scholarly journals Temporal Dynamics and Spatial Specificity of Arterial and Venous Blood Volume Changes during Visual Stimulation: Implication for Bold Quantification

2010 ◽  
Vol 31 (5) ◽  
pp. 1211-1222 ◽  
Author(s):  
Tae Kim ◽  
Seong-Gi Kim

Determination of compartment-specific cerebral blood volume ( CBV) changes is important for understanding neurovascular physiology and quantifying blood oxygenation level-dependent (BOLD) functional magnetic resonance imaging (fMRI). In isoflurane-anesthetized cats, we measured the spatiotemporal responses of arterial CBV ( CBVa) and total CBV ( CBVt) induced by a 40-second visual stimulation, using magnetization transfer (MT)-varied BOLD and contrast-agent fMRI techniques at 9.4 T. To determine the venous CBV ( CBVv) change, we calculated the difference between CBVt and CBVa changes. The dynamic response of CBVa was an order of magnitude faster than that of CBVv, while the magnitude of change under steady-state conditions was similar between the two. Following stimulation offset, Δ CBVa showed small poststimulus undershoots, while Δ CBVv slowly returned to baseline. The largest CBVa and CBVt response occurred after 10 seconds of simulation in cortical layer 4, which we identified as the stripe of Gennari by T1-weighted MRI. The CBVv response, however, was not specific across the cortical layers during the entire stimulation period. Our data indicate that rapid, more-specific arterial vasodilation is followed by slow, less-specific venous dilation. Our finding implies that the contribution of CBVv changes to BOLD signals is significant for long, but not short, stimulation periods.

2010 ◽  
Vol 31 (1) ◽  
pp. 82-89 ◽  
Author(s):  
Peter Dechent ◽  
Gunther Schütze ◽  
Gunther Helms ◽  
Klaus Dietmar Merboldt ◽  
Jens Frahm

One of the characteristics of the blood oxygenation level-dependent (BOLD) magnetic resonance imaging (MRI) response to functional challenges of the brain is the poststimulation undershoot, which has been suggested to originate from a delayed recovery of either cerebral blood volume (CBV) or cerebral metabolic rate of oxygen to baseline. Using bolus-tracking MRI in humans, we recently showed that relative CBV rapidly normalizes after the end of stimulation. As this observation contradicts at least part of the blood-pool contrast agent studies performed in animals, we reinvestigated the CBV contribution by dynamic T1-weighted three-dimensional MRI (8 seconds temporal resolution) and Vasovist at 3 T (12 subjects). Initially, we determined the time constants of individual BOLD responses. After injection of Vasovist, CBV-related T1-weighted signal changes revealed a signal increase during visual stimulation (1.7%±0.4%), but no change relative to baseline in the poststimulation phase (0.2%±0.3%). This finding renders the specific nature of the contrast agent unlikely to be responsible for the discrepancy between human and animal studies. With the assumption of normalized cerebral blood flow after stimulus cessation, a normalized CBV lends support to the idea that the BOLD MRI undershoot reflects a prolonged elevation of oxidative metabolism.


2011 ◽  
Vol 31 (7) ◽  
pp. 1599-1611 ◽  
Author(s):  
Jun Hua ◽  
Robert D Stevens ◽  
Alan J Huang ◽  
James J Pekar ◽  
Peter CM van Zijl

The poststimulus blood oxygenation level-dependent (BOLD) undershoot has been attributed to two main plausible origins: delayed vascular compliance based on delayed cerebral blood volume (CBV) recovery and a sustained increased oxygen metabolism after stimulus cessation. To investigate these contributions, multimodal functional magnetic resonance imaging was employed to monitor responses of BOLD, cerebral blood flow (CBF), total CBV, and arterial CBV (CBVa) in human visual cortex after brief breath hold and visual stimulation. In visual experiments, after stimulus cessation, CBVa was restored to baseline in 7.9 ± 3.4 seconds, and CBF and CBV in 14.8 ± 5.0 seconds and 16.1 ± 5.8 seconds, respectively, all significantly faster than BOLD signal recovery after undershoot (28.1 ± 5.5 seconds). During the BOLD undershoot, postarterial CBV (CBVpa, capillaries and venules) was slightly elevated (2.4 ± 1.8%), and cerebral metabolic rate of oxygen ( CMRO2) was above baseline (10.6 ± 7.4%). Following breath hold, however, CBF, CBV, CBVa and BOLD signals all returned to baseline in ∼20 seconds. No significant BOLD undershoot, and residual CBVpa dilation were observed, and CMRO2 did not substantially differ from baseline. These data suggest that both delayed CBVpa recovery and enduring increased oxidative metabolism impact the BOLD undershoot. Using a biophysical model, their relative contributions were estimated to be 19.7 ± 15.9% and 78.7 ± 18.6%, respectively.


2009 ◽  
Vol 30 (2) ◽  
pp. 449-458 ◽  
Author(s):  
Barış Yeşilyurt ◽  
Kevin Whittingstall ◽  
Kâmil Uğurbil ◽  
Nikos K Logothetis ◽  
Kâmil Uludağ

There is currently a great interest to combine electroencephalography (EEG) and functional magnetic resonance imaging (fMRI) to study brain function. Earlier studies have shown different EEG components to correlate well with the fMRI signal arguing for a complex relationship between both measurements. In this study, using separate EEG and fMRI measurements, we show that (1) 0.1 ms visual stimulation evokes detectable hemodynamic and visual-evoked potential (VEP) responses, (2) the negative VEP deflection at ∼80 ms (N2) co-varies with stimulus duration/intensity such as with blood oxygenation level-dependent (BOLD) response; the positive deflection at ∼120 ms (P2) does not, and (3) although the N2 VEP–BOLD relationship is approximately linear, deviation is evident at the limit of zero N2 VEP. The latter finding argues that, although EEG and fMRI measurements can co-vary, they reflect partially independent processes in the brain tissue. Finally, it is shown that the stimulus-induced impulse response function (IRF) at 0.1 ms and the intrinsic IRF during rest have different temporal dynamics, possibly due to predominance of neuromodulation during rest as compared with neurotransmission during stimulation. These results extend earlier findings regarding VEP–BOLD coupling and highlight the component- and context-dependency of the relationship between evoked potentials and hemodynamic responses.


2009 ◽  
Vol 29 (6) ◽  
pp. 1197-1207 ◽  
Author(s):  
Satoru Kohno ◽  
Nobukatsu Sawamoto ◽  
Shin-ichi Urayama ◽  
Toshihiko Aso ◽  
Kenji Aso ◽  
...  

We used magnetic resonance imaging (MRI) to investigate the temporal dynamics of changes in water diffusion and blood oxygenation level-dependent (BOLD) responses in the brain cortex of eight subjects undergoing visual stimulation, and compared them with changes of the vascular hemoglobin content (oxygenated, deoxygenated, and total hemoglobin) acquired simultaneously from intrinsic optical recordings (near infrared spectroscopy). The group average rise time for the diffusion MRI signal was statistically significantly shorter than those of the BOLD signal and total hemoglobin content optical signal, which is assumed to be the fastest observable vascular signal. In addition, the group average decay time for the diffusion MRI also was shortest. The overall time courses of the BOLD and optical signals were strongly correlated, but the covariance was weaker with the diffusion MRI response. These results suggest that the observed decrease in water diffusion reflects early events that precede the vascular responses, which could originate from changes in the extravascular tissue.


2002 ◽  
Vol 22 (3) ◽  
pp. 262-270 ◽  
Author(s):  
Mikko I. Kettunen ◽  
Olli H. J. Gröhn ◽  
M. Johanna Silvennoinen ◽  
Markku Penttonen ◽  
Risto A. Kauppinen

The balance between oxygen consumption and delivery in the rat brain after exposure to transient ischemia was quantitatively studied with single-spin echo T2-BOLD (blood oxygenation level–dependent) magnetic resonance imaging at 4.7 T. The rats were exposed to graded common carotid artery occlusions using a modification of the four-vessel model of Pulsinelli. T2, diffusion, and cerebral blood volume were quantified with magnetic resonance imaging, and CBF was measured with the hydrogen clearance method. A transient common carotid artery occlusion below the CBF value of approximately 20 mL·100 g−1·min−1 was needed to yield a T2 increase of 4.6 ± 1.2 milliseconds (approximately 9% of cerebral T2) and 6.8 ± 1.7 milliseconds (approximately 13% of cerebral T2) after 7 and 15 minutes of ischemia, respectively. Increases in CBF of 103 ± 75% and in cerebral blood volume of 29 ± 20% were detected in the reperfusion phase. These hemodynamic changes alone could account for only approximately one third of the T2 increase in luxury perfusion, suggesting that a substantial increase in blood oxygen saturation (resulting from reduced oxygen extraction by the brain) is needed to explain the magnetic resonance imaging observation.


2005 ◽  
Vol 26 (8) ◽  
pp. 1043-1051 ◽  
Author(s):  
Tsukasa Nagaoka ◽  
Fuqiang Zhao ◽  
Ping Wang ◽  
Noam Harel ◽  
Richard P Kennan ◽  
...  

2005 ◽  
Vol 25 (7) ◽  
pp. 852-857 ◽  
Author(s):  
Hiroshi Ito ◽  
Masanobu Ibaraki ◽  
Iwao Kanno ◽  
Hiroshi Fukuda ◽  
Shuichi Miura

Hypercapnia induces cerebral vasodilation and increases cerebral blood volume (CBV), and hypocapnia induces cerebral vasoconstriction and decreases CBV. Cerebral blood volume measured by positron emission tomography (PET) is the sum of three components, that is, arterial, capillary, and venous blood volumes. Changes in arterial blood volume ( Va) and CBV during hypercapnia and hypocapnia were investigated in humans using PET with H215O and 11CO. Arterial blood volume was determined from H215O PET data by means of a two-compartment model that takes Va into account. Baseline CBV and values during hypercapnia and hypocapnia in the cerebral cortex were 0.034 ± 0.003, 0.038 ± 0.003, and 0.031 ± 0.003 mL/mL (mean ± s.d.), respectively. Baseline Va and values during hypercapnia and hypocapnia were 0.015 ± 0.003, 0.025 ± 0.011, and 0.007 ± 0.003 mL/mL, respectively. Cerebral blood volume changed significantly owing to changes in PaCO2, and Va changed significantly in the direction of CBV changes. However, no significant change was observed in venous plus capillary blood volume (= CBV- Va). This indicates that changes in CBV during hypercapnia and hypocapnia are caused by changes in arterial blood volume without changes in venous and capillary blood volume.


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