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Figure 1—Lateral (A) and ventrodorsal (B) radiographic views of the cervical vertebral column of a 4-month-old Nubian doe with a history of progressive tetraparesis.

History A 4-month-old Nubian doe was evaluated at the University of Georgia Large Animal Teaching Hospital because of progressive tetraparesis of 5 weeks’ duration. Initial signs consisted of toe dragging of the left thoracic limb and both pelvic limbs and stumbling, which progressed to tetraparesis and eventually an inability to walk. The doe was obtained by the owner at 3 weeks of age as a pet, and no other goats were housed on the premises. No information was available about goats from the herd of origin. On initial evaluation, the goat was bright, alert, and responsive and in sternal recumbency. With the exception of a poor body condition (body condition score, 1/5), no abnormalities were found on physical examination. On neurologic examination, the goat’s mentation was considered normal. The goat was in sternal recumbency and was unable to walk or support weight without assistance. When supported, the goat had voluntary movement only in the pelvic limbs. Postural reaction testing was performed, and hopping responses were present but slow in the right thoracic limb and absent in the left thoracic and both pelvic limbs. The thoracic limbs were hypotonic and lacked withdrawal reflexes. The pelvic limbs had normal muscle tone, and withdrawal and patellar reflexes were intact bilaterally. The cutaneous trunci and perineal reflexes were intact. Tail and anal sphincter tone were considered normal. There also was generalized, symmetric muscle atrophy, which was most severe in the cervical and lumbar epaxial muscles. Cranial nerve reflexes were intact. The neuroanatomic diagnosis was consistent with an asymmetric lesion involving spinal cord segments C6 through T2, which was worse on the left side. Radiographs of the cervical vertebral column were obtained (Figure 1). Determine whether additional imaging studies are required, or make your diagnosis from Figure 1—then turn the page → This report was submitted by Caroline S. Monk, BS; Eli B. Cohen, DVM; Kelsey A. Hart, DVM, PhD; Marc Kent, DVM; David A. Jimenez, DVM; and Brent C. Credille, DVM; from the Departments of Large Animal Medicine (Monk, Hart, Credille), Anatomy and Radiology (Cohen, Jimenez), and Small Animal Medicine and Surgery (Kent), College of Veterinary Medicine, University of Georgia, Athens, GA 30602. Address correspondence to Dr. Credille ([email protected]). JAVMA, Vol 245, No. 7, October 1, 2014

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Figure 2—Same lateral (A) and ventrodorsal (B) radiographic images as in Figure 1. A—The C1-2 articulation is luxated with ventral displacement of the cranial aspect of C2 (long black arrows). The vertebral canal at C1 is widened (short black arrows). The C3-4 articulation is subluxated with severe narrowing of the vertebral canal (white arrows). Notice the markedly hypoplastic dens. B—A bulbous bony proliferation is present in the region of the dorsal articulations of C2 (white arrows).

Figure 3—T2-weighted sagittal plane (A) and transverse plane at the level of the caudal aspect of C2 (B) MRI images of the cervical vertebral column of the same goat in Figure 1. A—Notice the extradural spinal cord compression at the C3-4 articulation (long arrows) and at the C4-5 articulation (short arrows). No compression is present at the C1-2 articulation. B—Notice the linear hyperintensity extending obliquely between the pedicle and the lamina on the left dorsolateral aspect of C2 (arrow).

Diagnostic Imaging Findings and Interpretation On the right lateral view, the C1-2 articulation is luxated, with ventral displacement of the cranial end of C2 and resultant focal lordosis. The dens is hypoplastic (Figure 2). The C3-4 intervertebral disk space is wedged and subluxated with a dorsal step misalignment of the cranial aspect of C4 and focal kyphosis. The dorsal portion of the cranial aspect of C4 is immediately subjacent to the ventral aspect of the lamina of C3. The C2-3, C5-6, and C6-7 intervertebral disk spaces are wedged. On the ventrodorsal view, the left cranial and right caudal aspects of C2 are smooth and well-defined with bulbous bony processes. Additionally, the vertebral canal at C1 is subjectively wide, and the vertebral canal at C2, C3, and C4 is irregular with lack of vertebral alignment, likely secondary to scoliosis. 758

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On the basis of the results of the physical examination, neurologic evaluation, and radiography, a diagnosis of cervical vertebral malalignment and severe vertebral canal stenosis was made. The wedging at JAVMA, Vol 245, No. 7, October 1, 2014

C2-3, C5-6, and C6-7 likely represented congenital malformation, although vertebral malalignment secondary to previous trauma could not be ruled out. To better characterize the vertebral abnormalities and assess concurrent spinal cord pathological lesions, MRI of the cervical vertebral column was performed. T1-weighted and T2-weighted images were obtained in transverse and sagittal planes. The same vertebral abnormalities as observed radiographically were identified on T2-weighted images (Figure 3). At the C3-4 intervertebral disk space, the dorsal displacement of the cranial aspect of C4 resulted in severe extradural spinal cord compression and narrowing of the vertebral canal (minimum dimension, 0.2 cm). Extradural spinal cord compression also was present at C4-5, where the vertebral canal measured 0.4 cm in height. The C1-2 articulation was luxated with ventral displacement of C2. On the left side of C2, a discontinuity of the pedicle and dorsal lamina was evident, extending ventromedially to dorsolaterally. This finding was characterized by a hyperintense line interposed between hypointense cortical bone on T1-weighted and T2-weighted images. Severe bulbous proliferative bone was present involving the articular processes at the C2-3 articulation on the right. Aside from compression, changes in the spinal cord were not observed. All of the nucleus pulposi of the cervical and cranial thoracic intervertebral disks had decreased signal intensity on T2-weighted images consistent with desiccation. Results of the MRI examination corroborated radiographic findings and were most consistent with congenital vertebral malformation. Additional information provided by MRI included spinal cord compression at C3-4 and C4-5, suspected failure of neural arch fusion of C2, and intervertebral disk degeneration. Treatment and Outcome Because the goat was a pet, surgical decompression of the cervical spinal cord was discussed; however, given the poor prognosis, the owner elected euthanasia. Necropsy was not performed. Comments Congenital vertebral malformations are an uncommon finding in goats, but when they occur, they are most often due to genetic aberrations or environmental factors.1,2 Cervical vertebral malformation resulting in occipitoantlantoaxial malformation with atlantooccipital fusion and atlantoaxial subluxation has been reported in 2 goats.1,2 In these cases, the malformation was assumed to be congenital in origin on the basis of a progressive history, young age at onset of disease, and consistent radiographic findings. The goat of this report had multiple cervical vertebral malformations, including atlantoaxial joint instability. Unlike the previously reported caprine cases of occipitoantlantoaxial malformation, no areas of atlantooccipital fusion were evident on imaging studies in the goat of the present report. Similar congenital atlantoaxial joint instability has been commonly reported for dogs, with a predilection for toy and miniature breeds.3 In Arabian horses,

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congenital occipitoantlantoaxial malformation and atlantooccipital fusion has been reported and is believed to be inherited.4 Atlantoaxial joint instability results in excessive flexion, seen on radiographs as luxation of the atlantoaxial joint, which in turn compresses the spinal cord3 resulting in neuronal degeneration. Hypoplasia of the dens plays a key role in the development of atlantoaxial joint instability in such cases. In dogs, it is theorized that dens hypoplasia results from ischemic necrosis secondary to trauma in utero rather than lack of an ossification center.5 Regardless of causation, resultant instability and luxation of the atlantoaxial joint often result in neurologic deficits in affected dogs.6 The discrepancy between the neuroanatomic lesion localization (C6 through T2) due to absent withdrawal reflexes in the thoracic limbs and the extensive spinal cord compression more proximally (C3 through C5) identified on imaging modalities is puzzling but has been reported in dogs.7 Although the exact reason for this change is unclear, factors such as muscle atrophy and alterations in the withdrawal reflex pathways within the CNS with long-standing spinal cord compression have been proposed.7 In goat of the present report, without knowledge of the status of related goats or the rest of the herd of origin, it is difficult to definitely determine the etiology of the vertebral malformations. If unrelated herdmates were also affected, it would be more likely that the observed abnormalities were due to fetal infection or teratogen exposure. Potential teratogens that could result in such malformations include viruses, toxins, or maternal vitamin D imbalances.1 If related animals had similar lesions, a hereditary origin would be more likely. This is described in similar conditions in Arabian horses4 and small-breed dogs3 but, to the authors’ knowledge, is not documented in goats. In conclusion, although a definitive etiology for the cervical vertebral malformations in the goat of the present report was not identified, the imaging features of the cervical vertebral malformations are consistent with reports of idiopathic or hereditary vertebral malformations in goats, dogs, and horses. The most valuable diagnostic aid to detect these lesions across species is a lateral cervical radiograph. Magnetic resonance imaging may be used to corroborate radiographic findings and localize sites of spinal cord compression in preparation for potential surgical decompression and stabilization. 1. 2. 3. 4. 5. 6. 7.

Seva JI, Gómez S, Pallarés FJ, et al. Occipitoatlantoaxial malformation in an adult goat. J Vet Diagn Invest 2008;20:654–656. Ramadan RO. A dicephalic goat with other defects. Zentralbl Veterinarmed A 1996;43:337–343. Westworth DR, Sturges BK. Congenital spinal malformations in small animals. Vet Clin North Am Small Anim Pract 2010;40:951–981. Watson AG, Mayhew IG. Familial congenital occipitoatlantoaxial malformation (OAAM) in the Arabian horse. Spine (Phila Pa 1976) 1986;11:334–339. Watson AG, Stewart JS. Postnatal ossification centers of the atlas and axis in Miniature Schnauzers. Am J Vet Res 1990;51:264–268. Watson AG, de Lahunta A, Evans HE. Morphology and embryological interpretation of a congenital occipito-atlanto-axial malformation in a dog. Teratology 1988;38:451–459. Forterre F, Konar M, Tomek A, et al. Accuracy of the withdrawal reflex for localization of the site of cervical disk herniation in dogs: 35 cases (2004–2007). J Am Vet Med Assoc 2008;232:559–563.

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What is your diagnosis? Congenital vertebral malformations.

What is your diagnosis? Congenital vertebral malformations. - PDF Download Free
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