Cerebral blood flow and CO2 responsiveness as an indicator of collateral reserve capacity in patients with carotid arterial disease

1985 ◽  
Vol 72 (5) ◽  
pp. 348-351 ◽  
Author(s):  
R. Bullock ◽  
A. D. Mendelow ◽  
I. Bone ◽  
J. Patterson ◽  
W. N. Macleod ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Arterial Disease ◽  
Reserve Capacity ◽  
Carotid Arterial

Cerebral Blood Flow and CO2 Responsiveness as an Indicator of Collateral Reserve Capacity in Patients with Cartoid Arterial Disease

1986 ◽  
Vol 30 (3) ◽  
pp. 144
Author(s):  
R. BULLOCK ◽  
A. D. MENDALOW ◽  
I. BONE ◽  
J. PATTERSON ◽  
W. N. MACLEOD ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Arterial Disease ◽  
Reserve Capacity

Pressure Autoregulation and Positron Emission Tomography-derived Cerebral Blood Flow Acetazolamide Reactivity in Patients with Carotid Artery Stenosis

Neurosurgery ◽  
2004 ◽  
Vol 55 (1) ◽  
pp. 63-68 ◽  
Author(s):  
Pawan S. Minhas ◽  
Piotr Smielewski ◽  
Peter J. Kirkpatrick ◽  
John D. Pickard ◽  
Marek Czosnyka
Keyword(s):  
Blood Pressure ◽  
Positron Emission Tomography ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Carotid Artery ◽  
Arterial Disease ◽  
Emission Tomography ◽  
Positron Emission ◽  
Carotid Arterial ◽  
Pressure Autoregulation

Abstract OBJECTIVE: Testing autoregulation is of importance in predicting risk of stroke and managing patients with occlusive carotid arterial disease. The use of small spontaneous changes in arterial blood pressure and transcranial Doppler (TCD) flow velocity can be used to assess autoregulation noninvasively without the need for a cerebrovascular challenge. We have previously described an index (called “Mx”) that achieves this. Negative or low positive values (<0.4) indicate intact pressure autoregulation, whereas an Mx greater than 0.4 indicates diminished autoregulation. The objective of this study was to compare acetazolamide reactivity of positron emission tomography (PET)-derived cerebral blood flow (CBF) with Mx in patients with carotid arterial disease. METHODS: In 40 patients with carotid arterial disease, we used bilateral TCD recordings of the middle cerebral artery to derive Mx and compared this with PET-derived CBF measurements of acetazolamide reactivity. RESULTS: Mx correlated inversely with baseline PET CBF (P = 0.042, R = −0.349) but not with postacetazolamide CBF or cerebrovascular reactivity to acetazolamide. This may reflect discordance between pressure autoregulation and acetazolamide reactivity. Mx correlated significantly with degree of internal carotid artery stenosis (P = 0.022, R = 0.38), whereas CBF reactivity to acetazolamide did not correlate with Mx (P = 0.22). After the administration of acetazolamide, slow-wave activity in blood pressure and TCD flow velocity recordings was seen to diminish, rendering the calculation of Mx unreliable after acetazolamide. CONCLUSION: The measurement of Mx offers a noninvasive, safe technique for assessing abnormalities of pressure autoregulation in patients with carotid arterial disease.

133Xe-DSPECT: Normalwerte von zerebraler Ruhedurchblutung und Reservekapazität

1987 ◽  
Vol 26 (05) ◽  
pp. 192-197 ◽  
Author(s):  
T. Kreisig ◽  
P. Schmiedek ◽  
G. Leinsinger ◽  
K. Einhäupl ◽  
E. Moser
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebrovascular Disease ◽  
Correlation Coefficient ◽  
Regional Cerebral Blood Flow ◽  
Regression Line ◽  
Reserve Capacity ◽  
Regional Cerebral Blood ◽  
Quantitative Measurements ◽  
Before And After

Using the 133Xe-DSPECT technique, quantitative measurements of regional cerebral blood flow (rCBF) were performed before and after provocation with acetazolamide (Diamox) i. v. in 32 patients without evidence of brain disease (normals). In 6 cases, additional studies were carried out to establish the time of maximal rCBF increase which was found to be approximately 15 min p. i. 1 g of Diamox increases the rCBF from 58 ±8 at rest to 73±5 ml/100 g/min. A Diamox dose of 2 g (9 cases) causes no further rCBF increase. After plotting the rCBF before provocation (rCBFR) and the Diamox-induced rCBF increase (reserve capacity, Δ rCBF) the regression line was Δ rCBF = −0,6 x rCBFR +50 (correlation coefficient: r = −0,77). In normals with relatively low rCBF values at rest, Diamox increases the reserve capacity much more than in normals with high rCBF values before provocation. It can be expected that this concept of measuring rCBF at rest and the reserve capacity will increase the sensitivity of distinguishing patients with reversible cerebrovascular disease (even bilateral) from normals.

Hemoglobin, hematocrit, and changes in cerebral blood flow: the Second Manifestations of ARTerial disease-Magnetic Resonance study

2015 ◽  
Vol 36 (3) ◽  
pp. 1417-1423 ◽  
Author(s):  
Pieternella H. van der Veen ◽  
Majon Muller ◽  
Koen L. Vincken ◽  
Jan Westerink ◽  
Willem P.T.M. Mali ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Magnetic Resonance ◽  
Arterial Disease ◽  
Magnetic Resonance Study

The Effects of Paco2 on Regional Cerebral Blood Flow and Internal Carotid Arterial Pressure during Carotid Clamping

1971 ◽  
Vol 35 (3) ◽  
pp. 286-300 ◽  
Author(s):  
Gudru n ◽  
H. J. Ladegaard-Pedersen ◽  
H. Henriksen ◽  
L. Olesen ◽  
O. B. Paulson ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Arterial Pressure ◽  
Regional Cerebral Blood Flow ◽  
Internal Carotid ◽  
Regional Cerebral Blood ◽  
Carotid Arterial

scholarly journals Reduced parenchymal cerebral blood flow is associated with greater progression of brain atrophy: The SMART-MR study

2020 ◽  
pp. 0271678X2094861
Author(s):  
Rashid Ghaznawi ◽  
Maarten HT Zwartbol ◽  
Nicolaas PA Zuithoff ◽  
Jeroen de Bresser ◽  
Jeroen Hendrikse ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Atrophy ◽  
Brain Volume ◽  
Arterial Disease ◽  
Cerebral Hypoperfusion ◽  
Intracranial Volume ◽  
Total Brain Volume ◽  
Brain Parenchymal ◽  
Mr Study

Global cerebral hypoperfusion may be involved in the aetiology of brain atrophy; however, long-term longitudinal studies on this relationship are lacking. We examined whether reduced cerebral blood flow was associated with greater progression of brain atrophy. Data of 1165 patients (61 ± 10 years) from the SMART-MR study, a prospective cohort study of patients with arterial disease, were used of whom 689 participated after 4 years and 297 again after 12 years. Attrition was substantial. Total brain volume and total cerebral blood flow were obtained from magnetic resonance imaging scans and expressed as brain parenchymal fraction (BPF) and parenchymal cerebral blood flow (pCBF). Mean decrease in BPF per year was 0.22% total intracranial volume (95% CI: –0.23 to –0.21). Mean decrease in pCBF per year was 0.24 ml/min per 100 ml brain volume (95% CI: –0.29 to –0.20). Using linear mixed models, lower pCBF at baseline was associated with a greater decrease in BPF over time ( p =  0.01). Lower baseline BPF, however, was not associated with a greater decrease in pCBF ( p =  0.43). These findings indicate that reduced cerebral blood flow is associated with greater progression of brain atrophy and provide further support for a role of cerebral blood flow in the process of neurodegeneration.

Carotid Arterial Stiffness and Cerebral Blood Flow in Amnestic Mild Cognitive Impairment

2021 ◽  
Vol 17 (12) ◽  
pp. 1115-1125
Author(s):  
Tsubasa Tomoto ◽  
Jun Sugawara ◽  
Takashi Tarumi ◽  
Collin Chiles ◽  
Bryon Curtis ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Arterial Stiffness ◽  
Linear Regression Analysis ◽  
Systolic Pressure ◽  
Amnestic Mild Cognitive Impairment ◽  
Stiffness Index ◽  
Carotid Arterial

Background: Central arterial stiffness is an emerging risk factor of age-related cognitive impairment and Alzheimer’s disease (AD). However, the underlying pathophysiological mechanisms remain unclear. Objective: We tested the hypothesis that carotid arterial stiffness is associated with reduced cerebral blood flow (CBF) and increased cerebrovascular resistance (CVR) in patients with amnestic mild cognitive impairment (MCI), a prodromal stage of AD. Methods: Fifty-four patients with amnestic MCI and 24 cognitively normal subjects (CN) of similar age and sex to MCI patients underwent measurements of CBF and carotid β-stiffness index using ultrasonography and applanation tonometry. Total CBF was measured as the sum of CBF from both the internal carotid and vertebral arteries, and divided by total brain tissue mass (assessed with MRI) to obtain normalized CBF (nCBF). Results: Relative to CN subjects, MCI patients showed lower nCBF (53.3 ± 3.2 vs 50.4±3.4 mL/100 g/min, P < 0.001) and higher CVR (0.143 ± 0.019 vs 0.156 ± 0.023 mmHg/mL/min, P < 0.015). Multiple linear regression analysis showed that nCBF was negatively associated with carotid β-stiffness index (B = -0.822, P < 0.001); CVR was positively associated with carotid systolic pressure (B = 0.001, P < 0.001) after adjustment for age, sex, body mass index, and MCI status. Conclusion: These findings suggest that carotid artery stiffening may contribute at least in part to the reduced nCBF and increased CVR in patients with MCI associated with augmented carotid arterial pulsatility.

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