Rohdin, Cecilia
- Institutionen för kliniska vetenskaper, Sveriges lantbruksuniversitet
- Albano Animal Hospital
Forskningsartikel2020Vetenskapligt granskadÖppen tillgång
Rohdin, Cecilia; Ljungvall, Ingrid; Haggstrom, Jens; Leijon, Alexandra; Lindblad-Toh, Kerstin; Matiasek, Kaspar; Rosati, Marco; Wohlsein, Peter; Jaderlund, Karin Hultin
Background Thoracolumbar myelopathies associated with spinal cord and vertebral column lesions, with a similar clinical phenotype, but different underlying etiologies, occur in pugs. Objectives To further characterize the clinical and neuropathological characteristics of pugs with longstanding thoracolumbar myelopathy. Animals Thirty client-owned pure-bred pugs with a history of more than a month of ataxia and paresis of the pelvic limbs, suggesting a myelopathy localized to the thoracolumbar spinal cord, were included in the study. Methods Prospective clinicopathological study. Included pugs underwent a complete neurological examination and gross and histopathologic postmortem studies with focus on the spinal cord. Computed tomography (n = 18), magnetic resonance imaging (n = 17), and cerebrospinal fluid analysis (n = 27) were performed before or immediately after death. Results Twenty male and 10 female pugs had a median age at clinical onset of 84 months (interquartile range, 66-96). Affected pugs presented with a progressive clinical course and 80% were incontinent. There was circumferential meningeal fibrosis with concomitant focal, malacic, destruction of the neuroparenchyma in the thoracolumbar spinal cord in 24/30 pugs. Vertebral lesions accompanied the focal spinal cord lesion, and there was lympho-histiocytic inflammation associated or not to the parenchymal lesion in 43% of the pugs. Conclusions and Clinical Importance Meningeal fibrosis with associated focal spinal cord destruction and neighboring vertebral column lesions were common findings in pugs with long-standing thoracolumbar myelopathy.
ataxia; meninges; spinal cord
Journal of Veterinary Internal Medicine
2020, Utgivare: WILEY
Klinisk vetenskap
DOI: https://doi.org/10.1111/jvim.15716
https://res.slu.se/id/publ/104405