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Publications (5)9.26 Total impact

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    ABSTRACT: To describe the clinical phenotype of a new motor disorder in Labrador Retrievers. Case series study. Seven young male Labrador Retrievers presented for evaluation of stiff gait. All affected dogs had generalized muscular stiffness, persistent at rest and resulting in restricted joint movements. They showed a forward flexed posture, festinating gait, and bradykinesia. Signs developed between 2 and 16 months of age and tended to stabilize in adulthood. Needle electromyogram in the conscious state showed continuous motor unit activity in resting epaxial and proximal limb muscles. This activity was abolished by general anesthesia. Muscle and nerve histopathology was normal. In 2 dogs necropsied, astrocytosis was evident throughout the spinal cord gray matter, reticular formation and caudate nuclei. Decreased neuronal counts were selectively found in the spinal cord Rexed's lamina VII, but not in VIII and IX. Pedigree analysis showed that the affected dogs were from 5 related litters. This new hypertonicity syndrome in Labrador Retrievers is unique because of the selective distribution of the histological lesions, the lack of progression in adulthood, and its exclusive occurrence in male dogs. Pedigree analysis suggests an X-linked hereditary disease, although other modes of inheritance cannot be ruled out with certainty. We hypothesize that altered output from basal nuclei and reticular formation together with motor neuron disinhibition caused by a decreased number of spinal cord interneurons leads to the muscular stiffness.
    Journal of Veterinary Internal Medicine 07/2011; 25(5):1089-96. · 2.06 Impact Factor
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    ABSTRACT: Adult dogs with neosporosis can develop a variety of neurologic signs. No area of predilection within the nervous system so far has been identified in adult dogs. To document neosporosis as a cause of progressive cerebellar ataxia and cerebellar atrophy in dogs. Seven client-owned dogs. Retrospective, descriptive study. Age at diagnosis ranged from 1 year 6 months to 9 years 11 months. Neuroanatomic localization indicated cerebellar and brainstem disease in 6 dogs and a central vestibular lesion in 1 dog. In all 7 dogs, there was moderate to marked bilaterally symmetrical cerebellar atrophy, with the atrophied cerebellum being surrounded by a region of T2-weighted hyperintense and T1-weighted hypointense signal. Cerebrospinal fluid (CSF) analysis in all but 1 dog showed mononuclear pleocytosis and high protein concentration. Polymerase chain reaction testing for Neospora caninum performed on the CSF was positive in 4/5 dogs tested and there was a high titer of serum antibodies to N. caninum (> or = 1 : 800) in all 6 dogs tested. Postmortem examination in 1 dog confirmed cerebellar atrophy and multifocal nonsuppurative encephalitis with areas of malacia and leptomeningitis. All of the remaining 6 dogs were treated with some combination of clindamycin, trimethoprim, sulfadiazine, and pyrimethamine. Two dogs were euthanized because of deterioration or relapse of neurologic signs, but treatment of the remaining 4 dogs resulted in improvement (3 dogs) or resolution (1 dog) of neurologic signs. Neosporosis is an important cause of progressive cerebellar ataxia and cerebellar atrophy in adult dogs.
    Journal of Veterinary Internal Medicine 03/2010; 24(3):571-8. · 2.06 Impact Factor
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    ABSTRACT: A 7-month-old neutered male ferret was evaluated for episodic pelvic limb weakness of 2 weeks' duration. Neurologic examination revealed flaccid tetraparesis with decreased spinal reflexes suggestive of a neuromuscular disease. Results of hematologic and CSF analyses, thoracic radiography, and abdominal ultrasonography were unremarkable. Electrodiagnostic testing revealed subtle spontaneous activity localized to pelvic limb interosseous muscles, unremarkable motor nerve conduction velocities, and lower than typical compound muscle action potential (CMAP) amplitude for tibial nerve stimulation only. A severe decremental response of the CMAP was detected with repetitive nerve stimulation (45.5% at the third ulnar nerve). An esophagogram revealed mild megaesophagus. Intravenous neostigmine methylsulfate administration resulted in immediate resolution of muscle weakness. Cross-reacting anti-acetylcholine receptor (AChR) antibodies were detected in serum (0.35 nmol/L) by use of a canine- and feline-specific muscle extract. Clinical signs and ancillary test results were diagnostic of acquired myasthenia gravis. Pyridostigmine bromide was administered (1 mg/kg [0.45 mg/lb], PO, q 8 h), resulting in complete remission of clinical signs. However, 1 month after the diagnosis, the ferret was euthanized because of recurrence of weakness despite anticholinesterase treatment. To the authors' knowledge, this is the first report of acquired myasthenia gravis in a ferret and the first identification of anti-AChR antibodies in this species. Autoimmune myasthenia gravis should be considered in ferrets when weakness and flaccid paresis suggest a neuromuscular disease. Electrodiagnostic testing, anticholinesterase challenge, and AChR antibody titer determination were helpful for diagnosis of this condition.
    Journal of the American Veterinary Medical Association 12/2009; 235(12):1462-6. · 1.72 Impact Factor
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    ABSTRACT: A spontaneous demyelinating polyneuropathy in two young Miniature Schnauzer dogs was characterized clinically, electrophysiologically and histopathologically. Both dogs were related and a third dog, belonging to the same family, had similar clinical signs. On presentation, clinical signs were restricted to respiratory dysfunction. Electrophysiological tests showed a dramatic decrease in both motor and sensory nerve conduction velocities. Microscopic examination of peripheral nerve biopsies (light and electron microscopy, teased nerve fibers), showed that this neuropathy was characterized by segmental demyelination and focally folded myelin sheaths. Various clinical syndromes associated with tomacula or focal thickening of the myelin sheath of the peripheral nerves have been described in humans and shown to be caused by gene mutations affecting the myelin proteins, such as the hereditary neuropathy with liability to pressure palsies or the demyelinating forms of Charcot-Marie-Tooth disease. In animals, a tomaculous neuropathy has been reported in cattle and chickens but not in carnivores. Here we report a demyelinating peripheral neuropathy with tomacula in two Miniature Schnauzer dogs.
    Journal of the Neurological Sciences 10/2008; 275(1-2):100-5. · 2.24 Impact Factor
  • J Couturier, D Rault, L Cauzinille
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    ABSTRACT: The objectives of the study were (1) to report the incidence of Chiari-like malformation and syringomyelia in a normal French cavalier King Charles spaniel breeding population; (2) to precise the standard computed tomography dimensions of the caudal fossa and (3) to investigate the use of ultrasonography in diagnosis of this syndrome. Clinically normal adult cavalier King Charles spaniel underwent ultrasonographic examination of the spinal cord and caudal fossa. Computed tomography was used to measure the caudal fossa and magnetic resonance imaging allowed syringomyelia and cerebellar herniation identification. Of the 16 dogs in the study, seven had syringomyelia (43.7 per cent). All dogs had cerebellar herniation, suggesting Chiari-like malformation and also a tendency to occipital dysplasia. Computed tomography measurements of the caudal fossa are reported. In one dog, a syrinx was identified by ultrasonography. The only difference between dogs with or without syringomyelia was that dogs with Chiari-like malformation/syringomyelia were statistically older. The incidence of Chiari-like malformation and syringomyelia may be high in an asymptomatic population of cavalier King Charles spaniel . Computed tomography measurements reported in this study should now be compared with those of a symptomatic population to evaluate the hypothesis that dogs with Chiari-like malformation/syringomyelia syndrome have a smaller caudal fossa. This study did not identify a smaller caudal fossa in an asymptomatic cavalier King Charles spaniel population with syringomyelia. Ultrasonography probably has a low sensitivity for diagnosis of Chiari-like malformation/syringomyelia.
    Journal of Small Animal Practice 09/2008; 49(9):438-43. · 1.18 Impact Factor