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3.1




            Developmental disorders


















            Anomalies of the vertebral column                  compression atrophy, even in patients without overt
                                                               neurologic deficits. An uncommon vertebral anomaly,
            Vertebral malformation                             caudal articular facet hypoplasia or aplasia in the
            Malformations of the vertebrae are common, and       thoracolumbar vertebral  column, has been reported
            although some are clinically significant, many are seen as   with spinal cord compression due to contralateral facet
            incidental findings on imaging studies. Malformations   and ligamentum flavum hypertrophy. 6
            can be categorized as simple or complex, and a recent   The CT appearance of vertebral anomalies will vary
            review of spinal anomalies proposed specific classifica­  depending on the specific malformation, but common
            tion of anomalous vertebrae based on a similar scheme   findings include alteration in vertebral shape, reduced
            used in people.  Those anomalies that occur during the   attenuation when mineralization is incomplete, and ver­
                         1,2
            early  embryonic  period  include  centrum  median  cleft   tebral column curvature abnormalities. Vertebral canal
            (butterfly vertebrae), true hemivertebrae, mediolateral   stenosis suggests spinal cord impingement or compres­
            wedged vertebrae, and transitional vertebrae. Anomalies   sion, which can be documented using CT myelography
            that develop during the later fetal period include block   (Figures 3.1.1, 3.1.2). Lumbosacral transitional vertebrae
            vertebrae, articular process hypoplasia, and centrum   can predispose to cauda equina syndrome (Chapter 3.5),
            hypoplasia or aplasia (dorsoventral wedged vertebrae).    and asymmetrical transitional vertebra at this level can
                                                         1–3
            Vertebral anomalies can be further classified as arising   result in pelvic rotation leading to coxofemoral malar­
            from defects in formation (e.g. wedged, hemi‐, and   ticulation (Figure 3.1.3).
              butterfly vertebrae) versus incomplete or absent segmen­  MR features are similar to those seen with CT, and
            tation (e.g. block vertebrae).                     spinal cord pathology is often more clearly detected
              German  Shepherd Dogs are  overrepresented for   (Figure 3.1.2).
            developing transitional vertebrae at the lumbosacral
            junction.  Certain screw‐tailed breeds, such as Bulldogs,
                    4
            French Bulldogs, Pugs, and Boston Terriers, are highly   Craniocervical junction malformation
            predisposed to complex vertebral anomalies,  particularly   The term craniocervical junction malformation
            in the midthoracic region.  Vertebral anomalies can   includes anomalies of the occipital bone and the first
                                    5
            result in a combination of scoliosis, kyphosis, lordosis,   two cervical vertebrae.  The most common of these
                                                                                   7
            or rotational spinal abnormalities; can cause spinal canal   disorders, Chiari‐like malformation, is discussed in
            stenosis; and may predispose to spinal injury from what   Chapter 2.3. Other malformations involving the occip­
            might otherwise be clinically insignificant trauma. In   ital bone and atlanto‐occipital overlap are described
            animals with vertebral canal stenosis, spinal cord   in Chapter 1.4. Chiari‐like malformation aside, cranio­
              diameter is often focally decreased as a result of chronic   cervical junction malformations primarily affect



            Atlas of Small Animal CT and MRI, First Edition. Erik R. Wisner and Allison L. Zwingenberger.
            © 2015 John Wiley & Sons, Inc. Published 2015 by John Wiley & Sons, Inc.
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