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DOI:10.2214/AJR.04.1874
AJR 2006; 186:1256-1259
© American Roentgen Ray Society


Case Report

Multiple Posterior Vertebral Fusion Abnormalities: A Case Report and Review of the Literature

Joseph J. Chen1, Barton F. Branstetter, IV1,2 and William C. Welch3

1 Department of Radiology, University of Pittsburgh, 200 Lothrop St., PUH Rm. D132, Pittsburgh, PA 15213.
2 Department of Otolaryngology, University of Pittsburgh, Pittsburgh, PA 15213.
3 Department of Neurological Surgery, University of Pittsburgh, Pittsburgh, PA 15213.

Received December 9, 2004; accepted after revision February 28, 2005.

 
Address correspondence to B. F. Branstetter IV (bfb1{at}pitt.edu).

Keywords: congenital anomaly • CT • radiography • spine • trauma • vertebral column


Introduction
Top
Introduction
Case Report
Discussion
References
 
Congenital vertebral anomalies of the posterior spine can be difficult to distinguish from acute traumatic injuries on CT and conventional radiography [1]. To ensure that patients with congenital anomalies are not treated unnecessarily for spinal fractures, radiologists need a thorough understanding of the embryology of the spinal column and the potential manifestations of fusion failure. We present an unusual patient with multiple neural arch clefts of the spine that were initially misdiagnosed as traumatic injuries. We discuss the expected locations of congenital vertebral clefts and review the pertinent radiology literature.


Case Report
Top
Introduction
Case Report
Discussion
References
 
A healthy 25-year-old man with no history of back pain was rear-ended in a low-speed motor vehicle collision. He was restrained and had no loss of consciousness. Two days later, the patient presented to a community emergency department complaining of neck and lower back pain. On examination, there were no clinical signs of neurologic trauma and no focal neurologic defects. The patient complained of moderate tenderness to palpation along the cervical, thoracic, and lumbar vertebrae and paravertebral areas.

At the community emergency department, the patient underwent conventional radiography of the cervical and lumbar spine (Figs. 1A and 1B) and CT of the cervical spine (Figs. 1C, 1D, and 1E). The imaging findings were suggestive of acute fractures, and the patient was referred to our trauma center for further evaluation. The images were reevaluated at the trauma center, and the diagnosis of multiple congenital vertebral arch clefts was made. The patient was diagnosed with muscular strain and was treated conservatively. He had follow-up examinations in the neurosurgery clinic and has recovered completely.


Figure 1
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Fig. 1A —25-year-old man with no history of back pain who was rearended in low-speed motor vehicle collision 2 days earlier presented to community emergency department complaining of neck and lower back pain. On examination, there were no clinical signs of neurologic trauma and no focal neurologic defects. Patient complained of moderate tenderness to palpation along cervical, thoracic, and lumbar vertebrae and paravertebral areas. Lateral radiograph of cervical spine shows linear radiolucency (arrows) through posterior elements of C2 vertebra. This finding was initially interpreted as acute fracture.

 

Figure 2
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Fig. 1B —25-year-old man with no history of back pain who was rearended in low-speed motor vehicle collision 2 days earlier presented to community emergency department complaining of neck and lower back pain. On examination, there were no clinical signs of neurologic trauma and no focal neurologic defects. Patient complained of moderate tenderness to palpation along cervical, thoracic, and lumbar vertebrae and paravertebral areas. Lateral radiograph of lumbar spine shows linear radiolucency (arrows) through pars interarticularis of L3 vertebra.

 

Figure 3
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Fig. 1C —25-year-old man with no history of back pain who was rearended in low-speed motor vehicle collision 2 days earlier presented to community emergency department complaining of neck and lower back pain. On examination, there were no clinical signs of neurologic trauma and no focal neurologic defects. Patient complained of moderate tenderness to palpation along cervical, thoracic, and lumbar vertebrae and paravertebral areas. Multiple fusion abnormalities seen on unenhanced axial CT: spinous cleft (spina bifida occulta, arrows, C) of C2 vertebra (C), retrosomatic cleft (arrows, D) of C5 vertebra (D), and spondylolysis (arrows, E) of C2 vertebra (E).

 

Figure 4
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Fig. 1D —25-year-old man with no history of back pain who was rearended in low-speed motor vehicle collision 2 days earlier presented to community emergency department complaining of neck and lower back pain. On examination, there were no clinical signs of neurologic trauma and no focal neurologic defects. Patient complained of moderate tenderness to palpation along cervical, thoracic, and lumbar vertebrae and paravertebral areas. Multiple fusion abnormalities seen on unenhanced axial CT: spinous cleft (spina bifida occulta, arrows, C) of C2 vertebra (C), retrosomatic cleft (arrows, D) of C5 vertebra (D), and spondylolysis (arrows, E) of C2 vertebra (E).

 

Figure 5
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Fig. 1E —25-year-old man with no history of back pain who was rearended in low-speed motor vehicle collision 2 days earlier presented to community emergency department complaining of neck and lower back pain. On examination, there were no clinical signs of neurologic trauma and no focal neurologic defects. Patient complained of moderate tenderness to palpation along cervical, thoracic, and lumbar vertebrae and paravertebral areas. Multiple fusion abnormalities seen on unenhanced axial CT: spinous cleft (spina bifida occulta, arrows, C) of C2 vertebra (C), retrosomatic cleft (arrows, D) of C5 vertebra (D), and spondylolysis (arrows, E) of C2 vertebra (E).

 

Discussion
Top
Introduction
Case Report
Discussion
References
 
Patients with suspected spinal trauma have historically been screened with conventional radiography of the spine. However, CT is increasingly being used as a screening tool [2]. Although CT provides a more detailed analysis of bone anatomy, congenital anomalies still represent a potential source of false-positive findings.

The human vertebral system forms from somites, which are segmented mesoderm derivatives found in the embryo during early gestation [3]. These somites differentiate into three parts: the dermatome, which becomes the dermis; the myotome, which becomes the skeletal muscles of the posterolateral body wall; and the sclerotome, which becomes the vertebrae and ribs. Initially, these segmented somites consist of only mesenchymal tissue, but by week 6 of fetal development, six chondrification centers appear in each somite [3] (Fig. 2).


Figure 6
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Fig. 2 —Illustration shows developmental landmarks in idealized vertebra: primary ossification centers (dark gray), secondary ossification centers (black), and chondrification centers (light gray).

 
The chondrification centers fuse, and by week 8, the mesenchymal vertebral body has been replaced by a cartilaginous vertebral body. The cartilaginous vertebral body then begins the process of ossification [3]. Although different sections of the spine ossify in slightly different ways, the process essentially involves three ossification centers—one in the anterior arch and one on each side of the neural arch (Fig. 2). By the age of 7 years, most of these centers have fused, replacing the previous cartilage model with bone. Each vertebral body also has secondary ossification centers that form rings on the superior and inferior surfaces [3]. These rings appear at puberty and fuse with the vertebral body by the age of 25 years.

There are six types of posterior neural arch defects (Fig. 3). Their origins are congenital, acquired, or a predisposition to defects based on a congenital weakness. The embryology of the vertebral column explains three of the six types of neural arch defects—neurocentral synchondroses, paraspinous clefts, and spinous clefts [4-6]. The remaining three defects either have an unknown cause or are presumed to be caused by overuse (e.g., spondylolysis) [7-13].


Figure 7
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Fig. 3 —Illustration shows six types of posterior neural arch defects: neurocentral synchondrosis (1), retrosomatic cleft (2), spondylolysis (3), retroisthmic cleft (4), paraspinous cleft (5), and spina bifida occulta (6). (Adapted from [10])

 

The first type of defect, persistent neurocentral synchondrosis, results from the failure of the vertebral body growth plates to transform into bone (Fig. 3). At birth, almost the entire vertebral body and arch have converted from cartilage into bone. The neurocentral joints and the spinous process and costovertebral joints remain as cartilaginous growth plates to allow the vertebral arch to grow in response to the growing spinal cord. Normally, by the age of 3-6 years, these cartilaginous neurocentral joints fuse [4]. By the age of 6-14 years, evidence of these cartilage segments can no longer be observed on MR images [5]. Neurocentral synchondrosis is thought to be an ossification failure of these cartilage segments [4].

The second type of defect, the retrosomatic cleft, is a hypoplasia or aplasia of the vertebral pedicle [7, 8] (Fig. 3). The origin of this defect has not been elucidated. Possible causes include neurofibroma, vertebral artery erosion, neoplastic disease, or fracture of the neural arch [9]. Other studies have suggested that the abnormality is of congenital origin [10].

The third type of defect, spondylolysis, is a cleft that passes through the pars interarticularis, which connects the superior and inferior articular facets (Fig. 3). Although these defects have been classified into congenital and acquired defects, it is widely believed that most are acquired due to repeated microtrauma and overuse, eventually causing stress fractures of the pars interarticularis [11, 12]. As such, they are seen more frequently in athletes and soldiers who underwent strenuous training during World War II [12, 14]. The overall prevalence of spondylolysis is estimated to be 7.2% [15]. The L5 vertebral body accounts for 90% of the cases [15].

The fourth type of defect is the retroisthmic cleft. This defect has been described as "laminolysis" because the defect is through the lamina. Unlike spondylolysis, the defect is dorsal to the inferior articular facet (Fig. 3). The origin of this defect is inconclusive, but researchers have suggested stress fracture from chronic mechanical overload [13]. Retroisthmic cleft is the rarest of the six posterior fusion defects.

The fifth and sixth types of defect are the paraspinous cleft and the spinous cleft (spina bifida occulta) (Fig. 3). Although most of these defects occur in the lumbar spine, they may occur anywhere along the spinal column. The defects are due to the failure of neural tube closure during development, preventing muscle and bone from growing around the gap [7]. The incidence of neural tube defects in the United States is approximately 1 of every 2,000 births [16].

Congenital vertebral anomalies of the posterior spine can cause confusion in the assessment of patients with suspected spine trauma. A greater knowledge of the location and imaging characteristics of potential fusion defects will assist the radiologist in distinguishing congenital defects from acute injuries.


References
Top
Introduction
Case Report
Discussion
References
 

  1. Harris JH, Harris WH, Novelline R. Radiology of emergency medicine, 3rd ed. Baltimore, MD: Williams & Wilkins, 1993: 226-229
  2. Berlin L. CT versus radiography for initial evaluation of cervical spine trauma: what is the standard of care? AJR2003; 180:911 -915[Free Full Text]
  3. Moore KL, Persaud TVN. The developing human: clinically oriented embryology, 6th ed. Philadelphia, PA: Saunders,1998 : 382-399
  4. Leemans J, Deboeck M, Claes H, Boven F, Potvliege R. Computed tomography of ununited neurocentral synchondrosis in the cervical spine. J Comput Assist Tomogr 1984;8 : 540-543[Medline]
  5. Rajwani T, Bhargava R, Moreau M, et al. MRI characteristics of the neurocentral synchondrosis. Pediatr Radiol2002; 32:811 -816[CrossRef][Medline]
  6. Wynbrandt J, Ludman MD. The encyclopedia of genetic disorders and birth defects. New York, NY: Facts on File,1991 : 283-286
  7. Morin ME, Palacios E. The aplastic hypoplastic lumbar pedicle. Am J Roentgenol Radium Ther Nucl Med1974; 122:639 -642[Medline]
  8. Bardsley JL, Manelin LG. The unilateral hypoplastic lumbar pedicles. Radiology 1971;101 : 315-317[Medline]
  9. Wortzman G, Steinhardt MI. Congenitally absent lumbar pedicle: a reappraisal. Radiology 1984;152 : 713-718[Abstract/Free Full Text]
  10. Johansen JG, McCarty DJ, Haughton VM. Retrosomatic clefts: computed tomographic appearance. Radiology 1983;148 : 447-448[Abstract/Free Full Text]
  11. Sullivan CR, Bickell WH. The problem of traumatic spondylolysis. Am J Surg 1960;100 : 698-708[CrossRef]
  12. Nassim R, Burrows HJ. Modern trends in diseases of the vertebral column. New York, NY: Paul B. Hoeber, Inc.1958 : 271
  13. Wick LF, Kaim A, Bongartz G. Retroisthmic cleft: a stress fracture of the lamina. Skeletal Radiol 2000;29 : 162-164[CrossRef][Medline]
  14. Guanciale AF, Dillin WH, Watkins RG. Back pain in children and adolescents. In: Herkowitz HN, Rothman RH, Simeone FA, Balderston RA, eds.Rothman-Simeone: the spine, 4th ed. Philadelphia, PA: Saunders 1999: 197-198
  15. Moreton RD. Spondylolysis. JAMA1966; 195:671 -674[Abstract/Free Full Text]
  16. Northrup H, Volcik K. Spina bifida and other neural tube defects. Curr Probl Pediatr 2000;30 : 313-332[Medline]

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