Transient depression of pelvic limb reflexes in dogs with acute focal thoracolumbar myelopathy.

OBJECTIVE To determine the prevalence of depressed pelvic limb reflexes and changes in those reflexes over time in dogs with acute thoracolumbar myelopathy. DESIGN Prospective study. ANIMALS 34 dogs. PROCEDURES Dogs with acute pelvic limb paralysis caused by acute noncompressive nucleus pulposus extrusion (ANNPE), fibrocartilaginous embolism (FCE), or compressive intervertebral disk herniation (IVDH) within the T3-L3 spinal cord segments were enrolled in the study. Dogs with depressed or absent pelvic limb withdrawal reflexes as determined by 2 examiners were classified as affected and underwent additional testing to rule out multifocal lesions. Pelvic limb reflexes of affected dogs were reassessed every 12 hours until they returned to normal. Neurologic examinations were performed at 4 and 8 weeks after initial examination for some dogs. RESULTS Compressive IVDH, ANNPE, and FCE were diagnosed in 30, 1, and 3 dogs, respectively. Nine (5 with compressive IVDH and all 4 with FCE or ANNPE) of 34 (26%) dogs were classified as affected. Patellar reflexes were depressed in 2 of 9 affected dogs. The median time required for withdrawal reflexes to return to normal was 60 hours (range, 12 to 156 hours). Onset duration of paralysis was negatively associated with the odds of a dog being classified as affected. CONCLUSIONS AND CLINICAL RELEVANCE Results indicated that dogs with focal thoracolumbar spinal cord lesions, especially those with peracute onset of paralysis, can develop transient depression of pelvic limb reflexes. Awareness of this phenomenon is important for veterinarians to accurately localize lesions and develop appropriate diagnostic plans and prognoses.

Congenital Myasthenic Syndrome in a Mixed Breed Dog.

A 6-month-old, male, intact mixed breed dog was presented for a 3-month history of progressive generalized weakness. Neurologic examination revealed non-ambulatory tetraparesis, weakness of the head and neck, and decreased withdrawal reflexes in all limbs consistent with a generalized neuromuscular disorder. Electromyography and motor nerve conduction velocity were normal. Repetitive nerve stimulation showed a decremental response of the compound muscle action potential with improvement upon intravenous administration of edrophonium chloride. The serum acetylcholine receptor (AChR) antibody titer was within reference range. Cerebrospinal fluid analysis was unremarkable. A presumptive diagnosis of post-synaptic congenital myasthenic syndrome (CMS) was made. Treatment with pyridostigmine bromide was initiated with titrated increases in dosage resulting in an incomplete improvement in clinical signs. The dog was euthanized 2 months after initiation of treatment due to poor quality of life. Immunostaining for localization of antibodies against end-plate proteins in muscle biopsies was negative. Immunofluorescence staining for AChRs in external intercostal muscle biopsies showed absence of AChRs and biochemical quantitation showed a markedly decreased concentration of AChRs with no detectable AChR-bound autoantibody which confirmed the diagnosis of a CMS. Evaluation for the CHRNE mutation previously identified as the causative mutation of CMS in Jack Russell Terriers was performed and was negative. This is the first reported confirmed case of CMS in a mixed breed dog and provides a review of typical clinical and diagnostic findings as well as treatment considerations.

Pharmacokinetics of zonisamide following rectal administration to healthy dogs.

OBJECTIVE To evaluate the pharmacokinetics of zonisamide following rectal administration of 20 or 30 mg/kg suspended in sterile water or polyethylene glycol (PEG) to healthy dogs and determine whether either dose resulted in plasma zonisamide concentrations within the recommended therapeutic target range (10 to 40 µg/mL). ANIMALS 8 healthy mixed-breed dogs. PROCEDURES Each dog received each of 2 doses (20 or 30 mg/kg) of zonisamide suspended in each of 2 delivery substrates (sterile water or PEG) in a randomized crossover study with a 7-day washout period between phases. A blood sample was collected from each dog immediately before and at predetermined times for 48 hours after zonisamide administration. Plasma zonisamide concentrations were determined by high-performance liquid chromatography, and data were analyzed with a noncompartmental model. RESULTS Mean maximum plasma concentration, time to maximum plasma concentration, mean residence time, and elimination half-life did not differ significantly among the 4 treatments. The mean maximum plasma concentration for all 4 treatments was less than the therapeutic target range. The mean ± SD area under the concentration-time curve for the 30 mg/kg-in-water treatment (391.94 ± 237.00 h•µg/mL) was significantly greater than that for the 20 mg/kg-in-water (146.19 ± 66.27 h•µg/mL) and 20 mg/kg-in-PEG (87.09 ± 96.87 h•µg/mL) treatments. CONCLUSIONS AND CLINICAL RELEVANCE Results indicated that rectal administration of zonisamide at doses of 20 and 30 mg/kg failed to achieve plasma zonisamide concentrations within the recommended therapeutic target range. Therefore, rectal administration of zonisamide cannot be recommended as a suitable alternative to oral administration.

Multi-Center Retrospective Evaluation of Screw and Polymethylmethacrylate Constructs for Atlantoaxial Fixation in Dogs.

OBJECTIVE: To evaluate outcome and adverse events following ventral stabilization of the atlantoaxial (AA) joint in dogs with clinical AA subluxation using screw/polymethymethacrylate (PMMA) constructs in a retrospective, multi-center cohort study. STUDY DESIGN: Historical cohort study. ANIMALS: 35 client-owned dogs. METHODS: Medical records from 3 institutions were reviewed to identify dogs with AA subluxation treated with ventral screw and PMMA constructs. Data on signalment, pre- and postoperative neurologic status, imaging performed, and adverse events were retrieved. Neurologic examination data were abstracted to generate a modified Frankel score at admission, discharge, and re-examination. Telephone interview of owners >180 days postoperative was conducted. RESULTS: Thirty-five dogs with AA subluxation treated with ventral screw/PMMA constructs were included. Most dogs were young (median age 1 year), small breed dogs with acute onset of neurologic signs (median duration 22.5 hours). Most dogs were non-ambulatory at the time of admission (median modified Frankel score 3). Adverse events were identified in 15/35 dogs including 9 dogs with major adverse events. Four dogs required a second surgery due to vertebral canal violation (n = 2) or implant failure (n = 2). Re-examination at 4-6 weeks postoperative reported 15/28 dogs with improved neurologic status and 19/28 dogs were ambulatory. Telephone follow-up was available for 23/35 dogs with 23/23 reported as ambulatory (median follow-up 390 days). CONCLUSIONS: Ventral application of screw and PMMA constructs for AA subluxation, as described here, is associated with clinical improvement in the majority of dog. Major adverse events are infrequent and the technique is considered relatively safe.

Acute onset of encephalomyelitis with atypical lesions associated with dual infection of Sarcocystis neurona and Toxoplasma gondii in a dog.

A two-year-old male, neutered, basset hound-beagle mix with progressive neurological impairment was examined postmortem. Grossly, the dog had multiple raised masses on the spinal cord between nerve roots. Microscopically, the dog had protozoal myeloencephalitis. Toxoplasma gondii and Sarcocystis neurona were detected in the CNS by immunohistochemistry and polymerase chain reaction (PCR). Sarcocysts in formalin-fixed muscle were negative for Sarcocystis by PCR. Banked serum was negative for T. gondii using the modified agglutination test, suggesting an acute case of T. gondii infection or immunosuppression; however, no predisposing immunosuppressive diseases, including canine distemper, were found. To the authors' knowledge, this is the first report of dual T. gondii and S. neurona infection in a dog.

Use of the T2*-weighted gradient recalled echo sequence for magnetic resonance imaging of the canine and feline brain.

T2*-weighted magnetic resonance imaging (MRI) has been reported to help improve detection of intracranial hemorrhage and is widely used in human neuroimaging. To assess the utility of this technique in small animals, interpretations based on this sequence were compared with those based on paired T2-weighted and fluid-attenuated inversion recovery (FLAIR) sequences in 200 dogs and cats that underwent brain MRI for suspected intracranial disease. Two sets of images (T2 + FLAIR and T2*) were reviewed separately in random order unaccompanied by patient information and were interpreted as normal or abnormal based on whether intracranial abnormalities were seen. The number and location of intracranial lesions were recorded. Eighty-five studies were considered normal and 88 were considered abnormal based on both sets of images, with good agreement (κ = 0.731) between the two. Susceptibility artifact was present in 33 cases (16.5%) on T2*-weighted images. In 12 cases (6%) a total of 69 lesions were seen on T2*-weighted images that were not seen on T2/FLAIR, all of which were associated with susceptibility artifact caused by presumed intracranial hemorrhage. Pseudolesions were seen on T2*-weighted images in five cases, none of which were associated with susceptibility artifact. Abnormalities were seen on T2/FLAIR images that were not seen on T2*-weighted images in 35 cases, confirming that T2* does not replace standard spin echo sequences. These results support inclusion of T2*-weighted sequences in small animal brain MRI studies and indicate that that a large number of abnormalities (especially hemorrhagic lesions) can go undetected if it is not performed.