Differences In Cerebrovascular Reactivity Research Articles

Age‐related differences in cerebrovascular reactivity in response to COX inhibition

Reduced cerebral blood flow and reactivity may explain age‐related changes in cognitive function. We examined cerebrovascular reactivity, and the potential role of prostaglandins, in young and old healthy humans. Middle cerebral artery velocity (MCAv) responses to stepped hypercapnia were measured in young (26±2y; 6M/5F) and old (66±2y, 3M/4F) adults before (PRE) and 90 min after (POST) oral indomethacin (1.2mg/kg). To account for any changes in blood pressure, cerebrovascular conductance index (CVCi) was calculated as the MCAv divided by mean arterial pressure. Cerebrovascular reactivity slopes were calculated using linear regression between either MCA velocity or CVCi and end‐tidal CO2. There were no differences between young and old adults in height, weight, BMI, or brachial blood pressures. Young adults demonstrated greater MCAv (53.7±6.7 vs. 32.0±3.3), MCAv reactivity (1.62±0.21 vs. 0.94±0.10), and CVCi (0.66±0.08 vs. 0.39±0.04) compared with old adults at PRE (P<0.05 for all). In both young and old adults, MCAv, MCAv reactivity, CVCi, and CVCi reactivity decreased between PRE and POST measurements. Furthermore, any age‐related differences in these cerebrovascular variables were abolished by indomethacin. These results suggest that cerebral blood flow and cerebrovascular reactivity is attenuated in aging adults and that this reduction may be mediated by prostaglandins.NIH: AG16574‐11PP2

Gender differences in cerebrovascular reactivity to carbon dioxide during sevoflurane anesthesia in children: preliminary findings

Cerebrovascular reactivity to carbon dioxide (CO(2) R) is affected by age, gender and anesthetic agents. While gender differences in CO(2) R are described in adults, there are no such data in children. To examine the gender differences in CO(2) R in children during sevoflurane anesthesia. Five girls and five boys <15 years of age and ASA physical status I, undergoing general anesthesia for elective surgery were enrolled. Under steady-state anesthesia with <1.0 MAC sevoflurane, middle cerebral artery blood flow velocity changes were monitored using Transcranial Doppler ultrasound while endtidal carbon dioxide (EtCO(2)) was adjusted from 40 to 30 mmHg (hypocapnia) and then from 40 to 50 mmHg (hypercapnia). CO(2)R was calculated between EtCO(2) ranges 30-40 and 40-50 mmHg. Cerebrovascular resistance (eCVR) was estimated as MAP/Vmca and the change in eCVR (ΔeCVR) between EtCO(2) 30 and 40 mmHg and between EtCO(2) 40 and 50 mmHg was calculated. There was no gender difference in CO(2)R. However, both CO(2)R and ΔeCVR were lower in the EtCO(2) 40-50 mmHg range compared to EtCO(2) 30-40 mmHg range only in girls (P = 0.01 and P = 0.01, respectively). Vmca increased significantly with increase in CO(2) (P < 0.001) for both boys and girls. The coefficient of nonlinear correlation (r) between Vmca and EtCO(2) was 0.88 in girls vs 0.66 in boys. While there were no gender differences in CO(2)R within the individual EtCO(2) ranges examined, girls but not boys had a significantly lower CO(2)R and ΔeCVR in the higher EtCO(2) range during <1.0 MAC sevoflurane anesthesia.

The role of endothelial dysfunction in the pathogenesis of neuropsychiatric systemic lupus erythematosus

Neuropsychiatric manifestations of systemic lupus erythematosus are common and disabling yet their pathogenesis is poorly understood. We investigated the role of cerebrovascular endothelial dysfunction in systemic lupus erythematosus and its neuropsychiatric manifestations. Subjects with systemic lupus erythematosus were recruited prospectively along with matched healthy control subjects. The presence of neuropsychiatric systemic lupus erythematosus syndromes was ascertained according to standard definitions. Cerebrovascular reactivity, an indicator of endothelial function, was measured using transcranial Doppler ultrasound. Sixty-one subjects (58 female, 3 male) with systemic lupus erythematosus and 70 control subjects were assessed. Sixty patients (98%) reported at least one neuropsychiatric manifestation, the most prevalent being headache and cognitive dysfunction. There was no significant difference in cerebrovascular reactivity between cases and controls (3.06 vs 3.06, p=0.99). Subjects with systemic lupus erythematosus and a history of stroke and/or transient ischaemic attack had significantly higher cerebrovascular reactivity than those without (3.99 vs 2.79, p = 0.007). No association was found between the presence of other neuropsychiatric syndromes or systemic lupus erythematosus-related variables and altered cerebrovascular reactivity. In conclusion, cerebrovascular endothelial dysfunction is not present in the majority of subjects with systemic lupus erythematosus. However, the role of endothelial dysfunction in the pathogenesis of stroke and transient ischaemic attack in systemic lupus erythematosus merits further investigation. Lupus (2010) 19, 797-802.

Blood‐oxygen level dependent MRI measures of cerebrovascular reactivity using a controlled respiratory challenge: Reproducibility and gender differences

To evaluate the reproducibility and gender differences in cerebrovascular reactivity (CVR) measurements obtained using the blood-oxygen level dependent (BOLD) response to controlled changes in end-tidal partial pressure of carbon dioxide (PETCO(2)). We obtained ethical approval to image 19 healthy volunteers (10 men, 9 women) on a 1.5 Tesla (T) MRI scanner twice on two separate days using identical procedures. CVR images were generated by collecting BOLD MRI data during controlled changes in PETCO(2) induced by a sequential gas delivery system. Using the intraclass correlation coefficient (ICC), we demonstrated excellent within-day CVR measures in gray matter (GM) (ICC = 0.92) and white matter (WM) (ICC = 0.88) regions, excellent between-day reproducibility in GM (ICC = 0.81), and good between-day reproducibility in the WM (ICC = 0.66). CVR values between men and women were significantly different in the GM and WM. Men exhibited a 22 +/- 2% greater CVR in GM and a 17 +/- 2% greater CVR in WM compared with females. Our results demonstrate the reliability of BOLD MRI CVR measurements obtained using a controlled cerebrovascular challenge. Using this technique, we also revealed significantly increased BOLD response to CO(2) in males compared with females.

Transcranial Doppler study of cerebrovascular reactivity: Are migraineurs more sensitive to breath-hold challenge?

Transcranial Doppler sonography (TCD) of cerebrovascular reactivity has been used to study migraine interictally. However, the previous TCD findings had been quite varied at the post breath-hold period. Autonomic responses were usually studied with cardiac information. The aim of this study was to use TCD as a tool to examine difference in cerebrovascular reactivity between migraineurs and non-headache controls by measuring interictally the whole time course of cerebral blood flow velocity (CBFV) during and after a breath-hold challenge. The percentage change of CBFV was derived in the left and right middle cerebral arteries in 10 migraineurs and 10 controls during and after a 20 s breath-hold. Three phases of CBFV change were identified with an initial positive phase above baseline, a middle negative phase during breath-hold, and a late positive phase which started before the cessation of breath-hold and continued for a period after. In addition to CBFV, we also extracted and utilized the information of the cardiac cycle duration (CC) derived from the time course of CBFV. The percentage change of CC was derived from time intervals between every two points of inflexion in CBFV. Two undershoots of CC change were shown at the transitions of breathing motions. We found evidence that migraineurs had significant difference of CBFV change at the middle negative phase during breath-hold and the pronounced undershoots of CC change compared to non-headache controls.

Middle cerebral artery blood flow velocity, end-tidal pC02 and blood pressure in patients with obstructive sleep apnea and in healthy subjects during continuous positive airway pressure breathing

There is conflicting evidence in the literature as to the potential effect of continuous positive airway pressure (CPAP) on cerebral perfusion. Compromising cerebral perfusion could possibly outweigh the benefit of improved oxygenation. Patients with the obstructive sleep apnea syndrome (OSAS) have been claimed to have a higher cerebrovascular reactivity to changes in end-tidal pC02. In this study, we investigated 23 patients with OSAS and 7 6 healthy young adults in the waking state. Both groups performed a series of lOmin of normal breathing, 20min with 9 cmH20 nasal CPAP, and then TOmin of normal breathing while wearing a nasal CPAP mask. The following parameters were assessed: bilateral transcranial Doppler signal of the middle cerebral artery, systolic and diastolic blood pressure assessed manually, and cerebrovascular reactivity to changes in pC02 during hyperventilation and rebreathing into an airbag. Continuous end-tidal pC02 measurements were performed in 74 subjects. As compared with normal breathing middle cerebral artery blood flow velocity and pC02 remained unchanged during CPAP. Systolic and diastolic blood pressure increased slightly by 1.2mmHg (p = 0.015) and 1.1 mmHg (p = 0.007), respectively. Cerebrovascular reactivity did not differ in the two groups. Nasal CPAP of 9 cmH20 is a safe treatment with respect to the maintenance of cerebral blood flow. Our study gives further evidence for the autoregulation's capacity to maintain cerebral blood flow velocity constant during different levels of intrathoracic pressure and different cerebral perfusion pressures. We could not demonstrate any difference in cerebrovascular reactivity between patients with OSAS and healthy persons. [Neurol Res 1999; 21: 737-741]

Regional differences in cerebrovascular reactivity to acetazolamide in Alzheimer's disease

The cerebral blood flow and cerebrovascular reactivity to acetazolamide were investigated in Alzheimer's disease using stable xenon computed tomography (CT). Ten patients with Alzheimer's disease and 10 healthy controls were studied. The regional cerebral blood flow was measured using the xenon delivery and analysis system (AZ-7000 model, Anzai Sogyo, Tokyo, Japan) and CT (PreSage, Yokogawa Medical Systems, Tokyo, Japan). The subjects inhaled room air followed by a mixture of 30% xenon and 50% oxygen for 3 min. Serial scanning was performed once before xenon inhalation, three times in the wash-in process and five times in the washout process of 5 min. The xenon concentration in the end-tidal expired gas was recorded continuously by the thermoconductivity method. The regional cerebral blood flow was measured before and 20 min after i.v. injection of 17 mg/kg acetazolamide. The blood flows in the frontal lobe, parietal lobe and temporal lobe were reduced but the blood flows in the caudate nucleus, putamen and thalamus were normal in the Alzheimer's disease group. The cerebrovascular reactivity to acetazolamide was reduced in the frontal, parietal and temporal cortex but was normal in the other areas. There is a regional difference in the cerebral blood flow and the cerebrovascular reactivity to acetazolamide in Alzheimer's disease

364 Regional difference in cerebrovascular reactivity to acetazolamide in Alzheimer's disease

364 Regional difference in cerebrovascular reactivity to acetazolamide in Alzheimer's disease

Estimation of cerebrovascular reactivity in migraine without aura.

The nature and role of vascular abnormalities in migraine are controversial. In this study we evaluated cerebrovascular reactivity to hypercapnia in patients suffering from migraine without aura with unilateral headache. Using bilateral transcranial Doppler ultrasound, we studied the changes of flow velocity after hypercapnia in the anterior, middle, and posterior cerebral arteries of 16 migraine patients and 16 healthy control subjects. All patients were studied during an attack-free interval and during a migraine attack. Cerebrovascular reactivity was evaluated with the breath-holding index, obtained by dividing the percent increase in mean flow velocity occurring during breath-holding by the time (seconds) in which the subjects held their breath after a normal inspiration. The response to breath-holding was similar for all arteries considered in both control subjects and patients during the attack-free interval. During the migraine attack, the breath-holding index in patients was significantly lower than the migraine-free interval in all arteries (P < .001). No side-to-side difference in cerebrovascular reactivity was detected in migraine patients either outside or during attacks. These results suggest that a failure of cerebrovascular regulation occurs during attacks of migraine without aura.

Mode of action of Xanthinol-Nicotinate on the human ERG

To determine if arterial stiffness is associated with age-related differences in cerebrovascular conductance and reactivity, twenty-eight apparently healthy sedentary young (25 ± 1 years; n = 15) and older (67 ± 1 years; n = 13) adults were studied. Brachial-ankle pulse wave velocity (baPWV) was measured as an index of arterial stiffness. Cerebrovascular reactivity was determined by measuring changes in mean blood velocity in the middle cerebral artery under normocapnic, hypocapnic and hypercapnic conditions. Mean baPWV was greater (p < 0.05) in older compared with young adults. At baseline, mean cerebral blood flow velocity and cerebrovascular conductance index were lower (p < 0.05) in older compared with young adults under normocapnic, hypocapnic and hypercapnic conditions. There were no significant group differences in cerebrovascular reactivity when they were adjusted for stimuli (i.e., end-tidal CO2 concentrations) in most perturbation conditions except for the normocapnia to hypercapnia condition. baPWV was negatively associated with cerebrovascular conductance index at all conditions (all p < 0.05). We concluded that arterial stiffness was associated with age-related differences in cerebrovascular conductance and that there were no apparent age-associated differences in cerebrovascular reactivity.

G.P. Maternity Beds

<h3>BACKGROUND AND PURPOSE:</h3> Changes in cerebrovascular reactivity can be used to assess disease progression and response to therapy but require discrimination of pathology from normal test-to-test variability. Such variability is due to variations in methodology, technology, and physiology with time. With uniform test conditions, our aim was to determine the test-to-test variability of cerebrovascular reactivity in healthy subjects and in patients with known cerebrovascular disease. <h3>MATERIALS AND METHODS:</h3> Cerebrovascular reactivity was the ratio of the blood oxygen level–dependent MR imaging response divided by the change in carbon dioxide stimulus. Two standardized cerebrovascular reactivity tests were conducted at 3T in 15 healthy men (36.7 ± 16.1 years of age) within a 4-month period and were coregistered into standard space to yield voxelwise mean cerebrovascular reactivity interval difference measures, composing a reference interval difference atlas. Cerebrovascular reactivity interval difference maps were prepared for 11 male patients. For each patient, the test-retest difference of each voxel was scored statistically as z-values of the corresponding voxel mean difference in the reference atlas and then color-coded and superimposed on the anatomic images to create cerebrovascular reactivity interval difference z-maps. <h3>RESULTS:</h3> There were no significant test-to-test differences in cerebrovascular reactivity in either gray or white matter (mean gray matter, <i>P</i> = .431; mean white matter, <i>P</i> = .857; paired <i>t</i> test) in the healthy cohort. The patient cerebrovascular reactivity interval difference z-maps indicated regions where cerebrovascular reactivity increased or decreased and the probability that the changes were significant. <h3>CONCLUSIONS:</h3> Accounting for normal test-to-test differences in cerebrovascular reactivity enables the assessment of significant changes in disease status (stability, progression, or regression) in patients with time.