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. 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. Some spinal malformations or anomalies are associated with specific dog breeds. Examples are dermal sinus tracts in the Rhodesian Ridgeback, spinal dysraphism in the Weimaraner, hemivertebra in the French Bulldog and arachnoid diverticula,[6, 7] and cervical fibrotic stenosis in the Rottweiler.
The Basset Hound also has been associated with a specific vertebral malformation. 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. 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. In 1977, 3 young Basset Hounds were included in a larger retrospective study about cervical spondylomyelopathy in dogs. Since that time, this condition in Basset Hounds has commonly been referred to as cervical spondylomyelopathy.
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.
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- Material and Methods
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.
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. 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. 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. 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. 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. 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. 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. Vertebrae are derived from the sclerotomal part of the somites, paired segmental structures located along both sites of the neural tube. Sclerotomal cells migrate ventrally to surround the notochord, where they form the vertebral body and annulus fibrosus, and dorsolaterally to form the neural arch. 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. 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.