Shielded Gradients. And The General Solution To The Near Field Problem Of Electromagnet Design

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Normal adult brain of a 40-year-old male without neurological deficits.a Isotropic DW image is obtained by combining b0 image and three orthogonal unidirectional images (x,y,z axis).The bilateral globi pallidi have low signal on DW image as a result of physiological iron deposition (arrows). Corticospinal tracts have mildly high signal on DW image (arrowheads). Gray matter shows mildly high signal compared to white matter.These signal changes on isotropic DW imaging are normal and are caused by T2 contrast. b ADC map shows homogeneous ADC values in globi pallidi, corticospinal tracts, gray and white matter. c b0 image shows low signal in globi pallidi (arrows), high signal in corticospinal tracts (arrowheads),and the gray-white matter contrast. d-f Diffusion weighting is applied in xaxis (d),y axis (e), and zaxis (f)

Figure 2.2a-d

Cystic changes in the choroid plexus. a DW image shows hyper-intensity in cystic changes of the left choroid plexus (arrow). b ADC values of the cystic changes are lower than those of the CSF,which may represent viscous gelatinous materials, but higher than those of brain parenchyma (arrow). c T2-weighted image shows the cystic changes as hyperintensity (arrow). d Gadolinium-enhanced T1-weighted image with magnetization transfer contrast reveals no enhancement in it (arrow)

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2.3 Pediatric Brain

2.3.1 Diffusion-Weighted Imaging and ADC of the Pediatric Brain

The normal brain of neonates and infants has significantly higher ADC values than the adult brain [8-13] (Fig. 2.3). ADC in neonates and infants varies markedly within different areas of the brain and is higher in white matter (1.13 x 10-3 mm2/s) than in gray matter (1.02x 10-3 mm2/s) [13]. ADC at birth is higher in subcortical white matter (1.88 x 10-3 mm2/s) than in both the anterior (1.30 x 10-3 mm2/s) and posterior limbs of the internal capsule (1.09 x 10-3 mm2/s). It is also higher in cortex and the caudate nucleus (1.34 x 10-3 mm2/s) than in the thalamus and the lentiform nucleus (1.20x 10-3 mm2/s) [13]. With the exception of the cerebrospinal fluid (CSF), there is a trend of decreasing ADC with increasing maturation in most areas of the pediatric brain. These ADC changes seem to reflect a combination of different factors, including a reduction of overall water content, cellular maturation and white matter myelina-tion. In neonates and infants, ischemia is usually global and can therefore resemble the normal image with elevated DW signal and decreased ADC. White matter diseases can also be mimicked by the normal, age-related appearance of DW imaging and ADC. Out of necessity, the ADC values will therefore have to be age related for a correct interpretation of the DW images of the pediatric brains.

Concussion Mri
Figure 2.3a,b

Normal neonatal brain. a The appearance of the pediatric brain on DW images varies with age. In neonates it is normal to have low DW signal intensities in the frontal deep white matter (arrows). b ADC values of the corresponding areas are high in neonatal brain, especially in the white matter (arrows). These ADC changes seem to reflect a combination of factors, including a reduction of overall water content, cellular maturation, and white matter myelination

2.4 Conclusion

Good knowledge of the DW appearance of the normal adult and pediatric brain and variations is necessary to avoid misinterpretation. In children it is also important to match the findings with those of normal children of the same age.

References

1. Yoshiura T,Wu O, Sorensen AG (1999) Advanced MR techniques: diffusion MR imaging, perfusion MR imaging, and spectroscopy. Neuroimaging Clin N Am 9:439-453

2. Chun T, Filippi CG, Zimmerman RD, Ulug AM (2000) Diffusion changes in the aging human brain. Am J Neuroradi-ol 21:1078-1083

3. Engelter ST, Provenzale JM, Petrella JR, DeLong DM, MacFall JR (2000) The effect of aging on the apparent diffusion coefficient of normal-appearing white matter. Am J Roentgenol 175:425-430

4. Helenius J, Soinne L, Perkio J (2002) Diffusion-weighted MR imaging in normal human brains in various age groups. Am J Neuroradiol 23:194-199

5. Gideon P, Thomsen C, Henriksen O (1994) Increased self-diffusion of brain water in normal aging. J Magn Reson Imaging 4:185-188

6. Nusbaum AO, Tang CY, Buchsbaum MS, Wei TC, Atlas SW

(2001) Regional and global changes in cerebral diffusion with normal aging.Am J Neuroradiol 22:136-142

7. Abe O, Aoki S, Hayashi N, et al. (2002) Normal aging in the central nervous system: quantitative MR diffusion-tensor analysis. Neurobiol Aging 23:433-441

8. Sakuma H, Nomura Y, Takeda K, et al. (1991) Adult and neonatal human brain: diffusional anisotropy and myeli-nation with diffusion-weighted MR imaging. Radiology 180:229- 233

9. Morriss MC, Zimmerman RA, Bilaniuk LT, Hunter JV, Haselgrove JC (1999) Changes in brain water diffusion during childhood. Neuroradiology 41:929-934

10. Tanner SF, Ramenghi LA, Ridgway JP, et al. (2000) Quantitative comparison of intrabrain diffusion in adults and preterm and term neonates and infants. Am J Roentgenol 174:1643-1649

11. Neil JJ,Shiran SI,McKinstry RC,et al.(1998) Normal brain in human newborns: apparent diffusion coefficient and diffusion anisotropy measured by using diffusion tensor MR imaging. Radiology 209:57-66

12. Engelbrecht V, Scherer A, Rassek M, Witsack HJ, Modder U

(2002) Diffusion-weighted MR imaging in the brain in children: findings in the normal brain and in the brain with white matter diseases. Radiology 222:410-418

13. Forbes KP, Pipe JG, Bird CR (2002) Changes in brain water diffusion during the 1st year oflife.Radiology 222:405-409

Pitfalls and Artifacts of DW Imaging

In collaboration with A. Hiwatashi and J.Zhong

3.1 Introduction

There are many inherent artifacts and pitfalls in diffusion-weighted (DW) imaging of the brain that are important to recognize to avoid misinterpretations.

3.2 Influence of ADC

and T2 on the DW Appearance

Diffusion-weighted images are inherently T2 weighted and changes in T2 signal characteristics will thus influence the appearance of DW images independent of tissue diffusibility [1-16]. The effect of T2 prolongation, so-called "T2 shine-through", is well known. Less well known is the balance between apparent diffusion coefficient (ADC) and T2, sometimes called T2 washout. Also the effect of T2 shortening, or T2 blackout, and magnetic susceptibility effects will influence the DW appearance in many situations. This chapter will illustrate and discuss the effects of T2 and ADC on DW images.

3.2.1 Concepts

The signal intensity (SI) on DW images is influenced by T2,ADC,the b factor,the spin density (SD) and the echo time (TE), and is calculated as follows:

SI=SIb=0e-bADC

However,

SI=£SDe-TE/TVbADC

where k is a constant, TR is repetition time, and SIb=0 is the signal intensity on the spin-echo echo-planar image (b0 image) [1,2,5,7,8,10,12,16].

To evaluate the tissue T2 and ADC, we should pay attention to the images discussed below as well as isotropic DW images and b0 images [3-5,7,8,10,11, 13-16].

3.2.2 Apparent Diffusion Coefficient Maps

To evaluate the diffusibility, ADC is calculated as: ADC=-n (SI/SIb=0)/b

Subsequently, increased ADC causes decreased SI on DW images, and decreased ADC causes increased SI on DW images [3-5,7,10,15,16].

3.2.3 Exponential Images

To remove the T2-weighted contrast, the DW image can be divided by the b0 image to create an "exponential image" [4,7,10,15].

The signal intensity (SIeDWI) on the exponential image is calculated as:

Therefore, this image can eliminate the effect of T2. Contrary to ADC maps, hyperintensity on exponential DW images means decreased ADC, and hy-pointensity means increased ADC.

3.3 Clinical Conditions 3.3.1 T2 Shine-through

This is a well-known phenomenon that causes hy-perintensity on DW images by means of T2 prolon gation [3-5,7,8,10,11,15,16]. If ADC is decreased at the same time, this can result in an accentuation of the hyperintensity on DW images (Figs. 3.1, 3.2 and 3.3).

Wash Out Que Shines LesionsShine Through

Figure 3.1 a-e

T2 shine-through in a 35-year-old female with multiple sclerosis and weakness of the lower extremities. a T2-weighted image shows several hyperintense lesions,with the largest one in the right frontal lobe (arrow). b On T1-weighted image the lesion was hypointense (arrow) and did not enhance with contrast (not shown).c On DW image the lesion is hyperintense (arrow). d ADC map also shows hyperintensity in the lesion (1.2X10-3 mm2/s; arrow). e Exponential image eliminates the T2 effect and shows the lesion to be hypointense (arrow).This confirms that the hyperintensity on DW image is due to a T2 shine-through

Cortical Gray Matter Cytotoxic Edema
Figure 3.2 a-e

T2 shine-through in a 45-year-old female with seizures caused by anaplastic astrocytoma. a T2-weighted image shows a hyperintense lesion in the left frontal lobe (arrow). b On T1-weighted image the lesion is hypointense with peripheral hy-perintense area (arrow).The lesion did not enhance with contrast (not shown).c DW image shows hyperintensity (arrow). d ADC map also shows hyperintensity in the lesion (0.98-1.35X10-3 mm2/s;arrow).e Exponential image eliminates the T2 effect and shows the lesion to be hypointense (arrow).This confirms that the hyperintensity on DW image is due to a T2 shine-through

Caudate Nucleus Hemorrhage Swi
Figure 3.3 a-f

T2 shine-through and restricted diffusion in a 56-year-old male with right-sided weakness due to acute infarction.MR imaging obtained 24 hours after the onset of symptoms.a FLAIR image shows a hyperintense lesion in the left middle cerebral artery territory. b On T1-weighted image the lesion is hypointense. c On T2-weighted image (b0) the lesion is hyperintense. d DW image also shows hyperintensity in the lesion. e ADC map shows hypointensity in the lesion (0.27-0.45X10-3 mm2/s).f On the exponential image,which eliminates the T2 effect,the lesion remains hyperintense.This confirms that the DW hyperintensity is due to both restricted diffusion and T2 prolongation

3.3.2 T2 Washout

This implies that isointensity on DW images is the result of a balance between hyperintensity on T2-weighted images and increased ADC [13,14,16]. This is often seen in vasogenic edema, where the combination of increased ADC and hyperintensity on T2-

weighted images will result in isointensity on DW images (Fig. 3.4).

To the best of our knowledge there have been no systematic reports on pathological conditions with isointensity on DW images, caused by a balance of hypointensity on T2-weighted images and decreased ADC.

Figure 3.4 a-d

T2 washout in a 45-year-old female with hypertension, seizures and posterior reversible encephalopathy syndrome. a FLAIR image shows hyperintense lesions in the bilateral occipital lobe (arrows). b T2-weighted image (b0) also shows hyperintensity of the lesions (arrows). c DW image shows mild hyperintensity in the lesions. d ADC map shows hyper-intensity of the lesions (1.18-1.38X10-3 mm2/s; arrows). With the strong T2 prolongation one would expect more hyperintensi-ty on the DW image, but the T2 shine-through effect is reduced by the hyperintensity on the ADC, resulting in a balance between increased diffusibility and hyperintensity on the T2-weighted image (T2 wash-out)

Paramagnetic Hemoglobin

3.3.3 T2 Blackout cally seen in some hematomas [9,16]. Paramagnetic susceptibility artifacts may occur in this situation This indicates hypointensity on DW images caused (Figs. 3.5 and 3.6). by hypointensity on T2-weighted images and is typi-

Shine Through Artifact
Figure 3.5 a-e

T2 blackout in lung cancer metastasis in a 62-year-old male with adenocarcinoma of the lung. a T2-weighted image shows a hypointense mass (arrow) with surrounding edema in the left cerebellar hemisphere. b Gadolinium-enhanced T1-weighted image shows heterogeneous enhancement of the mass (arrow). c T2-weighted image (b0) also shows hypointensity in the lesion with surrounding hyperintense edema (arrow). d ADC map shows central hyperintensity (1.63-2.35X10-3 mm2/s;arrowhead) and peripheral hypointensity (1.13-1.38X10-3 mm2/s;arrow) of the mass.There is also hyperintensity of the surrounding tissue, consistent with vasogenic edema. e DW image shows heterogeneous hypointensity of the mass (arrow) and isointensity of the surrounding edema.The DW hypointensity of the mass (arrow) is due to the increased diffusibility and hypointensity on T2-weighted image.The isointensity in the surrounding edema is due to the balance between the increased diffusibility and hyperintensity on T2-weighted image (T2 washout)

Deoxyhemoglobin Mri

Figure 3.6 a-d

T2 blackout from susceptibility artifacts in acute hemorrhage (deoxyhemoglobin and intracellular met-hemoglobin) in a 74-year-old male with left-sided weakness.MR imaging was obtained 24 hours after the onset of symptoms. a T2-weight-ed image shows hypointense lesions in the right frontoparietal lobes (arrows deoxyhemoglobin and intracellular met-hemoglobin) with areas of surrounding hyperintensity consistent with edema (arrowheads). b T1-weighted image shows the heterogeneous lesion with hypointensity (arrow deoxyhemoglobin) and hyperintensity (arrowheads intracellular met-hemoglobin).c DW image shows hypointensity (arrows deoxy-hemoglobin and intracellular met-hemoglobin) and hyperintensity in region of edema (arrowhead).The surrounding hyperintense rims (smallarrowheads) are due to magnetic susceptibility artifacts.d ADC could not be calculated accurately in the T2 "dark"hematoma due to magnetic susceptibility artifacts (arrows).The surrounding areas of hypointensity (arrowhead) probably correspond to cytotoxic edema surrounding the hematoma. This example shows how T2 hypointensity from susceptibility effects can produce a complex appearance in and around cerebral hemorrhage

3.4 Artifacts

Numerous artifacts can be generated during acquisition of DW images. There are five main artifacts of single-shot DW echo-planar imaging:

1. Eddy current artifacts due to echo-planar imaging phase-encode and readout gradients, and motion-probing gradient pulses for diffusion weighting

2. Susceptibility artifacts

3. N/2 ghosting artifacts

4. Chemical shift artifacts

5. Motion artifacts

We will discuss each artifact separately.

3.4.1 Eddy Current Artifacts

Eddy currents are electrical currents induced in a conductor by a changing magnetic field. Eddy currents can occur in patients and in the MR scanner itself, including cables or wires, gradient coils, cryoshields and radiofrequency shields [17]. Eddy currents are particularly severe when gradients are turned on and off quickly, as in echo-planar imaging pulse sequences. Gradient waveforms are distorted due to eddy currents,which results in image artifacts, including spatial blurring and misregistration. In single-shot DW echo-planar imaging, eddy currents are due to both echo-planar imaging gradients and motion-probing gradients, which lead to image distortions (Fig. 3.7). Correction of image distortion is essential to calculate ADC values and especially to quantify anisotropy with diffusion tensor imaging. Correction methods: (1) correction of distortion by using post-processing [18-21], (2) pre-emphasis or pre-compensation, purposely distorting the gradient-driving currents [22,23], (3) shielded gradients, redesigning the magnet to incorporate shielding coils between the gradient coils and main windings [24].

3.4.2 Susceptibility Artifacts

Single-shot echo-planar imaging is sensitive to susceptibility artifacts, especially frequency and phase errors due to paramagnetic susceptibility effects. These artifacts are seen near the skull base, especially near the air in the sinus and mastoid (Fig. 3.8). Susceptibility artifacts are more severe along the phase-encoding direction and phase encoding should thus be along the anterior-posterior direction for axial DW images. Coronal and sagittal DW images are helpful in detecting lesions in certain locations, such as the hippocampus and brain stem, and to identify susceptibility artifacts (Fig. 3.9). Increased matrix size leads to elongation of readout time, which causes even larger image distortions. Correction methods: (1) multi-shot echo-planar imaging (to reduce the readout time, to enable high-resolution scan) [25,26],(2) line scan [27,28],(3) singleshot fast spin echo (SSFSE) [29,30], (4) periodically rotated overlapping parallel lines with enhanced reconstruction (PROPELLER) [31,32],(5) sensitive encoding (SENSE)/array spatial and sensitivity-encoding technique (ASSET), undersampling of k-space enables effective band width and shortens readout time, providing thin section and high-resolution matrix [33].

Eddy Current Artifact
Figure 3.7 a,b

Misregistration due to eddy current artifact. a, b Misregistration artifact is noted in the occipital regions (arrows) on DW image (a) and the ADC map (b). Gradient waveforms are distorted due to eddy currents, which results in this misregistration

Figure 3.8

Susceptibility artifact. Susceptibility artifacts are seen near the air content of the mastoids (arrows).This is generally prominent in echo-planar sequences

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Susceptibility artifact in coronal and sagittal plane DW images. Coronal DW image (a) and the ADC map (b) are used to evaluate the hippocampus,but susceptibility artifacts distort the image near the mastoids. Sagittal DW image (c) and the ADC map (d) show a pontine infarct as hyperintense with decreased ADC (arrowhead). Susceptibility artifacts are caused by air in the ethmoid and sphenoid sinuses (arrows)

Nyquist Artifact

3.4.3 N/2 Ghosting Artifact (Nyquist Ghost)

N/2 ghosting artifact occurs when there are differences between the even and odd lines of the k-space. Phase error is due to hardware imperfections (eddy currents, imperfect timing of even and odd echo, imperfect gradients, and magnetic field inhomogene-ity), which can be produced by on-off switching during readout gradients. The ghosts in this artifact are always shifted by half of the field of view in the phase-encoding direction (Fig. 3.10). This ghost can produce severe artifacts when ADC maps are calculated. Correction methods: (1) reduce eddy currents, (2) adjust gradients and magnetic field homogeneity, (3) high b-value, (4) fluid-attenuated inverse-recovery (FLAIR) DW imaging (reduce cerebrospinal fluid signal) [33,34].

3.4.4 Chemical Shift

In echo-planar DW imaging, chemical shift artifacts due to the different resonance frequencies in water and fat are produced along the phase-encoding direction, while they are along the frequency-encoding direction in conventional spin-echo type MR imaging. This artifact is more severe in echo-planar imaging than in conventional spin-echo type MR imaging. Effective fat suppression techniques, such as the chemical shift selective (CHESS) method and the spectral selective radiofrequency excitation method are necessary.

Correction methods: appropriate fat suppression techniques.

3.4.5 Motion Artifacts

The sources of motion artifacts include gross head motion, respiratory motions, cardiac-related pulsations and patient bed vibration due to gradient pulses. Single-shot DW echo-planar imaging has relatively low sensitivity to patient motion, because each image is acquired in about 100-300 ms and the total acquisition time is less than 40 s. If one of the x, y, z or b0 images is corrupted by motion artifacts during a scan, or if patient head motion occurs between scans, the isotopic DW images and the ADC maps will have these artifacts (Figs. 3.11 and 3.12). In those cases, unidirectional and b0 images from the raw data of DW imaging can be free from the motion artifacts and remain diagnostically useful. Long (tens of ms) gradient pulses to reach sufficient diffusion weighting often increase sensitivity to motion. Correction methods: (1) For a fixed b-factor, use high-gradient amplitude but reduce gradient pulse duration to minimize the sensitivity to motion, (2) post-processing to correct for phase error (Navigator method) [35-37], (3) elimination of phase-encode step (line scan method, projection reconstruction), (4) minimize time for phase error accumulation (single-shot echo-planar imaging, hybrid method with multishot echo-planar imaging), (5) SSFSE, (6) PROPELLER [38],(7) SENSE.

Phase Encoded Motion Artifact
Figure 3.10 a,b

N/2 ghosting artifact.a DW image shows N/2 ghosting artifacts (arrows), which are always shifted by half of the field of view in the phase-encoding direction. b On the ADC map severe N/2 ghosting artifacts are also seen (arrows)

Motion artifacts due to head motion during the scan of a patient with status epilepticus.a It is difficult to evaluate the DW image because of severe motion artifacts. b In the raw data of the DW imaging, the x axis image is corrupted by head motion during the scan. c The y axis image is free from the artifacts. This image shows a hy-perintense lesion in the left hippocampus (arrow). d ADC map of y axis image also shows decreased ADC of the lesion (transferred to a workstation for image processing, using a home-made code, which is based on the numerical computation software)

Cytotoxic Edema
Figure 3.12 a-f

Motion artifacts due to head motion between the scans.Chronic infarcts in the right basal ganglia.a DW image has motion artifacts due to head motion between the scans.This image appears overlapping of b0,and x,y,z axis images. b ADC map also shows severe motion artifacts.c b0,dxaxis,ey axis,fzaxis.b0 and unidirectional images are all free from the artifacts

3.5 Conclusion

Diffusion-weighted images are inherently T2 weighted and the interpretation of signal intensity on DW images requires a correlation between b0 images, ADC maps and exponential images to uncover the underlying pathophysiologic condition. It is also important to understand a variety of artifacts to avoid misinterpreting the DW images. Understanding inherent artifacts and the way to reduce the artifacts on DW imaging will improve the quality and accuracy of DW imaging.

References

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3. Warach S, Gaa J, Siewert B, Wielopolski P, Edelman RR (1995) Acute human stroke studied by whole brain echo planar diffusion-weighted magnetic resonance imaging. Ann Neurol 37:231-241

4. Provenzale JM, Engelter ST, Petrella JR, Smith JS, MacFall JR (1999) Use of MR exponential diffusion-weighted images to eradicate T2 "shine-through" effect. AJR Am J Roentgenol 172:537-539

5. Burdette JH, Elster AD, Ricci PE (1999) Acute cerebral infarction: quantification of spin-density and T2 shine-through phenomena on diffusion-weighted MR images. Radiology 212:333-339

6. Coley SC, Porter DA, Calamante F, Chong WK, Connelly A (1999) Quantitative MR diffusion mapping and cy-closporine-induced neurotoxicity. AJNR Am J Neuroradiol 20:1507-1510

7. Schaefer PW, Grant PE, Gonzalez RG (2000) Diffusion-weighted MR imaging of the brain. Radiology 217:331-345

8. Field A (2001) Diffusion and perfusion imaging. In: Elster AD, Burdette JH (eds). Questions and answers in magnetic resonance imaging. Mosby, St. Louis, Missouri pp 194-214

9. Maldjian JA, Listerud J, Moonis G, Siddiqi F (2001) Computing diffusion rates in T2-dark hematomas and areas of low T2 signal. AJNR Am J Neuroradiol 22:112-128

10. Engelter ST, Provenzale JM, Petrella JR,Alberts MJ, DeLong DM, MacFall JR (2001) Use of exponential diffusion imaging to determine the age of ischemic infarcts. J Neu-roimaging 11:141-147

11. Chen S, Ikawa F, Kurisu K, Arita K, Takaba J, Kanou Y (2001) Quantitative MR evaluation of intracranial epidermoid tumors by fast fluid-attenuated inversion recovery imaging and echo-planar diffusion-weighted imaging. AJNR Am J Neuroradiol 22:1089-1096

12. Geijer B, Sundgren PC, Lindgren A, Brockstedt S, Stahlberg F, Holtas S (2001) The value of b required to avoid T2 shine-through from old lacunar infarcts in diffusion-weighted imaging. Neuroradiology 43:511-517

13. Casey S (2001) "T2 washout": an explanation for normal diffusion-weighted images despite abnormal apparent diffusion coefficient maps. AJNR Am J Neuroradiol 22:1450-1451

14. Provenzale JM, Petrella JR, Cruz LC Jr, Wong JC, Engelter S, Barboriak DP (2001) Quantitative assessment of diffusion abnormalities in posterior reversible encephalopathy syn-drome.AJNR Am J Neuroradiol 22:1455-1461

15. Eastwood JD, Engelter ST, MacFall JF, Delong DM, Provenzale JM (2003) Quantitative assessment of the time course of infarct signal intensity on diffusion-weighted images. AJNR Am J Neuroradiol 24:680-687

16. Hiwatashi A, Kinoshita T, Moritani T, et al. (2003) Hy-pointensity on diffusion-weighted MRI related to T2 shortening and susceptibility effects.AJR Am J Roentgenol (in press)

17. Elster AD, Burdette JH (2001) Scanner hardware. In: Elster AD, Burdette JH (eds). Questions and answers in magnetic resonance imaging. Mosby, St. Louis, Missouri pp 54-71

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19. Horsfield MA (1999) Mapping eddy current induced fields for the correction of diffusion-weighted echo planar images. Magn Reson Imaging 17:1335-1345

20. Jezzard P, Barnett AS, Pierpaoli C (1998) Characterization of and correction for eddy current artifacts in echo planar diffusion imaging. Magn Reson Med 39:801-812

21. Calamante F, Porter DA, Gadian DG, Connelly A (1999) Correction for eddy current induced Bo shifts in diffusion-weighted echo-planar imaging. Magn Reson Med 41:95-102

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27. Maier SE, Gudbjartsson H, Patz S, et al. (1998) Line scan diffusion imaging: characterization in healthy subjects and stroke patients.AJR Am J Roentgenol 171:85-93

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Brain Edema

4.1 Characterization and Classification of Brain Edema

Brain edema is defined as accumulation of excess fluid in cells or in the extracellular space. Brain edema can be classified as cytotoxic (cellular), vasogenic [1] or interstitial. Cytotoxic and vasogenic edema usually coexist in pathological conditions such as infarction, hypoxic ischemic encephalopathy, trauma, or multiple sclerosis. The edema may primarily be either vasogenic or cytotoxic, but as the process evolves over time, the injury leads to a combination of cellular swelling and vascular damage. Interstitial edema occurs with hydrocephalus, water intoxication, or plasma hyposmolarity.

Conventional MR imaging does not always allow distinction between the different forms of edema. However, diffusion-weighted (DW) imaging, which is based on the microscopic movement of water molecules in brain tissue, can differentiate cytotoxic edema from vasogenic and interstitial edema [2].

4.2 Definition and Classification of Cytotoxic Edema

Cytotoxic or cellular edema is an abnormal uptake of fluid in the cytoplasm due to abnormal cellular os-moregulation. This kind of edema may accompany various processes that damage cells, such as ischemia, trauma, toxic metabolic disease, demyelina-

tion, and even the early phase of degeneration. Classification of the involved cell types may explain the pathophysiology and different prognosis of these conditions.

In normal brain tissues, the gray and white matters are mainly composed of neurons, glial cells, axons, and myelin sheaths (Fig. 4.1). In the gray matter, cy-totoxic edema occurs mainly in neurons and glial cells (Fig. 4.2). In the white matter, however, cytotoxic edema occurs in glial cells, axons (axonal swelling) (Fig. 4.3) and myelin sheaths (intramyelinic edema) (Fig. 4.4) [1].

4.3 Pathophysiology of Cytotoxic Edema 4.3.1 Energy Failure

In ischemia or hypoxia, cytotoxic edema is mainly caused by energy failure [3]. The insult initiates substrate depletion, which leads to a decrease in intracel-lular ATP used for oxidative phosphorylation, and a failure of the sodium-potassium pump. This will cause an influx of sodium and calcium into the cells, subsequently increasing the osmotic gradient and the transport of water into the cells, resulting in cellular swelling. Moreover, in an attempt to produce ATP, the cells switch from oxidative phosphorylation to anaerobic glycolysis, resulting in intracellular lac-tate. This will further increase the osmotic gradient across the cell membrane, which exacerbates the cy-totoxic edema.

Oligodendrocyte

Intramyelinic Edema
Fig. 4.1. Normal brain tissue is mainly composed of neurons,glial cells (astrocytes or oligodendrocytes), axons and myelin sheaths surrounded by an extracellular space
Oligodendrocyte Elongation
Figure 4.2

Cytotoxic edema occurs in neurons and glial cells (astrocytes and oligodendrocytes).These cells are vulnerable to ischemia.As cells increase in size,there is a shift of water from extracellular to intracellular compartments, which can occur without a net gain in water (compared with Fig.4.1).Cytotoxic edema results in increased intra-cellular space and decreased extracellular space,which may cause a decrease in ADC

Figure 4.4

Cytotoxic edema can occur in myelin sheaths in which edema is found in either the myelin sheath itself or in the intramyelinic cleft

Cytotoxic Brain Edema Radiographics

4.3.2 Excitotoxic Brain Injury

Energy failure is not the only mechanism responsible for the cytotoxic edema [3]. Membrane transporters can be triggered or inhibited by a range of excitatory neurotransmitters, such as glutamate and aspartate, but also other agents such as cytokines and free radicals [4]. Any cell, including neuron, glia, axon and myelin sheath can be a target of these toxic sub stances; however, reactive astrocytes play a significant role in cellular and tissue repair by detoxifying various noxious substances (such as glutamate, free radical, ammonia and metals). Neuropathologic examination shows that the acutely reactive astrocytes have swollen cytoplasm and neutrophil, consistent with cytotoxic edema [5].

High glutamate in the synaptic and extracellular space is one of the important mechanisms associated

Pre-synaptic neuron

Synaptic vesicles £>f glutamate

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