Three skeletally immature screw-tailed dogs were evaluated because of progressive pelvic limb ataxia. Dog 1 was a 6-month-old sexually intact male Pug, dog 2 was a 7-month-old sexually intact male English Bulldog, and dog 3 was a 4-month-old sexually intact male Pug. In all dogs, findings on physical examination were unremarkable, with the exception of palpable deviation of the normal contour of the thoracic vertebral column despite apparently normal epaxial muscle bulk. At the time of initial evaluation, all the dogs were ambulatory, although marked pelvic limb ataxia and paresis were evident; the condition of dog 2 deteriorated rapidly and it developed nonambulatory paraparesis within 24 hours of admission to the hospital. Neurologic examination of each dog revealed apparently normal function in the thoracic limbs; in the pelvic limbs, flexor and patellar reflexes were intact but there were deficits in responses to toe knuckling and hopping. Dog 1 had a crossed extensor reflex (from right to left) in the pelvic limbs. The panniculus reflex could not be elicited in dog 1, was weak caudal to the level of the T8 vertebra in dog 2, and was considered normal in dog 3. Signs of mild discomfort were evoked on forcible palpation of the midthoracic region of the vertebral column in each dog. These findings suggested that there was a lesion between the T3 and L3 spinal cord segments in all 3 dogs.
Radiography was performed on each dog and revealed marked kyphosis of the thoracic vertebral column that was centered on the region where there was 1 or more hemivertebrae. In dog 1 (the 6-month-old Pug), this region was centered on the T9 vertebra; the vertebral body was notably short in the craniocaudal plane and displaced dorsally with respect to the neighboring T8 vertebra. The T8 vertebral body was also shortened, and there was bone proliferation on the ventral aspect of the T8-9 intervertebral space. Ventrodorsal radiographic views of dog 1 did not reveal any lateral displacement of the affected or neighboring vertebrae. In dog 2 (the 7-month-old English Bulldog), there was abnormal curvature of the thoracic portion of the vertebral column that was centered on the T6-7 intervertebral junction; the T5, T6, and T7 vertebral bodies were markedly short craniocaudally. The T8 vertebra was wedge shaped, and the apex was directed dorsally (Figure 1). Ventrodorsal radiographic views of this region revealed an S-shaped deformity of the vertebral column. Several vertebrae at this level appeared to be incompletely developed and, in some instances, butterfly shaped. In dog 3 (the 4-month-old Pug), the T8 vertebra was trapezoid shaped on lateral radiographic views (the narrow edge was directed cranially) and malarticulated and dorsally displaced with respect to the T7 vertebra.
For each dog, T1-weighted (time to repeat, 600 to 800 ms; time to echo, 26 ms) and T2-weighted (time to repeat, 3,000 ms; time to echo, 80 ms) MR images were obtained by use of a 0.2-T permanent magneta (Figure 2). Sagittal MR images of dog 1 suggested that there was severe spinal cord compression associated with the region of severe kyphosis and the malformation and dorsal displacement of the T9 vertebral body. Transverse MR images confirmed that there was severe ventrodorsal spinal cord compression associated with gross reduction in the dorsoventral height of the pedicles (compared with findings expected in clinically normal dogs) at this site. The region of compression was only approximately 6 mm long. These images also revealed a component of ventrolateral cord compression that was apparently associated with the imperfectly formed dorsal aspect of the T9 vertebral body.
In dog 2, sagittal MR images confirmed that there were extensive abnormalities of the T4, T5, and T6 vertebral bodies, but because of the lateral deviation of the vertebral column at this level, it was difficult to define precisely the origin or degree of cord compression. Transverse MR images of this region confirmed that the vertebral canal was severely stenotic in both planes. The T1-weighted transverse scans indicated that there was lateral compression of the spinal cord associated with a mass to the right of the cord within the vertebral canal at T5; the mass was hyperintense, compared with both the spinal cord and the vertebral bone.
In dog 3, sagittal MR images confirmed the abnormal development and incomplete separation of T7 and T8 vertebrae (the intervertebral disk between these 2 vertebral bodies was absent) and suggested that this was associated with spinal cord compression. Transverse images indicated that there was severe dorsoventral attenuation of the vertebral canal over a distance of approximately 10 mm, which was associated with gross dorsoventral shortening of the pedicles.
Each dog was treated surgically. The precise surgical approach was determined by the origin and nature of the compressive lesion that was revealed via MR imaging. Thus, in dog 1, dorsal laminectomy over the T8, T9, and T10 vertebral bodies (where there was considerable ventrodorsal cord compression) was performed. In addition, the annuli of the T8-9 and T9-10 intervertebral disks were excised as completely as possible to allow the vertebral body of T9 to be displaced ventrally. Ventral displacement was accomplished through leverage obtained by implantation of positive-threaded external fixator pinsb into the vertebral bodies of T8, T9, and T10 (Figures 3 and 4). The vertebrae were then fixed in position by application of PMMA bone cementc (in a manner similar to its use for stabilization of vertebral fracture-dislocations1). In dog 2, a right-sided hemilaminectomy of T4, T5, and T6 vertebrae allowed resolution of laterally located compression caused by encroachment of a hypertrophic articular facet into the vertebral canal. The region was then stabilized by use of a unilateral construct of positive-threaded pinsb driven into the vertebral bodies and embedded in PMMA bone cement. In dog 3, a dorsal laminectomy was used to decompress the spinal cord within the T7 and T8 vertebrae, followed by segmental spinal stabilization2 with 1.0-mm-diameter Kirschner wires attached with 2-0 polypropylene sutured and PMMA bone cement (to prevent pin migration) to the spinous processes, articular facets, and rib heads from T3 through T12.
After surgery, neurologic recovery was slow in dog 1; after 2 months, the dog was mildly ataxic with persistent mild deficits in toe knuckling and hopping responses. This dog subsequently reached skeletal maturity and remained mildly ataxic in the pelvic limbs, despite only equivocal improvement in degree of kyphosis (Figure 3). In dog 2, there was early neurologic deterioration following surgery because of cord compression induced by bone cement (and an adjacent insulating gelatin spongee) encroaching on the hemilaminectomy site. Given the radiographic evidence of this, the dog underwent exploratory surgery during which the encroaching cement was identified and removed; new PMMA bone cement was placed more laterally to ensure that encroachment on the vertebral canal did not recur. The dog subsequently recovered and had mild ataxia and mild deficits in hopping responses by 12 weeks after surgery. Radiography revealed that the stabilized vertebrae maintained their immediate postoperative positions with respect to one another despite growth of neighboring vertebral bodies. Following surgery, dog 3 recovered rapidly and had a normal gait after 3 weeks; mild deficits in pelvic limb hopping responses were evident at that time and this level of function was maintained while growth was completed.
Vet MRI, Esaote, Genova, Italy.
Veterinary Instrumentation, Sheffield, UK.
Palacos R-20 with Gentamicin, Schering-Plough Europe, Brussels, Belgium.
Prolene, Johnson & Johnson Medical Ltd, Gargrave, Skipton, UK.
Spongostan, Johnson & Johnson Medical Ltd, Gargrave, Skipton, UK.
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