A 3-year-old 9-kg (19.8-lb) sexually intact male French Bulldog was referred to the neurology service of the Vetsuisse Faculty of the University of Zurich because of gait abnormalities and signs of pain that developed acutely 48 hours before. No traumatic events had been observed. The dog did not have a history of previous illness, and findings of physical examination were unremarkable. Results of neurologic examination indicated the dog was ambulatory with spastic paraparesis of the hind limbs. Proprioception was decreased in right and left hind limbs (right more affected than left), and spinal reflexes were exaggerated bilaterally. Severe signs of pain were detected during palpation of the lumbar portion of the vertebral column, and vertebrae were in a kyphotic position. No history of urine retention was reported, and palpation revealed the urinary bladder was moderately filled. The cutaneous trunci reflex was normal on the left side and absent on the right; the caudal extent of the reflex was the level of the fourth lumbar vertebra. Neuroanatomic localization of the lesion was determined to be in the T3-L3 spinal cord segment. The degree of neurologic impairment was graded as 2 of 5 on the scale of Sharp and Wheeler.1
The primary differential diagnoses included herniation of a degenerated intervertebral disk or vascular myelopathy resulting in spinal cord infarction or hemorrhage. Inflammatory and neoplastic diseases were considered less likely on the basis of the history and signalment of the dog. Results of hematologic and serum biochemical analyses were within reference ranges.
The dog was premedicated with an IV bolus of fentanyl and anesthetized with propofol. After endotracheal intubation, anesthesia was maintained with isoflurane in oxygen and MRI of the thoracolumbar vertebrae was performed with a 3-T device.a The MRI included T2-weighted turbo spin echo sagittal (echo time, 100 milliseconds; repetition time, 3,069 milliseconds; number of signal averages, 1; echo train length, 17; slice thickness, 2.5 mm; interslice gap, 0.75 mm; field of view, 234 mm; matrix, 588 × 461), T2-weighted turbo spin echo transverse (echo time, 8 milliseconds; repetition time, 2,073 milliseconds; number of signal averages, 3; echo train length, 5; slice thickness, 3 mm; interslice gap, 0.3 mm; field of view, 180 mm; matrix, 400 × 310), T2*-weighted fast field echo transverse (echo time, 16 milliseconds; repetition time, 33 milliseconds; flip angle, 7°; number of signal averages, 2; echo train length, 1; slice thickness, 2 mm; field of view, 180 mm; matrix, 328 × 274), and T1-weighted turbo spin echo transverse (echo time, 90 milliseconds; repetition time, 573 milliseconds; number of signal averages, 1; echo train length, 19; slice thickness, 3 mm; interslice gap, 0.3 mm; field of view, 180 mm; matrix, 400 × 299) sequences obtained before and after IV administration of contrast medium.b The nuclei pulposi of the lumbar intervertebral disks had moderate, inhomogenous signal loss in T2 sequence images, and the width of the intervertebral disk space at L3–4 was moderately narrowed (Figure 1). A moderate amount of material with variable, low T1- and T2-sequence signal intensity was detected in the ventral right aspect of the vertebral canal at the level of the intervertebral disk space at L3–4 and extended caudally (Figure 2). To calculate the volume of the extruded disk material and the spinal cord, the images were exported to a computer workstation.c Areas of interest were manually drawn around the areas of intervertebral disk material, spinal cord, and vertebral canal by one of the authors (MD). The volume was calculated by multiplication of the cross-sectional area by the MRI image slice thickness. The intervertebral disk material had an approximate volume of 0.16 cm3, and the area was 27.3% of the area of the vertebral canal at the level of the maximal size of the extruded material. The spinal cord area was 49.2% of the area of the vertebral canal at that same level, and the remainder of the area of the vertebral canal contained epidural fat and vasculature. The spinal cord had normal MRI signal intensity, was displaced dorsally and to the left, and was mildly compressed. The linings of the dorsal and ventral aspects of the subarachnoid spaces were interrupted from L1–2 to L4–5. Evaluation of the T2* MRI sequence images revealed no susceptibility artifacts. The lesion was not contrast enhanced after IV administration of gadolinium. The imaging diagnosis was mild, extradural spinal cord compression at the level of the intervertebral disk space L3–4 at the ventral right aspect with swelling of the subarachnoid space over 4 spinal cord segments. On the basis of the MRI findings, a diagnosis of sequestrated Hansen type 1 intervertebral disk extrusion was made.
Surgical and conservative treatment options were discussed with the owner. Because of the owners’ concerns regarding risks of surgery and the ambulatory status of the dog, the patient underwent nonsurgical treatment consisting of cage rest and restricted exercise on a leash for 4 weeks.
Nonsteroidal anti-inflammatory medicationd was administered for 10 days. The dog was discharged from the hospital 2 days after diagnosis, and the owners were advised to monitor ambulation and urinary tract function.
Five weeks after the initial examination, a neurologic follow-up examination was performed; results indicated neurologically normal gait and posture, and the dog ambulated without obvious neurologic deficits or signs of pain. The quality of spinal reflexes was clinically normal. A subtle delay in the proprioceptive positioning response was detected in the right hind limb. No signs of pain were elicited during palpation of the thoracolumbar portion of the vertebral column. The cutaneous trunci reflex was clinically normal on right and left sides.
At the owners’ request, MRI was repeated (by use of the same MRI settings that were used during initial MRI). Results indicated almost complete regression of the extradural lesion at the level of the intervertebral disk space L3–4. A small amount of residual material with low T1- and T2-sequence signal intensity was detected, but the spinal cord was not compressed (Figures 1 and 2). The volume of the material had decreased to 0.05 cm3, and the area was only 15% of the area of the vertebral canal at the level of the maximal extent of the extruded material; the area of the spinal cord was 59% of the area of the vertebral canal at that location. The material had mild contrast medium uptake. The displacement and compression of the spinal cord had resolved. On the basis of results of the second MRI, a diagnosis of almost complete regression of sequestrated extruded intervertebral disk material was made.
Ingenia 3T with dStream Coil Solution posterior, Philips SA, Zurich, Switzerland.
Omniscan, 0.5 mmol/mL, GE Healthcare SA, Glattbrugg, Switzerland.
OsiriX 64-bit DICOM viewer, version 4.1, OsiriX Foundation, Geneva, Switzerland.
Onsior/robenacoxib, Novartis Animal Health SA, Basel, Switzerland.
1. Sharp NJH, Wheeler SJ. Thoracolumbar disc disease. In: Small animal spinal disorders: diagnosis and surgery. 2nd ed. Philadelphia: Mosby, 2005;125.
2. Bergknut N, Egenvall A, Hagman R, et al. Incidence of intervertebral disk degeneration-related diseases and associated mortality rates in dogs. J Am Vet Med Assoc 2012; 240: 1300–1309.
3. Bergknut N, Smolders LA, Grinwis GC, et al. Intervertebral disc degeneration in the dog. Part 1: anatomy and physiology of the intervertebral disc and characteristics of intervertebral disc degeneration. Vet J 2013; 195: 282–291.
4. Smolders LA, Bergknut N, Grinwis GC, et al. Intervertebral disc degeneration in the dog. Part 2: chondrodystrophic and nonchondrodystrophic breeds. Vet J 2013; 195: 292–299.
6. Davies JV, Sharp NJ. A comparison of conservative treatment and fenestration for thoracolumbar intervertebral disc disease in the dog. J Small Anim Pract 1983; 24: 721–729.
8. Mann FA, Wagner-Mann CC, Dunphy ED, et al. Recurrence rate of presumed thoracolumbar intervertebral disc disease in ambulatory dogs with spinal hyperesthesia treated with anti-inflammatory drugs: 78 cases. J Vet Emerg Crit Care 2007; 17: 53–60.
9. Maigne JY, Deligne I. Computed tomographic follow-up study of 48 cases of nonoperatively treated lumbar intervertebral disc herniation. Spine 1992; 17: 1071–1074.
10. Levine JM, Levine GM, Porter BF, et al. Naturally occurring disk herniations in dogs: an opportunity for pre-clinical spinal cord injury research. J Neurotrauma 2011; 28: 678–688.
12. Saal JA, Saal JS, Herzog RJ. The natural history of lumbar intervertebral disc extrusions treated nonoperatively. Spine 1990; 15: 683–686.
13. Benson RT, Tavares SP, Robertson SC, et al. Conservatively treated massive prolapsed discs: a 7-year-follow-up. Ann R Coll Surg Engl 2010; 92: 147–153.
15. Jeffery ND, Blakemore WF. Spinal cord injuries in small animals. 1. Mechanisms of spontaneous recovery. Vet Rec 1999; 134: 407–413.
16. da Costa RC, Parent JM. One-year clinical and magnetic resonance imaging follow-up of Doberman Pinschers with cervical spondylomyelopathy treated medically or surgically. J Am Vet Med Assoc 2007; 231: 243–250.
17. De Decker S, Gielen IMVL, Duchateau L, et al. Evolution of clinical signs and predictors of outcome after conservative medical treatment for disk-associated cervical spondylomyelopathy in dogs. J Am Vet Med Assoc 2012; 240: 848–857.
18. Bergknut N, Rutges JPHI, Kranenburg HJC, et al. The dog as an animal model for intervertebral disc degeneration. Spine 2012; 37: 351–358.
19. Satoh K, Konno S, Nishiyama K, et al. Presence and distribution of of antigen-antibody complexes in the herniated nucleus pulposus. Spine 1999; 24: 1980–1984.
20. Ito T, Yamada M, Ikuta F, et al. Histologic evidence of absorption of sequestration-type herniated disc. Spine 1996; 21: 230–234.
21. Ahn SH, Ahn MW, Byun MW. Effect of transligamentous of lumbar disc herniations on their regression and the clinical outcome of sciatica. Spine 2000; 25: 475–480.
22. Matsui Y, Maeda M, Nakagami W. The involvement of matrix metalloproteinases and inflammation in lumbar disc herniation. Spine 1998; 23: 863–868.
23. Kranenburg HJC, Grinwis GC, Bergknut N, et al. Intervertebral disc disease in dogs—part 2: comparison of clinical, magnetic resonance imaging, and histological findings in 74 surgically treated dogs. Vet J 2013; 195: 164–171.
24. Besalti O, Pekcan Z, Sirin YS, et al. Magnetic resonance findings in dogs with thoracolumbar intervertebral disk disease: 69 cases (1997–2005). J Am Vet Med Assoc 2006; 228: 902–908.
25. Naudé SH, Lambrechts NE, Wagner WM, et al. Association of preoperative magnetic resonance imaging findings with surgical features in Dachshunds with thoracolumbar disk extrusion. J Am Vet Med Assoc 2008; 232: 702–708.