DOI: 10.1148/radiol.2392040224
(Radiology 2006;239:607-609.)
© RSNA, 2006
The Posterior Vertebral Scalloping Sign1
Suzanne L. Wakely, MD
1 From the Department of Radiology, Southampton General Hospital, Tremona Rd, Shirley, Southampton SO16 6YD, England. Received February 5, 2004; revision requested April 13; revision received April 29; accepted May 24.
Address correspondence to the author (e-mail: swakely{at}radiol.cam.ac.uk).
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APPEARANCE
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The posterior vertebral scalloping sign appears on a lateral radiograph of the spine as an exaggeration of the normal concavity of the posterior surface of one or more vertebral bodies (Fig 1a) (1). This sign can also be seen in images created with computed tomography (CT) and MR imaging of the spine in the transverse and sagittal planes.
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Figure 1a: Images of a 52-year-old woman with a long-standing, previously partially resected lipoma of the medullary cone and the cauda equina. (a) Lateral radiograph of the lumbar spine demonstrates florid posterior vertebral scalloping (arrows), which is maximal at L1 through L2. (b) Sagittal T1-weighted spin-echo 420/25 (repetition time msec/echo time msec) magnetic resonance (MR) image in the same patient demonstrates an extensive, principally high-signal-intensity intradural mass (arrows) which expands the spinal canal and causes posterior vertebral scalloping.
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EXPLANATION
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A minor degree of concavity in the posterior vertebrae is a normal physiologic variation and has been demonstrated in over 50% (56 of 100) of otherwise healthy individuals (1,2). However, there are a number of pathologic mechanisms described in the literature that result in increased concavity of the posterior vertebral body. The concavity itself is the result of abnormal bone subjected to normal forces or normal bone subjected to abnormal forces. Five pathologic explanations have been proposed as the cause of this sign (Table)(1,3). The posterior vertebral scalloping that results may be either focal or diffuse.
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DISCUSSION
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A common cause of localized posterior vertebral scalloping is increased intraspinal pressure secondary to an expanding mass. Widening of the interpediculate distance and alteration of the configuration of the pedicles are associated signs that may precede the development of posterior vertebral scalloping. Relatively large, slow-growing lesions that originate during a period of active skeletal growth and modeling (such as ependymomas of the terminal filum or medullary cone) are most likely to give rise to posterior vertebral scalloping (4). Other intraspinal masses such as dermoid cysts, epidermoid cysts, and lipomas also produce scalloping (1) (Fig 1b). On rare occasions, scalloping may be caused by intervertebral disk herniation (5). Diffuse scalloping in the absence of a mass has also been reported in cases of chronic raised intraspinal pressure due to communicating hydrocephalus (6).
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Figure 1b: Images of a 52-year-old woman with a long-standing, previously partially resected lipoma of the medullary cone and the cauda equina. (a) Lateral radiograph of the lumbar spine demonstrates florid posterior vertebral scalloping (arrows), which is maximal at L1 through L2. (b) Sagittal T1-weighted spin-echo 420/25 (repetition time msec/echo time msec) magnetic resonance (MR) image in the same patient demonstrates an extensive, principally high-signal-intensity intradural mass (arrows) which expands the spinal canal and causes posterior vertebral scalloping.
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Dural ectasia is thought to cause posterior vertebral scalloping due to loss of the normal protection provided to the vertebral body by a strong, intact dura. This results in diffuse scalloping that tends to be more marked in the lumbar region (1). The diagnosis of dural ectasia can be inferred from conventional radiographs or CT scans by the demonstration of posterior vertebral scalloping. Dural ectasia classically occurs in association with inherited connective tissue disorders such as Marfan syndrome and Ehlers-Danlos syndrome (1,7). This sign is a highly characteristic indicator of Marfan syndrome; it was observed by Fattori et al (8) on MR images of 76 of 83 (92%) affected patients. Posterior vertebral scalloping is also commonly seen in patients with neurofibromatosis, most often due to dural ectasia but also secondary to neurofibromas or a thoracic meningocele (9–12). Additional spinal abnormalities seen in patients with neurofibromatosis include scoliosis and syringomyelia. Dural ectasia resulting in posterior vertebral scalloping has also been reported in patients with ankylosing spondylitis; in these cases, the development of associated arachnoid cysts may give rise to cauda equina syndrome (13).
A number of congenital skeletal disorders are associated with posterior vertebral scalloping. It is a consistent feature in achondroplasia (Fig 2). In these patients, there is a progressive decrease of the interpediculate distance and vertebral body width in the more caudal segments, with diffuse short pedicles which cause lumbar spinal stenosis (14). Diffuse posterior vertebral scalloping is thought to develop as an adaptive response to growth of the spinal cord and membranes within this restricted spinal canal and is, in this case, most marked in the lumbar area of the spine (14).
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Figure 2: Sagittal T2-weighted fast spin-echo (5000/112) MR image of a 26-year-old woman with known achondroplasia and symptoms suggesting spinal stenosis demonstrates posterior vertebral scalloping (arrows) throughout the lumbar spine with multilevel spinal stenosis.
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The mucopolysaccharidoses, including Morquio syndrome and Hurler syndrome, are also associated with diffuse posterior vertebral scalloping, although the pathologic mechanism is not known. Caudal narrowing of the spinal canal is not a feature of the mucopolysaccharidoses (1,15), whereas it is a feature of anchondroplasia. Associated features include platyspondyly and anterior vertebral body beaks (16).
Acromegaly has been described as a further cause of diffuse posterior vertebral scalloping, probably because of a combination of soft-tissue hypertrophy in the spinal canal and increased bone resorption. In most tubular bones of acromegalic patients, bone deposition is greater than resorption, so that the net result is increased bone mass. In some regions of the skeleton, however, more resorption than deposition is thought to occur. For example, in the facial bones, predominant resorption gives rise to characteristic prominence of the frontal sinuses. Dominant bone resorption may contribute to the development of posterior vertebral scalloping in these patients (17). The prevalence of posterior vertebral scalloping in acromegaly is unclear. This was reported by Steinbach et al (17) in six out of 18 (33%) acromegalic patients while Stuber and Palacios (18) report some degree of posterior vertebral scalloping in all of the 38 acromegalic patients in their study, with moderate or substantial posterior vertebral scalloping demonstrated on lateral radiographs of the lumbar spine in 11 of 17 (65%) patients.
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FOOTNOTES
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| A trainee (resident or fellow) wishing to submit a manuscript for Signs in Imaging should first write to the Editor for approval of the sign to be prepared, to avoid duplicate preparation of the same sign.
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References
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- Larsen JL. The posterior surface of the lumbar vertebral bodies. I. Spine 1985;10(1):50–58.
- Leeds NE, Jacobson HG. Plain film examination of the spinal canal. Semin Roentgenol 1972;7(3):179–196.[CrossRef][Medline]
- Epstein BS. Spinal canal mass lesions. Radiol Clin North Am 1966;4:185–202.
- Berthelot JM, Maugars Y, Bertrand-Vasseur A, Lalande S, Prost A. Dorsal scalloping by calcified disc herniation. Spine 1995;20(1):106–107.[Medline]
- Shealy CN, Lemay M, Haddad FS. Posterior scalloping of vertebral bodies in uncontrolled hydrocephalus. J Neurol Neurosurg Psychiatry 1964;27:567–573.[Free Full Text]
- Macfarlane IL. Ehlers-Danlos syndrome presenting certain unusual features. J Bone Joint Surg Br 1959;41-B:541–545.
- Fattori R, Nienaber CA, Descovich B, et al. Importance of dural ectasia in phenotypic assessment of Marfan's syndrome. Lancet 1999;354(9182):910–913.[CrossRef][Medline]
- Leeds NE, Jacobson HG. Spinal neurofibromatosis. AJR Am J Roentgenol 1976;126(3):617–623.[Abstract]
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- Heard G, Payne EE. Scalloping of the vertebral bodies in von Recklinghausen's disease of the nervous system (neurofibromatosis). J Neurol Neurosurg Psychiatry 1962;25:345–351.[Free Full Text]
- Abello R, Rovira M, Sanz MP, et al. MRI and CT of ankylosing spondylitis with vertebral scalloping. Neuroradiology 1988;30(3):272–275.[CrossRef][Medline]
- Caffey J. Achondroplasia of pelvis and lumbosacral spine: some roentgenographic features. Am J Roentgenol Radium Ther Nucl Med 1958;80:449–457.[Medline]
- H Taybi. Metabolic disorders. In: Taybi H, Lachman R, eds. Radiology of syndromes, metabolic disorders and skeletal dysplasias. 4th ed. St Louis, Mo: Mosby, 1996; 670–672, 677–679.
- Langer LO Jr, Carey LS. The roentgenographic features of the KS mucopolysaccharidosis of Morquio (Morquio-Brailsford's disease). Am J Roentgenol Radium Ther Nucl Med 1966;97:1–20.[Medline]
- Steinbach HL, Feldman R, Goldberg MB. Acromegaly. Radiology 1959;72(4):535–549.[Medline]
- Stuber JL, Palacios E. Vertebral scalloping in acromegaly. Am J Roentgenol Radium Ther Nucl Med 1971;112(2):397–400.[Medline]
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