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Cerebral Blood Flow Velocity (cerebral + blood_flow_velocity)
Selected AbstractsBiofeedback-Assisted Relaxation in Migraine Headache: Relationship to Cerebral Blood Flow Velocity in the Middle Cerebral ArteryHEADACHE, Issue 3 2003Sachinder Vasudeva MD Objective.,To determine if migraineurs with aura respond differently to biofeedback/relaxation than those without aura and, if so, whether the variability in outcome can be explained by blood flow velocity. Background.,The relationship between cerebral blood flow velocity and treatment response to biofeedback/relaxation in migraine with and without aura is uncertain. Method.,Twenty migraineurs underwent 12 sessions of biofeedback/relaxation therapy, while 20 controls simply were told to relax on their own. Cerebral blood flow velocity was measured bilaterally in the middle cerebral artery with transcranial Doppler. Results.,The biofeedback group showed significant (P < .05) reductions in pain, depression, and anxiety compared to the control group. Patients with and without aura did equally well. There were significant (P < .05) left to right blood flow velocity differences only in the migraine with aura group. Maximum blood flow velocities were significantly higher (P < .05) in the migraine with aura group than in the cohort without aura. There was an inverse correlation between indicators of anxiety and blood flow velocity, perhaps related to hyperventilation-induced constriction in the small vessels distal to the middle cerebral artery. Conclusion.,The positive treatment response to biofeedback/relaxation in migraine headache is not related to presence of aura, nor to changes in blood flow velocity, but may be associated with reduction in anxiety and depression. [source] Cerebral Hemodynamics Changes During Retrograde Brain Perfusion in DogsJOURNAL OF NEUROIMAGING, Issue 2 2001Alexander Y. Razumovsky PhD ABSTRACT The objective of this study was to examine cerebral hemodynamics changes during hypothermic circulatory arrest (HCA) with and without retrograde cerebral perfusion (RCP). Thirteen colony-bred hound dogs were placed on cardiopulmonary bypass (CPB) and cooled to 18°C. Five dogs underwent 2 hours of HCA without RCP and 8 with RCP. The animals were then rewarmed on CPB until normothermic and weaned. Cerebral blood flow velocity (CBFV) and Gosling Pulsatility Index (PI) in the middle cerebral artery (MCA) were studied using transcranial Doppler (TCD) ultrasound. At baseline and during pre- and postarrest CPB, there was anterograde direction of blood flow in the MCA. During HCA with RCP, there was retrograde direction of blood flow in the MCA. There was no difference in CBFV between pre-, during, and postarrest CPB in the group with RCP; however, there was significantly increased CBFV during postarrest CPB in the group without RCP compared to the dogs with RCP. Later, at 3 hours after postarrest CPB, there was decreased CBFV in all animals accompanied by increased PI (2.4 ± 0.4 and 2.2 ± 0.6 for animals with RCP and without RCP, respectively) and abnormal TCD waveform changes including decreased diastolic compartment and sharp systolic peak. During hypothermic circulatory arrest, RCP provides CBFV in the MCA comparable to MCA CBFV during CPB. HCA dogs without RCP showed immediate hyperemia on reperfusion. The decreased CBFV and increased PI at 1 hour after postarrest CPB could be an indicator of progressive ischemic injury due to the increased intracranial pressure despite the implementation of RCP. [source] Low cerebral blood flow velocity and risk of white matter hyperintensitiesANNALS OF NEUROLOGY, Issue 3 2001Christophe Tzourio MD Cerebral blood flow velocity (CBF-V) measured by transcranial doppler was assessed in 628 elderly individuals who had cerebral magnetic resonance imaging performed as part of a population-based study on vascular aging. Cerebral white matter hyperintensities (WMHs) were associated with low CBF-V, such as the adjusted odds ratios of severe WMHs from highest (referent) to lowest quartile of mean CBF-V were 1.0, 1.7, 3.7, and 4.3 (p = 0.001). Further, CBF-V was found to be a stronger risk factor for WMHs than high blood pressure. These findings suggest that the assessment of CBF-V might be a powerful tool in future studies on WMHs. Ann Neurol 2001;49:411,414 [source] Transcranial Doppler Blood Flow Assessment in Patients With Mild Heart Failure: Correlates With Neuroimaging and Cognitive PerformanceCONGESTIVE HEART FAILURE, Issue 2 2008Raymond L. C. Vogels MD Cardiac output and cerebral perfusion are reduced in patients with advanced stages of heart failure. Our aim was to determine whether cerebral blood flow velocity measured by transcranial Doppler ultrasonography was reduced in outpatients with mild heart failure in comparison to controls and, if so, whether this reduction was related to cognitive performance and abnormalities of the brain diagnosed by magnetic resonance imaging. [source] Cerebral oxygenation decreases during exercise in humans with beta-adrenergic blockadeACTA PHYSIOLOGICA, Issue 3 2009T. Seifert Abstract Aim:, Beta-blockers reduce exercise capacity by attenuated increase in cardiac output, but it remains unknown whether performance also relates to attenuated cerebral oxygenation. Methods:, Acting as their own controls, eight healthy subjects performed a continuous incremental cycle test to exhaustion with or without administration of the non-selective beta-blocker propranolol. Changes in cerebral blood flow velocity were measured with transcranial Doppler ultrasound and those in cerebral oxygenation were evaluated using near-infrared spectroscopy and the calculated cerebral mitochondrial oxygen tension derived from arterial to internal jugular venous concentration differences. Results:, Arterial lactate and cardiac output increased to 15.3 ± 4.2 mm and 20.8 ± 1.5 L min,1 respectively (mean ± SD). Frontal lobe oxygenation remained unaffected but the calculated cerebral mitochondrial oxygen tension decreased by 29 ± 7 mmHg (P < 0.05). Propranolol reduced resting heart rate (58 ± 6 vs. 69 ± 8 beats min,1) and at exercise exhaustion, cardiac output (16.6 ± 3.6 L min,1) and arterial lactate (9.4 ± 3.7 mm) were attenuated with a reduction in exercise capacity from 239 ± 42 to 209 ± 31 W (all P < 0.05). Propranolol also attenuated the increase in cerebral blood flow velocity and frontal lobe oxygenation (P < 0.05) whereas the cerebral mitochondrial oxygen tension decreased to a similar degree as during control exercise (delta 28 ± 10 mmHg; P < 0.05). Conclusion:, Propranolol attenuated the increase in cardiac output of consequence for cerebral perfusion and oxygenation. We suggest that a decrease in cerebral oxygenation limits exercise capacity. [source] Twenty-four-hour non-invasive monitoring of systemic haemodynamics and cerebral blood flow velocity in healthy humansACTA PHYSIOLOGICA, Issue 1 2002M. DIAMANT ABSTRACT Acute short-term changes in blood pressure (BP) and cardiac output (CO) affect cerebral blood flow (CBF) in healthy subjects. As yet, however, we do not know how spontaneous fluctuations in BP and CO influence cerebral circulation throughout 24 h. We performed simultaneous monitoring of BP, systemic haemodynamic parameters and blood flow velocity in the middle cerebral artery (MCAV) in seven healthy subjects during a 24-h period. Finger BP was recorded continuously during 24 h by Portapres and bilateral MCAV was measured by transcranial Doppler (TCD) during the first 15 min of every hour. The subjects remained supine during TCD recordings and during the night, otherwise they were seated upright in bed. Stroke volume (SV), CO and total peripheral resistance (TPR) were determined by Modelflow analysis. The 15 min mean value of each parameter was assumed to represent the mean of the corresponding hour. There were no significant differences between right vs. left, nor between mean daytime vs. night time MCAV. Intrasubject comparison of the twenty-four 15-min MCAV recordings showed marked variations (P < 0.001). Within each single 15-min recording period, however, MCAV was stable whereas BP showed significant short-term variations (P < 0.01). A day,night difference in BP was only observed when daytime BP was evaluated from recordings in the seated position (P < 0.02), not in supine recordings. Throughout 24 h, MCAV was associated with SV and CO (P < 0.001), to a lesser extent with mean arterial pressure (MAP; P < 0.005), not with heart rate (HR) or TPR. These results indicate that in healthy subjects MCAV remains stable when measured under constant supine conditions but shows significant variations throughout 24 h because of activity. Moreover, changes in SV and CO, and to a lesser extent BP variations, affect MCAV throughout 24 h. [source] Impairment of cerebral autoregulation in diabetic patients with cardiovascular autonomic neuropathy and orthostatic hypotensionDIABETIC MEDICINE, Issue 2 2003B. N. Mankovsky Abstract Aims Impaired cerebrovascular reactivity and autoregulation has been previously reported in patients with diabetes mellitus. However, the contribution of cardiovascular diabetic autonomic neuropathy and orthostatic hypotension to the pathogenesis of such disturbances is not known. The purpose of this study was to evaluate cerebral blood flow velocity in response to standing in patients with diabetes and cardiovascular autonomic neuropathy with or without orthostatic hypotension. Methods We studied 27 patients with diabetes,eight had cardiovascular autonomic neuropathy and orthostatic hypotension (age 46.4 ± 13.5 years, diabetes duration 25.0 ± 11.0 years), seven had autonomic neuropathy without hypotension (age 47.3 ± 12.7 years, diabetes duration 26.4 ± 12.1 years), and 12 had no evidence of autonomic neuropathy (age 44.1 ± 13.8 years, diabetes duration 17.1 ± 10.2 years),and 12 control subjects (age 42.6 ± 9.7 years). Flow velocity was recorded in the right middle cerebral artery using transcranial Doppler sonography in the supine position and after active standing. Results Cerebral flow velocity in the supine position was not different between the groups studied. Active standing resulted in a significant drop of mean and diastolic flow velocities in autonomic neuropathy patients with orthostatic hypotension, while there were no such changes in the other groups. The relative changes in mean flow velocity 1 min after standing up were ,22.7 ± 16.25% in patients with neuropathy and orthostatic hypotension, +0.02 ± 9.8% in those with neuropathy without hypotension, ,2.8 ± 14.05% in patients without neuropathy, and ,9.2 ± 15.1% in controls. Conclusions Patients with diabetes and cardiovascular autonomic neuropathy with orthostatic hypotension show instability in cerebral blood flow upon active standing, which suggests impaired cerebral autoregulation. [source] Monitoring of CBFV and time characteristics of oxygen-induced acute CNS toxicity in humansEUROPEAN JOURNAL OF NEUROLOGY, Issue 7 2008A. E. Koch Background:, Hyperbaric oxygen can cause central nervous system (CNS) toxicity with seizures. We tested the hypothesis that CNS toxicity could be predictable by cerebral blood flow velocity (CBFV) monitoring. Method:, We monitored 369 mandatory oxygen tolerance tests (30 min, 280 kPa O2) by video-documentation and since May 2005 by additional CBFV registration (n = 61). Results:, The onset of early manifestations of CNS toxicity was documented in 11 of 369 tests within 22 ± 3 min. These included twitches and/or agitation, 6 of 11 and tonic,clonic seizures in 5 of 11 cases. In both cases with CBFV monitoring, an increase in CBFV preceded symptom onset, once followed by seizure, once without seizure after timely oxygen reduction. Conclusions:, During exposure to 280 kPa oxygen at rest a constant delay of approximately 20 min precedes the onset of central nervous oxygen toxicity. An increase in CBFV may indicate the impending seizure. [source] Biofeedback-Assisted Relaxation in Migraine Headache: Relationship to Cerebral Blood Flow Velocity in the Middle Cerebral ArteryHEADACHE, Issue 3 2003Sachinder Vasudeva MD Objective.,To determine if migraineurs with aura respond differently to biofeedback/relaxation than those without aura and, if so, whether the variability in outcome can be explained by blood flow velocity. Background.,The relationship between cerebral blood flow velocity and treatment response to biofeedback/relaxation in migraine with and without aura is uncertain. Method.,Twenty migraineurs underwent 12 sessions of biofeedback/relaxation therapy, while 20 controls simply were told to relax on their own. Cerebral blood flow velocity was measured bilaterally in the middle cerebral artery with transcranial Doppler. Results.,The biofeedback group showed significant (P < .05) reductions in pain, depression, and anxiety compared to the control group. Patients with and without aura did equally well. There were significant (P < .05) left to right blood flow velocity differences only in the migraine with aura group. Maximum blood flow velocities were significantly higher (P < .05) in the migraine with aura group than in the cohort without aura. There was an inverse correlation between indicators of anxiety and blood flow velocity, perhaps related to hyperventilation-induced constriction in the small vessels distal to the middle cerebral artery. Conclusion.,The positive treatment response to biofeedback/relaxation in migraine headache is not related to presence of aura, nor to changes in blood flow velocity, but may be associated with reduction in anxiety and depression. [source] Remifentanil and the brainACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 3 2008V. FODALE Background and aim: Remifentanil is an ultra-short-acting opioid, increasingly used today in neuroanesthesia and neurointensive care. Its characteristics make remifentanil a potentially ideal agent, but previous data have cast a shadow on this opioid, supporting potentially toxic effects on the ischemic brain. The aim of the present concise review is to survey available up-to-date information on the effects of remifentanil on the central nervous system. Method: A MEDLINE search within the past seven years for available up-to-date information on remifentanil and brain was performed. Results: Concise up-to-date information on the effects of remifentanil on the central nervous system was reported, with a particular emphasis on the following topics: cerebral metabolism, electroencephalogram, electrocorticography, motor-evoked potentials, regional cerebral blood flow, cerebral blood flow velocity, arterial hypotension and hypertension, intracranial pressure, cerebral perfusion pressure, cerebral autoregulation, cerebrovascular CO2 reactivity, cerebrospinal fluid, painful stimulation, analgesia and hyperalgesia, neuroprotection, neurotoxicity and hypothermia. Conclusion: The knowledge of the influence of remifentanil on brain functions is crucial before routine use in neuroanesthesia to improve anesthesia performance and patient safety as well as outcome. [source] The effect of nitrous oxide on cerebral blood flow velocity in children anesthetized with propofolACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 3 2003E. Wilson-Smith Background: Propofol for maintenance of anesthesia by continuous infusion is gaining popularity for use in pediatric patients. Nitrous oxide (N2O) has been shown to increase cerebral blood flow velocity (CBFV) in both children and adults. To determine the effects of N2O on middle cerebral artery blood flow velocity (Vmca) during propofol anesthesia in children, Vmca was measured with and without N2O using transcranial Doppler (TCD) sonography. Methods: Thirty ASA I or II children aged 18 months to 6 years undergoing elective urological surgery were enrolled. Anesthesia comprised propofol aimed at producing an estimated steady-state serum concentration of 3 µg·ml,1 and a caudal epidural block. A transcranial Doppler probe was used to measure middle cerebral artery blood flow velocity. Each patient was randomized to receive a sequence of either Air/N2O/Air or N2O/Air/N2O in 35% oxygen. Fifteen min after each change in the N2O concentration, three measurements of cerebral blood flow velocity, blood pressure and heart rate were recorded. Ventilatory parameters and EtCO2 were kept constant throughout the study period. Results: CBFV increased by 12.4% when air was replaced by N2O, and returned to baseline when N2O was subsequently removed. There was a 14% decrease in CBFV when N2O was replaced with air, which increased to baseline when air was subsequently replaced with N2O. Mean heart rate and blood pressure remained constant throughout the study period. Conclusion: The effects of nitrous oxide on CBFV are preserved in children during propofol anesthesia. [source] Surgical closure of patent ductus arteriosus reduces the cerebral tissue oxygenation index in preterm infants: a near-infrared spectroscopy and Doppler studyPEDIATRICS INTERNATIONAL, Issue 3 2006PATRIZIA ZARAMELLA Abstract Background: The aim of this study was to investigate the effects of patent ductus arteriosus (PDA) ligature on cerebral oxygen saturation, cerebral blood volume (CBV) and cerebral blood flow velocity by means of near-infrared spectroscopy (NIRS) and transcranial Doppler simultaneous examinations. Methods: This is an observational study considering 16 babies of gestational age 24,34 weeks diagnosed with PDA who underwent surgical ligation. The cerebral oxygen saturation, CBV and blood gases values were obtained 35 min before ligation, so also around the 14th and 27th min after the clip's insertion. Results: Cerebral oxygen saturation, measured as tissue oxygenation index (TOI), decreased significantly after PDA ligation from a basal value of 61.1 (3.8) before surgery to 56.6 (3.3) and 55.8 (2.6)%, for the 14th and 27th min, respectively (P < 0.04). CBV before and after clipping was unvaried. A negative correlation was found between ,pH and ,CBV after ligation (R = 0.52, P = 0.03), whilst a positive correlation was found between ,CBV and ,PaCO2 (R = 0.62, P = 0.009). pH increased at the 27th min post-ligation. Conclusions: NIRS is a tool for obtaining information on cerebral oxygen saturation and CBV changes during surgical PDA ligation at the bedside. A fall in TOI suggests an increased oxygen extraction during PDA surgery. The lack of increase in ,CBV or in diastolic flow velocity show that the PDA before the clipping did not limit cerebral blood flow, the drop in TOI suggests increased oxygen consumption over the clip and the need for accurate monitoring of oxygen utilization after the surgical treatment. [source] Enhanced vascular responses to hypocapnia in neurally mediated syncopeANNALS OF NEUROLOGY, Issue 3 2008Lucy Jane Norcliffe-Kaufmann PhD Objective The susceptibility to suffer neurally mediated syncope and loss of consciousness varies markedly. In addition to vasodilatation and bradycardia, hyperventilation precedes loss of consciousness. The resultant hypocapnia causes cerebral vasoconstriction and peripheral vasodilatation. We postulate that more pronounced cerebral and peripheral vascular responses to reductions in arterial CO2 levels underlie greater susceptibility to neurally mediated syncope. Methods We compared vascular responses to CO2 among 31 patients with histories of recurrent neurally mediated syncope and low orthostatic tolerance and 14 age- and sex-matched control subjects with no history of syncope and normal orthostatic tolerance. Vascular responses to CO2 were calculated after all subjects had fully recovered and their blood pressures and heart rates were stable. We measured blood flow velocity in the middle cerebral artery (transcranial Doppler) and in the left brachial artery (brachial Doppler), and end-tidal CO2 during voluntary hyperventilation and hypoventilation (end-tidal CO2 from 21,45mm Hg), and determined the slopes of the relations. Results Hypocapnia produced a significantly greater reduction in cerebral blood flow velocity and in forearm vascular resistance in patients with neurally mediated syncope than in control subjects. Opposite changes occurred in response to hypercapnia. In all subjects, the changes in cerebral blood flow velocity and forearm vasodilatation were inversely related with orthostatic tolerance. Interpretation Susceptibility to neurally mediated syncope can be explained, at least in part, by enhanced cerebral vasoconstriction and peripheral vasodilatation in response to hypocapnia. This may have therapeutic implications. Ann Neurol 2007 [source] Low cerebral blood flow velocity and risk of white matter hyperintensitiesANNALS OF NEUROLOGY, Issue 3 2001Christophe Tzourio MD Cerebral blood flow velocity (CBF-V) measured by transcranial doppler was assessed in 628 elderly individuals who had cerebral magnetic resonance imaging performed as part of a population-based study on vascular aging. Cerebral white matter hyperintensities (WMHs) were associated with low CBF-V, such as the adjusted odds ratios of severe WMHs from highest (referent) to lowest quartile of mean CBF-V were 1.0, 1.7, 3.7, and 4.3 (p = 0.001). Further, CBF-V was found to be a stronger risk factor for WMHs than high blood pressure. These findings suggest that the assessment of CBF-V might be a powerful tool in future studies on WMHs. Ann Neurol 2001;49:411,414 [source] Does caffeine impair cerebral oxygenation and blood flow velocity in preterm infants?ACTA PAEDIATRICA, Issue 9 2010MB Tracy Abstract Aim:, The aim of the study is to assess the effects of an intravenous 10 mg/kg loading dose of caffeine base in cerebral oxygenation, cerebral Doppler blood flow velocity and cardiac output in preterm infants. Methods:, Preterm neonates <34 weeks gestation were investigated at 1 and 4 h following the loading dose of caffeine using Doppler cerebral sonography, cardiac echocardiography and cerebral spatially resolved near-infrared spectroscopy. Results:, Forty infants were studied with a mean gestational age (mean ± standard deviation) of 27.7 (±2.5) weeks, birth weight of 1155 (±431) g and a postnatal age of 2.8 (±2.2) days. Mean Anterior Cerebral Artery peak and time average mean blood flow velocity fell significantly by 14% and 17.7%, respectively at 1 h post-caffeine loading dose, which recovered partially by 4 h. Cerebral Tissue Oxygenation Index fell from pre-dose levels by 9.5% at 1 h with partial recovery to 4.9% reduced at 4 h post-dose. There were no significant changes in left or right ventricular output, transcutaneous oxygen saturation, transcutaneous PCO2 or total vascular resistance. Conclusions:, A loading dose of 10 mg/kg caffeine base resulted in significant reduction at 1 h post-dose in cerebral oxygenation and cerebral blood flow velocity with partial recovery at 4 h. [source] Low cerebral blood flow velocity and head circumference in infants with severe hypoxic ischemic encephalopathy and poor outcomeACTA PAEDIATRICA, Issue 3 2009Pilvi Ilves Abstract Aims: To evaluate long-term changes in cerebral blood flow velocity (CBFV) and head circumference in asphyxiated infants. Methods: CBFV was measured in 83 asphyxiated and 115 healthy term infants in anterior and middle cerebral, basilar and internal carotid artery (ICA) up to the age of 60,149 days. The psychomotor development and head circumference was followed for 18 months. Results. Mean CBFV was increased (p < 0.05) during the first days after asphyxia in infants with severe hypoxic-ischemic encephalopathy (HIE) (n = 25) compared to control group or infants with mild to moderate HIE (n = 58) with maximum values found at the age of 36,71.9 h: in ICA (mean [95% CI]) 31.2 (25.5,36.6) cm/s in severe HIE infants compared to 13.0 (12.2,13.9) cm/s in controls. Decreased (p < 0.0001) mean CBFV developed in severe HIE infants by the age of 21,59 days: in ICA 14.1 (11.5,16.8) cm/s compared to 22.9 (21.4,24.4) cm/s in controls. Infants with severe HIE had similar mean height but lower head circumferences compared to controls (p < 0.05) at the age of 21,59 days. Conclusion: The high mean CBFV found in infants with severe HIE during the first days after asphyxia is temporary and low CBFV and head circumference develops by the age of 21,59 days. [source] | ||||||||||||||||||||||