Mean Cerebral Blood Flow Velocity Research Articles

19 Late Cord-Clamping Improves Circulation in Neonates

Aimwas to investigate the effects of late vs. early cord clamping on systemic circulation cerebral blood flow velocity (CBFV) in prematures infants < 1500g in a randomized trial.Subjects35 neonates were...

Risks for impaired cerebral autoregulation during cardiopulmonary bypass and postoperative stroke

Impaired cerebral autoregulation may predispose patients to cerebral hypoperfusion during cardiopulmonary bypass (CPB). The purpose of this study was to identify risk factors for impaired autoregulation during coronary artery bypass graft, valve surgery with CPB, or both and to evaluate whether near-infrared spectroscopy (NIRS) autoregulation monitoring could be used to identify this condition. Two hundred and thirty-four patients were monitored with transcranial Doppler and NIRS. A continuous, moving Pearson's correlation coefficient was calculated between mean arterial pressure (MAP) and cerebral blood flow (CBF) velocity, and between MAP and NIRS data, to generate the mean velocity index (Mx) and cerebral oximetry index (COx), respectively. Functional autoregulation is indicated by an Mx and COx that approach zero (no correlation between CBF and MAP); impaired autoregulation is indicated by an Mx and COx approaching 1. Impaired autoregulation was defined as an Mx ≥0.40 at all MAPs during CPB. Twenty per cent of patients demonstrated impaired autoregulation during CPB. Based on multivariate logistic regression analysis, time-averaged COx during CPB, male gender, Pa(CO(2)), CBF velocity, and preoperative aspirin use were independently associated with impaired CBF autoregulation. Perioperative stroke occurred in six of 47 (12.8%) patients with impaired autoregulation compared with five of 187 (2.7%) patients with preserved autoregulation (P=0.011). Impaired CBF autoregulation occurs in 20% of patients during CPB. Patients with impaired autoregulation are more likely than those with functional autoregulation to have perioperative stroke. Non-invasive monitoring autoregulation may provide an accurate means to predict impaired autoregulation. Clinical trials registration. www.clinicaltrials.gov (NCT00769691).

Effect of head and body positioning on cerebral blood flow velocity in patients who underwent cranial surgery

The aim of this study was to investigate the effects of head and neck positions on the cerebral blood flow velocity by transcranial Doppler ultrasound in patients who underwent cranial surgery. Inappropriate head elevation and body positioning in patients who undergo cranial surgery may affect cerebral blood flow and cerebral perfusion pressure. DESIGNED: Experimental clinical study. Our sample consisted of 38 patients who underwent cranial surgery between October 2009 and May 2010. The measurments of mean cerebral blood flow velocity were taken by the transcranial Doppler ultrasound through the temporal window. The mean cerebral blood flow velocity of the patients was measured in supine position with 0° and 30° head elevations, right and left lateral positions, right and left lateral positions with head flexion and extension. The measurements were taken before surgery and within 72 hours after surgery. The mean cerebral blood flow velocity of the middle cerebral arteries was increased in head elevations from 0° to 30°, in right and lateral positions with 30° head elevations, but the velocity was decreased in head flexion and extension positions in preoperative and postoperative periods. Head and body positioning, which is one of the nursing care activities, may affect intracranial pressure and cerebral perfusion pressure. Our results are similar with those of previous studies, which showed that head elevation did not affect the cerebral blood flow velocity. By the results of this study, the head elevation of the patients, who underwent cranial surgery, should be 30° during the nursing care to provide optimum cerebral blood flow. Right and left lateral positioning is safe and recommended for these patients if there is no medical contraindication.

Noninvasive optical evaluation of spontaneous low frequency oscillations in cerebral hemodynamics

Spontaneous low frequency oscillations (LFOs) around 0.1 Hz have been observed in mean arterial pressure (MAP) and cerebral blood flow velocity (CBFV). Previous studies have shown that cerebral autoregulation in major arteries can be assessed by quantification of the phase shift between LFOs of MAP and CBFV. However, many cerebral diseases are associated with abnormal microvasculature and tissue dysfunction in brain, and quantification of these abnormalities requires direct measurement of cerebral tissue hemodynamics. This pilot study used a novel hybrid near-infrared diffuse optical instrument to noninvasively and simultaneously detect LFOs of cerebral blood flow (CBF) and cerebral oxygenation (i.e., oxygenated/deoxygenated/total hemoglobin concentration: [HbO(2)]/[Hb]/THC) in human prefrontal cortex. Using the hybrid instrument and a finger plethysmograph, the dynamic changes of CBF, [HbO(2)], [Hb], THC and MAP were concurrently measured in 15 healthy subjects at rest, during 70° head-up-tilting (HUT) and during enforced breathing at 0.1 Hz. The LFOs were extracted from the measured variables using power spectral analysis, and the phase shifts and coherences of LFOs between MAP and each of the measured hemodynamic variables were calculated from the corresponding transfer functions. Levels of coherence (>0.4) were used to judge the success of LFO measurements. We found that CBF, [HbO(2)] and THC were reliable hemodynamic parameters in detecting LFOs and HUT was the most robust and stable protocol for quantifying phase shifts of hemodynamic LFOs. Comparing with other relevant studies, similar success rates for detecting cerebral LFOs have been achieved in our study. The phase shifts of LFOs in CBF were also close to those in CBFV reported by other groups, although the results in cerebral oxygenation measurements during enforced breathing varied across studies. Future study will investigate cerebral LFOs in patients with cerebral impairment and evaluate their cerebral autoregulation capabilities and neurocognitive functions via the quantification of LFO phase shifts.

Continuous Cerebral Blood Flow Autoregulation Monitoring in Patients Undergoing Liver Transplantation

Clinical monitoring of cerebral blood flow (CBF) autoregulation in patients undergoing liver transplantation may provide a means for optimizing blood pressure to reduce the risk of brain injury. The purpose of this pilot project is to test the feasibility of autoregulation monitoring with transcranial Doppler (TCD) and near-infrared spectroscopy (NIRS) in patients undergoing liver transplantation and to assess changes that may occur perioperatively. We performed a prospective observational study in 9 consecutive patients undergoing orthotopic liver transplantation. Patients were monitored with TCD and NIRS. A continuous Pearson's correlation coefficient was calculated between mean arterial pressure (MAP) and CBF velocity and between MAP and NIRS data, rendering the variables mean velocity index (Mx) and cerebral oximetry index (COx), respectively. Both Mx and COx were averaged and compared during the dissection phase, anhepatic phase, first 30min of reperfusion, and remaining reperfusion phase. Impaired autoregulation was defined as Mx≥0.4. Autoregulation was impaired in one patient during all phases of surgery, in two patients during the anhepatic phase, and in one patient during reperfusion. Impaired autoregulation was associated with a MELD score>15 (p=0.015) and postoperative seizures or stroke (p<0.0001). Analysis of Mx categorized in 5mmHg bins revealed that MAP at the lower limit of autoregulation (MAP when Mx increased to≥0.4) ranged between 40 and 85mmHg. Average Mx and average COx were significantly correlated (p=0.0029). The relationship between COx and Mx remained when only patients with bilirubin>1.2mg/dL were evaluated (p=0.0419). There was no correlation between COx and baseline bilirubin (p=0.2562) but MELD score and COx were correlated (p=0.0458). Average COx was higher for patients with a MELD score>15 (p=0.073) and for patients with a neurologic complication than for patients without neurologic complications (p=0.0245). These results suggest that autoregulation is impaired in patients undergoing liver transplantation, even in the absence of acute, fulminant liver failure. Identification of patients at risk for neurologic complications after surgery may allow for prompt neuroprotective interventions, including directed pressure management.

Linear and Nonlinear Modeling of Cerebral Flow Autoregulation Using Principal Dynamic Modes

Cerebral Flow Autoregulation (CFA) is the dynamic process by which cerebral blood flow is maintained within physiologically acceptable bounds during fluctuations of cerebral perfusion pressure. The distinction is made with “static” flow autoregulation under steady-state conditions of perfusion pressure, described by the celebrated “autoregulatory curve” with a homeostatic plateau. This paper studies the dynamic CFA during changes in perfusion pressure, which attains critical clinical importance in patients with stroke, traumatic brain injury and neurodegenerative disease with a cerebrovascular component. Mathematical and computational models have been used to advance our quantitative understanding of dynamic CFA and to elucidate the underlying physiological mechanisms by analyzing the relation between beat-to-beat data of mean arterial blood pressure (viewed as input) and mean cerebral blood flow velocity(viewed as output) of a putative CFA system. Although previous studies have shown that the dynamic CFA process is nonlinear, most modeling studies to date have been linear. It has also been shown that blood CO2 tension affects the CFA process. This paper presents a nonlinear modeling methodology that includes the dynamic effects of CO2 tension (or its surrogate, end-tidal CO2) as a second input and quantifies CFA from short data-records of healthy human subjects by use of the modeling concept of Principal Dynamic Modes (PDMs). The PDMs improve the robustness of the obtained nonlinear models and facilitate their physiological interpretation. The results demonstrate the importance of including the CO2 input in the dynamic CFA study and the utility of nonlinear models under hypercapnic or hypocapnic conditions.

Linear and Nonlinear Modeling of Cerebral Flow Autoregulation Using Principal Dynamic Modes

Cerebral Flow Autoregulation (CFA) is the dynamic process by which cerebral blood flow is maintained within physiologically acceptable bounds during fluctuations of cerebral perfusion pressure. The distinction is made with “static” flow autoregulation under steady-state conditions of perfusion pressure, described by the celebrated “autoregulatory curve” with a homeostatic plateau. This paper studies the dynamic CFA during changes in perfusion pressure, which attains critical clinical importance in patients with stroke, traumatic brain injury and neurodegenerative disease with a cerebrovascular component. Mathematical and computational models have been used to advance our quantitative understanding of dynamic CFA and to elucidate the underlying physiological mechanisms by analyzing the relation between beat-to-beat data of mean arterial blood pressure (viewed as input) and mean cerebral blood flow velocity(viewed as output) of a putative CFA system. Although previous studies have shown that the dynamic CFA process is nonlinear, most modeling studies to date have been linear. It has also been shown that blood CO2 tension affects the CFA process. This paper presents a nonlinear modeling methodology that includes the dynamic effects of CO2 tension (or its surrogate, end-tidal CO2) as a second input and quantifies CFA from short data-records of healthy human subjects by use of the modeling concept of Principal Dynamic Modes (PDMs). The PDMs improve the robustness of the obtained nonlinear models and facilitate their physiological interpretation. The results demonstrate the importance of including the CO2 input in the dynamic CFA study and the utility of nonlinear models under hypercapnic or hypocapnic conditions.

CO2-Dependent Vasomotor Reactivity of Cerebral Arteries in Patients with Severe Traumatic Brain Injury: Time Course and Effect of Augmentation of Cardiac Output with Dobutamine

Failing cerebral blood flow (CBF) autoregulation may contribute to cerebral damage after traumatic brain injury (TBI). The purpose of this study was to describe the time course of CO(2)-dependent vasoreactivity, measured as CBF velocity in response to hyperventilation (vasomotor reactivity [VMR] index). We included 13 patients who had had severe TBI, 8 of whom received norepinephrine (NE) based on clinical indication. In these patients, measurements were also performed after dobutamine administration, with a goal of increasing cardiac output by 30%. Blood flow velocity was measured with transcranial Doppler ultrasound in both hemispheres. All patients except one had an abnormal VMR index in at least one hemisphere within the first 24 h after TBI. In those patients who did not receive catecholamines, mean VMR index recovered within the first 48 to 72 h. In contrast, in patients who received NE within the first 48 h period, VMR index did not recover on the second day. Cardiac output and mean CBF velocity increased significantly during dobutamine administration, but VMR index did not change significantly. In conclusion, CO(2) vasomotor reactivity was abnormal in the first 24 h after TBI in most of the patients, but recovered within 48 h in those patients who did not receive NE, in contrast to those eventually receiving the drug. Addition of dobutamine to NE had variable but overall insignificant effects on CO(2) vasomotor reactivity.

Cerebral autoregulation is enhanced at higher levels of exercise intensity

Cerebral blood flow (CBF) changes in response to exercise are intensity dependent, but it is unclear how well cerebral autoregulation (CA) is maintained at higher intensities. We had ten healthy subjects perform cycle exercise at 50%, 85%, and 115% of their ventilatory threshold (Vt) as well as delta 90 for a 5 minute bout. CBF (transcranial Doppler), mean arterial pressure (MAP), heart rate and ventilatory response were measured continuously throughout, and exercise responses were compared to baseline values. CA was calculated via transfer‐function (0.04 – 0.5 Hz) gain between MAP and mean CBF velocity and analyzed via repeated measures ANOVA. CBF and MAP significantly increased from baseline (59.24±5.3 cm/s, 90.6±6.4 mmHg) to exercise (64.83±5.8 cm/s, 103.81±6.3 mmHg). We observed minimal changes in gain during submaximal intensities (i.e. 50–115%Vt), but saw a significant decrease in gain from baseline (1.57±0.28) to exercise (0.63±0.23) as intensity increased (i.e. delta90). We interpret this significant interaction (baseline/exercise x intensity) as evidence of improved CA during high‐intensity exercise. Therefore, during high levels of exercise CBF is adequately maintained despite greater effort and increased cerebral metabolism.

Lifelong Exercise Improves Cardiac Baroreflex Function But Not Dynamic Cerebral Autoregulation In Older Adults

Previous studies suggest that aerobic exercise training improves cardiac baroreflex function. However, the effects of aerobic exercise training on dynamic cerebral autoregulation (dCA) are not clear. The purpose of this study was to determine the effect of lifelong exercise on cardiac baroreflex function and dCA in older adults. Eleven Masters athletes (MA) (8 males, age 73±6 yrs, aerobic training&gt;15 yrs) and 9 healthy sedentary elderly (SE) (6 males, age 73±4 yrs) participated in this study. Blood pressure (BP), cerebral blood flow velocity (CBFV) and heart rate were measured continuously during resting conditions and repeated sitstand maneuvers. Baroreflex gain was assessed using transfer function analysis of spontaneous changes in systolic BP and RR‐interval in the low (0.05–0.15 Hz; LF) and high (0.15–0.35 Hz; HF) frequency ranges. dCA was assessed using transfer function analysis of induced changes in mean BP and CBFV during repeated sit‐stand maneuvers at 0.05 Hz (10s sit, 10s stand). MA showed higher cardiac baroreflex gain compared to SE (LF: MA: 7.69±7.95, SE: 3.13±1.22, ms/mmHg, P=0.001, HF: MA: 11.13±7.33, SE: 4.11±2.70, ms/mmHg, P=0.006). However, dCA was similar between the two groups (normalized gain: MA: 1.50±0.56, SE: 1.42±0.40, %CBFV/mmHg, P=0.743). These findings suggest that lifelong exercise improves cardiac baroreflex function, but does not alter dCA in older adults.

Cerebrovascular time constant: dependence on cerebral perfusion pressure and end-tidal carbon dioxide concentration

Objective: The cerebrovascular time constant (τ) describes the time to establish a change in cerebral blood volume after a step transient in arterial blood pressure (ABP). We studied the relationship between τ, ABP, intracranial pressure (ICP), and end-tidal carbon dioxide concentration (EtCO2).Method: Recordings from 46 anaesthetized, paralysed and ventilated New Zealand rabbits were analysed retrospectively. ABP was directly monitored in the femoral artery, transcranial Doppler (TCD) cerebral blood flow velocity (CBFV) from the basilar artery, and ICP using an intraparenchymal sensor. In nine animals end-tidal CO2 (EtCO2) was monitored continuously. ABP was decreased with injection of trimetophan (n = 11) or haemorrhage (n = 6) and increased by boluses of dopamine (n = 11). ICP was increased by infusion of normal saline into the lumbar cerebrospinal fluid space (n = 9). Changes in cerebral compliance (Ca) were estimated as a ratio of the pulse amplitude of the cerebral arterial blood volume (CBV) and the pulse amplitude of ABP. Changes in cerebrovascular resistance (CVR) were expressed as mean ABP or cerebral perfusion pressure (CPP) divided by mean CBFV. Time constant τ was calculated as the product of CVR and Ca.Results: The time constant changed inversely to the direction of the change in ABP (during arterial hypo- and hypertension) and CPP (during intracranial hypertension). Ca increased with decreasing CPP, while CVR decreased. During a decrease in CPP, changes in Ca exceeded changes in CVR. In contrast, during hypercapnia, the decrease in CVR was more pronounced than the increase in Ca, resulting in a decreasein τ.Conclusion: Cerebrovascular time constant τ is modulated by ABP, ICP, and EtCO2.

Melatonin does not attenuate dynamic cardiovascular and cerebrovascular reflex responses to acute hypotension in healthy men

BackgroundMelatonin has been shown to attenuate the reflex sympathetic increases that arise in response to orthostatic challenges. We tested the hypothesis that the attenuated sympathetic increase induced by melatonin premedication may weaken the arterial blood pressure (ABP) preserving the capability during acute hypotension, thereby altering dynamic cerebral autoregulation and causing a further decrease in cerebral blood flow (CBF).MethodsAcute hypotension was induced in 12 healthy subjects by releasing bilateral thigh cuffs before and after an oral dose of melatonin (0.2 mg/kg). Heart rate (HR), arterial blood pressure (ABP), Modelflow estimate of cardiac output (CO), total peripheral resistance (TPR) and cerebral blood flow velocity (CBFV) by transcranial Doppler were measured.ResultsSteady state HR, the mean arterial pressure and CBFV were not altered 60 minutes after melatonin ingestion. Reduced systolic arterial pressure (ΔSAP), changes in HR (ΔHR), CO (ΔCO), and TPR (ΔTPR), ΔHR/ΔSAP and percentage restoration of SAP were not affected after a temporal decrease in ABP induced by thigh cuff release. In the cerebral circulation, melatonin did not affect changes in CBFV, cerebrovascular resistance index, the rate of regulation and percentage restoration of CBFV following a sudden decrease in ABP.ConclusionsContrary to our hypothesis, melatonin did not affect the rapid vasodilatory and recovery responses of cardiovascular and dynamic cerebral autoregulation. These results suggest that melatonin premedication may not impair ABP and CBF preserving capability induced by sudden postural changes or hemorrhage.

Postural neurocognitive and neuronal activated cerebral blood flow deficits in young chronic fatigue syndrome patients with postural tachycardia syndrome

Neurocognition is impaired in chronic fatigue syndrome (CFS). We propose that the impairment relates to postural cerebral hemodynamics. Twenty-five CFS subjects and twenty control subjects underwent incremental upright tilt at 0, 15, 30, 45, 60, and 75° with continuous measurement of arterial blood pressure and cerebral blood flow velocity (CBFV). We used an n-back task with n ranging from 0 to 4 (increased n = increased task difficulty) to test working memory and information processing. We measured n-back outcomes by the number of correct answers and by reaction time. We measured CBFV, critical closing pressure (CCP), and CBFV altered by neuronal activity (activated CBFV) during each n value and every tilt angle using transcranial Doppler ultrasound. N-back outcome in control subjects decreased with n valve but was independent of tilt angle. N-back outcome in CFS subjects decreased with n value but deteriorated as orthostasis progressed. Absolute mean CBFV was slightly less than in control subjects in CFS subject at each angle. Activated CBFV in control subjects was independent of tilt angle and increased with n value. In contrast, activated CBFV averaged 0 in CFS subjects, decreased with angle, and was less than in control subjects. CCP was increased in CFS subjects, suggesting increased vasomotor tone and decreased metabolic control of CBFV. CCP did not change with orthostasis in CFS subjects but decreased monotonically in control subjects, consistent with vasodilation as compensation for the orthostatic reduction of cerebral perfusion pressure. Increasing orthostatic stress impairs neurocognition in CFS subjects. CBFV activation, normally tightly linked to cognitive neuronal activity, is unrelated to cognitive performance in CFS subjects; the increased CCP and vasomotor tone may indicate an uncoupling of the neurovascular unit during orthostasis.

Vasospasm Shortens Cerebral Arterial Time Constant

Cerebrovascular time constant (τ) estimates how fast cerebral blood arrives in cerebral arterial bed after each heart stroke. We investigate the pattern of changes in τ following subarachnoid hemorrhage (SAH), with specific emphasis on the temporal profile of changes in relation to the development of cerebral vasospasm. Simultaneous recordings of arterial blood pressure (ABP) and transcranial Doppler (TCD) blood flow velocity (CBFV) in MCA were performed daily in patients after SAH. In 22 patients (10 males and 12 females; median age: 48 years, range: 34-84 years) recordings done before spasm were compared to those done during spasm. Vasospasm was confirmed with TCD (mean CBFV in MCA > 120 cm/s and Lindegaard ratio > 3). τ was estimated as a product of compliance of cerebral arteries (C (a)) and cerebrovascular resistance (CVR). C (a) and CVR were estimated using mathematical transformations of ABP and CBFV waveforms. Vasospasm caused shortening of τ on both the spastic (before: 0.20 ± 0.05 s vs. spasm: 0.14 ± 0.04 s, P < 0.0008) and contralateral side (before: 0.22 ± 0.05 s vs. spasm: 0.16 ± 0.04 s, P < 0.0008). Before TCD signs of vasospasm were detected, τ demonstrated asymmetry with lower values on ipsilateral side to aneurysm, in comparison to contralateral side (P < 0.009), Cerebral vasospasm causes shortening of τ. Shorter τ at the side of aneurysm can be observed before formal TCD signs of vasospasm are observed, therefore, potentially reducing time to escalation of treatment.

Low Pulsatility Index on Transcranial Doppler Predicts Symptomatic Large-Vessel Vasospasm After Aneurysmal Subarachnoid Hemorrhage

Elevated mean cerebral blood flow velocity (mCBFV) on transcranial Doppler predicts vasospasm of the large intracranial arteries after aneurysmal subarachnoid hemorrhage (aSAH). The pulsatility index (PI) is a measure of distal vascular resistance, which may be low when there is compensatory distal vasodilatation following hypoperfusion caused by large-vessel vasospasm. To study the predictive value of low PI for symptomatic large-vessel vasospasm (SLVVS) after aSAH. Medical records of patients admitted with aSAH between January 2007 and April 2009 were reviewed. Transcranial color-coded duplex (TCCD) sonography was performed daily between days 2 and 14. Patients with unexplained acute neurological decline underwent catheter- or computed tomography-angiography. The lowest recorded PI and the highest mCBFV on TCCD were correlated to the occurrence of SLVVS, angiographic vasospasm, and delayed cerebral infraction in multivariate analysis by use of logistic regression. Functional outcome was assessed at first follow-up. Eighty-one patients met inclusion criteria. Mean lowest PI was 0.71 + 0.19. Median highest mCBFV was 135 cm/s (interquartile range 99-194 cm/s). SLVVS was seen in 21 of 81 (26%) patients, whereas 27 of 55 (49%) patients with repeat angiography had moderate or severe angiographic vasospasm. Following multivariate analysis, only the lowest PI was an independent predictor of SLVVS (P = .03, odds ratio 0.04, 95% confidence interval 0.001-0.54), whereas only the highest mCBFV was an independent predictor of angiographic vasospasm (P = .02, odds ratio 1.01, 95% confidence interval 1.002-1.02). SLVVS was independently associated with functional outcome at follow-up. Low PI on TCCD is an independent predictor of SLVVS after aSAH, whereas mCBFV is a better predictor of angiographic vasospasm.

Cerebral circulation during mild +Gz hypergravity by short-arm human centrifuge

We examined changes in cerebral circulation in 15 healthy men during exposure to mild +Gz hypergravity (1.5 Gz, head-to-foot) using a short-arm centrifuge. Continuous arterial pressure waveform (tonometry), cerebral blood flow (CBF) velocity in the middle cerebral artery (transcranial Doppler ultrasonography), and partial pressure of end-tidal carbon dioxide (ETco(2)) were measured in the sitting position (1 Gz) and during 21 min of exposure to mild hypergravity (1.5 Gz). Dynamic cerebral autoregulation was assessed by spectral and transfer function analysis between beat-to-beat mean arterial pressure (MAP) and mean CBF velocity (MCBFV). Steady-state MAP did not change, but MCBFV was significantly reduced with 1.5 Gz (-7%). ETco(2) was also reduced (-12%). Variability of MAP increased significantly with 1.5 Gz in low (53%)- and high-frequency ranges (88%), but variability of MCBFV did not change in these frequency ranges, resulting in significant decreases in transfer function gain between MAP and MCBFV (gain in low-frequency range, -17%; gain in high-frequency range, -13%). In contrast, all of these indexes in the very low-frequency range were unchanged. Transfer from arterial pressure oscillations to CBF fluctuations was thus suppressed in low- and high-frequency ranges. These results suggest that steady-state global CBF was reduced, but dynamic cerebral autoregulation in low- and high-frequency ranges was improved with stabilization of CBF fluctuations despite increases in arterial pressure oscillations during mild +Gz hypergravity. We speculate that this improvement in dynamic cerebral autoregulation within these frequency ranges may have been due to compensatory effects against the reduction in steady-state global CBF.

Correlation analysis between prefrontal oxygenation oscillations and cerebral artery hemodynamics in humans

The objective of this study is to assess the correlation between the prefrontal cerebral oxygenation oscillations measured by near-infrared spectroscopy (NIR) and cerebral artery hemodynamic parameters as measured by transcranial Doppler (TCD). A total of thirty subjects were recruited from the university to participate in this study. The cerebral oxygenation signal and TCD hemodynamic parameters were monitored on separate days. The cerebral oxygenation signal was monitored for 10min from the left prefrontal lobe using NIRS. TCD monitoring was performed to measure the hemodynamic parameters including end diastolic, peak systolic, and mean cerebral blood flow velocities. Pulsatility index (PI) and resistance index (RI) were calculated automatically. With spectral analysis based on wavelet transform of NIR signal, five frequency intervals were identified (I, 0.005–0.02Hz, II, 0.02–0.06Hz, III, 0.06–0.15Hz, IV, 0.15–0.50Hz and V, 0.50–2.0Hz). Significant negative correlation was found between the cerebral [Hb] and [HbO2] oscillations in frequency intervals from I to V and the PI or RI in left external carotid artery (ECA) (p<0.005). Also weak negative correlation was found between the cerebral [Hb] and [HbO2] oscillations in frequency intervals III, IV, V and the mean velocity in left middle cerebral artery (MCA) (p<0.05). The results suggested that the cerebral oscillations measured from the frontal lobe were closely related to the pulsatility of ECA and reflect partly the vessel stiffness of MCA.

Hypertension Impairs Vascular Reactivity in the Pediatric Brain

Chronic hypertension impairs cerebrovascular regulation in adults, but its effects on the pediatric population are unknown. The objective of this study was to investigate cerebrovascular abnormalities in hypertensive children and adolescents. Sixty-four children and adolescents aged 7 to 20 years underwent transcranial Doppler examinations of the middle cerebral artery at the time of rebreathing CO2. Time-averaged maximum mean cerebral blood flow velocity and end-tidal CO2 were used to quantify cerebrovascular reactivity during hypercapnia. Patients were clinically categorized as hypertensive, prehypertensive, or white coat hypertensive based on 24-hour ambulatory blood pressure measurements. Their reactivities were compared with 9 normotensive control subjects and evaluated against baseline mean blood pressure z-scores and loads. Untreated hypertensive children had significantly lower hypercapnic reactivity than normotensive children (2.556 +/- 1.832 cm/s x mm Hg versus 4.256 +/- 1.334 cm/s x mm Hg, P < 0.05). Baseline mean diastolic blood pressure z-scores (r = -0.331, P = 0.037) and diastolic blood pressure loads (r = -0.351, P = 0.026) were inversely related to reactivity. Untreated hypertensive children and adolescents have blunted reactivity to hypercapnia, indicating deranged vasodilatory reactivity. The inverse relationship between diastolic blood pressure indices and reactivity suggests that diastolic blood pressure may be a better predictor of cerebral end organ damage than systolic blood pressure.

Increased Pulsatile Cerebral Blood Flow, Cerebral Vasodilation, and Postsyncopal Headache in Adolescents

We hypothesize that, after a sudden decrease in cerebral blood flow velocity (CBFV) in adolescents, a faint, rapid hyperemic pulsatile CBFV occurs upon the patient's return to the supine position and is associated with postsyncopal headache. This case-control study involved 16 adolescent subjects with a history of fainting and headaches. We induced fainting during 70° tilt-table testing and measured mean arterial pressure, heart rate, end-tidal CO(2), and CBFV. Fifteen control subjects were similarly evaluated with a tilt but did not faint, and comparisons with fainters were made at equivalent defined time points. Baseline values were similar between the groups. Upon fainting, mean arterial pressure decreased 49% in the patients who fainted vs 6% in controls (P < .001). The heart rate decreased 15% in fainters and increased 35% in controls (P < .001). In patients who fainted, cerebrovascular critical closing pressure increased markedly, which resulted in reduced diastolic (-66%) and mean CBFV (-46%) at faint; systolic CBFV was similar to controls. Pulsatile CBFV (systolic-diastolic CBFV) increased 38% in fainters, which caused flow-mediated dilatation of cerebral vessels. When the fainters returned to the supine position, CBFV exhibited increased systolic and decreased diastolic flows compared with controls (P < .02). Increased pulsatile CBFV during and after faint may cause postsyncopal cerebral vasodilation and headache.

Low-Voltage aEEG as Predictor of Intracranial Hemorrhage in Preterm Infants

The objectives of this prospective cohort study were to identify amplitude-integrated electroencephalography (aEEG) background patterns predictive of severe intracranial hemorrhage. Thirty ventilated preterm newborns weighing <1,000 g were assessed by an aEEG cerebral function monitor and ultrasound measurement of cerebral blood flow velocity at time of surfactant administration and tracheal suctioning simultaneously during first 48 hours of life. Birth weight was 624 ± 200 g (mean ± S.D.) and gestational age was 25 ± 2 weeks. Background electrical activity was predominantly discontinuous in 72% of infants. A sharp increase in electrical activity/burst density was observed during surfactant administration and tracheal suctioning in most infants, with a 33.5% increase in mean cerebral blood flow velocity. Burst suppression with low voltage was identified in 57% infants with severe intracranial hemorrhage, whereas no infant without hemorrhage exhibited this pattern (P = 0.014). We conclude that aEEG low-voltage burst suppression might have useful clinical applications with 100% positive predictive value for severe intracranial hemorrhage.