Immunohistochemical evidence for immunoglobulin and complement deposition in spinal cord lesions in degenerative myelopathy in German shepherd dogs.

The purpose of this study was to examine the distribution of immunoglobulin and complement component C3 in spinal cord tissues of dogs with degenerative myelopathy. Sections of formalin-fixed paraffin-embedded spinal cord from five German Shepherd dogs with clinical and histological features consistent with degenerative myelopathy (DM) and one normal dog were tested immunohistochemically for deposition of immunoglobulin G (IgG) and the third component of complement (C3). In all dogs there was staining associated with large and small blood vessels. In addition, in the dogs with DM there was focal staining for IgG and C3 in spinal nerve tracts characteristically affected in DM. Deposition of IgG and C3 was found in histological lesions, and in addition, in other areas independent of visible lesions, suggesting that IgG and C3 deposition may precede histological evidence of spinal cord damage. These findings suggest a role for immune-mediated destruction of the spinal cord which may contribute to the pathogenesis of DM in German Shepherd dogs.     

Degenerative myelopathy in a cat

Degenerative myelopathy was diagnosed in a 6-year-old cat that had progressive ataxia, posterior paresis, and loss of conscious proprioception over a period of 8 months. Corticosteroid therapy did not alleviate clinical signs, and the cat was euthanatized. Microscopic examination of the spinal cord revealed diffuse degeneration of myelin attended by marked astrocytosis. The degenerative changes were most marked in the thoracolumbar segment. The cause of the degenerative lesions was not apparent.     

THE USE OF MAGNETIC RESONANCE IMAGING IN EVALUATING HORSES WITH SPINAL ATAXIA

To determine the accuracy of magnetic resonance imaging for diagnosing cervical stenotic myelopathy in horses, 39 horses with spinal ataxia and 20 control horses underwent clinical and neurologic examinations, cervical radiographs, euthanasia, magnetic resonance (MR) imaging of the cervical spine and necropsy. Twenty‐four horses were diagnosed with cervical stenotic myelopathy, 5 with cervical vertebral stenosis, 7 with idiopathic ataxia, 3 horses had other causes of ataxia, and 20 were controls. The MR images were assessed for spinal cord intensity changes, presence of spinal cord compression, spinal cord compression direction, shape of spinal cord, and the presence of synovial cysts, joint mice, and degenerative joint disease. The height, width, and area of the spinal cord, dural tube and vertebral canal were measured. The identification of spinal cord compression on MR images was significantly different in horses with cervical stenotic myelopathy (P < 0.02), but in the cervical stenotic myelopathy group the identification of spinal cord compression on MR images had poor to slight agreement with histopathologic evidence of compression (κ = 0.05). Horses with cervical stenotic myelopathy were more likely to have a T2 hyperintensity in the spinal cord (P < 0.05). Horses with cervical stenotic myelopathy or cervical vertebral stenosis were more likely to have degenerative joint disease than control horses or horses with other or idiopathic ataxia.     

Degenerative myelopathy in a German shepherd

A 9-year-old male German Shepherd had marked stumbling, staggering and weakness in both rear limbs. Pelvic radiographs revealed only mild hip dysplasia, while survey spinal radiographs and a myelogram revealed only areas of possible pachymeningitis. Results of CSF analysis were normal. Degenerative myelopathy was suspected, but a mitogen response assay failed to confirm this diagnosis. Another mitogen response assay, performed several months later, again failed to indicate degenerative myelopathy as the cause of clinical signs. The dog's condition worsened and the animal was euthanized. At necropsy, classic histopathologic lesions of degenerative myelopathy were noted in the thoracic spinal cord.     

Marginal siderosis and degenerative myelopathy: a manifestation of chronic subarachnoid hemorrhage in a horse with a myxopapillary ependymoma

Marginal siderosis is recognized in humans as an uncommon clinicopathologic entity characterized by degeneration of neural tissue at the surface of the brain and spinal cord, in association with the accumulation of hemosiderin, and resulting from chronic subarachnoid hemorrhage. The sources of hemorrhage are various and include neoplasms, malformations, cysts, and vasculopathy. Marginal siderosis of the spinal cord due to a myxopapillary ependymoma was diagnosed in a 19-year-old Dutch Warm Blood horse with clinical signs of myelopathy. There is only one previous report of marginal siderosis in the veterinary literature, also in a horse with clinical myelopathy.     

EVALUATION OF DIFFERENT COMPUTED TOMOGRAPHY TECHNIQUES AND MYELOGRAPHY FOR THE DIAGNOSIS OF ACUTE CANINE MYELOPATHY

Forty‐six dogs with either cervical (C1–C5 or C6–T2) or thoracolumbar (T3–L3) acute myelopathy underwent prospective conventional computed tomography (CT), angiographic CT, myelography, and CT myelography. Findings were confirmed at either surgery or necropsy. Seventy‐eight percent of lesions were extradural, 11% were extradural with an intramedullary abnormality, 7% were intramedullary, 2% were intradural–extramedullary, and 2% had nerve root compression without spinal cord compression. Intervertebral disc herniation was the most frequent abnormality regardless of signalment or neurolocalization. Twenty‐one of 23 Hansen type I disc extrusions but none of the Hansen type II disc protrusions were mineralized. Two chondrodystrophic dogs had acute myelopathy attributable to extradural hemorrhage and subarachnoid cyst. CT myelography had the highest interobserver agreement, was the most sensitive technique for identification of compression, demonstrating lesions in 8% of dogs interpreted as normal from myelography and enabling localization and lateralization in 8% of lesions incompletely localized on myelography due to concurrent spinal cord swelling. None of the imaging techniques evaluated permitted definitive diagnosis of spinal cord infarction or meningomyelitis but myelography and CT myelography did rule out a surgical lesion in those cases. While conventional CT was adequate for the diagnosis and localization of mineralized Hansen type I disc extrusions in chondrodystrophic breeds, if no lesion was identified, plegia was present due to concurrent extradural compression and spinal cord swelling, or the dog was nonchondrodystrophic, CT myelography was often necessary for correct diagnosis.     

Thoracolumbar spinal cord compression due to vertebral process degenerative joint disease in a family of Shiloh Shepherd dogs

Five young Shiloh Shepherd Dogs (4 males and 1 female) related by a common sire were studied because of progressive pelvic limb weakness and incoordination. All dogs had a spastic paraparesis and pelvic limb ataxia consistent with an upper motor neuron and general proprioceptive lesion between spinal cord segments T3 and L3. Proliferative lesions involving one or more of the articular processes from the 11th thoracic vertebrae to the 2nd lumbar vertebra were observed on radiographs of the thoracolumbar vertebrae. Dorsal compression of the spinal cord was identified during imaging studies at these sites. Abnormalities of the synovial joints and bony proliferation of the involved articular processes were identified at postmortem examination in 2 dogs. The articular processes and associated vertebral arches protruded into the vertebral canal, indenting the dorsal surface of the spinalcord. Degenerative joint disease (DJD) was identified histologically. A compressive myelopathy was diagnosed in the spinal cord. These dogs were affected by a compressive myelopathy as a consequence of vertebral process DJD that likely has a geneticcomponent. The DJD could have been caused by a primary vertebral malformation or an injury to the processes at a young age causing malarticulation.     

Myelopathy in Holstein x Gir calves in Brazil

This case report contains clinical and pathologic features of a degenerative myelopathy in Holstein X Gir crossbred calves in Brazil. The bilateral and symmetrical spinal cord white matter lesions were interpreted as a primary axonopathy that may be of the dying-back type.     

Spinal dural ossification causing neurological signs in a cat

A six-year-old Ragdoll cat underwent examination due to a six-month history of slowly progressive gait abnormalities. The cat presented with an ambulatory tetraparesis with a neurological examination indicating a C1-T2 myelopathy. Radiographs of the spine showed a radiopaque irregular line ventrally in the vertebral canal dorsal to vertebral bodies C3-C5. In this area, magnetic resonance imaging revealed an intradural extramedullary/extradural lesion compressing the spinal cord. The spinal cord was surgically decompressed. The cause of the spinal cord compression was dural ossification, a diagnosis confirmed by histopathological examination of the surgically dissected sample of dura mater. The cat gradually improved after the procedure and was ambulating better than prior to the surgery. The cat’s locomotion later worsened again due to ossified plaques in the dura causing spinal cord compression on the same cervical area as before. Oral prednisolone treatment provided temporary remission. Ten months after surgery, the cat was euthanized due to severe worsening of gait abnormalities, non-ambulatory tetraparesis. Necropsy confirmed spinal cord compression and secondary degenerative changes in the spinal cord on cervical and lumbar areas caused by dural ossification. To our knowledge, this is the first report of spinal dural ossification in a cat. The reported cat showed neurological signs associated with these dural changes. Dural ossification should be considered in the differential diagnosis of compressive spinal cord disorders in cats.     

Intramedullary cavernous malformation of the spinal cord in two dogs

Intramedullary cavernous malformations (CVMs) of the spinal cord were diagnosed in 2 adult dogs that presented for paraparesis. An intramedullary spinal cord lesion was identified on a myelogram in the first dog, and expansion of the vertebral canal was evident on radiographs in the second. Extensive intraparenchymal hemorrhage was found on gross postmortem examination in both dogs, and a distinct lobulated intramedullary mass was evident in the second dog. Microscopically, both lesions were composed of dilated, thin-walled vascular channels with little-to-no intervening neural parenchyma. Both dogs had evidence of channel thrombosis along with perilesional hemorrhage and hemosiderin accumulation. The second dog had additional degenerative changes, including thickened fibrous channel walls with hyalinization, foci of mineralization, and occasional tongues of entrapped gliotic neuropil. CVMs appear to be an uncommon cause of both acute and chronic spinal cord disease in the dog.     

Evaluation of magnetic resonance imaging for the differentiation of inflammatory,neoplastic, and vascular intradural spinal cord diseases in the dog

Magnetic resonance imaging (MRI) is a common test for dogs with suspected intradural spinal cord lesions, however studies on diagnostic performance for this test are lacking. Objectives of this multi‐institutional, retrospective, case‐control study were to estimate sensitivity and specificity of MRI for (1) distinguishing between histopathologically confirmed intradural spinal cord disease versus degenerative myelopathy in dogs, (2) categorizing intradural spinal cord diseases as neoplastic, inflammatory, or vascular; and (3) determining tumor type within the etiologic category of neoplasia. Additional aims were to (1) determine whether knowledge of clinical data affects sensitivity and specificity of MRI diagnoses; and (2) report interrater agreement for MRI classification of intradural spinal lesions. Cases were recruited from participating hospital databases over a 7‐year period. Three reviewers independently evaluated each MRI study prior to and after provision of clinical information. A total of 87 cases were sampled (17 degenerative myelopathy, 53 neoplasia, nine inflammatory, and eight vascular). Magnetic resonance imaging had excellent (>97.6%) sensitivity for diagnosis of intradural spinal cord lesions but specificity varied before and after provision of clinical data (68.6% vs. 82.4%, P = 0.023). Magnetic resonance imaging had good sensitivity (86.8%) and moderate specificity (64.7–72.5%) for diagnosing neoplasia. Sensitivity was lower for classifying inflammatory lesions but improved with provision of clinical data (48.1% vs. 81.5%, P = 0.015). Magnetic resonance imaging was insensitive for diagnosing vascular lesions (25.0%). Interrater agreement was very good for correctly diagnosing dogs with intradural lesions (? = 0.882–0.833), and good (? = 0.726–0.671) for diagnosing dogs with neoplasia.     

Intramedullary Spinal Cord Metastasis in the Dog

Intramedullary spinal cord metastasis (ISCM) was diagnosed in three dogs with signs of myelopathy. The clinicopathologic features of ISCM in these and previously reported cases in the veterinary and human literature were compared. Myelopathic signs associated with ISCM may be the initial clinical manifestation of malignancy or may develop in the patient with known malignancy. Pain, a frequent manifestation of extradural compressive myelopathy, is not a consistent feature of ISCM. Survey spinal radiographs are usually unrewarding and cerebrospinal fluid (CSF) abnormalities nonspecific. Myelography is indicated to differentiate intramedullary lesions from more common extradural compressive lesions. Myelographic interpretation may be difficult, and intramedullary tumors must be differentiated from spinal cord edema or hemorrhage. Evidence of widely disseminated malignancy should increase suspicion for ISCM; hemangiosarcoma and lymphosarcoma should be considered the most likely histologic types. CSF cytology may be helpful in the diagnosis of patients with lymphosarcoma. Prognosis is poor due to the frequent presence of disseminated disease, although temporary response to corticosteroid therapy may be achieved. More aggressive therapeutic approaches, such as spinal irradiation and microsurgical resection of metastases, have been advocated in humans but have not been reported in the dog. Although it is an uncommon complication of systemic malignancy, ISCM should be considered in the differential diagnosis of myelopathy in the dog.     

Unilateral degenerative joint disease of a cervical articular process joint between the fourth and fifth cervical vertebrae causing asymmetrical ataxia in a young horse

A 5-year-old horse was examined for investigation of asymmetrical, quadrilateral ataxia and paresis. Clinical examination was unremarkable, and a thorough neurological examination localised the lesion to the cervical spine. Following this, magnetic motor evoked potentials were acquired to allow for latency times to be determined. Abnormal conduction times were found to the right thoracic and right pelvic limbs, confirming that the horse had an asymmetrical cervical spinal myelopathy. Radiographs were acquired to ensure that the horse had no significant pathology which would contraindicate general anaesthesia. There were no abnormalities noted on these, so the horse underwent contrast-enhanced computed tomography of its cervical spine which revealed enlargement of the right articular process joint between C4 and C5 with dorsolateral impingement of the spinal canal and cord. Due to the poor prognosis for future performance, the horse was subsequently euthanised. A post-mortem examination confirmed the findings of degenerative joint disease, with some unexpected changes seen on histology of the spinal cord. The unilateral right-sided compression had caused degenerative changes to ascending and descending tract bilaterally indicating a dynamic component to this lesion, which would be more commonly understood to be static.     

Spinal oligodendroglioma with diffuse arachnoidal dissemination in a Japanese Black heifer

A gelatinous focus with cystic spaces, was found in the posterior funiculus of the 2nd to 3rd lumbar levels of the spinal cord of a Japanese Black heifer, 2 years old, with clinical signs of severe dysstasia. Histopathological examination revealed that the spinal lesion consisted of multifocal and diffuse proliferation of round cells with abundant vacuolar cytoplasm and hyperchromatic nuclei. In the lesions there was a number of cystic spaces containing aggregates of small round cells. The neoplastic foci showed a honeycomb structure divided by thin blood vessels, representing typical lesions of oligodendroglioma. Diffuse and multifocal proliferation of these round cells were also recognized in the subarachnoidal space in the sacral spinal cord. Immunohistochemically, the proliferating round cells were negative for glial fibrillary acidic protein. Based on these morphological features, the case was diagnosed as lumbar spinal oligodendroglioma with diffuse arachnoidal dissemination.     

Contrast-enhanced computed tomography and myelography in six horses with cervical stenotic myelopathy.

The cervical spines of 6 horses with cervical stenotic myelopathy (CSM) were examined using myelography and contrast-enhanced computed tomography (CECT). Histopathology of the spinal cord of these horses identified 10 neurologically significant compressive lesions. Myelography and CECT were both able to demonstrate all 10 spinal cord compressive lesions, but myelography falsely identified 2 sites and CECT falsely identified 1 site as compressive lesions of the spinal cord which were not supported by histopathology. Additional qualitative information was obtained by CECT regarding the source, severity and location of spinal cord compression. Computed tomography identified stenosis of the vertebral canal with circumferential loss of contrast agent and documented lateral compressive lesions of the spinal cord due to malformed articular facets. Compression of the peripheral nerve roots by malformed articular facets encroaching on the intervertebral foramen was easily identified by CECT in the axial plane. No compressive lesions were identified in 3 unaffected horses by either method. Minimum sagittal diameter (MSD) values obtained from CECT images were strongly correlated with necropsy measurements, validating CECT as an accurate method of obtaining MSD values. The MSD values in the CSM-affected horses were significantly narrowed (P less than 0.05) from C3C6 regardless of the site of spinal cord compression, when compared with the unaffected controls. This finding supports previous reports suggesting that generalised stenosis of the vertebral canal is an important feature in the pathogenesis of cervical stenotic myelopathy.     

Atlantoaxial subluxation and absence of transverse ligament of the atlas in a dog

Absence of the transverse ligament of the atlas was diagnosed at necropsy in an 8-month-old Shih Tzu with radiographic signs of atlantoaxial subluxation. Symmetric ataxia, tetraparesis, and signs of pain in the vertebral canal suggested a lesion in the cervical portion of the spinal cord. Necropsy revealed absence of the transverse ligament of the atlas and malformation of dens and atlas. In addition, the alar ligaments were distinct and thick, and the atlanto-occipital and atlantoaxial joint capsules were markedly thicker than normal. Histologic examination revealed focal compressive myelopathy of the spinal cord at the level of the atlantoaxial joint.     

A survey of more than 11 years of neurologic diseases of ruminants with special reference to transmissible spongiform encephalopathies (TSEs) in Greece

The first cases of scrapie were detected in Greece in a flock of sheep in October 1986. All the animals of the affected flock and all sheep in two flocks that were in contact were killed and buried. A systematic investigation of all available cases with signs indicating a neurological disease started in sheep and goats in late 1986, as well as in cattle in 1989. The investigation was based on clinical examination, necropsy or macroscopical examination of the brain and viscera, and histological examination of the brain in all animals except those with coenurosis. Histological examinations of specimens from the spinal cord and other tissues, and if considered necessary bacteriological, toxicological and serological examinations were also carried out. In October 1997, scrapie was diagnosed in sheep of a second flock (a mixed flock of sheep and goats), grazing in a pasture close to the place where scrapie was initially detected. All animals of the second flock were also killed and buried. Diagnosis in the first flock was based on clinical signs and histological lesions, and in the second immunoblotting was also used. Distinctive lesions of scrapie were found in the brain and/or the spinal cord of eight sheep with clinical signs from the two flocks. The lesions were revealed in the brain stem and/or in the cervical spinal cord, and tended to be symmetrical. In one sheep, severe lesions in the cortex of cerebral hemispheres and of the cerebellum were also found. In the brain of two sheep from the second flock the pathological isoform of PrP protein was detected. Despite the eradication scheme applied, scrapie in sheep reappeared after 11 years in a place close to where it occurred initially. This may indicate that the effectiveness of the eradication scheme implemented was not adequate and additional approaches may be needed.     

Invasive histiocytic sarcoma of the lumbar spine in a ferret (Mustela putorius furo)

This report describes the history, clinical examination and histopathology of a histiocytic sarcoma in a domestic ferret. Clinical signs were acute paraplegia and dysuria. Physical examination revealed a firm, smooth, touch‐sensitive mass in and around the lumbar vertebral column. Neurologic examination was consistent with a lesion between spinal cord segments T3 and L3. Magnetic resonance images revealed bone lesions of L2 and L3 combined with compression of the spinal cord due to a homogenous, isointense mass that was diagnosed as a malignant round cell tumour and the ferret was euthanased. Histopathology confirmed the diagnosis of an infiltrative histiocytic sarcoma.     

Evaluation of a proposed therapeutic protocol in 12 dogs with tentative degenerative myelopathy

The objective of this work was to evaluate the long-term efficacy of a proposed therapeutic protocol in 12 dogs with a tentative diagnosis of degenerative myelopathy, followed-up for a 6-month period. Twelve dogs fulfilling the antemortem inclusion criteria (breed, age, adequate vaccination, history of progressive posterior ataxia and/or paraparesis, no radiographic and myelographic abnormalities in the spinal cord and vertebral column) were allocated. All these dogs presented signs of thoracolumbar syndrome (T3-L3), scored as grade I (mild to moderate ataxia and paraparesis) in 10 and grade II (severe ataxia and ambulatory paraparesis) in 2 cases. Treatment included the use of epsilon-aminocaproic acid and N-acetylcysteine, supplemented with vitamins B, C and E. Prednisolone was given for the first two weeks and upon worsening of neurological signs. Daily exercise, performed as walking or swimming, was strongly recommended. Clinicopathological evaluation was normal in all 12 dogs, and survey radiographs and myelograms did not show spinal cord compression. Magnetic resonance imaging (MRI), performed only in 4 dogs, did not disclose compressive disorders or intramedullary lesions. Neurological signs were progressively worsening in all 12 animals, eventually resulting in severe paraparesis (grade III) or paraplegia (grade IV). The applied medications do not appear to be an attractive alternative to conservative management (physiotherapy) or euthanasia in canine degenerative myelopathy, irrespective of its chronicity.