation.

Drinking coffee causes caffeine-induced physiological alterations such as increases in arterial blood pressure, sympathetic nerve activity, cerebral vasoconstriction, etc., and these physiological alterations may be associated with a reduced risk of cerebral vascular disease. However, the effect of coffee drinking on dynamic cerebral blood flow (CBF) regulation remains unclear. The aim of this study was to test our hypothesis that coffee drinking enhances dynamic cerebral autoregulation. Twelve healthy young subjects participated in the present study. After a 5min baseline measurement in a semi-recumbent position on the hospital bed, each subject drank water (CON) as a placebo condition or coffee beverage (Coffee INT). Arterial blood pressure and middle cerebral artery blood velocity (MCAv) were measured continuously throughout the experiment. At 30min after the intake of either water or coffee, dynamic cerebral autoregulation was examined using a thigh cuffs occlusion and release technique. Each condition was randomly performed on a different day. Under Coffee INT condition, mean arterial blood pressure was increased (P=0.01) and mean MCAv was decreased (P=0.01) from the baseline. The rate of regulation (RoR), as an index of dynamic cerebral autoregulation, during coffee condition was significantly higher than that during CON (P=0.0009). The findings of the present study suggest that coffee drinking augments dynamic CBF regulation with cerebral vasoconstriction. This phenomenon may be associated with a reduction in the risk of cerebral vascular disease.

The effect of an acute increase in central blood volume on the response of cerebral blood flow to acute hypotension.

The purpose of the present study was to examine whether the response of cerebral blood flow to an acute change in perfusion pressure is modified by an acute increase in central blood volume. Nine young, healthy subjects voluntarily participated in this study. To measure dynamic cerebral autoregulation during normocapnic and hypercapnic (5%) conditions, the change in middle cerebral artery mean blood flow velocity was analyzed during acute hypotension caused by two methods: 1) thigh-cuff occlusion release (without change in central blood volume); and 2) during the recovery phase immediately following release of lower body negative pressure (LBNP; -50 mmHg) that initiated an acute increase in central blood volume. In the thigh-cuff occlusion release protocol, as expected, hypercapnia decreased the rate of regulation, as an index of dynamic cerebral autoregulation (0.236 ± 0.018 and 0.167 ± 0.025 s(-1), P = 0.024). Compared with the cuff-occlusion release, the acute increase in central blood volume (relative to the LBNP condition) with LBNP release attenuated dynamic cerebral autoregulation (P = 0.009). Therefore, the hypercapnia-induced attenuation of dynamic cerebral autoregulation was not observed in the LBNP release protocol (P = 0.574). These findings suggest that an acute change in systemic blood distribution modifies dynamic cerebral autoregulation during acute hypotension.

The Effect Of An Acute Increase In Central Blood Volume On Dynamic Cerebral Autoregulation

Previous investigations demonstrated that cerebral blood flow was influenced by changes in central blood volume and arterial blood pressure even within the range of cerebral autoregulation (60-150 mmHg). Recently, we found that during acute microgravity (parabolic flight condition), the acute increase in central blood volume decreased gradually arterial blood pressure via the arterial and cardiopulmonary baroreflexes. Despite the acute hypotension and central hypervolemia, steady-state cerebral blood flow was well maintained during this condition. However, the dynamic relationship between central blood volume and cerebrovascular control remains unclear. PURPOSE: The purpose of the present study was to examine dynamic cerebral autoregulation during an acute hypotension with central hypervolemia. METHODS: Nine young healthy subjects voluntarily participated in this study. In order to measure dynamic cerebral autoregulation, change in middle cerebral artery mean blood flow velocity (MCA Vmean) was analyzed during acute hypotension caused by two methods: 1) thigh-cuff occlusion release (without change in central blood volume) and 2) lower body negative pressure (-50 mmHg, LBNP) release (with acute increase in central blood volume). RESULTS: As expected, the thigh-cuff occlusion release caused acute hypotension and decrease in MCA Vmean accordingly, but MCA Vmean returned to the baseline value quickly. LBNP release increased and then decreased arterial blood pressure acutely. During the phase of decreased arterial blood pressure, however, the rate of regulation, as an index of dynamic cerebral autoregulation during LBNP release, was significantly lower than that during cuff release (0.112 ± 0.116 and 0.236 ± 0.053 sec-1, respectively, P=0.030). CONCLUSIONS: These findings suggest that an acute change in central blood volume modifies dynamic cerebral autoregulation.

The effect of an acute increase in central blood volume on hypercapnia‐induced attenuation in dynamic cerebral autoregulation

It is well established that hypercapnia attenuates dynamic cerebral autoregulation. The impact of central blood volume on cerebral blood flow is controversial. The purpose of the present study was to examine whether hypercapnia‐induced attenuation in dynamic cerebral autoregulation is modified by acute central hypervolemia. Nine young healthy subjects voluntarily participated in this study. In order to measure dynamic cerebral autoregulation during normocapnic and hypercapnic (5%) conditions, the change in middle cerebral artery mean blood flow velocity (MCA Vmean) was analyzed during acute hypotension caused by two methods: 1) thigh‐cuff occlusion release (without change in central blood volume) and 2) lower body negative pressure (‐50 mmHg, LBNP) release (with acute increase in central blood volume). As expected, hypercapnia decreased the rate of regulation, as an index of dynamic cerebral autoregulation (0.236±0.053 and 0.167±0.074 sec‐1, respectively, P=0.025). In contrast, this attenuation was disappeared during central hypervolemia (P=0.574). This phenomenon may be associated with hypervolemia‐induced attenuation of dynamic cerebral autoregulation (P=0.009). These findings suggest that an acute change in central blood volume modifies carbon dioxide‐induced changes in dynamic cerebral autoregulation.

A New Model-Free Index of Dynamic Cerebral Blood Flow Autoregulation

The classic dynamic autoregulatory index (ARI), proposed by Aaslid and Tiecks, is one of the most widely used methods to assess the efficiency of dynamic cerebral autoregulation. Although this index is often used in clinical research and is also included in some commercial equipment, it exhibits considerable intra-subject variability, and has the tendency to produce false positive results in clinical applications. An alternative index of dynamic cerebral autoregulation is proposed, which overcomes most of the limitations of the classic method and also has the advantage of being model-free. This new index uses two parameters that are obtained directly from the response signal of the cerebral blood flow velocity to a transient decrease in arterial blood pressure provoked by the sudden release of bilateral thigh cuffs, and a third parameter measuring the difference in slope of this response and the change in arterial blood pressure achieved. With the values of these parameters, a corresponding classic autoregulatory index value could be calculated by using a linear regression model built from theoretical curves generated with the Aaslid-Tiecks model. In 16 healthy subjects who underwent repeated thigh-cuff manoeuvres, the model-free approach exhibited significantly lower intra-subject variability, as measured by the unbiased coefficient of variation, than the classic autoregulatory index (p = 0.032) and the Rate of Return (p<0.001), another measure of cerebral autoregulation used for this type of systemic pressure stimulus, from 39.23%±41.91% and 55.31%±31.27%, respectively, to 15.98%±7.75%.

Sea-Level Assessment of Dynamic Cerebral Autoregulation Predicts Susceptibility to Acute Mountain Sickness at High Altitude

Dynamic cerebral autoregulation is impaired in subjects who develop acute mountain sickness (AMS), a neurological disorder characterized by headache. The present study examined if the normoxic sea-level measurement of dynamic cerebral autoregulation would predict subsequent susceptibility to AMS during rapid ascent to terrestrial high altitude. A dynamic cerebral autoregulation index was determined in 18 subjects at sea level from continuous recordings of middle cerebral artery blood flow velocity (Doppler ultrasonography) and arterial blood pressure (finger photoplethysmography) after recovery from transiently induced hypotension. Six hours after passive ascent to 3800 m (Mt Elbrus, Russia), the Lake Louise and Environmental Symptoms Cerebral Symptoms questionnaires were used to assess AMS. AMS scores increased markedly at high-altitude (Lake Louise: +3±2 points, P=0.001 and Environmental Symptoms Cerebral Symptoms: +0.6±0.9 points, P=0.0003 versus sea level). Inverse relationships were observed between the sea-level autoregulation index score and the high-altitude-induced increases in the Lake Louise (r=-0.62, P=0.007) and Environmental Symptoms Cerebral Symptoms (r=-0.78, P=0.01) scores. One subject with a history of high-altitude pulmonary and cerebral edema presented with the lowest sea-level autoregulation index score (3.7 versus group: 6.2±1.0 points) and later developed high-altitude cerebral edema at 4800 m during the summit bid. These findings suggest that a lower baseline autoregulation index may be considered a potential risk factor for AMS. This laboratory measurement may prove a useful screening tool for the expedition doctor when considering targeted pharmacological prophylaxis in individuals deemed "AMS-susceptible."

Exercise-induced oxidative-nitrosative stress is associated with impaired dynamic cerebral autoregulation and blood-brain barrier leakage

The present study examined whether dynamic cerebral autoregulation and blood-brain barrier function would become compromised as a result of exercise-induced oxidative-nitrosative stress. Eight healthy men were examined at rest and after an incremental bout of semi-recumbent cycling exercise to exhaustion. Changes in a dynamic cerebral autoregulation index were determined during recovery from continuous recordings of blood flow velocity in the middle cerebral artery (MCAv) and mean arterial pressure during transiently induced hypotension. Electron paramagnetic resonance spectroscopy and ozone-based chemiluminescence were employed for direct detection of spin-trapped free radicals and nitric oxide metabolites in venous blood. Neuron-specific enolase, S100β and 3-nitrotyrosine were determined by ELISA. While exercise did not alter MCAv, it caused a mild reduction in the autoregulation index (from 6.9 ± 0.6 to 5.5 ± 0.9 a.u., P < 0.05) that correlated directly against the exercise-induced increase in the ascorbate radical, 5-(diethoxyphosphoryl)-5-methyl-1-pyrroline N-oxide and N-tert-butyl-α-phenylnitrone adducts, 3-nitrotyrosine and S100β (r = -0.66 to -0.76, P < 0.05). In contrast, no changes in neuron-specific enolase were observed. In conclusion, our findings suggest that intense exercise has the potential to increase blood-brain barrier permeability without causing structural brain damage subsequent to a free radical-mediated impairment in dynamic cerebral autoregulation.

The effect of oxygen on dynamic cerebral autoregulation: critical role of hypocapnia

Hypoxia is known to impair cerebral autoregulation (CA). Previous studies indicate that CA is profoundly affected by cerebrovascular tone, which is largely determined by the partial pressure of arterial O(2) and CO(2). However, hypoxic-induced hyperventilation via respiratory chemoreflex activation causes hypocapnia, which may influence CA independent of partial pressure of arterial O(2). To identify the effect of O(2) on dynamic cerebral blood flow regulation, we examined the influence of normoxia, isocapnia hyperoxia, hypoxia, and hypoxia with consequent hypocapnia on dynamic CA. We measured heart rate, blood pressure, ventilatory parameters, and middle cerebral artery blood velocity (transcranial Doppler). Dynamic CA was assessed (n = 9) during each of four randomly assigned respiratory interventions: 1) normoxia (21% O(2)); 2) isocapnic hyperoxia (40% O(2)); 3) isocapnic hypoxia (14% O(2)); and 4) hypocapnic hypoxia (14% O(2)). During each condition, the rate of cerebral regulation (RoR), an established index of dynamic CA, was estimated during bilateral thigh cuff-induced transient hypotension. The RoR was unaltered during isocapnic hyperoxia. Isocapnic hypoxia attenuated the RoR (0.202 +/- 0.003/s; 27%; P = 0.043), indicating impairment in dynamic CA. In contrast, hypocapnic hypoxia increased RoR (0.444 +/- 0.069/s) from normoxia (0.311 +/- 0.054/s; +55%; P = 0.041). These findings indicated that hypoxia disrupts dynamic CA, but hypocapnia augments the dynamic CA response. Because hypocapnia is a consequence of hypoxic-induced chemoreflex activation, it may provide a teleological means to effectively maintain dynamic CA in the face of prevailing arterial hypoxemia.

Continuous estimates of dynamic cerebral autoregulation during transient hypocapnia and hypercapnia

Dynamic cerebral autoregulation (CA) is the transient response of cerebral blood flow (CBF) to rapid blood pressure changes: it improves in hypocapnia and becomes impaired during hypercapnia. Batch-processing techniques have mostly been used to measure CA, providing a single estimate for an entire recording. A new approach to increase the temporal resolution of dynamic CA parameters was applied to transient hypercapnia and hypocapnia to describe the time-varying properties of dynamic CA during these conditions. Thirty healthy subjects (mean +/- SD: 25 +/- 6 yr, 9 men) were recruited. CBF velocity was recorded in both middle cerebral arteries (MCAs) with transcranial Doppler ultrasound. Arterial blood pressure (Finapres), end-tidal CO(2) (ET(CO(2)); infrared capnograph), and a three-lead ECG were also measured at rest and during repeated breath hold and hyperventilation. A moving window autoregressive moving average model provided continuous values of the dynamic CA index [autoregulation index (ARI)] and unconstrained gain. Breath hold led to significant increase in ET(CO(2)) (+5.4 +/- 6.1 mmHg), with concomitant increase in CBF velocity in both MCAs. Continuous dynamic CA parameters showed highly significant changes (P < 0.001), with a temporal pattern reflecting a delayed dynamic response of CA to changes in arterial Pco(2) and a maximal reduction in ARI of -5.1 +/- 2.4 and -5.1 +/- 2.3 for the right and left MCA, respectively. Hyperventilation led to a marked decrease in ET(CO(2)) (-7.2 +/- 4.1 mmHg, P < 0.001). Unexpectedly, CA efficiency dropped significantly with the inception of the metronome-controlled hyperventilation, but, after approximately 30 s, the ARI increased gradually to show a maximum change of 5.7 +/- 2.9 and 5.3 +/- 3.0 for the right and left MCA, respectively (P < 0.001). These results confirm the potential of continuous estimates of dynamic CA to improve our understanding of human cerebrovascular physiology and represent a promising new approach to improve the sensitivity of clinical applications of dynamic CA modeling.

Dynamic cerebral autoregulation in carotid stenosis before and after carotid stenting

Impaired dynamic cerebral autoregulation (DCA) has been shown in patients with severe (> or =70%) internal carotid artery (ICA) stenosis, but DCA in moderate (50% to 69%) ICA stenosis, especially its response to carotid revascularization, has rarely been reported. Our study aimed to characterize DCA in severe and moderate ICA stenosis before and after carotid stenting. This study included 21 patients with ICA stenosis > or =50% who received carotid stenting. Data of arterial blood pressure and cerebral blood flow velocity of the middle cerebral artery, measured by transcranial Doppler, were collected for 10 minutes < or =24 hours before and after stenting. The DCA index, represented as aMx, was assessed by calculating the Pearson product-moment correlation coefficient of spontaneous arterial blood pressure and cerebral blood flow velocity fluctuations. The relationship between aMx and stenotic severity and also alternations of aMx before and after stenting were assessed. Carotid stenting was effective to improve the DCA in the stenting side but not in the contralateral nonstenting side. In considering individual ICAs, the average aMx (mean +/- SD) increased significantly from ICA stenosis <50% (0.117 +/- 0.091) to 50% to 69% (0.349 +/- 0.144), 70% to 99% (0.456 +/- 0.147), and total occlusion (0.557 +/- 0.210; P < .05, P < .01, and P < .01, compared with 50% to 69%, 70% to 99%, or total occlusion with <50% stenosis). The correlation between the degree of ICA stenosis and the aMx was also significant (r = 0.693, P < .005). The aMx improved significantly in the stented side after carotid stenting in both moderate and severe ICA stenosis, and this finding was not affected by age, sex, risk factors, or clinical symptoms. In addition to patients with severe carotid stenosis, patients with moderate carotid stenosis may also have impaired DCA that can be restored after carotid stenting.

Early morning impairment in cerebral autoregulation and cerebrovascular CO2 reactivity in healthy humans: relation to endothelial function

The reduction in cerebrovascular reactivity to CO(2) and/or endothelial function that occurs in the early hours after waking are potential causes for the increased risk for cardiovascular events at this time point. It is unknown whether cerebral autoregulation is reduced in the morning. We tested the hypothesis that early morning reduction in endothelium-dependent vascular reactivity would be linked to changes in cerebrovascular reactivity to CO(2) and cerebral autoregulation (CA). Overnight changes in a dynamic cerebral autoregulation index (ARI) were determined from continuous recordings of blood flow velocity in the middle cerebral artery (MCAv) and arterial blood pressure (BP) during transiently induced hypotension in 20 individuals. Frontal cortical oxygenation (near infrared spectroscopy) and cerebral haemodynamics were also monitored during hypercapnia and before and during 3 min of active standing. Brachial artery flow-mediated endothelium-dependent vasodilatation (FMD) and endothelium-independent dilatation (NFMD) were also monitored. From evening to morning, there was a significant lowering in ARI (5.3 +/- 0.5 versus 4.7 +/- 0.6 a.u.; P < 0.05), cerebrovascular reactivity to CO(2) (5.3 +/- 0.6 versus 4.6 +/- 1.1% mmHg(-1); P < 0.05) and FMD (7.6 +/- 0.9 versus 6.0 +/- 1.4%; P < 0.05). The lowered FMD was related to the decrease in cerebrovascular reactivity to CO(2) (r = 0.76; P < 0.05). Transient reductions in morning MCAv and cortical oxyhaemoglobin concentrations were observed upon resuming a supine-to-upright position (P < 0.05 versus evening). The early morning reduction in cerebral autoregulation may facilitate the onset of cerebrovascular accidents; this may be of particular relevance to at-risk groups, especially upon resuming the upright position.

The Effect of Sevoflurane on Dynamic Cerebral Blood Flow Autoregulation Assessed by Spectral and Transfer Function Analysis

Sevoflurane reduces autonomic neural control, which plays a significant role in cerebral autoregulation. Therefore, we hypothesized that sevoflurane influences cerebral autoregulation. We investigated the effects of sevoflurane on dynamic cerebral blood flow (CBF) autoregulation by using spectral and transfer function analysis between blood pressure variability and CBF velocity variability. Eleven healthy male subjects received 0.5%, 1.0%, and 1.5% sevoflurane via facemask. Dynamic cerebral autoregulation was evaluated by transfer function gain, phase, and coherence between CBF velocity in the middle cerebral artery measured by transcranial Doppler, and blood pressure in the radial artery. Coherence in the very low-frequency range (0.02-0.07 Hz) increased above 0.5 during administration of 0.5% and 1.0% sevoflurane. Transfer function gain in this frequency range (0.02-0.07 Hz), as an index of dynamic cerebral autoregulation, increased significantly with 0.5% and 1.0% sevoflurane. Transfer function gain and coherence in the low- and high-frequency ranges, however, remained unchanged during administration of sevoflurane. These results suggest that sevoflurane impairs dynamic cerebral autoregulation in the very-low-frequency range even with small concentrations, whereas dynamic cerebral autoregulation in the low- and high-frequency ranges remained unchanged.

Cerebral autoregulation and ageing

Little is known about the effects of ageing on cerebral autoregulation (CA). To examine the relationship between age and CA in adults, we conducted a prospective study using a non-invasive protocol without external stimuli. We studied 32 subjects, aged 23-68 years. They were assigned to a young group (28+/-5 years) and an old group (54+/-8 years). The groups were sex-matched. Transcranial Doppler ultrasonography (TCD) was used to record bilateral middle cerebral artery flow velocities (CBFV, cm/sec). Noninvasive beat-to-beat tonometric arterial blood pressure (ABP) measurement of the radial artery was used to record spontaneous blood pressure fluctuations. The Mx, an index of dynamic cerebral autoregulation (dCA), was calculated from a moving correlation between ABP and CBFV. We did not find a correlation between age and Mx. No statistically significant difference in the Mx between the groups (0.27+/-0.23, young, vs. 0.37+/-0.24, old) was demonstrated. Age does not affect dynamic cerebral autoregulation assessed by the Mx index in healthy adult subjects. This study supports findings from previous papers wherein CA was measured with protocols which require external stimuli. Further studies are needed to determine CA in subjects above 70 years of age.

Effects of High Altitude Exposure on Cerebral Hemodynamics in Normal Subjects

Acute mountain sickness (AMS) may be an early stage of high altitude cerebral edema. If so, AMS could result from an alteration of dynamic autoregulation of cerebral blood flow resulting in overperfusion of capillaries and vasogenic cerebral edema. We measured middle cerebral artery blood flow velocity (Vmca) by transcranial Doppler and arterial blood pressure by finger plethysmography at 490 m and 20 hours after arrival at 4559 m in 35 volunteers who had been randomized to tadalafil, dexamethasone, or placebo in a study on the pharmacological prevention of high altitude pulmonary edema. A dynamic cerebral autoregulation index (ARI) was calculated from continuous recordings of Vmca and blood pressure during transiently induced hypotension. Altitude was associated with an increase in a cerebral-sensible AMS (AMS-C) score (P<0.001) and with a decrease in arterial oxygen saturation (Sao2), whereas average Vmca or ARI did not change. However, at altitude, the subjects with the lowest ARI combined with the lowest Sao2 presented with the highest AMS-C score (P<0.03). In addition, a stepwise multiple linear regression analysis on arterial Pco2, Sao2, and baseline or altitude ARI identified altitude ARI as the only significant predictor of the AMS-C score (P=0.01). The AMS-C score was lower in dexamethasone-treated subjects compared with high altitude pulmonary edema-susceptible untreated subjects. Neither tadalafil nor dexamethasone had any significant effect on Vmca or ARI. High altitude hypoxia is associated with impairment in the regulation of the cerebral circulation that might play a role in AMS pathogenesis.

Cerebral autoregulation indicesare unimpaired by hypertensionin middle aged and older people

Background Hypertension is known to increase the limits of static cerebral autoregulation (CA) but its effects on other aspects of CA such as efficiency and latency are unknown. In this study we test the hypothesis that dynamic cerebral autoregulation and the efficiency of static cerebral autoregulation are impaired by untreated hypertension. Methods Cerebral blood flow velocity was recorded using transcranial Doppler ultrasound, along with noninvasive beat-to-beat blood pressure (BP), electrocardiogram, and transcutaneous carbon dioxide levels, with subjects at rest and during isometric hand grip, thigh cuff, and the Valsalva maneuver. Static and dynamic CA indices were calculated. Results No significant difference was seen in static or dynamic CA indices between normotensive and hypertensive groups for any pressor or depressor stimulus. Spearman's rank correlation showed no relation between static or dynamic CA indices and systemic BP levels for all maneuvers, but a significant relationship between age and static CA index, determined using isometric handgrip ( P = .002), was found. Conclusions In middle-aged and older people, sustained untreated hypertension does not alter dynamic CA or the efficiency of static CA within the BP limits studied.

Serial Changes in Static and Dynamic Cerebral Autoregulation after Acute Ischaemic Stroke

Background: The longitudinal changes in static and dynamic cerebral autoregulation (CA) following acute ischaemic stroke are unknown and were assessed in this study. Methods: Fifty-four ischaemic stroke patients were studied within 96 h of ischaemic stroke and again 7–14 days later, using transcranial Doppler techniques to measure CA. Results were compared to an age-, sex- and blood pressure (BP)-matched control group. Static BP pressor stimulus was produced by thigh cuff inflation and dynamic stimulus by rapid thigh cuff release. Results: Dynamic, but not static, CA was globally impaired at initial (mean dynamic CA index 3.9 ± 3.1 vs. 6.2 ± 2.3, p < 0.005) and follow-up studies (dynamic CA 3.9 ± 2.8 vs. 6.2 ± 2.3, p < 0.01) in stroke patients compared to controls. Static CA was similar in stroke patients and controls and was unchanged during follow-up. Conclusions: Dynamic, but not static, CA is impaired after acute ischaemic stroke and remains abnormal for at least 1–2 weeks post ictus. These changes are present in both the affected and non-affected hemispheres and are unrelated to previous antihypertensive treatment, baseline BP levels or BP changes after stroke, age or stroke type.