• Open Access

Cervical Vertebral Stenosis Associated with a Vertebral Arch Anomaly in the Basset Hound

Authors


Corresponding author: Steven De Decker, Department of Veterinary Clinical Sciences, Royal Veterinary College, University of London, Hawkshead Lane, North Mymms, Hatfield, Hertfordshire AL9 7TA, England; e-mail: sdedecker@rvc.ac.uk

Abstract

Objectives

To report the clinical presentation, imaging characteristics, treatment results, and histopathological findings of a previously undescribed vertebral malformation in the Basset Hound.

Animals and Methods

Retrospective case series study. Eighteen Basset Hounds presented for evaluation of a suspected cervical spinal cord problem. All dogs underwent computed tomography myelography or magnetic resonance imaging of the cervical region.

Results

Thirteen male and 5 female Basset Hounds between 6 months and 10.8 years of age (median: 1.4 years) were studied. Clinical signs varied from cervical hyperesthesia to nonambulatory tetraparesis. Imaging demonstrated a well-defined and smooth hypertrophy of the dorsal lamina and spinous process of ≥2 adjacent vertebrae. Although this bony abnormality could decrease the ventrodorsal vertebral canal diameter, dorsal midline spinal cord compression was predominantly caused by ligamentum flavum hypertrophy. The articulation between C4 and C5 was most commonly affected. Three dogs were lost to follow-up, 10 dogs underwent dorsal laminectomy, and medical management was initiated in 5 dogs. Surgery resulted in a good outcome with short hospitalization times (median: 4.5 days) in all dogs, whereas medical management produced more variable results. Histopathology confirmed ligamentum flavum hypertrophy and demonstrated the fibrocartilaginous nature of this anomaly.

Conclusions and Clinical Importance

Dorsal lamina and spinous process hypertrophy leading to ligamentum flavum hypertrophy should be included in the differential diagnosis of Basset Hounds with cervical hyperesthesia or myelopathy. Prognosis after decompressive surgery is favorable. Although a genetic component is suspected, additional studies are needed to determine the specific etiology of this disorder.

Abbreviations
BMP

bone morphogenetic protein

CSM

cervical spondylomyelopathy

CT

computed tomography

CT-m

computed tomography myelography

MRI

magnetic resonance imaging

NSAID

nonsteroidal anti-inflammatory drug

Clinical signs of cervical hyperesthesia, general proprioceptive ataxia, and tetraparesis in dogs can be caused by congenital, degenerative, inflammatory, neoplastic, traumatic, and vascular disorders affecting the cervical spinal cord.[1] Several congenital malformations affecting the vertebral column and spinal cord have been described in small animals. Classification of these disorders is difficult and has not yet been clearly defined.[2] Some spinal malformations or anomalies are associated with specific dog breeds. Examples are dermal sinus tracts in the Rhodesian Ridgeback,[3] spinal dysraphism in the Weimaraner,[4] hemivertebra in the French Bulldog[5] and arachnoid diverticula,[6, 7] and cervical fibrotic stenosis in the Rottweiler.[8]

The Basset Hound also has been associated with a specific vertebral malformation.[9] In 1968, a deformity of the 3rd cervical vertebral body was described in 6 related, young Basset Hounds. This deformity typically resulted in ventral extradural spinal cord compression between the 2nd and 3rd cervical vertebrae.[9] Later, the same authors considered this condition similar to a form of vertebral abnormality seen in ataxic Great Danes, Doberman Pinschers, Ridgebacks, and “wobbler” horses.[10] In 1977, 3 young Basset Hounds were included in a larger retrospective study about cervical spondylomyelopathy in dogs.[11] Since that time, this condition in Basset Hounds has commonly been referred to as cervical spondylomyelopathy.[12]

This study describes a previously unreported cervical vertebral anomaly in Basset Hounds. This disorder, apparently distinct from previously reported vertebral deformities, is characterized by dorsal lamina and spinous process hypertrophy leading to ligamentous hypertrophy. The aims of this study were to characterize the clinical presentation, imaging findings, treatment results, and histopathological lesions for this cause of cervical vertebral canal stenosis in the Basset Hound.

Material and Methods

Included Dogs

Eighteen Basset Hounds with a diagnosis of cervical vertebral canal stenosis associated with a dorsal lamina and spinous process anomaly were included in this study. The dogs were investigated between February 2005 and March 2012 at the Royal Veterinary College, University of London, England (n = 4 dogs); Centre of Small Animal Studies, Animal Health Trust, England (n = 7); Davies Veterinary Specialists, England (n = 4), and the Faculty of Veterinary Medicine, Ghent University, Belgium (n = 3). To be included in the study, computed tomography myelography (CT-m) or magnetic resonance imaging (MRI) of the cervical vertebral column had to be performed with complete medical records and imaging studies available for review. The following information was collected from the medical records: age at diagnosis, sex, body weight, presenting clinical signs, duration of clinical signs before diagnosis, and treatment received before presentation.

Imaging Studies

All imaging studies were performed under general anesthesia. Although anesthesia protocols could vary among individual cases, a commonly used protocol included premedication with a combination of acepromazine (0.01 mg/kg IV) and methadone (0.1–0.2 mg/kg IV), followed by induction with propofol (4–6 mg/kg IV) and maintenance of general anesthesia with isoflurane in oxygen. Included dogs underwent MRI as the only diagnostic technique (n = 12), a combination of radiography and MRI (n = 1), a combination of radiography, myelography, and CT-m (n = 4) or a combination of radiography, computed tomography (CT), and MRI (n = 1). Myelography was performed by cisternal injection of iohexol1a contrast medium (0.2 mL/kg with a maximal dose of 10 mL). Computed tomography was performed using a single row detector spiral CT2b (n = 3 dogs) or a 16-slice CT3c (n = 2) scanner. After completion of the transverse CT study, sagittal and three-dimensional reconstructions were made. Cervical MRI studies were acquired with either a 0.4T4d (n = 4) or 1.5T,5e,6f (n = 10) imaging system. Sequences could vary among individual cases, but most MRI studies included a minimum of T2- and T1- weighted sagittal and transverse images of the cervical region. Two of the investigators (SD, HV) reviewed the imaging studies individually, after which a consensus opinion was reached.

Treatment and Follow-up

Treatment details (surgical or medical), possible complications related to treatment, duration of hospitalization, and clinical status at the time of discharge were retrieved from the medical records. Short-term follow-up information was obtained from the medical records of reexamination visits. Long-term follow-up was obtained from reexamination visits or by contacting the referring veterinary surgeon or the owners by telephone. A standardized questionnaire (Appendix A) was used to guide telephone follow-up.

Histopathology

For 3 dogs, the surgically removed ligamentum flavum was submitted for histopathological evaluation. For 2 of these dogs, the surgically removed dorsal lamina with its intact spinous process also was submitted for histopathological evaluation. The tissue was fixed in 10% formalin. After fixation, vertebral tissue was decalcified in a formic acid solution7g at 37°C for 14 days. The decalcifying solution was changed every 3 days. When the tissue gained appropriate flexibility for sectioning, it was embedded in paraffin wax, sectioned at 8 μm and stained with hematoxylin and eosin (HE), Alician Blue (AB), and Alazarin Red (AR), according to standard techniques, and microscopically examined using a bright field microscope.

Results

Clinical Presentation

Eighteen Basset Hounds were included in this study. This group consisted of 13 male and 5 female dogs between 6 months and 10.8 years of age (median: 1.4 years; mean: 2.7 years) at the time of presentation. Fourteen of 18 (78%) dogs were <2 years of age at the time of presentation. Body weight varied between 21.8 and 32.3 kg (median: 25.7 kg; mean: 26.2 kg). Seventeen dogs (94%) were ambulatory at the time of presentation. One dog (6%) presented with cervical hyperesthesia without neurological deficits, 2 dogs (11%) presented with ataxia and paresis restricted to the pelvic limbs, 5 dogs (28%) with ataxia and paresis affecting all limbs, 9 dogs (50%) with ataxia affecting all limbs and paresis affecting predominantly the thoracic limbs, and 1 dog with nonambulatory tetraparesis (6%). Eight of the 17 Basset Hounds with neurological deficits also demonstrated cervical hyperesthesia. Neurological deficits were asymmetrical in 7 dogs. In 1 dog (a 10.8-year-old Basset Hound), no clinical signs of cervical hyperesthesia or gait abnormalities were noted before presentation for seizures. It was only during neurological examination that mild-to-moderate cervical hyperesthesia was demonstrated. Magnetic resonance imaging of the brain and CSF analysis were unremarkable in this dog. For the other dogs, reported duration of clinical signs before diagnosis ranged from 7 days to 3.2 years (median: 2 months; mean: 4.8 months). Eight dogs received treatment using nonsteroidal anti-inflammatory drugs (NSAIDs; n = 5 dogs) or corticosteroids (n = 3) before presentation. Treatment resulted in clinical improvement in 2 dogs, an unchanged clinical course in 2 dogs and further neurological deterioration in the remaining 4 dogs before presentation.

Imaging Findings

Twenty-eight sites of spinal cord compression were detected in 18 dogs. Eight dogs had 1 site of spinal cord compression, whereas 10 dogs had 2 sites of spinal cord compression. The C4–C5 intervertebral articulation was most often affected (n = 17 dogs). Other affected articulations were C3–C4 (n = 4) and C5–C6 (n = 7).

A well-defined and smooth abnormality involving the dorsal lamina and spinous process of ≥2 adjacent vertebrae was observed in all dogs (Figs 1-3). The dorsally enlarged caudal part of the lamina of the cranially affected vertebra formed a convex-shaped protuberance, which communicated with the concave-shaped, enlarged spinous process of the caudally affected vertebra. This protuberance extended dorsally (n = 19 sites of spinal cord compression) or both dorsally and ventrally (n = 9). The enlarged spinous process extended cranially (n = 21) or cranioventrally (n = 7). This deformation had the characteristics of cortical bone on all imaging techniques. The abnormally formed dorsal lamina and spinous process were separated by a cleft, which communicated with the vertebral canal. This area had imaging characteristics consistent with soft tissue on all imaging techniques. Although the dorsal lamina and spinous process abnormality could result in a variably decreased dorsoventral vertebral canal diameter, dorsal midline spinal cord compression predominantly was caused by hypertrophied ligamentous tissue. With the exception of 1 dog, the articular processes were not involved in the pathological process. In this 1 dog, the left caudal articular process of C4 had an abnormal, irregular, and enlarged shape. This dog had left-sided dorsolateral spinal cord compression. An intramedullary spinal cord hyperintense signal was observed on T2-weighted images for 11 of 14 dogs (79%) that underwent MRI. In 2 dogs, MRI disclosed the above-described vertebral abnormality at 2 sites (C3–C4 and C4–C5), with spinal cord compression only at C4–C5.

Figure 1.

Survey cervical radiographs of a 4-year-old Basset Hound with ambulatory tetraparesis and cervical hyperesthesia (A) and a 4-year-old Basset Hound without a cervical spinal disorder (B). Cranial is left. (A) The caudal part of the dorsal lamina of C5 is well-defined, smooth, and enlarged dorsally (arrow). Also, the spinous process of C6 is enlarged and extends cranially (arrowhead).

Figure 2.

Sagittal reconstructed (A) and C5–C6 transverse (B) cervical CT images of the same clinically affected Basset Hound as Figure 1A. Cranial is left. (A) The caudal part of the dorsal lamina of C5 forms a well-defined and smooth enlarged convex protuberance, which extends dorsally and ventrally (arrow). Also, the spinous process of C6 is enlarged and extends cranioventrally (arrowhead). Sagittal reconstructed (C) and C5–C6 transverse (D) CT images of the same unaffected Basset Hound as Figure 1B.

Figure 3.

T1-weighted sagittal (A) and C5–C6 transverse (B) MR images of the same clinically affected Basset Hound as Figures 1-31–3. Cranial is left. (A) The caudal part of the dorsal lamina of C5 forms a well-defined and smooth enlarged convex protuberance, which extends dorsally and ventrally (arrow). Also, the spinous process of C6 is enlarged and extends cranioventrally (arrowhead). Obvious dorsal spinal cord compression is present at this level. Similar abnormalities, but to a lesser extent, are present between C4 and C5. (B) Dorsal midline compression can be appreciated. Sagittal (C) and C5–C6 transverse (D) T1-weigthed MR images of a 7-year-old Basset Hound without cervical spinal disease.

One dog underwent 2 MRI studies within a period of 6 months (Fig 4). The 1st MRI study demonstrated an abnormally shaped dorsal lamina and spinous process at the levels of C4–C5 and C5–C6 with intramedullary spinal cord hyperintensity and minimal dorsal spinal cord compression at the level of C4–C5. The 2nd MRI study identified severe dorsal spinal cord compression at the level of C4–C5 and moderate spinal cord compression at the level of C5–C6. The 2nd MRI scan disclosed increased soft tissue proliferation in comparison with the initial MRI scan.

Figure 4.

Sagittal T2-weighted (A) and transverse C4–C5 T1-weighted (B) MR images of a 1-year-old Basset Hound with ataxia and paresis affecting all limbs. Although a vertebral malformation affecting the dorsal aspects of C4–C5 and C5–C6 can be seen, only minimal spinal cord compression is present (arrow). There is intramedullary spinal cord hyperintensity (compared with normal gray matter) at the level of C4–C5. Sagittal T2-weighted (C) and transverse C4–C5 T1-weighted (D) MR images of the same dog, 6 months later. (C) Now obvious spinal cord compression is present at the level of C4–C5 (arrow) and, to a lesser extent, at the level of C5–C6 (arrowhead). (D) Severe dorsal midline spinal cord compression by tissue with soft tissue intensity is observed.

Treatment and Outcome

Information related to treatment was available for 15 of the 18 Basset Hounds. The 3 remaining dogs were exclusively referred to one of the participating institutions for diagnostic investigations. For these cases, treatment was carried out by the referring veterinary surgeon.

Ten of the remaining 15 dogs underwent surgery. One of these dogs initially was treated medically for a period of 6 months. The owners of this dog elected for surgery because of neurological deterioration. Surgery consisted in each case of a dorsal cervical laminectomy. The operated sites were C4–C5 in 4 dogs, a combination of C4–C5 and C5–C6 in 4 dogs, C3–C4 and C4–C5 in 1 dog, and 2 separate laminectomies at C3–C4 and C5–C6 in 1 dog. Surgery confirmed the dorsal lamina and spinous process abnormalities in each case with hypertrophied ligamentum flavum as the cause of dorsal spinal cord compression (Fig 5). Intraoperative hemorrhage of the internal vertebral venous plexus occurred in 1 dog. No intraoperative complications were recorded for the other dogs. One dog was neurologically worse the 1st day after surgery. This dog was already nonambulatory before surgery and experienced hemorrhage of the internal vertebral venous plexus during surgery. No postoperative neurological deterioration was noted for the other dogs. Postoperative care included analgesia, consisting of a combination of opioids and NSAIDs, cage rest, and physical therapy. Duration of postoperative hospitalization ranged from 3 to 7 days (median: 4.5 days; mean: 4.7 days). At discharge, all dogs were able to ambulate independently. Owners were advised to use a body harness, and provide anti-inflammatory medications orally for 5 to 10 days and restricted exercise for 4 weeks. One dog was lost to follow-up. The 9 remaining dogs were still alive at the time of this study and had improved markedly after surgery. In 3 dogs, the neurological examination was unremarkable at 4 months, 3.1 years, and 3.6 years postoperatively, respectively. According to the referring veterinary surgeon (n = 4 dogs) or owner (n = 2), 5 dogs had recovered completely, whereas 1 dog experienced very mild intermittent gait abnormalities after long walks. Follow-up time for all surgically treated dogs ranged from 3 months to 6.9 years (median: 3.1 years; mean: 3.0 years).

Figure 5.

Intraoperative picture of the same clinically affected Basset Hound as Figures 1-41–4. Right is cranial. The abnormal spinous process of C6 (*) and dorsally enlarged caudal lamina of C5 (**) can be appreciated, which are separated by a cleft.

Medical treatment, consisting of restricted activity for 4 weeks and the use of a body harness, was initiated in 5 dogs. A tapering dose of an anti-inflammatory dose of prednisolone administered orally was started in 3 dogs, whereas the 2 other dogs were not given any medication. At the time of data capture, 4 dogs were still alive and 1 dog was euthanized 1 month after presentation for reasons unrelated to this study (uncontrollable seizures). The follow-up period for the remaining 4 dogs ranged from 2.9 to 3.4 years (median: 3.3 years; mean: 3.2 years). According to the referring veterinary surgeon (n = 2 dogs) or owner (n = 2), 1 dog had recovered completely, 1 dog still demonstrated intermittent signs of cervical hyperesthesia and gait abnormalities, and the 2 remaining dogs were neurologically worse, but still ambulatory.

Histopathology

Histopathological examination of the ligamentum flavum (Fig 6) identified dense fibrous connective tissue with abundant intercellular collagen and foci of degeneration. Neovascularization and fibrous remodeling was noted. Parts of the ligament demonstrated a marked basophilic matrix containing cells of chondrocytic morphology. There was no evidence of inflammation. These changes indicated hyperplasia and remodeling of the ligamentum flavum. Histopathological examination of the surgically removed dorsal lamina and spinous process (Fig 7) indicated that both fragments contained dense, compact bone. They were connected ventrally by the ligamentum flavum and dorsally by the interspinous ligament. A fissure, containing fibrous tissue, separated both bony fragments. The adjacent interosseous borders were characterized by a margin of periosteum followed by fibrocartilage tissue. This fibrocartilaginous tissue demonstrated signs of disintegration and fibrochondrocytes organized in large clusters, which could represent a response to chronic abnormal forces. Active bone remodeling was observed in the area of transition between bone and calcified fibrocartilage.

Figure 6.

(A) HE stained ligamentum flavum (LF) with magnified square showing marked vascularization (arrow), suggesting active remodeling. (B) Distinct area of basophilic matrix in LF (M) and magnified view of cells of chondrocyte like morphology (arrows). Scale bars, 100 μm.

Figure 7.

(A) Macroscopic view of the C5 dorsal lamina and C6 spinous process of the same clinically affected Basset Hound as Figures 1-41–4 and 6. Inset pictures presenting the highlighted region histologically. (B) AR -and AB-staining demonstrating compact bone (B), fibrocartilage (FC), and interspinous ligament (IL) with marked disintegration and high number of blood vessels (arrows). Ligamentum flavum (LF) connects the 2 bony parts. (C) HE and AR-AB (smaller picture) staining from the magnified square of the previous picture. Visible periosteum (PO). Disintegrated fibrocartilage (FC), containing groups of cell clusters (arrows) as a possible response to stress. (D) HE stained section from the transition area between bone, pseriosteum, and fibrocartilage, presenting active bone remodeling (black arrows), and new osteon formation (red arrows). Scale bars, 100 μm.

Discussion

In this study, we describe a previously unreported vertebral malformation in the Basset Hound. The described anomaly was characterized by a smooth and well-defined hypertrophy of the dorsal part of 2 adjacent vertebrae. The C4 and C5 vertebrae were affected most often, and the occurrence of multiple sites of spinal cord compression was not uncommon. Male dogs were more often affected than female dogs and although most affected Basset Hounds were <2 years of age, clinical signs also were noted in older dogs. The majority of dogs were ambulatory at the time of diagnosis and the most common clinical presentation consisted of generalized ataxia with neurological deficits affecting predominantly the thoracic limbs. This clinical presentation also is observed in other conditions causing dorsal midline compression of the cervical spinal cord, such as spinal arachnoid diverticulae.[6, 7] This has been referred to as central cord syndrome and can be explained by the somatotopic organization of the cervical spinal cord.[13]

Although the abnormal and enlarged dorsal lamina and spinous process could cause variable degrees of vertebral canal stenosis, spinal cord compression was predominantly caused by hypertrophy of the ligamentum flavum. One dog in this study underwent 2 MRI studies with an interval of 6 months between each diagnostic procedure. Both imaging studies disclosed the characteristic vertebral malformation, but the 2nd MRI identified a markedly increased degree of ligamentum flavum hypertrophy causing more severe spinal cord compression compared to the 1st MRI scan. This finding suggests that the observed ligamentum flavum hypertrophy occurs secondary to the primary bony abnormalities. When vertebral malformations occur, abnormal forces can act on the surrounding soft tissue structures.[14] Hypertrophy of these tissues can cause or contribute to vertebral canal stenosis and associated clinical signs.

Abnormalities of the dorsal part of the vertebral column have been reported in small animals.[2, 14] Spinal neural tube defects are congenital malformations of the vertebral column and spinal cord that occur secondary to abnormal closure of the developing neural tube. This typically results in a defective neural arch through which meninges or neural elements may herniate.[2] In contrast, the anomaly reported here was not associated with a defective vertebral arch, but instead a hypertrophic vertebral arch. Therefore, we believe this abnormality in the Basset Hound does not represent a neural tube defect. The combination of a malformed vertebral lamina and ligamentum flavum hypertrophy also has been associated with cervical spondylomyelopathy (CSM) in young adult giant breed dogs.[14-18] This type of abnormality is commonly seen in combination with deformed articular processes.[14, 17, 18] In general, no specific abnormalities are seen on survey radiographs of CSM affected dogs with vertebral arch malformation.[18] This is in marked contrast with the obvious radiographic abnormalities seen in the Basset Hounds described herein. Furthermore, vertebral arch malformations with ligamentum flavum hypertrophy have not yet been described in the Basset Hound, and with the exception of 1 dog in the present study, the articular processes were not involved in the disease process. Finally, CSM has been reported in the Basset Hound and is, in contrast with the dorsal midline compressions reported herein, typically associated with 1 or more ventral extradural compressions in the cranial cervical vertebral column.[9, 12] For these reasons, it seems unlikely that the vertebral arch malformation presented herein represents a form of CSM. Cranial cervical spinal cord compression caused by enlarged and fibrotic ligamentum flavum has been reported in young adult Rottweiler dogs.[8] However, vertebral abnormalities were not present in these dogs. Previously, a case of thoracolumbar vertebral canal stenosis was reported in a 3-month-old female Basset Hound.[19] This compression was caused by a smooth bony malformation involving the caudal lamina of the 12th and the cranial lamina of the 13th thoracic vertebrae.[19] It is possible that the malformation in the Basset Hounds reported herein represent a similar malformation in the cervical region.

The underlying cause of most congenital spinal anomalies remains unknown, but a genetic predisposition or mutation has been identified in some cases.[2-4] The occurrence of this characteristic vertebral malformation in a specific breed, the Basset Hound, could indicate a potential genetic predisposition. Embryogenesis of vertebral formation is a complex process, involving different gene families, transcription factors, and signaling molecules.[20] Vertebrae are derived from the sclerotomal part of the somites, paired segmental structures located along both sites of the neural tube.[20] Sclerotomal cells migrate ventrally to surround the notochord, where they form the vertebral body and annulus fibrosus, and dorsolaterally to form the neural arch.[21] The last region of the vertebra to be formed is its mediodorsal portion, which closes the arch and develops as the spinous process.[21, 22] Expression of the Msx1 and Msx2 genes is closely related to development of the dorsal part of the vertebra.[23-25] Bone morphogenetic proteins (BMPs), especially BMP2 and BMP4, are important signaling molecules stimulating Msx gene expression and promoting cartilage and bone formation.[22, 25-27] Therefore, BMP expression is required for spinous process differentiation. BMP-producing cells grafted dorsally to the neural tube cause overexpression of Msx1 and Msx2 genes, resulting in differentiation of ectopic cartilage, hypertrophy of the dorsal vertebral cartilage, enlargement of the dorsal part of the vertebra, and, in some cases, formation of an enlarged spinous process-like structure dorsally.[25] Although the vertebral anomaly described in this report also was characterized by hypertrophy of the dorsal vertebral structures, additional studies are necessary to determine the underlying cause of this specific anomaly in the Basset Hound.

According to the owner, 1 dog in this study did not have clinical signs of neck pain or gait abnormalities before presentation for another condition. Cervical hyperesthesia and marked spinal cord compression only were identified by neurological examination and MRI. In 2 other dogs, abnormally formed laminae and spinous processes were seen at multiple sites along the cervical vertebral column, whereas spinal cord compression was seen only at 1 site. These findings may indicate that dorsal lamina and spinous process anomalies in the Basset Hound do not necessarily result in spinal cord compression and clinical signs. This is in agreement with findings in both human and veterinary medicine, where subjects with vertebral malformations often remain asymptomatic.[2, 28] However, additional studies are warranted to confirm this hypothesis and assess the incidence of vertebral arch anomalies in the clinically normal Basset Hound.

Surgical treatment of the Basset Hounds reported here was associated with good clinical outcome, rapid recovery, and short hospitalization. Furthermore, no clinical relapses were reported by the owners or referring veterinary surgeons. This is remarkable because variable results have been reported for neurological recovery and morbidity after dorsal cervical laminectomy.[15, 29-31] This surgical technique has been associated with severe tissue disruption, prolonged operation time, immediate transient postoperative neurological deterioration, and possible recurrence of clinical signs caused by excessive scar tissue formation at the laminectomy site.[14, 15, 18] It remains unclear why the Basset Hounds in this study experienced such uneventful clinical recoveries after dorsal cervical laminectomy. Possible reasons could be the relatively mild degree of neurological deficits before surgery, the limited number of adjacent operated sites, minimal spinal cord manipulation required to remove the hypertrophied ligamentum flavum, and the specific location and nature of the dorsal midline compression by the ligamentum flavum. This ligament is a comparatively soft structure, which may not cause sustained spinal cord deformation in the same way a bony malformation perhaps could.

In summary, this report describes a novel vertebral malformation characterized by well-defined and smooth hypertrophy of the dorsal lamina and spinous process of ≥1 cervical vertebrae. Although this abnormality can be readily recognized on survey radiographs, advanced imaging is necessary to demonstrate spinal cord compression. Outcome seems favorable after decompressive surgery. Dorsal lamina and spinous process hypertrophy with ligamentum flavum hypertrophy should be included in the differential diagnosis of Basset Hounds with signs of cervical hyperesthesia or myelopathy. Additional studies are indicated to investigate the underlying cause of this vertebral malformation and to assess the occurrence and incidence of this specific anomaly in the clinically normal Basset Hound.

Acknowledgment

Conflict of Interest Declaration: Authors disclose no conflict of interest.

Footnotes

  1. 1

    Omnipaque 240 mg I/mL, GE Healthcare, Diegem, Belgium

  2. 2

    Prospeed, GE Medical Systems, Milwaukee, WI

  3. 3

    PQ 500, Universal Systems, Solon, OH

  4. 4

    0.4 Tesla Open permanent magnet, Aperto, Hitachi, Tokyo, Japan

  5. 5

    1.5 Tesla Intera, Philips Medical Systems, Eindhoven, the Netherlands

  6. 6

    1.5 Tesla Sigma Echospeed System, GE Medical Systems

  7. 7

    Immunocal, Decal, Tallman, NY

Ancillary