Diffusion Spectroscopy in Living Systems

Zijl, Peter C.M. van; Davis, Delphine; Moonen, Chrit

doi:10.1016/b978-0-12-283980-1.50016-8

Cited by 29 publications

(36 citation statements)

References 51 publications

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“…These applications employ both the directional anisotropy that can be measured by DTI 4,5 as well as removal of this anisotropy through the use of the tensor trace. [6][7][8] For example, DTI is presently being explored as a research tool to study brain development, 9,10 multiple sclerosis, 11,12 amyotrophic lateral sclerosis (ALS), 13 stroke, 14,15, schizophrenia 16,17 and reading disability, 18 while trace imaging has become an essential part of clinical acute stroke assessment. [19][20][21][22] As first shown by Basser et al, 4 the diffusion ellipsoid obtained from DTI can not only provide a quantitative orientation-independent measure of diffusion anisotropy, 23,24 but also the predominant direction of water diffusion in image voxels.…”

Section: Introductionmentioning

confidence: 99%

Fiber tracking: principles and strategies – a technical review

2002

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The state of the art of reconstruction of the axonal tracts in the central nervous system (CNS) using diffusion tensor imaging (DTI) is reviewed. This relatively new technique has generated much enthusiasm and high expectations because it presently is the only approach available to non-invasively study the three-dimensional architecture of white matter tracts. While there is no doubt that DTI fiber tracking is providing exciting new opportunities to study CNS anatomy, it is very important to understand its limitations. In this review we therefore assess the basic principles and the assumptions that need to be made for each step of the study, including both data acquisition and the elaborate fiber reconstruction algorithms. Special attention is paid to situations where complications may arise, and possible solutions are reviewed. Validation issues and potential future directions and improvements are also discussed.

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Section: Introductionmentioning

confidence: 99%

Fiber tracking: principles and strategies – a technical review

2002

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“…[18][19][20][21][22][23][24][25] Most of the studies concerning the diffusion of NAA in brain tissue have been performed using a single diffusion time and by acquiring only few data points with relatively low b values. [18][19][20][21][22][23] Only in one study the effect of diffusion time on NAA diffusion was evaluated 24,25 but in all these studies [18][19][20][21][22][23][24][25] only a monoexponential decay was observed. Recently, preliminary results on in vitro brain at 25°C demonstrated the existence of two NAA populations.…”

Section: Introductionmentioning

confidence: 99%

In vivo andin vitro bi-exponential diffusion ofN -acetyl aspartate (NAA) in rat brain: a potential structural probe?

Assaf

Cohen

1998

NMR Biomed.

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Diffusion measurements were performed on the N ‐acetyl aspartate (NAA) signal in in situ brains (in vivo and post‐mortem) and on in vitro brain tissue at 37 °C using wide ranges of b‐values (from 0 up to 4.5 × 106 s/cm2 and 35.8 × 106 s/cm2 for the in vivo and the in vitro cases, respectively). In vivo and in vitro NAA signals attenuation due to diffusion was measured at fixed diffusion times (t D ). In the in vitro cases the effect of t D on the apparent diffusion coefficients (ADCs) of NAA was evaluated. From these experiments the following observations and conclusions were made: (1) NAA signal attenuation both in vivo and in vitro is not mono‐exponential and could be fitted by bi‐exponential fitting function; (2) analysis of the low b‐value range only (up to 0.5 × 106 s/cm2 ) gives a mono‐exponential decay (r = 0.999); (3) in both cases the obtained ADCs are sensitive to the diffusion time; (4) the ADCs of the pre‐ and post‐mortem cases are nearly similar; (5) the ADCs obtained from the bi‐exponential fitting function decrease when the diffusion time increases; and (6) both the fast and the slow diffusing components of NAA show a considerable restriction by what seems to be a non‐permeable barrier from which two compartments were identified, one having a size of 6–8 μm and the other of ∼1–2 μm in size. It seems conceivable that the two populations identified in the diffusion experiments represent primarily the NAA in the cell body (soma) and in the neurital space (axons and proximal dendrites). © 1998 John Wiley & Sons, Ltd.

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“…[38][39][40] Contrary to the large number of studies devoted to water diffusion in brain, only a few have dealt with the diffusion of metabolites in brain. [41][42][43][44][45][46][47] Most were performed with a single diffusion time, [41][42][43][44][45][46] and all these studies showed only a mono-exponential signal decay due to diffusion. [41][42][43][44][45][46][47] We recently demonstrated that, in in situ brain, the attenuation due to diffusion of the Nacetyl aspartate (NAA) signal is bi-exponential.…”

mentioning

confidence: 99%

“…[41][42][43][44][45][46][47] Most were performed with a single diffusion time, [41][42][43][44][45][46] and all these studies showed only a mono-exponential signal decay due to diffusion. [41][42][43][44][45][46][47] We recently demonstrated that, in in situ brain, the attenuation due to diffusion of the Nacetyl aspartate (NAA) signal is bi-exponential. 38,39 In the present study we investigated the diffusion characteristics of metabolites (NAA, choline, and creatine) in bovine optic nerve, and compared the results to our recent findings on NAA diffusion in brain tissue.…”

mentioning

confidence: 99%