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Abstract

  1. Top of page
  2. Abstract
  3. Introduction
  4. Materials and methods
  5. Results
  6. Discussion
  7. References

Objectives: To describe the clinical and magnetic resonance imaging features of cervical vertebral malformation-malarticulation in Bernese mountain dogs.

Methods: Seven Bernese mountain dogs (four males and three females) were diagnosed with cervical vertebral malformation-malarticulation by magnetic resonance imaging. The following data were evaluated retrospectively: (1) abnormalities of the cervical vertebral column and spinal cord, (2) spinal cord compression, (3) intervertebral disc degeneration and herniation, (4) severity of clinical signs pretreatment and after treatment, (5) type of treatment and (6) outcome.

Results: Spin echo T1-weighted and T2-weighted images disclosed multi-level, extradural compressive spinal cord lesions (ventral, dorsolateral or both) spanning from intervertebral disc spaces C3-4 to C6-7. In all seven dogs, T2-weighted images disclosed one or more intramedullary hyperintensities associated with extradural spinal cord compression. Surgery was performed in five dogs. Two dogs were managed medically. The prognosis for surgical or conservative management in Bernese mountain dogs was similar to cervical vertebral malformation-malarticulation in other breeds.

Clinical Significance: Cervical vertebral malformation-malarticulation is an important differential diagnosis for young to middle-aged Bernese mountain dogs with a C1-5 or C6-T2 neuroanatomic localisation. Dorsolateral spinal cord compression associated with articular process hypertrophy was the most common feature of cervical vertebral malformation-malarticulation in the seven Bernese mountain dogs evaluated.


Introduction

  1. Top of page
  2. Abstract
  3. Introduction
  4. Materials and methods
  5. Results
  6. Discussion
  7. References

Cervical vertebral malformation-malarticulation (CVMM; also referred to as wobbler syndrome, cervical spondylomyelopathy and cervical vertebral stenotic myelopathy) is a common neurological disorder of the cervical vertebral column in large breed dogs (da Costa and others 2006). The aetiopathogenesis of CVMM is believed to be complex and likely varies between individual cases. Vertebral column malformation, relative vertebral canal stenosis, intervertebral disc (IVD) degeneration, vertebral column instability, various nutritional factors and chronic microtrauma are speculated mechanisms underlying spinal cord lesion development in dogs and other species (Trotter and others 1976, Van Gundy 1989, da Costa and others 2006, Levine and others 2007).

The most common vertebral column abnormalities associated with CVMM include (1) vertebral malformation (stenosis of the vertebral foramen secondary to shortened pedicles and/or misshapen cervical vertebral bodies resulting in instability or vertebral “tipping”), (2) chronic IVD degeneration and herniation, (3) ligamentous hypertrophy (dorsal longitudinal and interarcuate ligaments) and vertebral remodelling (thickening of the vertebral dorsal lamina), (4) proliferation of the joint capsule of the articular processes with or without cyst formation and (5) osteoarthrosis of the articular processes (Seim and Withrow 1982, Van Gundy 1989, Summers and others 1995). Typically, a combination of these factors leads to a compressive cervical myelopathy characterised by variable degrees of cervical hyperaesthesia, tetraparesis and general proprioceptive (GP) ataxia.

Dobermanns and great Danes are overrepresented among dog breeds with CVMM, however, the syndrome has been described sporadically in several other large dog breeds (Lewis 1989). A single Bernese mountain dog (BMD) has been documented with CVMM in a retrospective case series (Lewis 1989); however, CVMM has not been established as a breed-associated disorder in the BMD. We have evaluated seven BMDs that were diagnosed with CVMM from 2003 to 2007. The clinical features, magnetic resonance imaging (MRI) findings and management of these cases are described in this report.

Materials and methods

  1. Top of page
  2. Abstract
  3. Introduction
  4. Materials and methods
  5. Results
  6. Discussion
  7. References

Case selection

The medical databases from the University of Georgia College of Veterinary Medicine, Canada West Veterinary Specialists and Ocean State Veterinary Specialists were searched for pure-bred BMDs with cervical spinal cord diseases. Inclusion criteria necessitated an MRI diagnosis of CVMM based on the presence of a minimum of two of the following: (1) vertebral canal malformation or vertebral canal remodelling (for example spinal stenosis), (2) ventral, extradural spinal cord compression associated with IVD herniation ± dorsal longitudinal ligament hypertrophy and (3) dorsolateral, extradural spinal cord compression associated with articular process hypertrophy. Dogs with IVD herniation in the absence of other lesions were excluded to ensure that the CVMM group consisted only of BMDs with multi-factorial spinal cord compression.

Clinical data collection

Age, sex, weight, onset and duration of clinical signs, and neuroanatomic localisation were retrieved from the medical records. Results of other vertebral column imaging studies and cerebrospinal fluid (CSF) analysis also were reviewed.

Magnetic resonance imaging

A 1.5 Tesla MRI unit (Siemens Medical Solutions USA, Inc.) with a cervical coil was used to image five of seven dogs; a single dog (dog 7) was imaged with a 1.0 Tesla MRI unit (Siemens Medical Solutions USA, Inc.) with a spine coil.

Before anaesthesia, dogs received various premedications including medetomidine (Domitor; Pfizer Animal Health); midazolam (Abbott Laboratories); morphine (ESI-Lederle Generics), butorphanol (Torbutrol; Fort Dodge Animal Health) or hydromorphone (Dilaudid; Abbott Laboratories). Propofol (PropoFlo; Abbott Laboratories) was utilised for anaesthesia induction and maintenance with a constant rate infusion at 0·1 to 0·2 mg/kg/min. All dogs received oxygen either by mask or by endotracheal intubation.

All dogs were positioned in dorsal recumbency with the thoracic limbs extended caudally. On the 1.5 Tesla MRI, the majority of images were acquired using a 3·0 mm slice thickness with 0·3 mm spacing (sagittal and transverse), except for one dog that was imaged with a 2·0 mm slice thickness. On the 1.0 Tesla MRI, images were acquired with a 3·0 mm slice thickness and 0·2 mm spacing (sagittal and transverse). The repetition time (TR) and time to echo (TE) were adjusted to acquire the best images for each dog.

T1-weighted (T1W) spin echo (TR=11 to 25, TE=5 to 6) was acquired as localiser images in dorsal and sagittal planes. The T1W spin echo (TR=380 to 700, TE=11 to 14) and T2-weighted (T2W) spin echo (TR=2800 to 4400, TE=81 to 130) sagittal images initially were acquired. The T1W spin echo (TR=480 to 830, TE=11 to 15) and T2W spin echo (TR=3820 to 8640, TE=84 to 125) transverse images subsequently were obtained from the C2-3 IVD space through the C6-7 IVD space, inclusive. The transverse images were obtained contiguously from the mid-vertebral bodies of C2 through C7. T2W gradient echo (TR=1930, TE=60, flip angle=30 degrees) transverse images were obtained in one dog. Transverse plane, postcontrast T1W spin echo images were acquired in one dog. Gadolinium 10-(2-hydroxy-propyl)-1,4,7,10 tetraazacyclododecane-1,4,7-tracetic acid diethylenetriaminepentaacetic acid (Gadoteridol; ProHance, Bracco Diagnostics) was used as the paramagnetic contrast agent (0·1 mmol/kg iv).

Abnormalities of the cervical vertebral column and spinal cord

The following components of CVMM were assessed in all dogs in T1W and T2W MRI in both the transverse and sagittal planes: (1) presence of vertebral canal malformation or vertebral canal remodelling (for example vertebral canal stenosis), (2) ventral, extradural spinal cord compression associated with IVD herniation ± dorsal longitudinal ligament hypertrophy, (3) dorsolateral, extradural spinal cord compression associated with articular process hypertrophy and (4) intramedullary hyperintensity (T2W only) at the level of spinal cord compression.

Spinal cord compression

The presence of non-disc-associated spinal cord compression was assessed based on (1) the loss of subarachnoid space and epidural fat on T2W transverse images compared with adjacent slices, (2) shape of the spinal cord and (3) the cross-sectional area of the spinal cord compared with the mid-body of the vertebrae immediately cranial and caudal to the site affected (da Costa and others 2006). The cross-sectional area of the spinal cord was measured in square centimetres (cm2) using OsiriX v.2.7 software (The OsiriX Foundation). If the cross-sectional area of the spinal cord at the site of compression was less than the cross-sectional area of the spinal cord at the mid-body of the vertebrae immediately cranial to and caudal to the site affected, the spinal cord was deemed to be compressed. The degree of compression also was calculated as a percentage of the cross-sectional area of the spinal cord at the mid-body of the vertebrae immediately cranial and caudal to the site of the lesion.

Degeneration and herniation of cervical IVDs

The degree of degeneration (dehydration) of the IVDs was assessed subjectively in all dogs. The degree of IVD degeneration was based on a loss of signal intensity in the nucleus pulposus on T2W sagittal imaging (Lipsitz and others 2001).

The degree of IVD herniation was assessed in all dogs by T1W and T2W MR imaging in both the transverse and sagittal planes. The modified spinal cord compression scale (Kasai and Uchida 2001) was used to grade the degree of IVD herniation: grade 0, no compression; grade 1, partial subarachnoid space compression; grade 2, complete subarachnoid space compression and grade 3, spinal cord compression.

Severity of clinical signs, pretreatment and after treatment, treatment outcome and follow-up

Treatment method (surgical versus medical management) and outcome were retrieved from the medical records for each of the seven BMDs in the study.

A modified Frankel score (MFS) was used to retrospectively grade dogs (before and after treatment) as having tetraplegia or paraplegia with no deep nociception (grade 0), tetraplegia or paraplegia with no superficial nociception (grade 1), tetraplegia or paraplegia with nociception (grade 2), non-ambulatory tetraparesis or paraparesis (grade 3), ambulatory tetraparesis or paraparesis and ataxia (grade 4), spinal hyperaesthesia only (grade 5) or no dysfunction (Frankel and others 1969, Levine and others 2006).

At the time of data collection, follow-up phone calls were made to all owners to determine if the dog was still alive, whether clinical signs had resolved, improved, remained unchanged or had progressed. Owners also were asked if the dog was being treated medically for CVMM.

Results

  1. Top of page
  2. Abstract
  3. Introduction
  4. Materials and methods
  5. Results
  6. Discussion
  7. References

Clinical data

Thirteen BMDs with cervical spinal cord diseases were identified. Seven BMDs (four males and three females) met inclusion criteria and had various degrees of IVD degeneration; ventral, extradural spinal cord compression associated with IVD herniation±dorsal longitudinal ligament hypertrophy; and dorsolateral, extradural spinal cord compression associated with articular process hypertrophy (Table 1). Five BMDs with only IVD-related, ventral spinal cord compression (but no other major features of CVMM) were excluded. One BMD was excluded because it was diagnosed with a combination of steroid responsive meningitis-arteritis (SRMA) and subclinical CVMM.

Table 1. Summery of clinical and MRI findings in seven Bernese mountain dogs with CVMM
NumberSignalmentNeuroanatomic localisation/MFSCervical hyperaesthesiaChronicityDegenerative discsSite of ventral compression and gradeSite of dorsolateral compression and CS%Parenchymal hyperintensity (T2W imaging)TreatmentDuration of follow-upFollow-up MFS
  1. CVMM cervical vertebral malformation-malarticulation. CS% Cross-sectional area of the spinal cord at the site of compression/cross-sectional area of the spinal cord at the mid-body cranial and caudal to the site of compression, respectively, multiplied by 100, T2W T2-weighted, MFS Modified Frankel score, FS Female spayed, D Decreased signal, A Absent signal, MC Male castrated, L Left, R Right, HSA Hemangiosarcoma, Sl. Slightly, GDV Gastric dilatation-volvulus, NSAIDS Nonsteroidal anti-inflammatory drugs.

Dog 1Six years, FS, 42·9 kgC1-5, MFS=4YesFive to seven daysC3-4 (D), C4-5 (D), C5-6 (D), C6-7 (D), C7-T1 (A)C3-4(3), C4-5 (1)C4-5 (79%, 69%); C5-6 (78%, 79%)C3-4, C5-6Surgery – C3/4 ventral slot; C4/5, C5/6 plug2·7 yearsNormal
Dog 2Four years, MC, 40·0 kgC1-5, MFS=4NoThree monthsC4-5 (D), C6-7 (D), C7-T1 (A)C6-7 (1)C4-5 (77%, 68%); C5-6 (56%, 53%); C6-7 (41%, 52%)C3-4, C5-6, C6-7Surgery – C5/6, C6/7 plug11 weeksMFS=2, patient euthanased at that time
Dog 3Five years, MC, 63·0 kgC6-T2 (L>R), MFS=4NoTwo monthsC6-7 (D), C7-T1 (D)C6-7 (1)C5-6 (73%, 70%); C6-7 (55%, 75%)C6-7Anti-inflammatory prednisone3·5 yearsMFS=4 to 5, euthanased because of HSA
Dog 4Two years, MC, 48·0 kgC1-5, MFS=4No18 monthsC5-6 (sl.D), C6-7 (sl. D)C3-4 (2)C4-5 (59%, 80%); C5-6 (83%, 74%); C6-7 (64%, 80%)C3-4, C4-5, C6-7Surgery – C4/5, C5/6, C6/7 plug12 weeksMFS=5, euthanased because of uncontrollable cervical hyperaesthesia secondary to vertebral osteomyelitis at surgical site
Dog 518 months, MC, 57·3 kgC1-5, MFS=4NoChronic ataxia, acute worsening five days before presentationC5-6 (sl.D), C6-7 (sl. D), C7-T1 (sl. D)C2-3 (2), C3-4 (2)C3-4 (78%, 74%); C4-5 (66%, 56%); C5-6 (82%, 77%)C4-5Surgery – C3/4, C4/5, C5/6, plug15 monthsNormal, patient died at that time secondary to GDV surgical complications
Dog 6Seven years, FS, 43·7 kgC6-T2, MFS=3YesSeven daysC2-3 (D), C3-4 (D), C4-5 (D), C5-6 (D), C6-7 (A), C7-T1 (A)C6-7 (3)C4-5 (84%, 68%); C5-6 (70%, 77%)C3-4, C4-5Surgery – C6/7 ventral slot5·5 monthsNormal
Dog 7Six years, FS, 55·5 kgC1-5, MFS=4Yes14 daysC6-7 (A), C7-T1 (A)C6-7 (2)C5-6 (95%, 83%); C6-7 (67%, 76%)C5-6Physical rehabilitation, acupuncture, NSAIDs, tramadol16 daysMFS=2, patient euthanased

The age of presentation ranged from 18 months to seven years (median 5·2 years); weight ranged from 40·0 to 63·0 kg (mean 50·1 kg). All dogs had progressive clinical signs ranging in duration from five days to 18 months (median two months).

Five dogs (dogs 1, 2, 4, 5 and 7) had a neuroanatomic localisation of C1-5. Of the five dogs, four (dogs 2, 4, 5 and 7) were presented with tetraparesis and GP ataxia in all four limbs and one dog (dog 1) was presented with paresis and GP ataxia that were appreciable in the pelvic limbs only. All five dogs that localised C1-5 were ambulatory and each had an MFS of 4. Two dogs (dogs 3 and 6) had a neuroanatomic localisation of C6-T2, one of which (dog 3) had lower motor neuron paresis in the thoracic limbs and upper motor neuron paresis and GP ataxia in the pelvic limbs (MFS of 4); the other dog (dog 6) was severely tetraparetic and non-ambulatory (MFS of 3). Three of seven dogs (dogs 1, 6 and 7) had cervical hyperaesthesia (low head carriage, resistant to range of motion of the neck) at the time of evaluation.

Survey vertebral column radiography and CSF analysis

One dog (dog 3) was evaluated by survey radiography of the entire vertebral column, which did not reveal any abnormalities. One dog (dog 4) was evaluated by survey radiography of the cervical vertebral column, which did not reveal any abnormalities. CSF analysis was performed for two dogs (dogs 3 and 5), both of which had normal protein levels, cell counts and cytology.

MRI abnormalities of the cervical spine and spinal cord

Dorsal spinal cord compression was evident in one dog (dog 7) at the C5-6 IVD space, and this was presumed to be associated with hypertrophy of the interarcuate ligament, remodelling of the dorsal lamina within the vertebral canal or both.

Bilateral dorsolateral compression of the spinal cord at the level of the articular processes was present in all dogs (Fig 1). The periarticular extradural lesions were hypointense (on both T1W and T2W) to the spinal cord parenchyma and consequently they were difficult to differentiate from the vertebral column. Four dogs (dogs 1, 3, 6 and 7) were affected at two sites and three dogs (dogs 2, 4 and 5) were affected at three sites. The sites involved spanned from C3-4 to C6-7, inclusive. Three (dogs 3, 4 and 5) of the seven dogs had asymmetric compression (Fig 2), whereas four dogs (dogs 1, 2, 6 and 7) had relatively symmetric dorsolateral spinal cord compression.

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Figure 1. Dog 4. T2-weighted transverse image through the level of C5-6. There is bilateral dorsolateral compression of the spinal cord present secondary to hypointense tissue associated with the articular processes (long arrow). The shape of the spinal cord is altered from round to triangular. The epidural fat/cerebrospinal fluid hyperintensity surrounding the spinal cord is preserved on the right side (short arrow), but it is lost on the left side

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image

Figure 2. Dog 5. T2-weighted transverse image through the level of C3-4. There is loss of the hyperintense epidural fat/cerebrospinal fluid around the right side of the spinal cord and unilateral spinal cord compression is present secondary to hypointense tissue associated with the articular process (arrow). The shape of the spinal cord is altered secondary to the compression

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On T2W imaging, all dogs were noted to have at least one intramedullary hyperintensity present at a level of concurrent spinal cord compression (Fig 3, 4, 5). Three (dogs 3, 5 and 7) of seven dogs had a single parenchymal hyperintensity, while the other four dogs (dogs 1, 2, 4 and 6) had two or more hyperintense areas. Given the concurrent spinal cord compression, differentials for the hyperintense abnormalities included hydromyelia secondary to spinal cord atrophy, oedema and gliosis (Lipsitz and others 2001).

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Figure 3. Dog 1. T2-weighted transverse image through the level of C5-6. There is bilateral dorsolateral compression of the spinal cord present secondary to hypointense tissue associated with the articular processes (arrow). The shape of the spinal cord is altered from round to trapezoid. The epidural fat/cerebrospinal fluid hyperintensity around the spinal cord is preserved. There is an area of hyperintensity in the dorsal funiculus

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image

Figure 4. Dog 4. T2-weighted transverse image through the level of C6-7. There is bilateral dorsolateral compression of the spinal cord present secondary to hypointense tissue associated with the articular processes (arrows). The shape of the spinal cord is altered from round to triangular. The epidural fat/cerebrospinal fluid hyperintensity around the spinal cord is preserved (short arrow). There is an area of hyperintensity at the level of the central canal

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image

Figure 5. Dog 4. T2-weighted transverse image through the level of C4-5. There is bilateral dorsolateral compression of the spinal cord present secondary to hypointense tissue associated with the articular processes (arrows). The shape of the spinal cord is altered from round to square shaped. The epidural fat/cerebrospinal fluid hyperintensity is absent on lateral and ventral aspects of the spinal cord but is retained dorsally. There is an area of hyperintensity at the level of the central canal

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T1W postcontrast imaging in one dog (dog 6) disclosed no areas of enhancement.

Intervertebral disc degeneration and herniation

Various degrees and anatomic sites of IVD degeneration and herniation were present throughout the cervical vertebral column from C2-3 through C7-T1 in all seven dogs (Table 1).

Five of the seven dogs had grade 1 to 2 ventral spinal cord compressions secondary to IVD herniation. Of these five dogs, one dog had two sites of IVD herniation (dog 5) and the other four dogs (dogs 2, 3, 4 and 7) had one site of IVD herniation. Two of the seven dogs (dogs 1 and 6) had grade 3 spinal cord compression at single sites. One of these two dogs (dog 1) also had a grade 1 compression at a second site.

Treatment

Ventral slot decompression was performed in two (dogs 1 and 6) of seven dogs, both of which had grade 3 spinal cord compression. Dog 1 had a ventral slot decompression at C3-4 with removal of extruded nucleus pulposus from the spinal canal, followed by distraction-stabilisation using a modified cement plug technique at C4-5 and C5-6. This procedure has been described previously and utilises polymethylmethacrylate plugs and cortical bone screws for distraction-stabilisation of the cervical vertebral column (Dixon and others 1996, McKee and Sharp 2003). Dog 6 had a ventral slot decompressive procedure at C6-7 only and fresh, extruded nucleus pulposus was removed from the spinal canal. Three dogs (dogs 2, 4 and 5) had the distraction-stabilisation procedure using the modified cement plug technique at C5-6, C6-7; C4-5, C5-6, C6-7; and C3-4, C4-5, C5-6, respectively.

Postoperative pain was controlled with acetaminophen-oxycodone hydrochloride (Percocet; Endo Laboratories LLC). None of the dogs that were managed surgically were treated with postoperative nonsteroidal anti-inflammatory drugs (NSAIDs) or glucocorticoids.

Surgery was declined by the owners of two dogs (dogs 3 and 7), and conservative management was pursued. One dog (dog 3) was managed medically with strict rest for one month and prednisone at 0·1 mg/kg every other day for the duration of the dog’s life (3·5 years). One dog (dog 7) was managed medically with NSAIDs, tramadol (Mutual Pharmaceutical Co., Inc.), physical rehabilitation and acupuncture for two weeks at which time the dog was euthanased.

Outcome – surgical management

Surgical follow-up ranged from 12 weeks to 3·5 years. Dog 1 (preoperative MFS of 4) had a normal neurological examination at 10·5 weeks postoperatively. At the time of manuscript submission, the dog had maintained a normal neurological status for 2·7 years postoperatively. Dog 2 (preoperative MFS of 4) had improved subjectively at six weeks (although maintained a MFS of 4) but deteriorated to tetraplegic (MFS of 2) 11 weeks postoperatively, and it was euthanased. Dog 4 (preoperative MFS of 4) had intermittent neck pain seven weeks postoperatively (MFS of 5) and was euthanased 12 weeks postoperatively because of vertebral osteomyelitis at the surgical site. Dog 5 (preoperative MFS of 4) had improved markedly four months postoperatively (MFS of 5) and it was assessed to be normal 15 months postoperatively when it died from complications of a gastric dilatation-volvulus. Dog 6 (preoperative MFS of 3) was normal as per the owner’s report within two to three weeks after surgery and it had had no recurrence 5·5 months postoperatively.

Outcome – conservative management

Dog 3 (preoperative MFS of 4) had one to two episodes per month of intermittent neck pain and pelvic limb weakness (MFS of 4 to 5). Dog 3 was euthanased on account of a hemangiosarcoma that was diagnosed 3·5 years after the diagnosis of CVMM. Dog 7 (preoperative MFS of 4) was euthanased 16 days after the diagnosis of CVMM because of decline in neurological status (MFS of 2).

Discussion

  1. Top of page
  2. Abstract
  3. Introduction
  4. Materials and methods
  5. Results
  6. Discussion
  7. References

CVMM has been recognised for decades in large breed dogs and there are numerous reports of the associated clinical features, diagnostic tests, treatments and pathological findings (Trotter and others 1976, Denny and others 1977, Lewis 1989). The Dobermann and great Dane are overrepresented among dogs with CVMM; however, numerous other breeds have been reported sporadically (Wright and others 1973. Lewis 1989). A single BMD was included in a case series of 224 dogs with CVMM (Lewis 1989). Our descriptive study was pursued because it has been the authors’ clinical impression that CVMM is a key differential for cervical spinal cord disease in young to middle-aged BMDs.

Common differentials for cervical spinal cord disease in large breed dogs include IVD herniation, CVMM, SRMA, discospondylitis, neoplasia and fibrocartilaginous embolic myelopathy. Young to middle-aged BMDs are overrepresented for SRMA (Tipold 2000). The BMD also has a genetic predisposition for the development of histiocytic sarcoma, a neoplasm with a grave prognosis (Voegeli and others 2006). Because of the overlap in clinical signs in the differential diagnosis, a complete neurological work-up including MRI and CSF analysis is recommended for BMDs with clinical signs of a cervical myelopathy.

The typical signalment for CVMM varies among breeds. In the Dobermann and the great Dane, clinical signs may develop from three months to 11 years of age (Lewis 1989). In the BMDs reported here, the age of presentation ranged from 18 months to seven years. Multiple reports suggest that male dogs are overrepresented for CVMM (Read and others 1983, Lewis 1989), although one report identified no sex predilection (Burbidge and others 1994). In this relatively small group of seven BMDs, male and female dogs were affected evenly. In light of the small number of cases in this study, we cautiously conclude that CVMM affects young to middle-aged BMDs with insufficient data to determine gender predilection.

Because CVMM has variable forms and clinical presentations, numerous attempts have been made to subcategorise the so-called “wobbler syndrome”. Dobermanns with CVMM typically manifest clinical signs after two years of age with a peak incidence between four and eight years of age (Lewis 1991, Burbidge and others 1994, McKee and others 1999). The most common pathological features of CVMM in Dobermanns include protrusion of the caudal cervical IVDs (Hansen Type II IVD diseases) and hypertrophy of the interarcuate ligament (Seim and Withrow 1982, Van Gundy 1988, 1989, Summers and others 1995). Because IVD protrusion is such a predominating feature in Dobermanns with CVMM, the term disc-associated wobbler syndrome (DAWS) has been proposed (Van Gundy 1988, McKee and Sharp 2003). In our case search, we identified five BMDs with IVD herniation without additional features of CVMM. The authors chose to exclude dogs without evidence of multi-factorial compression to reduce the possibility of selection bias. The impact of errors in case selection is especially important in small, descriptive case series, as inclusion of animals without the disease of interest may produce faulty data and inaccurate conclusions (Grimes and Schulz 2002).

In contrast to Dobermanns with DAWS, great Danes with CVMM typically present with a cervical myelopathy by two years of age. Features of CVMM in great Danes include dorsal or dorsolateral spinal cord compression secondary to osteoarthrosis of the articular processes, hypertrophy of the joint capsules of the articular facets and hypertrophy of the interarcuate ligament (Lewis 1989, Braund 1994, Sharp and others 1995, Summers and others 1995). Any site(s) from C3-4 to C6-7 may be affected, although C5-6 and C6-7 are most common (Braund 1994, Sharp and Wheeler 2005). Similar to the situation in great Danes, the most prominent feature of CVMM in the BMD appears to be articular process-associated, dorsolateral and caudal cervical spinal cord compression.

In the seven BMDs with CVMM, MRI disclosed dorsolateral spinal cord compression secondary to overgrowth of the articular processes (Figs 1 to 5). It is noteworthy that midline sagittal images did not disclose spinal cord compression in six of seven dogs, suggesting that transverse imaging of the cervical spine should be completed in all suspect cases of CVMM. In all dogs, the articular process overgrowth altered the normal shape of the spinal cord. In addition, the cross-sectional area at the level of the compressed spinal cord was reduced compared with that immediately cranial and caudal to all articular process lesions. This approach was utilised to account for the natural variation in spinal cord diameter in the cervicothoracic area. Interestingly, on T2W transverse imaging, the hyperintensity comprising CSF in the subarachnoid space and epidural fat typically was preserved despite an obvious change in shape and cross-sectional area of the spinal cord (Fig 4). This may reflect spinal cord atrophy secondary to chronic compression; however, post-mortem tissues were not available to confirm this consideration (Sharp and others 1995).

The articular process and facet lesions associated with CVMM are considered to be a form of osteochondrosis dissecans by some investigators (Lincoln 1992). In BMDs, it is unclear whether the articular-process-associated spinal cord compression is secondary to periarticular bone formation or proliferation of the joint capsule or both. MR imaging cannot differentiate between the two, as both osseous and fibrous tissues are hypointense on T1W and T2W imaging. Cervical radiography performed in two dogs disclosed no osseous abnormalities. Another important differential for dorsolateral compression is synovial cyst formation; however, T2W MRI did not disclose evidence of high signal lesions associated with the articular processes (Levitski and others 1999). Visualisation of the vertebral articulations was not possible during surgery because of the ventral approach utilised in all cases. Post-mortem examinations will be necessary to determine the histopathological features of the articular process lesions in the future.

In addition to articular process hypertrophy, mild to moderate ventral, IVD-associated spinal cord compression was present in seven dogs. In two dogs, ventral slot decompression disclosed a moderate amount of fresh nucleus pulposus within the spinal canal at the level of herniated IVDs (Hansen type I IVDD). The Hansen classification in the remaining dogs was not determined. In an MRI study of 21 large breed dogs with CVMM (including 14 great Danes), all dogs had dorsolateral spinal cord compression associated with articular process changes, but only two dogs had evidence of disc herniation (Hansen type II IVDD) (Lipsitz and others 2001). Hansen type I IVD herniation typically is not a feature of CVMM, suggesting that a combination of two disease processes occurred in the two BMDs with CVMM and IVD extrusion. Another interesting finding was the presence of IVD degeneration/dehydration in all BMDs evaluated. In the Lipsitz study, only six of 21 large breed dogs had evidence of degenerative IVDs. This suggests that primary cervical IVDD may be more common in the BMD or that CVMM in this breed is a predisposing factor to the development of a cervical disc herniation.

While articular process compression is an important similarity between BMDs and great Danes with CVMM, it may be premature to conclude that the two breed-associated disorders are analogous. An important signalment difference is that the majority of the BMDs were presented with clinical signs after four years of age, whereas great Danes typically were presented before the age of two. In addition, great Danes with CVMM commonly are affected by dorsal spinal cord compression (because of hypertrophy of the interarcuate ligament), whereas only one BMD showed this feature in addition to a separate articular-process-associated lesion. Finally, the definitive histopathological changes associated with the articular process overgrowth and ligamentous changes within the spinal canal have yet to be elucidated in the BMD. In light of the limited cases evaluated and the current lack of histopathology, comparisons to the great Dane or other breeds with CVMM should be made cautiously.

The small number of BMDs with CVMM evaluated here also limits our ability to draw definitive conclusions on the disease prognosis. The procedure utilised in all but one surgically treated case was a ventral distraction-stabilisation technique. One of the goals of this surgery is to decrease or abolish movement at the vertebral articulation. Fusion in dogs has been shown to cause regression of the interarcuate ligament and decrease excessive bone formation around the articular processes (McKee and others 1990, Galano and others 2005). Additionally, distraction-fusion likely enlarges the area through which the spinal cord traverses vertebral articulations by stretching the interarcuate ligament and inducing lordosis (Bayley and others 1995). Various surgical techniques have been described for the treatment of CVMM (Sharp and Wheeler 2005).

To date, there have been no published studies that compare dorsal and ventral surgical techniques for the treatment of articular-process-associated spinal cord compression. The only study comparing dorsal and ventral surgical techniques evaluated cases of DAWS (Jeffery and McKee 2001). Therefore, the potential therapeutic value of an alternative surgical approach such as a continuous dorsal laminectomy for BMD with CVMM currently is unknown. Although the number of BMDs included in this report is small, long-term outcome appeared similar to that which has been reported in other breeds with CVMM after surgical intervention (Seim 1986, Van Gundy 1988, Dixon and others 1996, Rusbridge and others 1998, McKee and others 1999, De Risio and others 2002).

In conclusion, CVMM is an important differential for cervical spinal cord disease in young to middle-aged BMDs. The most common and clinically relevant feature of CVMM present in this cohort was articular-process-associated spinal cord compression. Other features of CVMM in this group of dogs included IVD degeneration, IVD herniation and interarcuate ligament hypertrophy. Further investigations including gross and histopathology, incidence studies and dynamic MRI studies should be pursued to better characterise CVMM in the BMD.

References

  1. Top of page
  2. Abstract
  3. Introduction
  4. Materials and methods
  5. Results
  6. Discussion
  7. References
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