A 12-year-old 31-kg (68.2-lb) sexually intact female Boxer was referred because of progressive weakness of 2 weeks' duration and signs of pain associated with the vertebral column. During physical examination, the dog was reluctant to stand and remained in sternal recumbency. The body condition score was 3.5/5.0. Rectal temperature was 37.8°C (100.0°F). A complete neurologic examination revealed nonambulatory tetraparesis and spinal hyperesthesia. Conscious proprioceptive reactions were decreased in all limbs. Spinal segmental reflexes in the pelvic limbs were consistent with an upper motor neuron lesion, whereas the reflexes in the thoracic limbs indicated a lower motor neuron lesion. No other abnormalities were detected during general physical examination.
What is the problem? Where is the lesion? What are the most probable causes of this problem? What is your plan to establish a diagnosis? Please turn the page.
Assessment
Anatomic diagnosis
| Problem | Rule out location |
|---|---|
| Progressive nonambulatory tetraparesis; asymmetric weakness of the thoracic limbs | C6-T2 spinal cord segment with asymmetric compromise of the right side |
| Hyperesthesia on palpation of the cervical and thoracic vertebral column segments | Meninges, vertebrae, nerve roots or spinal nerves, or paraspinal musculature at the site of hyperesthesia |
Likely location of 1 lesion
| Given the asymmetric signs associated with nonambulatory tetraparesis, a right-sided spinal cord lesion involving the C6-T2 spinal cord segment was suspected. |
Etiologic diagnosis—The results of the neurologic examination indicated a neuroanatomic localization consistent with a C6-T2 myelopathy, with more involvement on the right side. The differential diagnoses for this asymmetric C6-T2 myelopathy included degenerative conditions (Hansen type II disk herniation, caudal cervical vertebral stenosis, degenerative myelopathy, articular process joint arthrosis, or intraspinal articular or meningeal cysts), immune-mediated or inflammatory conditions (spinal cord–only meningoencephalomyelitis of unknown origin), vertebral neoplasia (extradural, intradural-extramedullary, or intramedullary), infectious diseases (diskospondylitis, vertebral empyema, or bacterial, viral, fungal, or protozoal myelitis), syrinx, and trauma. The initial diagnostic plan included clinicopathologic analysis (CBC and serum biochemical analysis) and CSF sample analysis. Planned diagnostic imaging included conventional radiography and CT of the cervical, cervicothoracic, and thoracic portions of the vertebral column.
Diagnostic test findings—The CBC revealed mild normocytic, normochromic, nonregenerative anemia (Hct, 35%; reference range, 37% to 50%) and mild leukopenia (7,800 WBCs/μL; reference range, 8,000 to 14,000 WBCs/μL) with lymphopenia and monocytopenia consistent with an inflammatory leukogram. Serum biochemical analysis revealed low aspartate aminotransferase activity and high alkaline phosphatase activity.
Conventional radiographic examination revealed ventral mild spondylosis from C6 to T2 on lateral and dorsoventral views of the vertebral column. Because MRI equipment was not available in our hospital, the dog was anesthetized and CT scans (without contrast medium administration) of the cervical, cervicothoracic, and thoracolumbar regions of the vertebral column were performed with a helical CT scanner unit.a Settings used in image acquisitions were as follows: interval of 2 mm, thickness of 2 mm, 120 kV, 85 mA, and 178 mAs. Computed tomography revealed a linear calcific density around the dorsolateral dural sac at the vertebral levels of C4, C5, C6, C7, T1, and T2, consistent with dural ossification. Transverse, sagittal, and dorsal planar noncontrast CT images revealed an irregular, sharply demarcated, extensive area of hyperdense (235 to 580 HU) excrescence measuring 7.8 × 3.15 × 20 mm, which was consistent with calcification attached to the dura mater. The dural-based mass was compressing and encircling the spinal cord at the C7 vertebral level, compatible with dural ossification and impingement of the spinal cord (Figure 1). On the basis of the CT imaging findings, the dog was suspected to have spinal dural ossification. However, although a neoplastic lesion was considered unlikely, it could not be completely ruled out.
Transverse (A), sagittal (B) and dorsal (C) CT images (obtained with a bone window setting and without contrast medium administration) of the C5-T2 vertebral segment of a 12-year-old Boxer that was evaluated because of a 2-week history of slowly progressive ambulatory tetraparesis. In panel A, notice a hyperdense (235 to 580 HU) dural-based excrescence indicative of dural ossification compressing the left dorsolateral aspect of the spinal cord at C7.
Citation: Journal of the American Veterinary Medical Association 254, 1; 10.2460/javma.254.1.67
Surgical intervention was recommended; however, the owner declined surgery because of financial concerns, and conservative treatment was started in an attempt to improve mobility in the dog's hind limbs. Medical and supportive treatments were initiated, with administration of dexamethasone (1 mg/kg [0.45 mg/lb], PO, q 24 h) for 1 week and tramadol (3 mg/kg [1.36 mg/lb], PO, q 8 h) for 5 days. During the 10 days after initiation of treatment, the dog became slightly ambulatory with minimal assistance. Further follow-up information was not available because the owner relocated.
Comments
Dural ossification (dural mineralization, dural osseous metaplasia, ossifying pachymeningitis, senile ossification of the spinal dura mater, or idiopathic hypertrophic spinal pachymeningitis) is a common metaplastic and degenerative aging change of the inner surface of the dura mater that develops generally in large-breed dogs1,2; typically, there are no associated inflammatory changes.3 The cause of the dura mater calcification in the dog of the present report was not evident, but the probable cause was considered to be degeneration attributable to physiologic aging.4,5 In humans, the mechanism of ectopic ossification within the dural sac may involve development of an intradural hematoma, presence of bone fragments from traumatic injury, metabolic entities (hyperthyroidism), heterotopic osseous metaplasia associated with neoplasia, or neighboring ossification of the posterior longitudinal ligament.6 Also, it is hypothesized that ossification of dura mater in humans is probably attributable to effects of osteogenic cytokines from the ossified ligamentum flavum.7 The dura mater of the cervical and lumbar intumescences is particularly affected at the ventral or ventrolateral aspect; however, dural ossification can develop at any level of the spinal cord and extend over several segments. These plaque-like mineralizations of the spinal dura mater are usually incidental aging changes that are often identified in association with vertebral spondylosis and are rarely associated with spinal cord lesions. There are few reports1,2,8 in veterinary medicine in which neurologic examination, diagnostic imaging, and pathological findings were directly indicative of osseous metaplasia of the spinal dura mater. Occasionally, these mineralized plaques are attached to the underlying spinal cord, resulting in neurologic signs. The chronic spinal cord compression caused by the plaques results in spinal cord atrophy and loss of neurons and their myelin sheaths.8 The dog of the present report had disease entities (dural ossification and spondylosis deformans) associated with chronic spinal conditions. Results of previous studies2,8 indicate that dural ossification in dogs is frequently accompanied by spondylosis deformans, as was found in the case described in the present report. Signs of pain in affected dogs are believed to be associated with focal compression of the spinal cord or spinal nerve roots.
Radiographic findings of dural ossification are single or multiple linear radiopaque densities along the vertebral canal. In dogs, the most common sites for dural ossification are at the vertebral levels of C2-C4, C7, and L1-L7.1,2 Dural ossification is difficult to identify with MRI, and lesions are hypointense in T1- and T2-weighted sequences.8,b Computed tomography is the most sensitive diagnostic tool for detection of these dural calcifications; such calcifications can be detected by visual assessment of CT images and when the hyperdense area recorded as calcification has a maximum calculated attenuation value > 100 HU.9 The CT characteristics of dural ossification in the dog of the present report included hyperdense linear and circumferential thickening around the spinal cord. In humans, there are 2 CT signs indicative of dural ossification that are evident in images obtained with a bone window setting: hyperdense bony excretions with a hyperdense center, and so-called comma signs created by ossification of half of the circumference of the spinal dura mater.10 The tail of the comma indicates that the ossification extends to the lateral or ventral aspect of the dura mater.10
The lack of histopathologic confirmation of the diagnosis was the main limitation of the case described in the present report; however, CT findings are considered the most accurate for the diagnosis of this condition. Because of financial concerns, no additional evaluation or surgical treatment of the dog was performed, and the owner opted for conservative treatment. Hemilaminectomy, durotomy, and surgical excision of the bone plaque would have been necessary to reduce the compression of the spinal cord secondary to the dural ossification.8
Dural ossification is a very uncommon cause of dural thickening that has a characteristic CT appearance and rarely results in chronic progressive neurologic signs. Differential diagnoses include epidural hematoma, epidural abscess, and spinal meningioma, although these conditions have different imaging and clinical characteristics. Spinal dural ossification should be considered a differential diagnosis for an uncommon cause of progressive myelopathy in dogs. Surgical resection of the spinal dural ossification segment has a favorable prognosis for improvement of neurologic function in humans.
Acknowledgments
The authors thank Kelly Zammit, BVSc, from Edanz Group (www.edanzediting.com/ac), for editing a draft of this manuscript.
Footnotes
Picker PQ 6000, Picker International, Cleveland, Ohio.
Mandara MT, Lepri E, Sforna M, et al. Pathological findings associated with osseous dural metaplasia, an underestimated spinal syndrome (abstr). J Vet Intern Med 2005;19:275.
References
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