(Radiology. 1999;212:761-762.)
© RSNA, 1999
The Radial Bands Sign1
Timothy A. Bernauer, MD
1 From the Department of Radiology, Indiana University Medical Center, Indianapolis. Received March 30, 1998; revision requested May 6; revision received July 22; accepted January 7, 1999. Address reprint requests to the author, 16 Southbrooke Place, Mt Zion, IL 62549.
Index terms: Brain, diseases, 13.1832, 30.1832 • Brain, MR, 13.121411, 13.121413, 13.121417 • Nervous system, diseases, 13.1832, 30.1832 • Signs in Imaging, 13.1832
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APPEARANCE
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The radial bands sign is a finding that is sometimes seen on magnetic resonance (MR) images of the brain (1). Images with this finding show linear or curvilinear areas of abnormal signal intensity that extend in a radial fashion from the periventricular to subcortical regions of the cerebral hemispheres (Figs 1, 2).
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Figure 1. Radial bands sign. Axial fluid-attenuated inversion-recovery MR image (repetition time msec/echo time msec/inversion time msec, 10,002/148/2,200) through the upper lateral ventricles shows linear areas of abnormal white matter with high signal intensity (arrows) extending from the periventricular to subcortical regions of the cerebral hemispheres.
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Figure 2. Radial bands sign. Axial, T1-weighted magnetization transfer image (repetition time msec/echo time msec, 500/9) obtained in the same patient as in Figure 1 after administration of a gadolinium-based contrast material, shows the same radiating linear white matter lesions (arrows) as those in Figure 1.
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EXPLANATION
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The radial bands sign is believed by some authors to represent a manifestation of abnormal migration of dysplastic stem cells along the course of the radial glial-neuronal unit in patients with tuberous sclerosis (1–3). This finding has also been called migration tracts or linear abnormalities (2,4). The abnormal signal intensity of the white matter in the radial bands sign represents clusters of giant cells with varying neuronal differentiation, astrocytic differentiation, and cells that are not easily classified (1,5,6). The same giant cell can differ in classification with different histologic techniques. This suggests that tuberous sclerosis may be the product of a dysgenetic event that occurs early in development and results in cells with aberrant or incomplete astrocytic or neuronal differentiation.
Similar histopathologic features are found in the other major intracranial manifestations of tuberous sclerosis (1). The abnormal signal intensity of the white matter lesions presumably relates to a lack of normal myelination and to differences in cellular or interstitial fluid content compared with these findings in the normal brain parenchyma.
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DISCUSSION
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Tuberous sclerosis was described by von Recklinghausen (7). Bourneville (8), who provided a detailed report of the neurologic symptoms and gross cerebral pathologic features of tuberous sclerosis, identified it as a distinct clinical syndrome. Tuberous sclerosis is now recognized as the second most frequently occurring neurocutaneous syndrome after neurofibromatosis type 1 (9) and is characterized by dysplasias and neoplasias of organs derived from all three embryonic germ layers (1). The clinical diagnosis of this disease in the past typically depended on the identification of the characteristic cutaneous manifestations of tuberous sclerosis and the classic triad of seizures, mental retardation, and facial angiofibromas. The advent of diagnostic radiology and subsequent improvements in imaging technology have since altered the approach to diagnosing tuberous sclerosis.
The four major intracranial manifestations of tuberous sclerosis are subependymal nodules, subependymal giant cell astrocytomas, cortical tubers, and white matter abnormalities (1). Before the use of cross-sectional imaging, only the periventricular manifestations could be discerned radiologically. Conventional radiographs showed the calcifications within subependymal nodules in a minority of cases. Pneumoencephalography demonstrated the characteristic "candle wax" appearance of periventricular lesions, but this procedure was invasive. Computed tomography (CT) and MR imaging have revolutionized the radiologic evaluation of this disorder in the past few decades; these modalities now enable confident diagnosis in virtually all cases (6).
Numerous white matter abnormalities have been identified by using cross-sectional imaging. These include wedge-shaped, tumefactive, and linear or curvilinear (ie, radial band) lesions in the cerebral hemispheres and multiple linear bands extending from a conglomerate focus near the fourth ventricle into the cerebellar hemispheres (1). Migration tracts may be seen connecting with cortical tubers, subependymal nodules, or both (4). The migration tracts are almost always hypointense to isointense on T1-weighted images and hyperintense on T2-weighted images in adults. In neonates and young children, they are hyperintense to premyelinated white matter on T1-weighted images and isointense to hypointense compared with premyelinated white matter on T2-weighted images (1). For unknown reasons, enhancement after contrast material administration is seen in a minority of cases.
White matter abnormalities are commonly seen at CT, but they are generally more numerous and conspicuous at MR imaging (4,9). Magnetization transfer and fluid-attenuated inversion-recovery images are particularly sensitive to these abnormalities; these modalities have shown substantially more lesions than has CT or other MR images in previous studies (10,11). Consequently, MR imaging findings may be dominated by white matter changes in some patients with tuberous sclerosis. Visualization of radial bands, which appear to be specific to tuberous sclerosis (1), may be helpful in distinguishing this disease from other possible entities such as demyelinating or dysmyelinating processes, infection, tumor, or ischemic changes. This is particularly true when subependymal nodules and cortical tubers are inconspicuous, and visualization of the radial bands should lead the observer to review the imaging study closely for these findings (Fig 3).
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Figure 3. Coronal T2-weighted fast multiplanar inversion-recovery image (5,000/108/120) obtained in the same patient as in Figures 1 and 2 shows a cortical tuber (arrow) in the right temporal lobe. A few small (2-3-mm) subependymal nodules (not shown) also were present.
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At pathologic examination, the white matter lesions of tuberous sclerosis show clusters of giant cells that characteristically align in rows that appear to follow the path of neuronal migration tracts (1). This distribution closely resembles the patterns of heterotopic gray matter distribution and thus suggests that the cerebral manifestations of tuberous sclerosis may be due to abnormal migration of dysplastic cells from the germinal zone (1). In theory, the dysplastic stem cells give rise to dysplastic glia and neurons that are unable to differentiate, migrate, or organize properly (2). It is hoped that future clinical and laboratory studies will substantiate this hypothesis and lead to a better understanding of the pathogenesis of the cerebral abnormalities in tuberous sclerosis.
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References
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Bourneville DM. Contribution a l'etude de l'idiote. Arch Neurol 1882; 1:81-91.
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