Magnetic Resonance Imaging Findings in a Dog with Sensory Neuronopathy

A 3-year-old, male neutered Miniature Dachshund was presented for investigation of an acute onset, slowly progressive ataxia of 2 months’ duration. Serum titers for Toxoplasma gondii and Neospora caninum evaluated before referral were negative. General physical examination was within normal limits. Neurological examination identified a “bouncy” generalized ataxia with exaggerated movements of all of the limbs, neck and head. No apparent paresis was present. The dog had proprioceptive deficits in all limbs manifested by a delay in hopping and paw placement. Clinical signs and neurological abnormalities were more severe in the pelvic limbs. The dog had bilaterally decreased menace responses and palpebral reflexes. The remainder of the neurologic examination was within normal limits. A diffuse or multifocal neuro-anatomic localization was considered most likely. Results of a CBC and serum biochemistry profile were within reference intervals. The dog was premedicated with butorphanol (0.2 mg/kg IV) and anesthesia was induced with propofol (3.5 mg/kg IV) and maintained with sevoflurane in oxygen. Magnetic resonance imaging (MRI) of the brain and cervical spinal cord included T2-weighted (repetition time, [TR] [ms], echo time [TE] [ms] 3333/110) sagittal and transverse images and transverse fluid attenuation inversion recovery (TR/TE, 6000/120) images. Sagittal and transverse plane T1-weighted images (TR/TE, 515/15) were acquired before and after IV injection of gadolinium contrast material. Slice thickness was 3.5 mm in all planes with an interslice gap of 0.9 mm in the sagittal and 1 mm in the transverse planes. No abnormalities were identified on MRI of the brain. In the cervical spinal cord, a linear, intra-parenchymal signal, hyperintense on T2-weighted images, delineated the dorsal funiculus (Fig 1). No contrast enhancement was observed. Differential diagnoses at this time included an inflammatory spinal cord disorder, a neurodegenerative disorder involving the cervical spinal cord, or a sensory neuronopathy. Analysis of cerebrospinal fluid, obtained by cisternal and lumbar punctures was within normal limits. Based on these findings, a sensory neuronopathy was considered the most likely diagnosis. Neurologic re-examination 1 month later identified worsening of the dog’s ataxia, decreased patellar reflexes and decreased nociception in the digits of all limbs. Electrodiagnostic evaluation and spinal ganglion biopsy were offered, but declined by the owner. The dog was presented 15 months after its initial clinical presentation for assessment of perceived vision loss and further worsening of clinical signs. There was a known familial history of progressive retinal atrophy. Neurologic examination identified severe deterioration of clinical signs. Although paresis still was not apparent, the severity of the dog’s ataxia impeded ambulation. Other findings included wide head and neck excursions, proprioceptive deficits in all limbs, absent bilateral menace responses, absent bilateral palpebral and corneal reflexes, bilaterally decreased responses after stimulation of the nasal mucosa, decreased pupillary light reflexes bilaterally (direct and indirect), absent patellar reflexes bilaterally and decreased nociception in the digits of all limbs. The remainder of the neurologic examination was within normal limits. A complete ophthalmic examination confirmed visual impairment and abnormalities of ocular reflexes as described above. Rudimentary corneal esthesiometry (ie, use of cottontipped applicator and the noncontact air-puff technique) indicated decreased corneal sensation. General anesthesia was induced and maintained by using the previously described protocol. A mixed rod-cone electroretinogram (ERG) disclosed no visible ERG in the right eye and a markedly diminished ERG in the left eye with barely discernible a and b waves. Findings of the ophthalmic and ERG examinations were in agreement with From the Department of Clinical Science and Services, Royal Veterinary College, University of London, North Mymms, Hatfield UK (Hamzianpour, Kenny, Sanchez, Volk, De Decker); and the Department of Pathology and Pathogen Biology, The Royal Veterinary College, University of London, North Mymms, Hertfordshire UK (Eley). This case report has been presented in part at the 26 Annual Symposium of the European Society of Veterinary Neurology – European College of Veterinary Neurology, 26-28 September 2013, Paris. Corresponding author: S. De Decker, Department of Clinical Science and Services, Royal Veterinary College, University of London, Hawkshead Lane, AL9 7TA North Mymms, Hatfield, UK; e-mail: [email protected]. Submitted January 28, 2015; Revised May 14, 2015; Accepted June 17, 2015. Copyright © 2015 The Authors. Journal of Veterinary Internal Medicine published by Wiley Periodicals, Inc. on behalf of the American College of Veterinary Internal Medicine. This is an open access article under the terms of the Creative Commons Attribution-NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes. DOI: 10.1111/jvim.13582 Abbreviations: