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Pediatric Imaging |
1 From the Institute of Diagnostic Radiology, Heinrich-Heine-University of Düsseldorf, PO Box 101007, D-40001 Düsseldorf, Germany. Received February 20, 2001; revision requested March 21; revision received June 11; accepted July 5. Address correspondence to V.E. (e-mail: engelbre@uni-duesseldorf.de).
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTS DISCUSSIONREFERENCES |
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MATERIALS AND METHODS: Diffusion-weighted magnetic resonance (MR) imaging was performed in 44 children (age range, 7 days to 7.5 years) without brain abnormalities and in 13 children with proved leukodystrophy. Apparent diffusion coefficient (ADC) and apparent anisotropy (AA) were measured in 11 regions of interest within white matter. Age-related changes were analyzed with regression analysis.
RESULTS: During normal brain myelination, ADCs in different anatomic regions were high at birth (range, 1.04 x 10-9 m2/sec ± 0.05 [SD] to 1.64 x 10-9 m2/sec ± 0.09) and low after brain maturation (range, 0.75 x 10-9 m2/sec ± 0.02 to 0.92 x 10-9 m2/sec ± 0.02). AA was low at birth (range, 0.05 ± 0.01 to 0.52 ± 0.04) and high after brain maturation (range, 0.25 ± 0.02 to 0.85 ± 0.03). Age relationship could be expressed with monoexponential functions for all anatomic regions. Anisotropy preceded the myelination-related changes at MR imaging. ADC and AA in four children with Pelizaeus-Merzbacher disease were identical with results in healthy newborn children and showed no age dependency. In peroxisomal disorders, Krabbe disease, and mitochondriopathy, demyelination on T1- and T2-weighted MR images led to expected findings at diffusion-weighted MR imaging, with high ADC and low AA, whereas in Canavan disease and metachromatic leukodystrophy, the opposite findings were revealed, with low ADC within the demyelinated white matter.
CONCLUSION: During early brain myelination, diffusion restriction in normal white matter increases. Anisotropy precedes myelination changes that are visible at MR imaging. Compared with T1- and T2-weighted MR imaging, diffusion-weighted MR imaging in white matter diseases reveals additional information.
Index terms: Brain, diseases, 13.871, 13.873, 15.871, 15.873 • Brain, white matter, 13.87 • Magnetic resonance (MR), diffusion study, 13.12144, 15.12144 • Myelin
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTS DISCUSSIONREFERENCES |
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ADC values have been measured in the brain in adults and children (4–10). These studies revealed that ADC values in the white matter in adults and children during 1 year are generally lower than those in neonates, whereas anisotropy is higher with increasing age. Changes in water diffusion, including the development of anisotropic motion, are expected to parallel the known course of maturation of the brain, especially in the white matter, as has been shown in animal models (11). The number of children with a normal brain older than neonatal age and younger than 2 years in whom ADC values were reported is still small (4,6,9). This age group, however, is of interest for comparison between MR assessment of myelination and diffusion-weighted MR imaging because age-related changes in signal intensity are visible predominantly during the first 2 years of life (12).
Whereas acute ischemia leads to cytotoxic edema with diffusion restriction and decreased ADC values, vasogenic edema with increased water motion in the extracellular space shows increased ADC values (13). Increased ADC values are seen especially in subacute and chronic ischemia, in inflammatory brain diseases, and in peritumoral edema (13). Leukodystrophies are characterized by destruction of myelin and by increased water in the extracellular space, which might lead to increased ADC values and a decrease of anisotropy. However, results of diffusion-weighted MR imaging of the brain in leukodystrophies are still limited (14–17). The purpose of our study was to establish quantitative standards for the age-related changes in diffusion restriction of cerebral white matter in children with a normal brain and to compare the data with the results in children with white matter diseases.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTS DISCUSSIONREFERENCES |
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MR imaging performed in 101 of the 173 children revealed a broad variety of pathologic changes. Among these were ischemic lesions, brain tumors, encephalitis, congenital abnormalities, and white matter diseases (in 13 children). Twenty-eight of the 173 children without pathologic changes at MR imaging were excluded because of clinical signs of developmental delay or because clinical data were insufficient.
The remaining 44 of the 173 children were selected for further evaluation to establish quantitative standards for diffusion MR imaging. By using the guidelines of Barkovich et al (12) and of van der Knaap and Valk (18), the MR images in these children were evaluated independently by two authors (V.E., A.S.), and they disclosed a normal degree of myelination and no pathologic changes. The indication for MR examination in these children varied; MR examination was performed for analysis in children who had seizures and in children who were suspected of having a brain tumor or encephalitis. Children with a developmental delay were excluded on the basis of findings of a complete clinical examination performed by the pediatric neurologist. Children’s age was corrected for prematurity and ranged from 1 week to 89 months, with a mean age of 24.7 months. Twenty-three children were male and 21 were female. No child was examined more than once. The age distribution of 44 children without brain abnormalities is included in Table 1.
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Image postprocessing was performed with a workstation (Ultrasparc 1; Sun Microsystems, Mountain View, Calif) and homebuilt software. On three images per section, the ADC was calculated and gray-scale encoded, with the diffusion-sensitizing gradient in x, y, and z directions. On a fourth image, the directionally averaged ADC was calculated and gray-scale encoded as the average of the three directional coefficients. The postprocessed images were transferred to a computer, where signal intensity measurement in regions of interest (ROIs) was performed with software (Osiris; University Hospital of Geneva, Switzerland). Polygonal and circular ROIs with a minimum pixel size of 20 were hand placed by two authors (V.E., A.S.), in consensus, on reference scans (b value = 0 sec/mm2) in 11 predefined anatomic areas (the cerebrospinal fluid, the frontal and occipital white matter, the genu and splenium of the corpus callosum, the anterior and posterior limbs of the internal capsule, the mesencephalon [midbrain], the anterior and posterior pons, and the middle cerebellar peduncle).
The system’s software automatically transferred the ROIs to the same regions on the three corresponding diffusion-weighted images (b value = 1,000 sec/mm2). The ADC value was measured within the ROI as a mean and SD. Apparent anisotropy (AA) was calculated with the measured ADC values by using the equation: AA = (ADCmax - ADCmin)/ ADCmax, where ADCmax is the highest of the three directional coefficients and ADCmin is the lowest. Data analysis was performed with a computer (Mac II; Apple, Cupertino, Calif) by using software (KALEIDAGRAPH 2.1.3; Synergy Software, Reading, Pa). A nonlinear least squares Marquardt algorithm was used for each anatomic region to fit the ADC and AA values with the children’s age to a monoexponential function. In addition, alternative models with spline functions were applied.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTS DISCUSSIONREFERENCES |
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Different results were seen in the children with Canavan disease and MLD. On images obtained in the 17-month-old boy with Canavan disease, demyelination in the outer parts of white matter was revealed, whereas the periventricular areas showed a normal signal intensity. In contrast to findings in the other children with leukodystrophies, ADC values (range, [0.81–0.92] x 10-9 m2/sec) within the demyelinated white matter were normal or lower (Fig 7). AA values were within the normal range. Findings at MR imaging of the brain in the 4
-year-old child with MLD disclosed severely demyelinated central white matter. The ADC values (range, [0.67–0.78] x 10-9 m2/sec) within these regions, especially within the corpus callosum, were lower, whereas ADC within demyelinated white matter of outer parts of the centrum semiovale was mildly increased (range, [1.1–1.2] x 10-9 m2/sec). Instead of the restricted diffusion in the corpus callosum, AA values (range, 0.08–0.10) revealed an almost complete loss of apparent anisotropy (Fig 8).
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTS DISCUSSIONREFERENCES |
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Although the ADC value is best determined from many b values, two-point fits, as performed in our examinations, have become a standard practice and yield reproducible and accurate ADC values within a short imaging time (20,21). With diffusion-weighted MR imaging, the signal intensity in white matter in the brain depends on the direction of the diffusion-sensitizing gradient. These signal intensity differences, owing to anisotropy, can be eliminated by acquiring the diffusion tensor (22). To characterize diffusion within a tract completely, it is necessary to measure the diffusion along a large number of at least six directions. Because this is time consuming, we acquired directional-independent ADC images by averaging three ADC maps measured with diffusion gradients along orthogonal axes. This process enables the comparison of our database for the ADC values in children from infancy through early adulthood with examination findings in other groups because almost all clinical sites that perform diffusion imaging use the three-axis approach (9,19).
In the white matter in the brain in newborns, we found the highest ADC values in the centrum semiovale. These results compare favorably with data from other researchers (7,9,10) who performed diffusion-weighted MR imaging in preterm and term neonates, whereas our ADC values are slightly higher than equivalent measurements made by Huppi et al (8) and somewhat lower than those made by Toft et al (5). However, the latter data were acquired with a measurement technique in which the diffusion-sensitizing gradient was applied along only a single direction. The lowest ADC values in newborns were found in the posterior limb of the internal capsule, the middle cerebellar peduncle, the mesencephalon, and the dorsal pons. Very few results for these regions are in the literature. For the posterior limb of the internal capsule, our data are confirmed by findings in studies of Neil et al (7) and Morriss et al (9); however, we found slightly lower ADC values in the dorsal pons and the mesencephalon than did Morriss et al (9).
Owing to the regression analysis we performed with the data in the children in this study, calculation of the theoretical ADC values in the newborn was possible. In the equation y = a - b x e-x/c, the term a - b represents the ADC value in a term newborn. Signal intensity measurements in ROIs are especially critical in newborns because of the small size of the anatomic structures and the low signal-to-noise ratio. Thus, our calculated ADC values might be more reliable because of a more comprehensive database.
ADC values decrease during brain myelination, which leads to a reduced contrast between gray and white matter on ADC images. Our data from newborn to early childhood confirm the results of Nomura et al (4), who performed single-section diffusion-weighted MR imaging in 32 newborns and children, and the data from Morriss et al (9), who performed multisection diffusion-weighted MR imaging in 30 newborns and children. Morriss et al (9) presented their results in tables with ADC values for seven age groups, but we tried to establish normative graphs with the age dependency of ADC values in 11 anatomic regions. We found that monoexponential functions reliably expressed the age dependency.
From these graphs, we were able to calculate a theoretic ADC level for the time after complete brain maturation. The lowest ADC values were in the corpus callosum, the mesencephalon, the middle cerebellar peduncle, and the pons. In comparison with the results in the brain of the newborn, the differences in ADC values among the different anatomic regions were small. We compared our results with ADC values in young healthy adults and found good correspondence (4,10,23,24). In adults older than 40 years, high ADC values were found in cerebral white matter with increasing age. This finding may be caused by increased extracellular water volume (23).
The decrease in diffusion in the white matter during brain maturation has been explained initially in terms of the development of myelin, which acts as a barrier to diffusion (4–6). All diffusion-weighted MR imaging examination findings in the maturing brain confirmed diffusion restriction before the onset of visible myelination signs on T1- or T2-weighted MR images. Additionally, animal study findings revealed diffusion restriction before myelination (11,25). Thus, additional points must be named to explain the decreasing ADC values during brain myelination. Here, water loss in the developing brain (7), early wrapping of axons by the oligodendroglial process (8), increasing concentration of the macromolecule, a greater membrane surface-to-cell volume ratio (25), and an increase in axonal diameters and in microtubule-associated proteins (11) must be addressed.
Examination of diffusion anisotropy is another approach to describe diffusion restriction in the maturing brain. First, anisotropy has been described qualitatively by signal intensity changes on diffusion-weighted MR images with differently oriented diffusion-sensitizing gradients. For a more quantitative approach, anisotropy has been estimated by calculation of the so-called anisotropic ratios. The values of ADC (90) in which the diffusion-sensitive gradients were perpendicular to the white matter fibers and of ADC (0) in which the gradients were parallel to the neurofibers were calculated. Then, the anisotropic ratio (ADC [90]/ADC [0]) was calculated (6). Scatterplots of age dependency of these anisotropic ratios in the optic radiation and the frontal lobe disclosed curves similar to those in our graphs of age dependency of apparent anisotropy. Morriss et al (9) proposed the use of a calculated AA value that can be obtained from three ADC images with orthogonal diffusion-sensitizing gradients.
We used this simple approach to establish a normative database of AA values in subjects from newborn to early adulthood. However, it must be kept in mind that this method works well only if the fibers are aligned perfectly within the gradient direction. In all other cases, the anisotropy will be underestimated (9,19). Until now, diffusion anisotropy measurement, performed by using diffusion-tensor MR imaging, has only been performed in preterm and term infants (7,8). A comparison of AA values with results from diffusion-tensor MR imaging in the maturing brain would be a promising approach to further evaluate the suitability of AA values in the brain of children to describe the degree of diffusion anisotropy.
Only few results from diffusion-weighted MR imaging in the brain in children with white matter diseases have been reported. These results were in a child with PMD (15), a child with Alexander disease and a child with Krabbe disease (16), 11 children with ALD (17), and four children with white matter demyelination in congenital muscular dystrophy (14). In the latter four children, however, only diffusion-weighted MR imaging without ADC calculation was performed. Therefore, changes in diffusion could not be differentiated from changes in T2. We examined four children with genetically proved PMD. This rare X-linked disease is characterized by dysmyelination of the central nervous system and is associated with mutations in the PLP gene (26). Instead of the reported heterogeneity of the phenotypes in this disease, findings in these four children were relatively uniform, with an almost total lack of myelination, at MR imaging examination.
All patients had increased ADC values without age-related changes. Despite the lack of myelination on T1- and T2-weighted MR images, we found clear signs of anisotropy in regions with tightly packed fibers, such as the corpus callosum. This underlines the fact that diffusion restriction and anisotropy can be seen without brain myelination. To our knowledge, the only case reported so far with diffusion-weighted MR imaging in PMD disclosed similar results. Despite the nonprogressive hypomyelination of white matter, findings of the diffusion-weighted MR imaging examination proved clearly that anisotropy existed in the cerebral white matter in this child with PMD (15). Diffusion-weighted MR imaging in an animal study with the jimpy mouse as a model of dysmyelination in PMD revealed normal or subnormal anisotropy, but diffusion-weighted MR imaging in the twitcher mouse as a model for demyelination in Krabbe disease disclosed markedly reduced diffusional anisotropy (27).
The same authors (16) reported the case of a child with Krabbe disease in whom diffusional anisotropy was lost in areas with demyelination. The child with Krabbe disease in our study showed increased ADC values and loss of anisotropy within demyelinated white matter lesions. The changes can be explained by a breakdown of myelin and a destruction of the axons and, thus, a loss of diffusion barriers. The same mechanism can be discussed with respect to children who have demyelination caused by ALD, Zellweger syndrome, and Leigh disease in whom we found increased ADC and reduced AA within demyelinated white matter. Melhelm et al (17) found significantly lower ADC values and higher fractional anisotropy values in affected white matter of patients with proved ALD.
In our study group, one child with genetically proved ALD and an unknown phenotype had slightly increased ADC values in white matter areas without signs of demyelination. Because early differentiation between childhood ALD and adrenomyeloneuropathy, the so-called adult-type ALD, is essential for the earliest possible beginning of bone marrow transplantation in childhood ALD, further examinations should be performed to investigate if diffusion-weighted MR imaging is a helpful tool for early differentiation between these two phenotypes of ALD.
We obtained unexpected results in the diffusion-weighted MR imaging examinations in the child with Canavan disease and the child with MLD. In Canavan disease, an autosomal recessive disease caused by a reduced activity of the enzyme aspartoacylase, demyelination spreads centripetally, with the most severe abnormalities being in the subcortical white matter. Instead of the severe demyelination signs on MR images, the ADC values in the child in this study were clearly reduced within the demyelinated white matter, which indicated a further reduced diffusivity. ADC values in normal-appearing white matter were normal, and AA values in the still normal-appearing corpus callosum were within the normal range. The child with MLD, an autosomal recessive disorder caused by reduced activity of the enzyme arylsulfatase A, had severe demyelination of white matter from which only small subcortical areas were spared.
ADC values in the inner parts of the centrum semiovale and in the corpus callosum were clearly reduced, whereas ADC values in peripheral areas of demyelination at the border to normal-appearing white matter were slightly increased. AA values in the severely demyelinated corpus callosum were almost completely lost. This unexpected finding—reduced ADC values in demyelinated white matter—might be explained by histologic findings. The reduced activity of arylsulfatase A results in accumulation of sulfatides within the oligodendrocytes. This progressive increase in sulfatides and decrease in cerebrosides results in increasing instability of the myelin membrane with subsequent demyelination. The metachromatic material (mainly the sulfatides) is stored in the cytoplasm of proliferated glia cells and macrophages (28). The inclusions are bound by a membrane of lysosomal origin.
All these changes can cause diffusion restriction as water is bound to an increasing amount of macromolecules and the number of membranes, especially lysosomal membranes, is increased. Histologically, a relative sparing of the axons in the demyelinated areas in MLD was found. The loss of AA in the corpus callosum is difficult to explain. Most probably, the increase in membranes and macromolecules leads to a randomly oriented diffusion restriction that exceeds the anisotropic diffusion restriction of the naked axons in the corpus callosum. The most striking histologic findings in Canavan disease are myelin vacuolation and loss accompanied by severe astrogliosis (29). At electron microscopy, the vacuoles are formed as a result of separation of myelin layers, with intramyelinic vacuole formation. These changes lead to an increase in the distance between the currently unorganized myelin layers, which might explain the lower ADC values and the loss of AA.
In conclusion, this study reveals a normative database of diffusion-weighted MR imaging findings in children at different ages from newborn to early adulthood, with graphs that represent the age dependency of ADC and the AA values; in children with dysmyelination or demyelination of white matter, diffusion-weighted MR imaging provides information that is not apparent on conventional T1- or T2-weighted MR images. Our results show that diffusion restriction precedes brain myelination and is further increased during myelination.
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FOOTNOTES |
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Author contributions: Guarantors of integrity of entire study, V.E., A.S., M.R.; study concepts, V.E., M.R.; study design, V.E.; literature research, V.E., M.R.; clinical studies, V.E., A.S.; data acquisition, V.E., A.S., M.R.; data analysis/interpretation, V.E., A.S., H.J.W.; statistical analysis, V.E., M.R., H.J.W.; manuscript preparation and editing, V.E., A.S.; manuscript definition of intellectual content, V.E., A.S., M.R., H.J.W.; manuscript revision/review and final version approval, all authors.
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTS DISCUSSIONREFERENCES |
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) compared with the values in children without brain diseases (
). Whereas AA values in normal white matter in older children were clearly higher than they were in younger children, patients with PMD revealed no age-dependent differences in AA.
