| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
2002 ARRS Executive Council Award 1 |
1 All authors: Department of Radiology, Duke University Medical Center, Box 3808, Durham, NC 27710.
Received February 14, 2002;
accepted after revision June 10, 2002.
Address correspondence to P. McGraw.
Abstract
 Top Abstract IntroductionMaterials and MethodsResultsDiscussionReferences |
|---|
MATERIALS AND METHODS. We retrospectively analyzed anisotropy maps derived from diffusion tensor imaging studies performed in 66 pediatric patients (age range, 4 days—71 months; mean age, 18.6 months) who underwent clinical MR imaging and were found to have no abnormalities on conventional MR images. Anisotropy was measured in three compact white matter structures (corpus callosum, internal capsule, cerebral peduncle) and two regions of noncompact white matter (corona radiata and peripheral white matter). Patients were assigned to one of the three following groups on the basis of age: group 1, younger than 12 months (n = 40); group 2, 12-35 months (n = 11); and group 3, 36-71 months (n = 15). First, we compared anisotropy values of noncompact white matter with those of compact white matter for each age group. Second, we compared the increase over time in anisotropy of noncompact white matter regions with that seen in compact white matter structures.
RESULTS. Among all three age groups, anisotropy measurements in compact white matter structures were higher than those in noncompact white matter (p < 0.01). The mean anisotropy values in noncompact white matter for groups 1, 2, and 3, respectively, were 0.349, 0.480, and 0.531. The mean anisotropy values in compact white matter for groups 1, 2, and 3, respectively, were 0.494, 0.646, and 0.697. When age groups were compared, a statistically significant increase in anisotropy was seen in both compact white matter and noncompact white matter (p < 0.01). However, the increase in anisotropy was significantly greater in non-compact white matter regions than in compact white matter structures when comparing group 1 with group 3 (p < 0.01) as well as group 1 with group 2 (p < 0.01).
CONCLUSION. Although anisotropy measurements were higher in compact than non-compact white matter in all three age groups, the increase in anisotropy was greater in non-compact white matter across each of the three groups. These data suggest that although myelination is initially greater in compact white matter, the change in myelination may be greater in noncompact white matter during the first few years after infancy.
|
TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
|---|
Diffusion tensor imaging is a newer and more complete method of evaluating myelination than previous methods. MR signal is sensitized to the smallest movement of water molecules with diffusion tensor imaging. Cell membranes and myelin sheaths restrict the movement of water molecules in white matter tracts, causing water to move faster and farther parallel to the white matter tracts, rather than perpendicular to them. This directional movement of water molecules is termed anisotropic diffusion, whereas completely random movement is termed isotropic diffusion [2].
Derivation of a diffusion tensor allows calculation of anisotropy values. Anisotropy values are known to be highest in regions of white matter, as compared with regions of gray matter, because of more directed movement of water molecules along white matter fiber tracts. Anisotropy has also been measured to be higher in the white matter structures of adults than in those of neonates and infants [6, 7]. Diffusion tensor imaging is also known to be sensitive to internal changes of myelination because anisotropy values increase with increased myelin formation. Anisotropy measurements, therefore, provide a unique marker for white matter maturation [8].
To our knowledge, milestones of anisotropy changes in both peripheral and central white matter of the maturing brain during infancy and childhood have not yet been identified in the same sample population [7, 9]. Knowledge of normal age-dependent anisotropy parameters may prove valuable in the clinical evaluation of neonates, infants, and children with various white matter disorders.
For these reasons, we undertook a study that focused on measuring anisotropy in a number of white matter regions in neonates, infants, and children. Our study had two purposes. The first purpose was to study the degree of anisotropy within various white matter areas in three pediatric age groups. Previous studies using diffusion tensor imaging have primarily focused on compact white matter structures such as the internal capsule and the corpus callosum [7]. In our study, we compared anisotropy values in compact white matter structures with those in noncompact white matter areas for each age group. Our hypothesis was that anisotropy values would be higher in compact white matter structures in all age groups studied.
The second purpose of this study was to compare increases in anisotropy in various white matter regions across age groups to provide a better understanding of the rates of myelination within these structures in healthy neonates, infants, and children. Our hypothesis was that the increase in anisotropy would be higher in noncompact white matter than in compact white matter. This hypothesis was based on the fact that compact white matter structures begin to have features consistent with myelination on conventional MR images in infants during the first year of life and, therefore, would be expected to have developed a high degree of anisotropy during this period. However, noncompact white matter develops features consistent with myelination on conventional MR images over the course of the next few years.
A prior histologic study with myelin staining of autopsy specimens identified mature myelin in approximately 90% of the specimens of the corpus callosum and the posterior limb of the internal capsule by 1 year of age. Peripheral white matter specimens, such as frontal—parietal lobe white matter, however, revealed mature myelin in less than 50% of the specimens at 1 year [10, 11]. Therefore, if compact white matter structures have completed a greater percentage of the normal myelination process in utero or during the first months of life, then noncompact white matter would be expected to have a greater increase in myelination during early childhood; these changes would be reflected in a greater increase in anisotropy in noncompact white matter.
|
TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
|---|
The patient population consisted of 66 neonates, infants, and young children (44 boys and 22 girls). The indications for MR imaging in these patients included a variety of clinical symptoms and signs, of which the most common were headache and seizure. Inclusion criteria consisted of the following: normal findings on an MR imaging examination of the brain and the absence of significant neurologic impairment as determined by a review of patient records. To decrease the possibility of including patients whose MR examinations were interpreted as normal but who actually had neurologic abnormalities, we retrospectively reviewed all patient records. Additional clinical information was available for 47 of the 66 patients. For the patients who underwent additional clinical evaluation, the range of clinical follow-up was 1-12 months (mean, 4.8 months).
Patients in our study population ranged in age from 4 days to 71 months with a mean age of 18.6 months. Each patient's age was corrected for prematurity and rounded down to the last full month. Subjects were classified into one of three groups on the basis of age for direct comparison of anisotropy and analysis of each age group. Three age groups were configured: group 1, younger than 12 months old (n = 40 patients); group 2, 12-35 months (n = 11 patients); and group 3, 36-71 months (n = 15 patients).
All imaging was performed on a 1.5-T clinical MR imaging scanner (Signa; General Electric Medical Systems, Milwaukee, WI). A standard head coil was used. The diffusion tensor imaging protocol consisted of a single-shot spin-echo echoplanar imaging sequence with a TR/TE of 12,000/101 and an inversion time of 2200 msec. Sixty-six patients underwent diffusion tensor imaging using 2 excitations, four patients underwent imaging using 1 excitation, and one patient underwent imaging using 4 excitations. Diffusion gradients were encoded in six directions with a b value of 1000 sec/mm2 as well as an additional image with no diffusion gradient (b = 0 sec/mm2). Imaging was performed through the entire brain. The slice thickness was 5 mm, and the interslice gap was 2.5 mm. The field of view was 40 x 20 cm with a 128 x 64 matrix. An acquisition time of approximately 4 min 48 sec was required for the 2-excitation sequence.
Region-of-interest (ROI) measurements were defined on diffusion tensor
images using an Advantage Windows workstation (General Electric Medical
Systems) and Functool software (General Electric Medical Systems). The six
independent elements of the diffusion tensor—Dxx,
Dyy, Dzz, Dxy, Dxz, and
Dyz—were statistically calculated for each voxel
using the method described by many researchers
[12,13,14,15]
and based on the following equation:
 |
 |
A neuroradiologist placed a uniform ROI on each side of the midline in the following seven regions of white matter: the peripheral frontal lobe white matter, the peripheral parietal lobe white matter, the corona radiata (Fig. 1A,1B,1C), the genu of the corpus callosum, the splenium of the corpus callosum, the posterior limb of the internal capsule (referred to as the internal capsule) (Fig. 2A,2B,2C), and the cerebral peduncle (Fig. 3A,3B,3C). Each ROI was drawn semiautomatically using Functool software and was a standard size—44 ± 2 mm2, which is equivalent to 3-5 pixels. Oval ROIs were drawn for placement in the genu and splenium of the corpus callosum and in the internal capsule to better conform to the morphology of these structures.
|
|
|
|
|
|
|
|
|
The values from the two ROIs for each structure were averaged to provide one mean value for each of the white matter areas in each patient. In addition, a mean value was obtained for peripheral white matter by averaging the measurements for the frontal lobe white matter and parietal lobe white matter. In a similar manner, a mean value for the corpus callosum was obtained by averaging anisotropy measurements for the genu and splenium of the corpus callosum.
The sites of ROI placement were categorized as either compact or noncompact white matter. Compact white matter consisted of the corpus callosum, internal capsule, and cerebral peduncle. Noncompact white matter consisted of the frontal—parietal white matter and corona radiata. These five white matter regions were chosen to reflect a spectrum of white matter fiber tracts in the brain so that both fractional anisotropy values and the rate of change of anisotropy in compact and noncompact white matter tracts during early childhood could be compared.
All measurements were performed on anisotropy maps that were oriented in the axial plane. ROIs for the cerebral peduncle, the internal capsule, and the genu and splenium of the corpus callosum were drawn within the midportion of these structures, which were readily identified on diffusion tensor imaging. Anatomic landmarks were chosen to ensure ROI placement was consistent for anisotropy measurements of the other white matter regions that were evaluated. ROIs in the corona radiata were routinely configured on the axial slice at the level of the roof of the lateral ventricle. The frontal and parietal white matter ROIs were drawn on the image one slice superior to the roof of the lateral ventricle. These ROIs were placed in the most peripheral portion of the white matter of the frontal and parietal lobes that could still accommodate a standard-sized ROI. Anisotropy measurements were performed on color-coded anisotropy maps. The ROI cursor was manually manipulated after visual inspection of the anisotropy map to ensure documentation of the highest anisotropy within each structure.
Two different methods were used to analyze anisotropy values. The first method consisted of comparison of mean anisotropy values across the five white matter areas in each age group as well as for groups of compact white matter and noncompact white matter using a paired two-group t test with the Bonferroni adjustment. The second method of analysis consisted of comparison of anisotropy differences between each of the five white matter regions as well as between compact and noncompact white matter regions across the three age groups. For this second analysis, anisotropy values were expressed as the ratio of the mean anisotropy values within any two white matter structures (e.g., the ratio of the mean anisotropy value in the internal capsule to the mean anisotropy value in the corpus callosum). Two-group t tests with the Bonferroni adjustment between the logarithms of these ratios were then computed between different age groups to determine whether the ratios increase or decrease with age. The logarithm was used to minimize possible right skewing caused by expressing the data as ratios. However, to control for the choice of logarithmic transformation on our results, we also compared the simple ratios using two-group t tests with the Bonferroni adjustment. The resulting probability values for comparisons using logarithms of the ratios and comparisons using ratios alone were similar and did not result in changes between significant p values and nonsignificant p values for comparison across age groups.
|
TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
|---|
Individual comparisons of mean anisotropy values among the five white matter areas were performed using paired two-group t tests with the Bonferroni adjustment. The comparisons produced statistically significant (p < 0.01) differences between each of the regions evaluated except for the direct comparison between the two noncompact white matter areas and the comparison between the corpus callosum and the internal capsule. The mean anisotropy value was found to be significantly higher in compact than in noncompact white matter regions (p < 0.01).
Group 2.—This patient group consisted of 11 infants and young children who ranged in age from 12 to 35 months (mean age, 26.5 months). The mean anisotropy values of each structure of compact white matter were 0.737 for the corpus callosum, 0.655 for the internal capsule, and 0.547 for the cerebral peduncle. The mean anisotropy value for all compact white matter structures was 0.646. The mean anisotropy values for noncompact white matter were 0.528 for the frontal—parietal white matter and 0.433 for the corona radiata (Fig. 4). The mean anisotropy value for all noncompact white matter was 0.480. Anisotropy values in all compact white matter structures were higher than those in noncompact white matter (Fig. 5).
|
|
Individual comparisons of mean anisotropy values among the five white matter areas were performed using paired two-group t tests with the Bonferroni adjustment. The comparisons produced statistically significant (p < 0.02) differences between each of the structures evaluated except for the direct comparison of the frontal—parietal white matter and the cerebral peduncle. The mean anisotropy value in compact white matter was found to be significantly higher than that in noncompact white matter (p < 0.01).
Group 3.—This group consisted of 15 young children who ranged in age from 36 to 71 months (mean age, 52.1 months). The mean anisotropy measurements of each structure of compact white matter were 0.784 for the corpus callosum, 0.695 for the internal capsule, and 0.605 for the cerebral peduncle. The mean anisotropy value for all compact white matter structures was 0.697. The mean anisotropy values for noncompact white matter were 0.566 for the frontal—parietal white matter and 0.494 for the corona radiata. The mean anisotropy value for all noncompact white matter structures was 0.531. The anisotropy values in all compact white matter structures were higher than those in noncompact white matter regions.
Individual comparisons of mean anisotropy values among the five white matter regions were performed using paired two-group t tests with the Bonferroni adjustment. The comparisons produced statistically significant (p < 0.01) differences of each of the areas evaluated except for the direct comparison between the frontal—parietal white matter and the cerebral peduncle. The mean anisotropy value in compact white matter was found to be significantly higher than that in noncompact white matter (p < 0.01).
Differences in Anisotropy Between Age Groups
Group 1 versus group 3.—The percentage increase in
anisotropy over time between group 1 and group 3 for each white matter
structure evaluated were as follows. In compact white matter structures, a 32%
increase was documented in the internal capsule, 44% increase in the cerebral
peduncle, and 46% increase in the corpus callosum. Therefore, the average
increase in anisotropy in compact white matter structures was 41%. Among
noncompact white matter regions, a 47% increase was seen in the corona radiata
and a 57% increase in the frontal—parietal white matter, giving an
average increase in anisotropy of 52%.
A statistically significant increase in anisotropy values was seen in both compact and noncompact white matter (p < 0.01) using a two-group t test with the Bonferroni adjustment on the logarithm of the anisotropy ratios (Fig. 4). The increase in anisotropy was significantly greater in noncompact white matter than that in compact white matter (p < 0.01) as determined by comparison of the difference of logarithms using a two-group t test on the paired differences (Fig. 5).
Comparison of individual structures in the same manner across the same two groups showed a statistically significant difference in the increase of anisotropy in the frontal—parietal white matter compared with the internal capsule (p < 0.01). The increase in anisotropy in the frontal—parietal white matter was higher than that seen in the corpus callosum, but the difference was not statistically significant (p < 0.1). A trend toward a more rapid increase in anisotropy in the corona radiata than in compact white matter structures was seen, but this difference was not statistically significant.
Group 1 versus group 2.—In compact white matter structures, a 25% increase in anisotropy was seen in the internal capsule, 30% increase in the cerebral peduncle, and 37% increase in the corpus callosum. Therefore, the average increase in anisotropy in compact white matter was 31%. Among noncompact white matter regions, a 29% increase was seen in the corona radiata and a 46% increase in the frontal—parietal white matter, giving an average increase in anisotropy of 38% (Fig. 5).
A statistically significant increase in anisotropy was seen in both compact and noncompact white matter (p < 0.01) applying a two-group t test with the Bonferroni adjustment to the logarithm of the anisotropy measurements. A higher rate of increase in anisotropy was seen in noncompact white matter, but the difference was not statistically significant.
Comparison of the difference of logarithms of individual structures between compact white matter and noncompact white matter showed a statistically significantly greater increase in anisotropy in the frontal—parietal white matter than in the internal capsule (p < 0.01). The increase in anisotropy in the frontal—parietal white matter was higher than the increases for all other compact white matter structures, but the differences were not statistically significant.
Group 2 versus group 3.—In compact white matter structures, a 6% increase in anisotropy was seen in the internal capsule, 6% increase in the corpus callosum, and 10% increase in the cerebral peduncle, giving an average anisotropy increase of 7%. In noncompact white matter regions, a 7% increase was seen in the frontal—parietal white matter and a 14% increase in the corona radiata, giving an average increase in anisotropy of 11%.
A statistically significant increase in anisotropy (p < 0.01) was seen for both compact and noncompact white matter as determined by a two-group t test with the Bonferroni adjustment applied to the logarithm of the anisotropy ratios. A higher increase in anisotropy was seen in noncompact white matter, but the difference was not statistically significant. A higher increase in anisotropy was seen in the frontal—parietal white matter and corona radiata than in the internal capsule and corpus callosum, but the differences were not statistically significant.
|
TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
|---|
Recently, different MR imaging sequences, such as phase-sensitive inversion recovery, magnetization transfer, and diffusion-weighted, have been applied to assess myelination [7, 17, 18]. Initial diffusion-weighted imaging studies investigating brain maturation used diffusion-weighted images obtained by applying diffusion gradients in three or fewer orthogonal directions rather than the six required for determination of the rotationally invariant diffusion tensor [6, 19,20,21]. One study evaluated myelination in the frontal and occipital lobe white matter in neonates, infants, and children by applying diffusion gradients in two directions. These investigators found that by the age of 6 months, infants exhibit the same pattern of myelination seen in adults [20]. Another study used three-direction (so-called trace) diffusion-weighted imaging to examine 30 pediatric patients ranging in age from 1 day to 17 years. These investigators reported that apparent anisotropy in compact white matter was higher than that in the noncompact white matter structures of the corona radiata and centrum semiovale [6]. These investigators also reported age-related increases in anisotropy in all white matter structures evaluated, and they observed that anisotropy values had increased in children by the age of 3 years to the value seen in adults [6]. However, studies using fewer than six directions for diffusion-weighted imaging are limited because anisotropy measurements are inaccurate as a result of the inability to fully trace the diffusion tensor. Diffusion tensor imaging is not biased by variables such as white matter fiber orientation that might occur with other forms of diffusion-weighted imaging [22].
More recently, studies have applied diffusion tensor imaging to the evaluation of brain maturation [7, 8]. In one study, 22 neonates of various gestational ages were reported to have lower anisotropy values than adults; in some instances, anisotropy values were found to correlate with gestational age [8]. However, the patient population in that study consisted solely of neonates. A more recent diffusion tensor imaging report of 153 pediatric patients who varied in age from 1 day to 11 years identified stereotypic time courses of anisotropy changes associated with brain development in central white matter [7]. However, that study assessed solely compact white matter structures, such as the corpus callosum and internal capsule, and therefore differs from our study. Based on these findings shown by previous investigators, our objective was to compare rates of anisotropy increases in compact white matter with those seen in noncompact white matter. One recent diffusion tensor imaging study showed that substantial increases in anisotropy were seen in both the genu of the corpus callosum and the frontal white matter in children without brain abnormalities [23]. However, that study did not specifically focus on the degree of change at various ages and included a smaller population of neonates, in whom anisotropy changes would be expected to be greatest, than our study.
The age-related changes in anisotropy appear to reflect well-described histologic changes. With increasing maturity, myelin proliferates and maturing neurons and glia increase in size. These internal microscopic changes of myelination lead to a decrease in the size of the extracellular space with less water diffusion and higher anisotropy [9]. These histologic changes of myelination occur at different rates in various white matter tracts. One of the purposes of this study was to compare the rates of increasing anisotropy, thought to reflect increases in myelination, in two types of white matter structures: compact and noncompact white matter. To our knowledge, comparisons of the rate of change in anisotropy between different types of white matter have not been previously described.
Our findings showed that anisotropy is higher in compact than noncompact white matter in all three age groups studied. These differences were shown to be statistically significant for most direct comparisons of individual white matter regions as well as for comparisons of groups of white matter (i.e., compact and noncompact white matter) within each age group. Therefore, our first hypothesis—that is, anisotropy values are higher in compact white matter structures—was verified. Measurements of anisotropy are sensitive to tissue microstructure, which includes microscopic factors (degree of myelination, tissue hydration, and fiber diameter) and macroscopic factors (regularity or order of axonal orientation) [8]. Anisotropy tends be highest in regions in which the white matter is packed into essentially parallel bundles and in those regions with greatest myelination.
Compact white matter structures have relatively high degrees of axonal packing and relatively high degrees of myelination; therefore, these characteristics account for the higher anisotropy ratios recorded along these fiber tracts. In contrast, noncompact white matter initially has neither high degrees of axonal packing nor extensive myelination. Therefore, comparatively lower measured anisotropy ratios would be expected along these white matter tracts, as reported in this study and another study [6].
This relationship of relative anisotropy values remains consistent whether the noncompact and compact white matter regions are considered as individual structures or as a group of structures because the properties of axonal packing and the degree of myelination do not change. The consistency of these relationships account for the finding of highest anisotropy at birth in the corpus callosum, internal capsule, and cerebral peduncle, respectively, and the lowest anisotropy in the corona radiata and frontal—parietal white matter, respectively. Changes in anisotropy during early childhood, however, would primarily reflect myelination because the orientation of white matter tracts would not be expected to change significantly. Other changes associated with brain maturation, such as total water content of the brain and development of cellular components, likely also account for changes in white matter anisotropy. However, these variables are believed to be less important than axon myelination in producing differences in anisotropy measurements between various white matter structures during early childhood [24, 25].
Comparison of changes in anisotropy in our patients showed a proportionally greater increase in anisotropy in noncompact than compact white matter in all three age groups. Group 1 and group 3 showed a statistically significant difference in the increase in anisotropy in noncompact white matter compared with compact white matter. Therefore, our second hypothesis was verified. Although anisotropy in noncompact white matter structures is less than that seen in compact white matter structures during infancy (as well as later in childhood), the increase of anisotropy is greater in noncompact white matter structures than in compact white matter structures during the first few years of life after infancy. This finding is in agreement with previous histologic studies of the myelination process [10, 11]. In these studies, compact white matter structures, which have completed a greater percentage of the myelination process than noncompact white matter structures before 1 year of age, have been found to myelinate at a slower rate after the first year of life than noncompact white matter structures [10, 11].
The anisotropy measurements in compact white matter structures in our study were similar to those seen in previous studies, including a progressive age-related increase in anisotropy that was greatest during the first few years of life [6,7,8]. Two regions of noncompact white matter in our investigation also showed similar age-related increases in anisotropy. Comparison between group 1 and group 3 of anisotropy changes in frontal—parietal white matter with measurements in the internal capsule showed a statistically significant difference, and comparison with the corpus callosum revealed a nearly statistically significant difference. The noncompact white matter tract of frontal—parietal white matter showed a greater percentage increase in anisotropy than that measured in the individual compact white matter structures during the time period evaluated. Comparison of anisotropy in the other noncompact white matter area, the corona radiata, revealed a greater increase in anisotropy than in the internal capsule and corpus callosum during the same time period, but this difference was not statistically significant. Therefore, whether considered as a group of white matter tracts (noncompact white matter) or as individual white matter tracts (the frontal—parietal white matter and the corona radiata), these peripheral white matter fibers have a greater percentage increase in anisotropy during the first few years of life after infancy than do central compact white matter structures. These findings imply that more myelination occurs in noncompact white matter than in compact white matter because anisotropy has been shown to correlate with myelin growth [9, 12].
Interestingly, our investigation also showed differences in the degree of anisotropy increases between fiber tracts with the same type of axonal organization. Comparisons across group 1 and group 3 of differences in anisotropy among the corpus callosum, the internal capsule, and the cerebral peduncle showed a greater percentage increase in myelination in the corpus callosum, followed by the cerebral peduncle; however, these findings were not statistically significant. The difference between the increase of anisotropy in the corona radiata and in the frontal—parietal white matter, both areas of noncompact white matter, was also not statistically significant.
The anisotropy values in our study tended to be of higher magnitude than those measured in previous studies [7, 8]. This discrepancy may reflect differences in patient populations or methodologic differences related to the placement of the ROIs. For instance, we specifically sought the area of highest anisotropy, which was determined after moving a standard-sized ROI through the general region of highest anisotropy as depicted on a color-coded map. In one previous study, anisotropy values were also obtained by relying on the identification of visible anisotropy within the central portion of each structure but without regard for internal variation within each structure [7]. Although our method should not cause internal discrepancy concerning comparison of anisotropy changes of various structures, it may limit direct comparison of anisotropy values with other studies if our technique is not used. Signal-to-noise ratio is another factor that can influence anisotropy values. For instance, low signal-to-noise ratios can cause overestimation of anisotropy in areas of low anisotropy. This factor was unlikely to have affected our study because almost all the examinations in our study were performed using a 2-excitation tensor pulse sequence, which is known to improve signal-to-noise ratios compared with the 1-excitation tensor sequence in use at many institutions. Differences in the examination times or the absence of cardiac gating might also contribute to differences in relative magnitudes of anisotropy observed in otherwise similar studies [22].
In summary, we found that regions of non-compact white matter, such as the frontal—parietal white matter and the corona radiata, initially have lower anisotropy values than those found in compact white matter structures, such as the corpus callosum, posterior limb of the internal capsule, and the cerebral peduncle. However, increases in anisotropy after the first year of life are proportionally greater in noncompact white matter. Changes in anisotropy have been shown to correlate with changes in myelination [9, 12]. Therefore, our findings appear to indicate that myelination occurs at a faster rate in noncompact white matter after the first year of life, a finding that has been substantiated by histologic studies [10, 11].
The anisotropy measurements in our study may serve as a baseline against which similar measurements in various white matter diseases may be compared. Future studies comparing the increase in anisotropy in pediatric patients who have white matter disorders against the normal values provided in our study may prove valuable for understanding these disorders and assessing therapies.
Acknowledgments
We thank David DeLong, Duke University Medical Center, Durham, NC, for
assistance with statistical analysis used in this investigation.
|
TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
|---|
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
This article has been cited by other articles:
|
|
 |
|
  M. I. Makki, R. Munian Govindan, B. J. Wilson, M. E. Behen, and H. T. Chugani Altered Fronto-Striato-Thalamic Connectivity in Children with Tourette Syndrome Assessed with Diffusion Tensor MRI and Probabilistic Fiber Tracking J Child Neurol, June 1, 2009; 24(6): 669 - 678. [Abstract] [PDF]
|
|
|
|
 |
|
 H. Chahboune, L. R. Ment, W. B. Stewart, D. L. Rothman, F. M. Vaccarino, F. Hyder, and M. L. Schwartz Hypoxic Injury during Neonatal Development in Murine Brain: Correlation between In Vivo DTI Findings and Behavioral Assessment Cereb Cortex, April 20, 2009; (2009) bhp068v1. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 W. Gao, W. Lin, Y. Chen, G. Gerig, J.K. Smith, V. Jewells, and J.H. Gilmore Temporal and Spatial Development of Axonal Maturation and Myelination of White Matter in the Developing Brain AJNR Am. J. Neuroradiol., February 1, 2009; 30(2): 290 - 296. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Mukherjee, J.I. Berman, S.W. Chung, C.P. Hess, and R.G. Henry Diffusion Tensor MR Imaging and Fiber Tractography: Theoretic Underpinnings AJNR Am. J. Neuroradiol., April 1, 2008; 29(4): 632 - 641. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M.I. Makki, D.C. Chugani, J. Janisse, and H.T. Chugani Characteristics of Abnormal Diffusivity in Normal-Appearing White Matter Investigated with Diffusion Tensor MR Imaging in Tuberous Sclerosis Complex AJNR Am. J. Neuroradiol., October 1, 2007; 28(9): 1662 - 1667. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. M. Provenzale, L. Liang, D. DeLong, and L. E. White Diffusion Tensor Imaging Assessment of Brain White Matter Maturation During the First Postnatal Year Am. J. Roentgenol., August 1, 2007; 189(2): 476 - 486. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. D. Warner, M. Behnke, F. D. Eyler, K. Padgett, C. Leonard, W. Hou, C. W. Garvan, I. M. Schmalfuss, and S. J. Blackband Diffusion Tensor Imaging of Frontal White Matter and Executive Functioning in Cocaine-Exposed Children Pediatrics, November 1, 2006; 118(5): 2014 - 2024. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. M. Provenzale, S. Mukundan, and D. P. Barboriak Diffusion-weighted and Perfusion MR Imaging for Brain Tumor Characterization and Assessment of Treatment Response. Radiology, June 1, 2006; 239(3): 632 - 649. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. Barnea-Goraly, V. Menon, M. Eckert, L. Tamm, R. Bammer, A. Karchemskiy, C. C. Dant, and A. L. Reiss White Matter Development During Childhood and Adolescence: A Cross-sectional Diffusion Tensor Imaging Study Cereb Cortex, December 1, 2005; 15(12): 1848 - 1854. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. McGraw, L. Liang, M. Escolar, S. Mukundan, J. Kurtzberg, and J. M. Provenzale Krabbe Disease Treated with Hematopoietic Stem Cell Transplantation: Serial Assessment of Anisotropy Measurements--Initial Experience Radiology, July 1, 2005; 236(1): 221 - 230. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. van Pul, J. Buijs, M. J. A. Janssen, G. F. Roos, M. T. Vlaardingerbroek, and P. F. F. Wijn Selecting the Best Index for Following the Temporal Evolution of Apparent Diffusion Coefficient and Diffusion Anisotropy After Hypoxic-Ischemic White Matter Injury in Neonates AJNR Am. J. Neuroradiol., March 1, 2005; 26(3): 469 - 481. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. M. Provenzale, P. McGraw, P. Mhatre, A. C. Guo, and D. Delong Peritumoral Brain Regions in Gliomas and Meningiomas: Investigation with Isotropic Diffusion-weighted MR Imaging and Diffusion-Tensor MR Imaging Radiology, August 1, 2004; 232(2): 451 - 460. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. Zhai, W. Lin, K. P. Wilber, G. Gerig, and J. H. Gilmore Comparisons of Regional White Matter Diffusion in Healthy Neonates and Adults Performed with a 3.0-T Head-only MR Imaging Unit Radiology, December 1, 2003; 229(3): 673 - 681. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
