The medical records of 29 dogs unable to close their mouths due to flaccid paralysis or paresis of the muscles innervated by the mandibular branch of the trigeminal nerve, were reviewed. Idiopathic trigeminal neuropathy was diagnosed in 26 dogs based on complete resolution of clinical signs and lack of any long-term neurological disease. Of these dogs, golden retrievers were overrepresented. No age, sex, or seasonal predispositions were identified. Trigeminal sensory innervation deficits were observed in 35% (9/26), facial nerve deficits were observed in 8% (2/26), and Horner's syndrome was observed in 8% (2/26) of dogs. Electromyographic examination of the muscles of mastication revealed abnormalities in seven of nine dogs. Results of cerebrospinal fluid analysis were abnormal in seven of eight dogs. Corticosteroid therapy did not affect the clinical course of the disease. Mean time to recovery was 22 days. Lymphosarcoma, Neospora caninum infection, and severe polyneuritis of unknown origin were diagnosed in three of 29 dogs at necropsy.

A 5-year-old, castrated male mixed-breed dog was presented for paraparesis, ataxia, hyperesthesia, and thrombocytopenia of 5 months' duration and recurrent seizures during the preceding 2 weeks. Multifocal neurological, ophthalmological, pulmonary, and cardiac diseases were identified. Magnetic resonance imaging and cerebrospinal fluid analysis supported a tentative diagnosis of neoplastic or inflammatory disease. A computed tomography-guided biopsy provided both cytopathological and histopathological evidence of intravascular lymphoma. The disease progressed despite chemotherapy with prednisone, L-asparginase, and vincristine. Postmortem histopathological examinations suggested intravascular lymphoma in the central and peripheral nervous systems as well as in multiple other organ systems. This is the first description of an antemortem diagnosis and treatment of intravascular lymphoma involving the central nervous system of a dog.

A n 8-year-old female spayed Bernese Mountain Dog (BMD) presented to the Bush Veterinary Neurology Service (BVNS) for paraparesis. The dog had been seen at the BVNS 13 months earlier for evaluation of progressive pelvic limb weakness. At that time, the dog had a short-strided gait in the pelvic limbs, mild postural reaction deficits in the right pelvic limb, normal segmental reflexes, and laxity of the right coxofemoral joint. The dog was treated with meloxicam (0.15 mg/kg PO q24h) for 3 days, amantidine (2 mg/kg PO q24h) for 1 month, and doxycycline (6 mg/kg PO q12h) for 2 weeks with no improvement noted. The dog had a previous history of hypothyroidism that had been treated with 0.3 mg levothyroxine PO q12h.Asymmetric general proprioceptive ataxia and spastic paraparesis were present on neurologic examination. Postural reactions were delayed in both pelvic limbs and segmental reflexes were normal. Initial diagnostic tests included a CBC, serum biochemistry, and thoracic and spinal radiographs. The results of all tests were within normal limits. A DNA test for the SOD1:c.118G 4 A mutation commonly associated with canine degenerative myelopathy (DM) was normal (homozygous for the G allele).1 Physiotherapy was initiated. Sixteen months after the initial presentation, signs had progressed to paraplegia with preservation of pain perception. Decreased patellar and withdrawal reflexes were present in both pelvic limbs and suggested neurodegeneration that had progressed to include the lower motor neurons associated with the femoral and sciatic nerves. Analysis of cerebrospinal fluid obtained by atlantooccipital puncture revealed mild albuminocytologic dissociation with a protein concentration of 30 mg/dL and no nucleated cells. Magnetic resonance imaging of the spinal cord was performed 21 months after the initial presentation with a 1.5 T unit, a T2-weighted (T2W), T1-weighted (T1W), and half Fourier acquisition single-shot turbo spin echo (HASTE) sagittal sequences were acquired from the foramen magnum to the sacrum. Transverse T2W, T1W, and T1W postcontrast b weighted images were acquired from T12 to L4. Spondylosis and a mildly increased signal within the dorsal funiculus of the spinal cord were noted at the T12-13 disc space on T2W images. The T12-13 disc was well hydrated and similar in size to adjacent discs.The dog was euthanized 21 months after the initial presentation because the disease had progressed to include fecal and urinary incontinence. Histopathologic evaluation of formalin-fixed spinal cord was performed at the University of Missouri Veterinary Medical Diagnostic Laboratory. Spinal cord cross sections were stained by standard methods with luxol fast blue (LFB), and periodic acid Schiff (PAS) as a counter stain. Immunostaining was performed to detect phosphorylated neurofilament and glial fibrillary acid protein (GFAP) as a measure of axonal loss and gliosis, respectively. Deparaffinized sections were treated with rabbit anti-GFAP antibody c without pretreatment, and binding was detected with horser...

BackgroundExtraparenchymal spinal cord hematoma has been described in veterinary medicine in association with neoplasia, intervertebral disk disease, and snake envenomation. There are rare reports of spontaneous extraparenchymal spinal cord hematoma formation with no known cause in human medicine. Multiple cases of spontaneous extraparenchymal spinal cord hematoma have not been described previously in veterinary medicine.ObjectivesTo describe the signalment, clinical findings, magnetic resonance imaging (MRI) features, and surgical outcomes in histopathologically confirmed extraparenchymal spinal cord hematomas in dogs with no identified underlying etiology.AnimalsSix dogs had MRI of the spinal cord, decompressive spinal surgery, and histopathologic confirmation of extraparenchymal spinal cord hematoma not associated with an underlying cause.MethodsMulti‐institutional retrospective study.ResultsSix patients had spontaneous extraparenchymal spinal cord hematoma formation. MRI showed normal signal within the spinal cord parenchyma in all patients. All hematomas had T2‐weighted hyperintensity and the majority (5/6) had no contrast enhancement. All dogs underwent surgical decompression and most patients (5/6) returned to normal or near normal neurologic function postoperatively. Follow‐up of the patients (ranging between 921 and 1,446 days) showed no progression of neurologic clinical signs or any conditions associated with increased bleeding tendency.Conclusions and Clinical ImportanceBefore surgery and histopathology confirming extraparenchymal hematoma, the primary differential in most cases was neoplasia, based on the MRI findings. This retrospective study reminds clinicians of the importance of the combination of advanced imaging combined with histopathologic diagnosis. The prognosis for spontaneous spinal cord extraparenchymal hematoma with surgical decompression appears to be favorable in most cases.

Severe hypomagnesemia (0.8 mg/dl; reference range, 1.6 to 2.3 mg/dl), hypocalcemia, and protein-losing enteropathy were identified in a 5-year-old castrated male 3-kg (6.6 lb) Shih Tzu examined because of anorexia, lethargy, paresis, and abdominal distention. Histologic examination of intestinal biopsy specimens revealed lymphangiectasia and lymphocytic, plasmacytic, neutrophilic infiltrates. Initial treatment included administration of magnesium (0.80 mEq/kg [0.36 mEq/lb]) of body weight in a balanced electrolyte solution. This treatment resulted in normalization of the serum magnesium concentration (1.7 mg/dl); resolution of the lethargy, paresis, and tachycardia; and an increase in the serum parathyroid hormone and ionized calcium concentrations. Findings were consistent with secondary hypoparathyroidism attributable to hypomagnesemia. Magnesium concentration should be monitored in all dogs with gastrointestinal tract disease, especially those with protein-losing enteropathy, anorexia, and weakness.