CASE DESCRIPTION An 11-year-old English Cocker Spaniel was evaluated because of chronic progressive ataxia of the hind limbs.
CLINICAL FINDINGS The dog had no history of previous illness, and findings of physical examination and laboratory tests were unremarkable. Neurologic examination revealed that the dog was ambulatory with severe ataxia of the hind limbs. Proprioception was decreased in the right and left hind limbs (right affected more than left), and spinal reflexes were bilaterally unremarkable. Moderate signs of pain were detected during palpation of the lumbar portion of the vertebral column. Findings suggested a lesion within the thoracolumbar or lumbar segments of the spinal cord. Magnetic resonance imaging revealed extradural spinal cord compression attributable to an extradural space-occupying lesion originating from or infiltrating the L4 lamina on the right side.
TREATMENT AND OUTCOME Hemilaminectomy was performed to remove the extradural lesion. Histologic findings for tissue samples collected during the procedure were consistent with a neurenteric cyst. The late onset and progression of clinical signs of this rare congenital malformation were suspected to have been the result of enlargement of the neurenteric cyst through continuous production of mucus by goblet cells. The dog responded favorably to surgical decompression and was clinically normal 1 year after surgery. It was euthanized 2 years after surgery for an unrelated reason (end-stage heart disease), and no neurologic deficits were evident before that point.
CLINICAL RELEVANCE Congenital neurenteric cysts should be considered as a differential diagnosis for neoplastic disease in dogs in which results of diagnostic imaging indicate the presence of an extradural mass affecting vertebral structures.
Objective—To describe the presence and amount of apoptotic ligamentous cells in different areas of partially ruptured canine cranial cruciate ligaments (prCCLs) and to compare these findings with apoptosis of ligamentous cells in totally ruptured cranial cruciate ligaments (trCCLs).
Animals—20 dogs with prCCLs and 14 dogs with trCCLs.
Procedures—Dogs with prCCLs or trCCLs were admitted to the veterinary hospital for stifle joint treatment. Biopsy specimens of the intact area of prCCLs (group A) and the ruptured area of prCCLs (group B) as well as specimens from trCCLs (group C) were harvested during arthroscopy. Caspase-3 and poly (ADP-ribose) polymerase (PARP) detection were used to detect apoptotic ligamentous cells by immunohistochemistry.
Results—No difference was found in the degree of synovitis or osteophytosis between prCCLs and trCCLs. No difference was found in degenerative changes in ligaments between groups A and B. A substantial amount of apoptotic cells could be found in > 90% of all stained slides. A correlation (rs = 0.71) was found between the number of caspase-3-and PARP-positive cells. No significant difference was found in the amount of apoptotic cells among the 3 groups. No significant correlation could be detected between the degree of synovitis and apoptotic cells or osteophyte production and apoptotic cells.
Conclusions and Clinical Relevance—The lack of difference between the 3 groups indicates that apoptosis could be a factor in the internal disease process leading to CCL rupture and is not primarily a consequence of the acute rupture of the ligament.
Objective—To compare oral administration of lomustine and prednisolone with oral administration of prednisolone alone as treatment for granulomatous meningoencephalomyelitis (GME) or necrotizing encephalitis (NE) in dogs.
Design—Retrospective cohort study.
Animals—25 dogs with GME and 18 dogs with NE (diagnosis confirmed in 8 and 5 dogs, respectively).
Procedures—Records of dogs with GME or NE were reviewed for results of initial neurologic assessments and clinicopathologic findings, treatment, follow-up clinicopathologic findings (for lomustine-treated dogs), and survival time. Dogs with GME or NE treated with lomustine and prednisolone were assigned to groups 1 (n = 14) and 3 (10), respectively; those treated with prednisolone alone were assigned to groups 2(11) and 4 (8), respectively.
Results—Prednisolone was administered orally every 12 hours to all dogs. In groups 1 and 3, mean lomustine dosage was 60.3 mg/m2, PO, every 6 weeks. Median survival times in groups 1 through 4 were 457, 329, 323, and 91 days, respectively (no significant difference between groups 1 and 2 or between groups 3 and 4). Within the initial 12 months of treatment, median prednisolone dosage was reduced in all groups; dosage reduction in group 1 was significantly larger than that in group 2 at 6, 9, and 12 months. Combination treatment most frequently caused leukopenia, but had no significant effect on liver enzyme activities.
Conclusions and Clinical Relevance—In dogs with GME and NE, oral administration of lomustine and prednisolone or prednisolone alone had similar efficacy. Inclusion of lomustine in the treatment regimen was generally tolerated well.
Objective—To evaluate the evolution of clinical signs and their correlation with results of magnetic resonance imaging (MRI) and transcranial magnetic stimulation (TMS) and to assess potential prognostic variables after conservative medical treatment for disk-associated cervical spondylomyelopathy (DA-CSM) in dogs.
Design—Prospective cohort study.
Animals—21 client-owned dogs with DA-CSM.
Procedures—After neurologic grading, dogs underwent low-field MRI and TMS with measurement of onset latencies and peak-to-peak amplitudes from the extensor carpi radialis and cranial tibial muscles. Dimensions calculated from MRI images were remaining spinal cord area, spinal cord compression ratio, vertebral occupying ratio, vertebral canal height-to-body height ratio, vertebral canal height-to-body length ratio, and vertebral canal compromise ratio. Intraparenchymal signal intensity changes were graded. Dogs were reevaluated 1, 3, 6, 12, and 24 months after initial diagnosis.
Results—Outcome was successful in 8 of 21 dogs. Negative outcomes were characterized by rapid progression of clinical signs. All dogs with more severe clinical signs of DA-CSM 1 month after diagnosis had unsuccessful outcomes. Outcome was associated with the remaining spinal cord area and vertebral canal compromise ratio. Prognosis was not associated with severity of clinical signs or results of TMS. There were no significant correlations among clinical signs, MRI findings, and TMS results.
Conclusions and Clinical Relevance—Conservative medical treatment of DA-CSM was associated with a guarded prognosis. Selected MRI variables and clinical evolution 1 month after diagnosis can be considered prognostic indicators. The lack of correlation among clinical signs, results of diagnostic imaging, and results of electrophysiologic evaluation in dogs with DA-CSM warrants further investigation.