Objective—To adapt and standardize neural tissue mobilization exercises, quantify nerve root movement, and assess the anatomic effects of lumbar spinal nerve and dural mobilization in dogs.
Animals—15 canine cadavers.
Procedures—5 cadavers were used in the preliminary part of the study to adapt 3 neural tissue mobilization physical therapy exercises to canine anatomy. In the other 10 cadavers, the L4 to L7 nerve roots and the dura at the level of T13 and L1 were isolated and marked. Movements during the physical therapy exercises were standardized by means of goniometric control. Movement of the nerve roots in response to each exercise was digitally measured. The effects of body weight and crownrump length on the distance of nerve root movement achieved during each exercise were also assessed. Each exercise was divided into 4 steps, and the overall distance of neural movement achieved was compared with distances achieved between steps.
Results—Neural tissue mobilization exercises elicited visible and measurable movement of nerve roots L4 to L7 and of the dura at T13 and L1 in all cadavers.
Conclusions and Clinical Relevance—The physical therapy exercises evaluated had measurable effects on nerve roots L4 to L7 and the dura mater in the T13 and L1 segments. These exercises should be evaluated in clinical trials to validate their efficacy as primary treatments or ancillary postsurgical therapy in dogs with disorders of the thoracolumbar and lumbosacral segments of the vertebral column.
Objective—To establish the reference ranges for motor evoked potential (MEP) latency and amplitude in clinically normal Doberman Pinschers, compare the MEPs of Doberman Pinschers with and without clinical signs of cervical spondylomyelopathy (CSM; wobbler syndrome), and determine whether MEP data correlate with neurologic or magnetic resonance imaging (MRI) findings.
Animals—16 clinically normal and 16 CSM-affected Doberman Pinschers.
Procedures—Dogs were classified according to their neurologic deficits. After sedation with acepromazine and hydromorphone, transcranial magnetic MEPs were assessed in each dog; latencies and amplitudes were recorded from the extensor carpi radialis and cranial tibial muscles. Magnetic resonance imaging was performed to evaluate the presence and severity of spinal cord compression.
Results—Significant differences in cranial tibial muscle MEP latencies and amplitudes were detected between clinically normal and CSM-affected dogs. No differences in the extensor carpi radialis MEP were detected between groups. There was a significant correlation (r = 0.776) between the cranial tibial muscle MEP latencies and neurologic findings. Significant correlations were also found between MRI findings and the cranial tibial muscle MEP latencies (r = 0.757) and amplitudes (r = −0.453).
Conclusions and Clinical Relevance—Results provided a reference range for MEPs in clinically normal Doberman Pinschers and indicated that cranial tibial muscle MEP latencies correlated well with both MRI and neurologic findings. Because of the high correlation between cranial tibial muscle MEP data and neurologic and MRI findings, MEP assessment could be considered as a screening tool in the management of dogs with spinal cord disease.
Objective—To compare morphologic and morphometric features of the cervical vertebral column and spinal cord of Doberman Pinschers with and without clinical signs of cervical spondylomyelopathy (CSM; wobbler syndrome) detected via magnetic resonance imaging (MRI).
Animals—16 clinically normal and 16 CSM-affected Doberman Pinschers.
Procedures—For each dog, MRI of the cervical vertebral column (in neutral and traction positions) was performed. Morphologically, MRI abnormalities were classified according to a spinal cord compression scale. Foraminal stenosis and intervertebral disk degeneration and protrusion were also recorded. Morphometric measurements of the vertebral canal and spinal cord were obtained in sagittal and transverse MRI planes.
Results—4 of 16 clinically normal and 15 of 16 CSM-affected dogs had spinal cord compression. Twelve clinically normal and all CSM-affected dogs had disk degeneration. Foraminal stenosis was detected in 11 clinically normal and 14 CSM-affected dogs. Vertebral canal and spinal cord areas were consistently smaller in CSM-affected dogs, compared with clinically normal dogs. In neutral and traction positions, the intervertebral disks of CSM-affected dogs were wider than those of clinically normal dogs but the amount of disk distraction was similar between groups.
Conclusions and Clinical Relevance—The incidence of intervertebral disk degeneration and foraminal stenosis in clinically normal Doberman Pinschers was high; cervical spinal cord compression may be present without concurrent clinical signs. A combination of static factors (ie, a relatively stenotic vertebral canal and wider intervertebral disks) distinguished CSM-affected dogs from clinically normal dogs and appears to be a key feature in the pathogenesis of CSM.
Objective—To measure 15F2t isoprostane concentrations in the urine of dogs undergoing ovariohysterectomy (OHE) and dogs undergoing surgery because of intervertebral disk disease (IVDD) and to assess relationships between urinary concentrations of 15F2t isoprostanes and neurologic score in dogs with IVDD.
Animals—11 dogs undergoing OHE and 32 dogs with IVDD undergoing hemilaminectomy.
Procedures—Paired urine samples were obtained at induction of anesthesia and approximately 1 hour after OHE (controls) and were collected from dogs with IVDD at induction of anesthesia (28 samples) and approximately 1 hour after hemilaminectomy (31 samples); 26 paired urine samples were obtained from dogs with IVDD. Urinary isoprostane concentrations were measured by use of a commercial ELISA, and results were adjusted on the basis of urinary creatinine concentrations. Differences in the mean isoprostane-to-creatinine ratio were analyzed. Neurologic score was determined in dogs with IVDD by use of the modified Frankel scoring system.
Results—Urinary isoprostane-to-creatinine ratios were significantly higher in dogs with IVDD than in control dogs before and after surgery. There was no significant difference between values before and after surgery for either group. There was a significant correlation of neurologic score and urinary isoprostane-to-creatinine ratio because dogs that had higher neurologic scores (ie, less severely affected) generally had higher isoprostane-to-creatinine ratios.
Conclusions and Clinical Relevance—Urinary isoprostane-to-creatinine ratios were higher in dogs with IVDD before and after surgery. Analysis of these data suggests that dogs with IVDD are in a state of oxidative stress and that preemptive treatment with antioxidants warrants further investigation.
Objective—To evaluate the numbers and proportions of olfactory ensheathing cells (OECs) in cell cultures derived from the olfactory bulb (OB) and olfactory mucosa of dogs.
Procedures—OB tissue and olfactory mucosa from the nasal cavity and frontal sinus were obtained from euthanatized dogs and prepared for cell culture. At 7, 14, and 21 days of culture in vitro, numbers and proportions of OECs, astrocytes, and fibroblasts were determined via immunocytochemistry. Antibody against the low-affinity nerve growth factor receptor p75 was used to identify OECs, antibody against glial fibrillary acidic protein was used to identify astrocytes, and antibody against fibronectin was used to identify fibroblasts.
Results—Cultured OECs derived from the olfactory mucosa of the nasal cavity and frontal sinus had similar characteristics. However, whereas OECs in the OB cell cultures constituted approximately 50% of the cells at 7 days and approximately 75% at 21 days the proportion of OECs in cultures derived from both mucosal types was much lower, with approximately 40% OECs at 7 days and approximately 25% at 21 days. Analysis of OEC numbers revealed that these changes were accompanied by corresponding decreases and increases in the population of cells with fibronectin receptors.
Conclusions and Clinical Relevance—Although olfactory mucosal cell cultures yielded a sufficient number of OECs for spinal cord transplantation procedures in dogs, modification of culture conditions would be required to ensure that the derived cell population contained a sufficient proportion of OECs.
Objective—To assess the use of CSF testing with an indirect fluorescent antibody test (IFAT) for diagnosis of equine protozoal myeloencephalitis (EPM) caused by Sarcocystis neurona.
Sample Population—Test results of 428 serum and 355 CSF samples from 182 naturally exposed, experimentally infected, or vaccinated horses.
Procedure—EPM was diagnosed on the basis of histologic examination of the CNS. Probability distributions were fitted to serum IFAT results in the EPM+ and EPM-horses, and correlation between serum and CSF results was modeled. Pairs of serum-CSF titers were generated by simulation, and titer-specific likelihood ratios and post-test probabilities of EPM at various pretest probability values were estimated. Post-test probabilities were compared for use of a serum-CSF test combination, a serum test only, and a CSF test only.
Results—Post-test probabilities of EPM increased as IFAT serum and CSF titers increased. Post-test probability differences for use of a serum-CSF combination and a serum test only were ≤ 19% in 95% of simulations. The largest increases occurred when serum titers were from 40 to 160 and pre-test probabilities were from 5% to 60%. In all simulations, the difference between pre- and post-test probabilities was greater for a CSF test only, compared with a serum test only.
Conclusions and Clinical Relevance—CSF testing after a serum test has limited usefulness in the diagnosis of EPM. A CSF test alone might be used when CSF is required for other procedures. Ruling out other causes of neurologic disease reduces the necessity of additional EPM testing.
Objective—To detect matrix metalloproteinase (MMP)-9 in serum and CSF and determine relationships between MMP activity and severity of disease, duration of clinical signs, and duration of hospitalization in dogs with acute intervertebral disk disease (IVDD).
Animals—35 dogs with acute IVDD and 8 clinically normal control dogs.
Procedure—CSF and serum were collected from affected and control dogs. Zymography was used to detect MMP-9.
Results—Activity of MMP-9 in CSF was detected in 6 of 35 dogs with IVDD; activity was significantly more common in dogs with duration of signs < 24 hours. Paraplegic dogs were more likely to have MMP-9 activity in the CSF than non-paraplegic dogs. No significant difference in hospitalization time was detected in dogs with IVDD between those with and without activity of MMP-9 in the CSF. Serum MMP-9 was detected more frequently in dogs with IVDD than in control dogs.
Conclusions and Clinical Relevance—Data were consistent with results of experimental rodent spinal cord injury studies that indicate that MMP-9 is expressed early during secondary injury.
Objective—To determine whether equine motor neuron disease (EMND) could be induced in adult horses fed a diet low in vitamin E and high in copper and iron.
Animals—59 healthy adult horses.
Procedure—Horses in the experimental group (n = 8) were confined to a dirt lot and fed a concentrate low in vitamin E and high in iron and copper in addition to free-choice grass hay that had been stored for 1 year. Control horses (n = 51) were fed a concentrate containing National Research Council–recommended amounts of copper, iron, and vitamin E. The hay fed to control horses was the same as that fed to experimental horses, but it had not been subjected to prolonged storage. Control horses had seasonal access to pasture, whereas experimental horses had no access to pasture. Horses that developed clinical signs of EMND were euthanatized along with an age-matched control horse to determine differences in hepatic concentrations of vitamin E, vitamin A, copper, iron, and selenium.
Results—4 experimental horses developed clinical signs of EMND. Plasma concentrations of vitamin E decreased in all 8 experimental horses. There were no significant changes in plasma concentrations of vitamin A, selenium, and copper or serum concentrations of ferritin. There were no significant differences in those analytes between experimental horses with EMND and experimental horses that did not develop EMND. No control horses developed EMND.
Conclusions and Clinical Relevance—Results suggest that lack of access to pasture, dietary deficiency of vitamin E, or excessive dietary copper are likely risk factors for EMND.