Decrease In Cerebral Blood Flow Velocity Research Articles

Cerebral blood flow and end-tidal CO2 predict lightheadedness during head-up tilt in patients with orthostatic intolerance.

Orthostatic intolerance (OI) is a common problem. Reliable markers of OI are missing, as orthostatic blood pressure and heart rate poorly correlate with orthostatic symptoms. The objective of this study was to assess the relationship between orthostatic lightheadedness and cerebral blood flow. In this retrospective study patients with OI were evaluated at the Autonomic Laboratory of the Department of Neurology, Brigham and Women's Faulkner Hospital, Boston. The 10-minute head-up tilt test was performed as a part of autonomic testing. Orthostatic lightheadedness was evaluated at every minute of the head-up tilt. Heart rate, blood pressure, capnography, and cerebral blood flow velocity (CBFv) in the middle cerebral artery using transcranial Doppler were measured. Repeated-measures design with a linear mixed-effects model was used to evaluate the relationship between orthostatic lightheadedness and hemodynamic variables. Correlation analyses were done by calculating Pearson's coefficient. Twenty-two patients with OI were compared to nineteen controls. Orthostatic CBFv and end-tidal CO2 decreased in OI patients compared to controls (p < 0.001) and predicted orthostatic lightheadedness. Orthostatic heart rate and blood pressure failed to predict orthostatic lightheadedness. The lightheadedness threshold, which marked the onset of lightheadedness, was equal to an average systolic CBFv decrease of 18.92% and end-tidal CO2 of 12.82%. The intensity of lightheadedness was proportional to the CBFv and end-tidal CO2 decline. Orthostatic lightheadedness correlated with systolic CBFv (r=-0.6, p < 0.001) and end-tidal CO2 (r=-0.33, p < 0.001) decline. In conclusion, orthostatic CBFv and end-tidal CO2 changes predict orthostatic lightheadedness and can be used as objective markers of OI.

Stellate Ganglion Block and Intraarterial Spasmolysis in Patients with Cerebral Vasospasm: A Retrospective Cohort Study

BackgroundIn patients with symptomatic cerebral vasospasm (CV) following aneurysmal subarachnoid hemorrhage who do not respond to medical therapy, urgent treatment escalation has been suggested to be beneficial for brain tissue at risk. In our routine clinical care setting, we implemented stellate ganglion block (SGB) as a rescue therapy with subsequent escalation to intraarterial spasmolysis (IAS) with milrinone for refractory CV.MethodsIn this retrospective analysis from 2012 to 2021, patients with CV following aneurysmal subarachnoid hemorrhage who received an SGB or IAS were identified. Patients were assessed through neurological examination and transcranial Doppler. Rescue therapy was performed in patients with mean cerebral blood flow velocity (CBFV) ≥ 120 cm/s and persistent neurological deterioration/intubation under induced hypertension. Patients were reassessed after therapy and the following day. The Glasgow Outcome Scale was assessed at discharge and 6-month follow-up.ResultsA total of 82 patients (mean age 50.16 years) with 184 areas treated with SGB and/or IAS met the inclusion criteria; 109 nonaffected areas were extracted as controls. The mean CBFV decrease in the middle cerebral artery on the following day was − 30.1 (± 45.2) cm/s with SGB and − 31.5 (± 45.2) cm/s with IAS. Mixed linear regression proved the significance of the treatment categories; other fixed effects (sex, age, aneurysm treatment modality [clipping or coiling], World Federation of Neurological Surgeons score, and Fisher score) were insignificant. In logistic regression, the presence of cerebral infarction on imaging before discharge from the intensive care unit (34/82) was significantly associated with unfavorable outcomes (Glasgow Outcome Scale ≤ 3) at follow-up.ConclusionsStellate ganglion block and IAS decreased CBFV the following 24 h in patients with CV. We suggest SGB alone for patients with mild symptomatic CV (CBFV < 180 cm/s), while subsequent escalation to IAS proved to be beneficial in patients with refractory CV and severe CBFV elevation (CBFV ≥ 180 cm/s).

Continuous monitoring of cerebral blood flow during general anaesthesia in infants

BackgroundGeneral anaesthesia is associated with neurocognitive deficits in infants after noncardiac surgery. Disturbances in cerebral perfusion as a result of systemic hypotension and impaired autoregulation may be a potential cause. Our aim was to study cerebral blood flow (CBF) velocity continuously during general anaesthesia in infants undergoing noncardiac surgery and compare variations in CBF velocity with simultaneously measured near-infrared spectroscopy (NIRS), blood pressure, and heart rate. MethodsNeoDoppler, a recently developed ultrasound system, was used to monitor CBF velocity via the anterior fontanelle during induction and maintenance of general anaesthesia until the start of surgery, and during recovery. NIRS, blood pressure, and heart rate were monitored simultaneously and synchronised with the NeoDoppler measurements. ResultsThirty infants, with a median postmenstrual age at surgery of 37.6 weeks (range 28.6–60.0) were included. Compared with baseline, the trend curves showed a decrease in CBF velocity during induction and maintenance of anaesthesia and returned to baseline values during recovery. End-diastolic velocity decreased in all infants during anaesthesia, on average by 59%, whereas peak systolic- and time-averaged velocities decreased by 26% and 45%, respectively. In comparison, the reduction in mean arterial pressure was only 20%. NIRS values were high and remained stable. When adjusting for mean arterial pressure, the significant decrease in end-diastolic velocity persisted, whereas there was only a small reduction in peak systolic velocity. ConclusionsContinuous monitoring of CBF velocity using NeoDoppler during anaesthesia is feasible and may provide valuable information about cerebral perfusion contributing to a more targeted haemodynamic management in anaesthetised infants.

Cerebral vasomotor reactivity during hypo- and hypercapnia across the adult lifespan

Age is the strongest risk factor for cerebrovascular disease; however, age-related changes in cerebrovascular function are still not well understood. The objective of this study was to measure cerebral vasomotor reactivity (CVMR) during hypo- and hypercapnia across the adult lifespan. One hundred fifty-three healthy participants (21–80 years) underwent measurements of cerebral blood flow velocity (CBFV) via transcranial Doppler, mean arterial pressure (MAP) via plethysmograph, and end-tidal CO2 (EtCO2) via capnography during hyperventilation (hypocapnia) and a modified rebreathing protocol (hypercapnia). Cerebrovascular conductance (CVCi) and resistance (CVRi) indices were calculated from the ratios of CBFV and MAP. CVMRs were assessed by the slopes of CBFV and CVCi in response to changes in EtCO2. The baseline CBFV and CVCi decreased and CVRi increased with age. Advanced age was associated with progressive declines in CVMR during hypocapnia indicating reduced cerebral vasoconstriction, but increases in CVMR during hypercapnia indicating increased vasodilation. A negative correlation between hypo- and hypercapnic CVMRs was observed across all subjects (CBFV%/ EtCO2: r = −0.419, CVCi%/ EtCO2: r = −0.442, P < 0.0001). Collectively, these findings suggest that aging is associated with decreases in CBFV, increases in cerebrovascular resistance, reduced vasoconstriction during hypocapnia, but increased vasodilatory responsiveness during hypercapnia.

Dynamic cerebral autoregulation is impaired in Veterans with Gulf War Illness: A case-control study.

Neurological dysfunction has been reported in Gulf War Illness (GWI), including abnormal cerebral blood flow (CBF) responses to physostigmine challenge. However, it is unclear whether the CBF response to normal physiological challenges and regulation is similarly dysfunctional. The goal of the present study was to evaluate the CBF velocity response to orthostatic stress (i.e., sit-to-stand maneuver) and increased fractional concentration of carbon dioxide. 23 cases of GWI (GWI+) and 9 controls (GWI) volunteered for this study. Primary variables of interest included an index of dynamic autoregulation and cerebrovascular reactivity. Dynamic autoregulation was significantly lower in GWI+ than GWI- both for autoregulatory index (2.99±1.5 vs 4.50±1.5, p = 0.017). In addition, we observed greater decreases in CBF velocity both at the nadir after standing (-18.5±6.0 vs -9.8±4.9%, p = 0.001) and during steady state standing (-5.7±7.1 vs -1.8±3.2%, p = 0.042). In contrast, cerebrovascular reactivity was not different between groups. In our sample of Veterans with GWI, dynamic autoregulation was impaired and consistent with greater cerebral hypoperfusion when standing. This reduced CBF may contribute to cognitive difficulties in these Veterans when upright.

Hypocapnic cerebral hypoperfusion: A biomarker of orthostatic intolerance.

The objective of the study was to identify markers of hypocapnic cerebral hypoperfusion (HYCH) in patients with orthostatic intolerance (OI) without tachycardia and without orthostatic hypotension. This single center, retrospective study included OI patients referred for autonomic evaluation with the 10 min tilt test. Heart rate, end-tidal CO2 (ET-CO2), blood pressure, and cerebral blood flow velocity (CBFv) from middle cerebral artery were monitored. HYCH was defined by: (1) Symptoms of OI; (2) Orthostatic hypocapnia (low ET-CO2); (3) Abnormal decline in orthostatic CBFv due to hypocapnia; 4) Absence of tachycardia, orthostatic hypotension, or other causes of low CBFv or hypocapnia. Sixteen subjects met HYCH criteria (15/1 women/men, age 38.5±8.0 years) and were matched by age and gender to postural tachycardia patients (POTS, n = 16) and healthy controls (n = 16). During the tilt, CBFv decreased more in HYCH (-22.4±7.7%, p<0.0001) and POTS (-19.0±10.3%, p<0.0001) compared to controls (-3.0±5.0%). Orthostatic ET-CO2 was lower in HYCH (26.4±4.2 (mmHg), p<0.0001) and POTS (28.6±4.3, p<0.0001) compared to controls (36.9 ± 2.1 mmHg). Orthostatic heart rate was normal in HYCH (89.0±10.9 (BPM), p<0.08) and controls (80.8 ±11.2), but was higher in POTS (123.7±11.2, p<0.0001). Blood pressure was normal and similar in all groups. It is concluded that both HYCH and POTS patients have comparable decrease in CBFv which is due to vasoconstrictive effect of hypocapnia. Blood flow velocity monitoring can provide an objective biomarker for HYCH in OI patients without tachycardia.

Knee-high compression socks minimize head-up tilt-induced cerebral and cardiovascular responses following dynamic exercise.

In healthy individuals during a non-exercised state, knee-high compression socks (CS) may reduce the magnitude of lower limb venous pooling during orthostasis but are not effective at minimizing the incidence of pre-syncopal symptoms. However, exaggerated reductions in cerebral blood flow velocity (CBV) and cardiac stroke volume (SV) occur during passive head-up tilt (HUT) testing following dynamic exercise. It is unknown if CS can minimize post-exercise HUT-induced decrements in CBV and SV in this population. To test the hypothesis that CS will attenuate the reductions in SV and CBV during 60° HUT following 60minutes of moderate-intensity (60% VO2 peak) cycling exercise. Ten healthy volunteers (22.6±2.1years, 24.1±2.5kg/m2 ) completed pre- and post-exercise 15-minute HUT tests during randomized CS and Control (no CS) conditions. Changes in blood pressure (finger plethysmography), SV (Modelflow® method), and CBV (Transcranial Doppler) were measured during HUT and preceding supine rest periods. Pre-exercise HUT-induced similar (all, P>.47) reductions in SV (Control; -23.1±11.5%, CS; -20.5±10.9%) and CBV (Control; -18.1±6.3%, CS; -15.3±9.0%). However, larger post-exercise decreases in SV and CBV during HUT were observed in the Control versus CS condition. Specifically, CS attenuated the drop in SV (Control: -32.9±5.6%, CS: -24.3±11.6%; P=.01) and CBV (Control: -25.1±5.8%, CS: -17.6±7.8%; P=.02) during the post-exercise HUT test. These results indicate that CS attenuated HUT-induced reductions in SV and CBV following moderate-intensity cycling exercise and suggest that CS may be an effective countermeasure to reduce the incidence of post-exercise syncope in vulnerable populations.

Indexes of cerebral autoregulation do not reflect impairment in syncope: insights from head-up tilt test of vasovagal and autonomic failure subjects.

The study of dynamic cerebral autoregulation (CA), which adapts cerebral blood flow to arterial blood pressure (ABP) fluctuations, has been limited in orthostatic intolerance syndromes, mainly due to its stationary prerequisites hardly to meet during maneuvers to provoke syncope itself. New techniques of continuous estimates of CA could overcome this pitfall. We aimed to evaluate CA during head-up tilt test in common conditions causing syncope. We compared three groups: eight controls; eight patients with autonomic failure due to familial amyloidotic polyneuropathy; eight patients with vasovagal syncope (VVS). ABP and cerebral blood flow velocity (CBFV) were measured with Finometer® and transcranial Doppler. We calculated cerebrovascular resistance index (CVRi), critical closing pressure (CrCP) and resistance area product (RAP), and derived CA continuously from autoregulation index [ARI(t)]. With HUTT, AF subjects showed a pronounced decrease in CBFV (-36±17 versus -7±6%, p<0.0001), ABP (-29±27 versus 7±12%, p<0.0001) and RAP (-17±23 versus 3±18%, p<0.0001) but not CVRi (p=0.110). VVS subjects showed progressive cerebral vasoconstriction prior to syncope, (reduced CBFV 19±15 versus 1±6, p<0.000; increased RAP 12±18 versus 2±3%, p=0.024 and CVRi 12±18 versus 2±3%, p=0.005). ARI(t) increased significantly in AF patients (5.7±1.2 versus 6.9±1.2, p=0.040) and VVS (5.8±1.2 versus 7.3±1.2, p=0.015) in response to ABP fall during syncope. Our data suggest that dynamic cerebral autoregulatory response to orthostatic challenge is neither affected by autonomic dysfunction nor in neutrally mediated syncope. This study also emphasizes that RAP+CrCP model is more informative than CVRi, mainly during cerebral vasodilatory response to orthostatic hypotension.

Cerebrovascular adaptations to cocaine-induced transient ischemic attacks in the rodent brain.

Occurrence of transient ischemic attacks (TIA) and cerebral strokes is a recognized risk associated with cocaine abuse. Here, we use a rodent model along with optical imaging to study cocaine-induced TIA and the associated dynamic changes in cerebral blood flow velocity (CBFv) and cerebrovasculature. We show that chronic cocaine exposure in mice resulted in marked cortical hypoperfusion, in significant arterial and venous vasoconstriction, and in a sensitized vascular response to an acute cocaine injection. Starting after 10 days of exposure, an acute cocaine challenge to these mice resulted in a TIA, which presented as hemiparalysis and was associated with an abrupt exacerbation of CBFv. The severity of the TIA correlated with the decreases in cortical CBFv such that the greater the decreases in flow, the longer the TIA duration. The severity of TIA peaked around 17-22 days of cocaine exposure and decreased thereafter in parallel to a reorganization of CBFv from superficial to deep cortical layers, along with an increase in vessel density into these layers. Here, we document for the first time to our knowledge evidence of a TIA in an animal model of chronic cocaine exposure that was associated with profound decreases in CBFv, and we revealed that while the severity of the TIA initially increased with repeated exposures, it subsequently improved in parallel to an increase in the vessel density. This suggests that strategies to accelerate cerebrovascular recovery might be therapeutically beneficial in cocaine abusers.

The relationship between widespread changes in gravity and cerebral blood flow.

We investigated the dose-effect relationship between wide changes in gravity from 0 to 2.0Gz (Δ0.5Gz) and cerebral blood flow (CBF), to test our hypothesis that CBF has a linear relationship with levels of gravity. Ten healthy seated men were exposed to 0, 0.5, 1.0, 1.5, and 2.0Gz for 21min, by using a tilt chair and a short-arm human centrifuge. Steady-state CBF velocity (CBFV) in the middle cerebral artery by transcranial Doppler ultrasonography, mean arterial pressure (MAP) at the heart level (MAPHeart), heart rate, stroke volume, cardiac output and respiratory conditions were obtained for the last 6min at each gravity level. Then, MAP in the middle cerebral artery (MAPMCA), reflecting cerebral perfusion pressure, was estimated. Steady-state CBFV decreased stepwise from 0.5 to 2.0Gz. Steady-state heart rate, stroke volume, estimated MAPMCA and end-tidal carbon dioxide pressure (ETCO2) also changed stepwise from hypogravity to hypergravity. On the other hand, steady-state MAPHeart and cardiac output did not change significantly. Steady-state CBFV positively and linearly correlated with estimated MAPMCA and ETCO2 in most subjects. The present study demonstrated stepwise gravity-induced changes in steady-state CBFV from 0.5 to 2.0Gz despite unchanged steady-state MAPHeart. The combined effects of reduced MAPMCA and ETCO2 likely led to stepwise decreases in CBFV. We caution that a mild increase in gravity from 0 to 2.0Gz reduces CBF, even if arterial blood pressure at the heart level is maintained.

Compromised cerebrovascular modulation in chronic anxiety: evidence from cerebral blood flow velocity measured by transcranial Doppler sonography

Cerebral autoregulation (CA) is the mechanism by which constant cerebral blood flow is maintained despite changes in cerebral perfusion pressure. CA can be evaluated by dynamic monitoring of cerebral blood flow velocity (CBFV) with transcranial Doppler sonography (TCD). The present study aimed to explore CA in chronic anxiety. Subjects with Hamilton anxiety scale scores ≥14 were enrolled and the dynamic changes of CBFV in response to an orthostatic challenge were investigated using TCD. In both the anxious and the healthy subjects, the mean CBFV was significantly lower in the upright position than when supine. However, the CBFV changes from supine to upright differed between the anxious and the healthy groups. Anxious subjects showed more pronounced decreases in CBFV with abrupt standing. Our results indicate that cerebrovascular modulation is compromised in chronic anxiety; anxious subjects have some insufficiency in maintaining cerebral perfusion after postural change. Given the fact that anxiety and impaired CA are associated with cardiovascular disease, early ascertainment of compromised cerebrovascular modulation using TCD might suggest interventional therapies in the anxious population, and improve the primary prevention of cardiovascular disease.

Exercise plus volume loading prevents orthostatic intolerance but not reduction in cerebral blood flow velocity after bed rest

This study tested the hypothesis that reduction in cerebral blood flow (CBF) during orthostatic stress after bed rest can be ameliorated with volume loading, exercise, or both. Transcranial Doppler was used to measure changes in CBF velocity during lower body negative pressure (LBNP) before and after an 18-day bed rest in 33 healthy subjects. Subjects were assigned into four groups with similar age and sex: 1) supine cycling during bed rest (Exercise group; n = 7), 2) volume loading with Dextran infusion after bed rest to restore reduced left ventricular filling pressure (Dextran group; n = 7), 3) exercise combined with volume loading to prevent orthostatic intolerance (Ex-Dex group; n = 7), and 4) a control group (n = 12). LBNP tolerance was measured using a cumulative stress index (CSI). After bed rest, CBF velocity was reduced at a lower level of LBNP in the Control group, and the magnitude of reduction was greater in the Ex-Dex group. However, reduction in orthostatic tolerance was prevented in the Ex-Dex group. Notably, volume loading alone prevented greater reductions in CBF velocity after bed rest, but CSI was reduced still by 25%. Finally, decreases in CBF velocity during LBNP were correlated with reduction in cardiac output under all conditions (r(2) = 0.86; P = < 0.001). Taken together, these findings demonstrate that volume loading alone can ameliorate reductions in CBF during LBNP. However, the lack of associations between changes in CBF velocity and orthostatic tolerance suggests that reductions in CBF during LBNP under steady-state conditions by itself are unlikely to be a primary factor leading to orthostatic intolerance.

077 Cerebrovascular autoregulation during orthostatic stress after spinal cord injury

077 Cerebrovascular autoregulation during orthostatic stress after spinal cord injury

Impact of Aging and Life‐long Exercise on Cerebral Vasomotor Reactivity

This study investigated the impact of aging and life-long aerobic exercise training on cerebral vasomotor reactivity to changes in end-tidal CO2. We used transcranial Doppler to measure cerebral blood flow velocity (CBFV) in response to hypocapnia and hypercapnia induced by hyperventilation and CO2 rebreathing method. Eleven sedentary healthy young (SY, 27 ± 5 yr, 5 women), 10 sedentary seniors (SS, 72 ± 4 yr, 3 women) and 10 Masters Athletes (MA, 72 ± 6 yr, 1 woman) participated in this study. Compared with SY, resting CBFV was reduced and cerebrovascular resistance was increased in both SS and MA (P < 0.05). The relative changes in CBFV (%) in response to hypercapnia were greater in SS and MA than in SY (79 ± 21, 96 ± 23 vs. 56 ± 11 %, P < 0.01), but the absolute increases in CBFV were similar among 3 groups ( 39 ± 19, 41 ± 17 vs. 35 ± 8 cm/s, P > 0.2). During hypocapnia, both relative and absolute decreases in CBFV were less in SS and MA than in SY (P < 0.05). These decreases also were less in MA than in SS (P < 0.05). The cerebral vasomotor reactivity, in the sedentary and physically active elderly, was preserved or enhanced to hypercapnia, but reduced to hypocapnia. It suggests that there are probably defense mechanisms against chronic cerebrovascular constriction in the elderly which improve cerebral perfusion efficiently in hypercapnia and keep the brain of hypoperfusion in hypocapnia. This study was supported by R01HL102457-01.

The effects of sevoflurane on cerebral blood flow autoregulation and flow-metabolism coupling during cardiopulmonary bypass

previous studies on non-cardiac surgical patients have shown that cerebral pressure-flow autoregulation and cerebral flow-metabolism coupling are maintained with sevoflurane. The effects of sevoflurane on cerebral blood flow (CBF) autoregulation and flow-metabolism coupling during cardiopulmonary bypass (CPB) have not been studied previously. the effects of sevoflurane-induced burst suppression, monitored with electroencephalography (EEG), on cerebral blood flow velocity (CBFV), cerebral oxygen extraction (COE) and flow autoregulation, were studied in 16 patients undergoing cardiac surgery. The experimental procedure was performed during non-pulsatile CPB with mild hypothermia (34 degreesC) in fentanyl/droperidol-anesthetized patients. Middle cerebral artery transcranial Doppler flow velocity, right jugular vein bulb oxygen saturation and jugular venous pressure were measured continuously. Autoregulation was tested during changes in the mean arterial pressure (40-90 mmHg), induced by sodium nitroprusside and norepinephrine before (control), and during additional sevoflurane administration, in a dose that resulted in an EEG burst-suppression level of 4-6/min. sevoflurane, at an inspired concentration of 3.36 ± 0.03%, induced a 17% decrease in CBFV (P<0.05) and a 22% decrease in COE (P<0.05) compared with the control. The slope of the positive relationship between CBFV and cerebral perfusion pressure was steeper with sevoflurane (p<0.01) compared with control measurements, as was the slope of the negative relationship between cpp and coe (p<0.01). burst-suppression doses of sevoflurane exert an intrinsic cerebral vasodilatory effect, which impairs CBF autoregulation during mildly hypothermic CPB. Furthermore, during sevoflurane administration, CBF is in excess relative to oxygen demand, indicating a partial loss of the cerebral flow-metabolism coupling.

Cerebral Autoregulation is affected in Postural Tachycardia Syndrome

Orthostatic intolerance (OI) is defined by symptoms and signs while upright, relieved by recumbency. Included are symptoms of CNS malperfusion. Chronic OI, also known as postural tachycardia syndrome (POTS), is associated with excessive upright tachycardia. We hypothesized that CNS symptoms are due to defects of dynamic and static cerebral autoregulation (CA). Nine normocapnic POTS patients and 6 control subjects, ages 15‐27, were continuously monitored for heart rate (HR), mean blood pressure (MAP), end‐tidal CO2, and cerebral blood flow velocity (CBFV) during a supine period and 70° head‐up tilt. Transfer function analysis, with low frequency (LF) between 0.04‐0.15 Hz and high frequency (HF) between 0.15‐0.40 Hz, compared MAP and CBFV. During tilt, POTS had a higher HR than controls (112 ± 14 vs. 83 ± 9 bpm) and lower systolic BP (110 ± 11 vs. 123 ± 4 mmHg). Supine CBFV decreased during tilt in POTS from 66 ± 21 to 54 ± 15.3 cm/s; whereas, in controls it dropped from 67 ± 16.5 to 61 ± 14.9 cm/s. Analysis during tilt showed that POTS exhibited a higher LF and HF coherence than controls (LF: 0.85 ± 0.11 vs. 0.30 ± 0.09; HF: 0.81 ± 0.16 vs. 0.24 ± 0.09). The greater decrease of CBFV during tilt in POTS compared to controls shows decreased static CA affecting CNS perfusion. The high coherence between MAP and CBFV in POTS implies decreased dynamic CA, which permits BP oscillations to further compromise phasic CBF.

Relationship Between Ventilatory Threshold and Cerebral Blood Flow During Maximal Exercise in Humans

Background: This work studied the relationship between changes in cerebral blood flow velocity (CBFV) through the middle cerebral artery (MCA) with non-invasive ventilatory threshold (VT) measurements determined by gas- exchange during upright maximal cycle ergometry. Methods: Fourteen (M=8, F=6) healthy, young (23.1 ± 3.9 yr) participants volunteered for this study and performed a cy- cle ergometer protocol to maximal exertion. The CBFV was monitored continuously through the MCA by transcranial Doppler ultrasound and was assessed at rest, VT, and at maximal exertion (VO2max). Ventilatory threshold was assessed using three common methods: 1) V-slope, 2) nadir of the ventilatory equivalent for carbon dioxide production (VE/VCO2), and 3) maximal partial pressure of carbon dioxide (PETCO2). Results: Analysis of variance demonstrated significant (p<0.001) main effects for CBFV, volume of oxygen consumed (VO2), volume of carbon dioxide produced (VCO2), and PETCO2. Bonferroni post hoc analysis demonstrated an increase in CBFV from rest to a peak CBFV (p<0.01) with a decrease from peak CBFV to VO2max (p<0.01). Stepwise linear re- gression suggest the only predictor of a reduction in CBFV during maximal exercise is the nadir of VE/VCO2 (p<0.01). Conclusion: These data demonstrate an increase in CBFV during dynamic upright exercise up to approximately 78% VO2max after which CBFV decreases significantly to VO2max. This decrease in CBFV was closely related to common non-invasive measures of ventilatory threshold suggesting a close relationship between cerebral blood flow and the threshold for ventilatory compensation.

Disparate cardio-cerebral vascular modulation during standing in multiple system atrophy and Parkinson disease

Purpose The dynamic variance of cerebral blood flow velocity (CBFV), monitored by transcranial doppler (TCD), can reveal the integrated effects of cardio-cerebral vascular autoregulation. We investigated the characteristics of CBFV curve during active standing in multiple system atrophy (MSA), Parkinson's disease (PD) and healthy volunteers. Methods The CBFV curve of middle cerebral arteries was recorded using TCD in 22 patients with probable MSA; 20 PD patients and 20 volunteers matched for age. All individuals started in a supine posture, followed by abrupt standing for 2 min before returning to supine. The features of CBFV curve were compared among the groups. Results In the healthy volunteers, the CBFV decreased following standing up but quickly rebounded and reached the same or greater level as the supine baseline. Afterwards, the CBFV decreased abruptly to a sustained level, lower than the supine baseline, forming a spike wave that appeared in CBFV curve. This spike wave was present in 5/22 of MSA, significantly less than PD patients (18/20) and volunteers (20/20) ( P < 0.001). The CBFV decrease after standing showed no significant difference between MSA than PD (9 ± 7 vs. 6 ± 3 cm/s, P = 0.163). Conclusions The different pattern of CBFV curves during active standing suggests MSA may possess cardio-cerebral vascular modulation different from PD. The clinical value of the CBFV curve in differentiating MSA from PD needs further investigation.

Lateralization of cerebral hemodynamics during Wisconsin Card Sorting Test: a functional transcranial Doppler sonography study

Objective Studies on lateralization of cerebral metabolism during Wisconsin Card Sorting Test (WCST), a well-known paradigm of category learning, have shown mixed results. Moreover, sorting dimension (number, color and shape) is a cofounder of laterality in WCST. Functional transcranial Doppler sonography (fTCD) has a high temporal resolution and allows the measurement of mean cerebral blood flow velocity (CBFV) in the middle (MCA) and anterior cerebral arteries (ACA), which supply lateral and medial parts of the frontal and parietal lobes, respectively. We used fTCD to investigate CBFV changes occurring in both MCA and ACA during WCST and different sorting dimensions. Methods Twenty-one subjects underwent twice two distinct phases of the WCST, namely maintaining a rule (maintaining set) and searching for a new rule (set shifting), during bilateral fTCD of the MCA and ACA. Results There was a left-sided dominance of CBFV during maintaining set and set shifting in the MCA. CBFV was not associated with test performance. The sorting dimension number caused the highest CBFV increase in both MCA and ACA during maintaining set, and the sorting dimension shape caused lowest CBFV decrease in both MCA during set shifting. Conclusions This study confirms results that cerebral blood flow (CBF) lateralizes to the left side during WCST. The 3 sorting dimensions provoked distinct processing speed during maintaining set and set shifting, but caused no effect on hemispheric lateralization. Significance Functional transcranial Doppler sonography can be used to assess CBFV during WCST and different sorting dimensions, and the latter modulate reaction time and cerebral hemodynamics.

Noninvasive Monitoring of Cerebral Oxygenation during Vasomotor Reactivity Tests by a New Near-Infrared Spectroscopy Device

Background: Spatially resolved spectroscopy is a recently developed technique for noninvasive monitoring of cerebral tissue oxygenation using the photon diffusion theory. Methods: We studied this technique with a new, commercial near-infrared spectroscopy (NIRS) device during vasomotor reactivity tests in 28 healthy volunteers (mean age 31.0 years; SD 10.6 years) and compared it with values assessed by the modified Beer-Lambert law and indices from simultaneous transcranial Doppler sonography of both middle cerebral arteries. We measured O₂ reactivity as percentage change of cerebral blood flow velocity (CBFV), as absolute change in the concentrations (measured in µmol/l) of oxygenated (HbO₂), deoxygenated (Hb) and total hemoglobin (HbT), and as change in the tissue oxygenation index (TOI) during inhalation of 100% oxygen. CO₂ reactivity was calculated as percentage change of CBFV (NCR), as absolute change in the concentrations of HbO₂, Hb, and HbT (µmol/l), and as change in TOI (%) per 1% increase in end-tidal CO₂. Results: One hundred percent oxygen inhalation lead to a decrease in CBFV (mean ± SD: left –8.0 ± 7.0%, p = 0.000; right –9.6 ± 7.6%, p = 0.000), an increase in HbO₂ (0.99 ± 1.07 µmol/l), Hbdiff (2.23 ± 1.72 µmol/l), and TOI (3.1 ± 1.5%), and a decrease in Hb (–1.22 ± 0.74 µmol/l), significant from baseline values (p = 0.0000). CO₂ reactivity was: NCR left 25.4 ± 14.7%; NCR right 25.9 ± 13.4%; HbO₂ 1.99 ± 0.97 µmol/l; Hb –1.24 ± 0.81 µmol/l; HbT 0.81 ± 1.0 µmol/l, and TOI 3.7 ± 2.2%. O₂ reactivity in TCD did not correlate with NIRS reactivities (Pearson p > 0.05), but NCR did correlate with changes in HbO₂, Hb, and TOI (Pearson p < 0.01). TOI was closely related to indices derived from the Beer-Lambert law (Pearson p < 0.03), but not with mean arterial blood pressure or skin blood flow during vasomotor reactivity tests. Conclusion: Spatially resolved spectroscopy provides an encouraging, noninvasive new tool to study cerebral tissue oxygenation during vasomotor reactivity tests consistent with physiological changes.