Western College of Veterinary Medicine for further evaluation. Clinical Findings. The dog on presentation preferred to rest

Transcription

1 CASE REPORT SYRINGOMYELIA AND SPINA BIFIDA OCCULTA IN A SAMOYED DOG R. W. FURNEAUX, C. E. DOIGE AND M. M. KAYE* Introduction Congenital defects involving the spinal cord and vertebral column are uncommon in domestic animals. A number of congenital defects are grouped under the term "status dysraphicus", indicating inadequate or abnormal midline fusion of the developing neural tube. Pathological changes may involve cutaneous, mesodermal and/or neural tissues and vary from spina bifida occulta to the more severe conditions of cranium bifidum and various forms of meningoceles and meningomyelodysplasias (2). Although spina bifida occulta is. reported to be a common incidental radiological finding in man (1), there are few recent reports of this condition in the canine species (7, 9). Syringomyelia or tubular cavitation of the spinal cord has been described in the Weimaraner dog (8) and in other breeds (4, 7). An extensive review of the literature regarding spina bifida and syringomyelia in the canine species has been published by Kalter (6). The purpose of this communication is to report both spina bifida occulta and syringomyelia in a Samoyed dog. History A two-month-old, female Samoyed was first seen by the referring veterinarian because the owner complained that the dog had a peculiar hind limb gait. On presentation, the dog had posterior ataxia which was likened to a duck waddle. No other abnormalities were observed. Some three weeks later the dog was returned to the referring veterinarian for a further examination. At that time the dog's condition had deteriorated to the extent that it was no longer able to walk on a smooth surface but was still able to walk with difficulty on carpeting. At that time, a positive anterior drawer sign was obtained from the right stifle and the left stifle joint appeared lax. The dog was then referred to the clinic of College of Veterinary Medicine, University of Saskatchewan, Saskatoon, Saskatchewan. CAN. VET. JOUR., vol. 14, no. 12, December, 1973 Western College of Veterinary Medicine for further evaluation. Clinical Findings The dog on presentation preferred to rest in a crouched position with the hind limbs stretched out behind. The shoulder, elbow, hip and stifle joints were all lax. There was a medial luxation of each patella. The dog's hind limb movement on initial exercise was that of a bilateral hop. As it became fatigued, its hind limbs lay flaccidly behind it while the forelimbs were used for locomotion. The muscles on all four limbs were flaccid. On neurological examination, the only reflexes present were those involving simple reflex arcs. Radiological Findings The lateral view (Figure 1) of the cervical spine, which was taken while the dog was fully anesthetized and with traction placed upon the cervical spine, revealed an apparent dorsal displacement as well as anterior angulation of the vertebral bodies of C5, 6 and 7 producing an apparent developmental kyphosis of the distal cervical spine. The most severe discontinuity in the relative width of the joint spaces and angulations of the vertebral bodies appeared to be associated with the intervertebral spaces at C5, 6 and 7. The FIGURE 1. Lateral view of thoracic vertebral column. lower cervical and 317

2 CANADIAN VETERINARY JOURNAL FIGURE 3. Lateral view of lower cervical and thoracic myelogram. FIGURE 2. Ventrodorsal view of lower cervical and thoracic vertebral column. lateral view of the distal thoracic as well as lumbar spine failed to reveal any obvious discontinuity in the osseous structures. On the ventrodorsal view (Figure 2) the dorsal spinous processes appeared to be missing from T-1 through T-9 with only a faint shadow at T-10. Careful examination of the roentgenogram suggested that from T-1 through T-5 the dorsal spinous processes were attached to the left side of the vertebral midline, while from T-6 through T-9 they were attached to the right side. There was scoliosis and lordosis of the thoracic spine. This was probably due to muscle tension on the abnormal spinous processes and arches, since no anomalous vertebral bodies were noted. Based on the examination of plain radiographs, a diagnosis of multiple congenital anomalies of the thoracic vertebrae, including atypical spina bifida was made. The bodies of the vertebrae appeared normal; anomalies were limited to the arches and spinous processes. A tentative diagnosis of a cervical cord or upper motor neuron neuropathy or syringomyelia was made. The client was advised to exercise the dog in water for half-hour periods 318 FIGURE 4. and thoracic Ventrodorsal view of lower cervical myelograms. three times a day and to return with the dog in two weeks. At that time there was a slight improvement in the gait and muscle tone of all four limbs. The dog was admitted to hospital for a further radiological evaluation, which was to include contrast myelography, using iophendylate.1 On lateral view (Figure 3), myelography indicated cavitation and dilatation of subarachnoid space at T-4, 5 with the space lethiodan, B.D.H. Pharmaceuticals, Toronto, Ontario.

3 SYRINGOMYELIA apparently displaced 2-3 cm dorsal to the thoracic vertebral bodies. There was evidence of cord compression and rupture of the dura at T6-7 with the apparent diameter reduced to less than 0.5 cm from a diameter of approximately 2 cm immediately cranial to the area of constriction. The cord and dura appeared to re-enter the spinal canal of vertebral bodies at T8. On the ventro-dorsal view (Figure 4), the dura and cord appeared to follow the line of scoliosis of the thoracic spine. The distal column reached a level of T2 and indicated dorsal displacement of the cord and dura, 2-4 mm dorsal to the osseous neural arch within the thoracic spine. The cervical myelogram indicated ventral subarachnoid compression at the anterior margins of C3, C4, C5 and C6. Based on the above findings, the following diagnoses were made: Spondylolisthesis - C3, 5, 6 and 7; Spina bifida - T1-8; Lordosis and scoliosis of proximal thoracic spine T1-8; and spinal cord compression at T5-6. The client was advised that the animal had an irreversible disease and euthanasia was recommended. Permission for necropsy was obtained and a postmortem examination was performed. FIGURE 5. Third thoracic vertebra. Vertebral laminae have failed to fuse leaving a cleft vertebra. Postmortem Findings Gross postmortem findings were restricted to the spinal cord and vertebral column. Incomplete fusion of the lamellae which normally unite to form the dorsal vertebral arches was observed in the second, third and fourth thoracic vertebrae. Partial fusion of lamellae was evident at T2 and T4, whereas at T3 fusion was completely lacking, leaving a cleft vertebra (Figure 5). At this site the spinal cord was situated in the dorsal portion of vertebral canal. The spinal cord was compressed laterally and, in cross section, was elongated dorsoventrally (Figure 6). In addition, the posterior border of the dorsal process of T4 was fused to the corresponding anterior portion of T5. All other vertebrae were judged to be normal. An area of cavitation (3X2 mm in diameter) was found in the lumbar portion of the spinal cord (Figure 7). This area of cavitation was irregular in outline, extended from the level of L3 to L5 and was filled with clotted blood. Microscopically, at the level of T2-T4, the normal architecture of the spinal cord was distorted. The central canal was enlarged, only...'... FIGURE 6. Gross-section of spinal cord at the level of T3. The cord is compressed laterally and normal architecture is lost. Hematoxylin and eosin, approximately IOX. 319

4 FIGURE 7. Cross-section of spinal cord at the level of L4. Note the area of cavitation present. Hematoxylin and eosin, approximately lox. partially lined by ependymal cells and was elongated dorsoventrally. Numerous swollen, eosinophilic axons were apparent in the ventral and lateral portions of the spinal cord. Granulocytes were present in the dura and lentomeninges. Sections of spinal cord cut at the level of L3-L5 had a large area of cavitation dorsolateral to the central canal. The cavity contained masses of red blood cells and appeared to compress the surrounding portion of the spinal cord. Loss of substance, degeneration of axons and areas of recent hemorrhage were observed in the tissue adjacent to the area of cavitation. Gliosis was not observed. No communication between the area of cavitation and the central spinal canal was demonstrated. On the basis of the above findings, a diagnosis of spina bifida occulta, fusion of spines of thoracic vertebrae and syringomyelia was made. Discussion Spina bifida or cleft spine is the result of non-union of the vertebral laminae which normally fuse to form the dorsal portion of the vertebral arch and dorsal spinous processes. Non-union is thought to be the result of defective closure of the neural tube (5). There may be no external abnormalities (spina bifida occulta) or there may be meningeal protrusion (spina bifida manifesta). In man, and in animals, spina bifida may be accompanied by local cutaneous lesions, e.g. a tuft of hair, or dimpling of the overlying skin (3, 7, 9). Spina bifida occulta may or may not result in abnormal clinical signs. Posterior paralysis CANADIAN VETERINARY JOURNAL 320 has been described in a five-week-old pup with spina bifida occulta (7). In man, a variety of clinical signs including paralysis of the urinary bladder and reotum as well as muscular weakness of the legs, have been associated with spina bifida occulta (3). In the animal described in the present report, the location of the vertebral defect was unusual, lesions most commonly being present in the lumbosacral area (9). Compression and distortion of the spinal cord at the level of T2-T4 were considered to be at least partly responsible for the clinical signs observed. Syringomyelia may be congenital or acquired in post-natal life. Although many different factors have been reported to be involved in the pathogenesis (2, 7, 10), Mc- Grath (8) believed syringomyelia in the Weimaraner dog to be associated with an abnormal vascular pattern in local areas of the spinal cord which led to low-grade ischemia, degeneration, rarefaction and eventually cavitation. Based on experimental studies in dogs, Woodward and Freeman (10) reported that the basic change leading to syringomyelia was venous insufficiency secondary to spinal cord edema. The significance of cavitation of the spinal cord of the animal described in this report was difficult to interpret. Since the cavity was found to be filled with clotted blood at the time of postmortem examination and since there was little cellular reaction in the surrounding neural tissue, the possibility of an iatrogenic lesion was considered. Fluids were not injected at the site of cavitation, although spinal punctures were done in this area. A lack of cellular response in tissues adjacent to areas of cavitation has been observed by other workers. McGrath (8) reported that, in a series of Weimaraner dogs with cavity formation, gliosis as frequently described in human syringomyelia was not observed. Others (10) have reported that hematoxylineosin sections failed to show definite glial hyperplasia in the vicinity of cavitation, although gold chloride preparations showed hypertrophied astrocytes. A lack of gliosis is perhaps consistent with the pathogenesis as proposed by McGrath, i.e. low-grade ischemia leading to degeneration, rarefaction and cavitation rather than acute necrosis. Summary A case of spina bifida occulta with fusion of thoracic vertebrae and syringomyelia in a Samoyed dog is presented. Clinical, radiological and postmortem findings are described.

5 SYRINGOMYELIA RMsum' Les auteurs rapportent un cas de spina bf occulta, avec fusion des vert6bres thoraciques et syringomy'lie, chez un chien Samoymde. ILs decrivent leurs observations cliniques et radiologiques, ainsi que celles de la necropsie. References 1. ANDERSON, F. M. Occult spinal dysraphism. Diagnosis and management. J. Pediat. 73: BENDA, C. E. Dysraphic states. J. Neuropath. exp. Neurol. 18: BoYD, W. A Textbook of Pathology. Structure and Function in Disease. 8th Edition. p Philadelphia: Lea & Febiger GEIB, L. W. and S. I. BISTNER. Spinal cord dysraphism in a dog. J. Am. vet. med. Ass. 150: JUBB, K. V. F. and P. C. KENNEDY. Pathology of Domestic Animals. 2nd Edition. Vol. 2. pp New York and London: Academic Press KALTER, H. Teratology of the Central Nervous System. Induced and Spontaneous Malfornations of Laboratory, Agricultural and Domestic Mammals. pp Chicago and London: The University of Chicago Press McGRATH, J. T. Neurologic Examination of the Dog. 2nd Edition. pp Philadelphia: Lea & Febiger McGRATH, J. T. Spinal dysraphism in the dog with comments on syringomyelia. Path. Vet. Supp PUTrNAM, R. W. and J. ARCHIBALD. Diseases of the locomotor system. In Canine Medicine. First Edition. E. J. Catcott, editor. pp Santa Bar ara, California: American Veterinary Publications, Inc WOODWARD, J. S. and L. W. FREEMAN. Ischemia of the spinal cord. An experimental study. J. Neurosurg. 13: CONCOURS "SCHERING" POUR ETUDIANTS EN MEDECINE VETERINAIRE Les prix "Schering" sont offerts aux finissants de chacun des trois colleges v6t6rinaires du Canada. Une serie de prix sera disponible pour chaque college: Un premier prix de... $100 Un deuxieme prix de Un troisieme prix de Un quatrieme prix de 25 REGLEMENTS 1. lligibilite: Le concours ne s'adresse qu'aux finissants d'un college v6t6rinaire du Canada. 2. Les prix seront attribu6s aux auteurs des meilleurs rapports de cas cliniques (de pr6f6rence: 300 a 1,000 mots), r6dig6s sous forme convenable pour fin de publication dans la "Revue vet6rinaire canadienne". Veuillez consulter les "Directives aux auteurs" et les demiers num6ros de la revue pour renseignements sur la forme et la presentation. 3. Les textes peuvent etre soumis en frangais ou en anglais. 4. Un "Comit6 de Selection" dans chaque college sera responsable du choix des dix meilleurs rapports de cas cliniques et les fera parvenir, avant le 1 mars 1974, a l'adresse suivante: President, Comit6 de Redaction L'Association canadienne des v6terinaires 360 avenue Bronson Ottawa, Ontario KIR 6J3 pour jugement final par le "Comit6 de Redaction" de l'association canadienne des veterinaires. 5. Les prix seront remis a, roccasion d'une ceremonie officielle. 6. La Revue se reserve le droit de publier, selon les regles habituelles de r6dition, les articles primes. 321