Quantifying CBF, with pulsed ASL: technical and pulse sequence factors. J Magn Reson Imaging: JMRI
University of California, San Diego, La Jolla, California CA 92093-0677, USA. Journal of Magnetic Resonance Imaging
(Impact Factor: 3.21).
12/2005; 22(6):727-31. DOI: 10.1002/jmri.20459
We summarize here current methods for the quantification of CBF using pulsed arterial spin labeling (ASL) methods. Several technical issues related to CBF quantitation are described briefly, including transit delay, signal from larger arteries, radio frequency (RF) slice profiles, magnetization transfer, tagging efficiency, and tagging geometry. Many pulsed tagging schemes have been devised, which differ in the type of tag or control pulses, and which have various advantages and disadvantages for quantitation. Several other modifications are also available that can be implemented as modules in an ASL pulse sequence, such as varying the wash-in time to estimate the transit delay. Velocity-selective ASL (VS-ASL) uses a new type of pulse labeling in which inflowing arterial spins are tagged based on their velocity rather than their spatial location. In principle, this technique may allow ASL measurement of cerebral blood flow (CBF) that is insensitive to transit delays.
Available from: PubMed Central
- "The difference between the control and tag images provides an image that is CBF-weighted. Although there are several parameters that must be measured, or more typically assumed, absolute quantification in ASL is relatively straight forward (Wong, 2005; van Osch et al., 2009). The ASL signal difference (i.e., control – tag images) divided by the initial magnetization (i.e., related to the proton density weighting) is directly proportional to perfusion in units of mL/100 g/min. "
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ABSTRACT: The global burden of stroke continues to grow. Although stroke prevention strategies (e.g., medications, diet, and exercise) can contribute to risk reduction, options for acute interventions (e.g., thrombolytic therapy for ischemic stroke) are limited to the minority of patients. The remaining patients are often left with profound neurological disabilities that substantially impact quality of life, economic productivity, and increase caregiver burden. In the last decade, however, the future outlook for such patients has been tempered by movement toward the view that the brain is capable of reorganizing after injury. Many now view brain recovery after stroke as an area of scientific research with large potential for therapeutic advances, far into the future (Broderick and William, 2004). As a probe of brain anatomy, function and physiology, magnetic resonance imaging (MRI) is a non-invasive and highly versatile modality that promises to play a particularly important role in such research. Here we provide a basic review of MRI physical principles and applications for assessing stroke, looking toward the future role MRI may play in improving stroke rehabilitation methods and stroke recovery.
Available from: Mark W Bondi
- "Resting brain blood perfusion was measured with pulsed ASL using a modified flow-sensitive alternating inversion recovery sequence with both presaturation pulses and PICORE QUIPSS 2 postinversion saturation pulses and a spiral readout with four interleaves to reduce signal dropout due to susceptibility effects (Liu and Wong, 2005; Wong et al, 1998). Imaging parameters of the ASL scan were 22 Â 22 cm field of view, a 64 Â 64 matrix, 3.2 ms echo time, 2,500 ms repetition time, postsaturation and inversion times of TI1 = 600 ms and TI2 = 1,600 ms, tag thickness 10 cm, tag to proximal slice gap 1 cm, 20 5 mm axial slices, and 40 volumes for 20 tag + control image pairs (Wong, 2005). A scan with the 901 excitation pulse turned off for the first eight repetitions was acquired to obtain the equilibrium magnetization of cerebrospinal fluid (CSF) (a 36-second scan with repetition time = 4 seconds, echo time = 3.4 ms, number of excitations (NEX) = 9). "
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ABSTRACT: Using whole-brain pulsed arterial spin labeling magnetic resonance imaging, resting cerebral blood flow (CBF) was measured in 20 mild cognitive impairment (MCI; 11 ɛ3 and 9 ɛ4) and 40 demographically matched cognitively normal (CN; 27 ɛ3 and 13 ɛ4) participants. An interaction of apolipoprotein (APOE) genotype (ɛ3 and ɛ4) and cognitive status (CN and MCI) on quantified gray-matter CBF corrected for partial volume effects was found in the left parahippocampal and fusiform gyri (PHG/FG), right middle frontal gyrus, and left medial frontal gyrus. In the PHG/FG, CBF was elevated for CN ɛ4 carriers but decreased for MCI ɛ4 carriers. The opposite pattern was seen in frontal regions: CBF was decreased for CN ɛ4 carriers but increased for MCI ɛ4 carriers. Cerebral blood flow in the PHG/FG was positively correlated with verbal memory for CN ɛ4 adults (r=0.67, P=0.01). Cerebral blood flow in the left medial frontal gyrus was positively correlated with verbal memory for MCI ɛ4 adults (r=0.70, P=0.05). Findings support dynamic pathophysiologic processes in the brain associated with Alzheimer's disease risk and indicate that cognitive status and APOE genotype have interactive effects on CBF. Correlations between CBF and verbal memory suggest a differential neurovascular compensatory response in posterior and anterior cortices with cognitive decline in ɛ4 adults.
Available from: Shana Hall
- "The high - resolution T1 - weighted image and partial volume segmentations were registered in ASL space , and partial volume segmentations were down - sampled to the resolution of the ASL data . CBF was calculated from the signal difference between tag and control images ( Wong , 2005 ) and converted to absolute units ( ml ⁄ 100 g ⁄ min ) using the CSF image as a reference signal ( Chalela et al . , 2000 ) . "
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ABSTRACT: Although there are multiple indications that alcohol can alter many physiological brain functions, including cerebral blood flow (CBF), studies of the latter have generally used small- or modest-sized samples. Few investigations have yet evaluated how CBF changes after alcohol relate to subsets of subjects with elevated alcoholism risks, such as those with lower levels of response (LR) to alcohol. This study used arterial spin labeling (ASL) after alcohol administration to evaluate a large sample of healthy young men and women with low and high alcohol responses, and, thus, varying risks for alcohol use disorders (AUD).
Healthy young adult social drinkers with low and high LR (N=88, 50% women) matched on demography and drinking histories were imaged with whole-brain resting ASL ~1 hour after ingesting ~3 drinks of ethanol and after a placebo beverage (i.e., 178 ASL sessions). The relationships of CBF changes from placebo to alcohol for subjects with low and high LR were evaluated.
CBF increased after alcohol when compared to placebo in 5 frontal brain regions. Despite identical blood alcohol concentrations, these increases with alcohol were less prominent in individuals who required more drinks to experience alcohol-related effects (i.e., had a lower LR to alcohol). The LR group differences remained significant after covarying for recent drinking quantities.
The results confirm that alcohol intake is associated with acute increases in CBF, particularly in frontal regions. Less intense CBF changes were seen in subjects with a genetically influenced characteristic, a low LR to alcohol, that relates to the future risk of heavy drinking and alcohol problems.
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