CASE DESCRIPTION A 16-month-old neutered male Continental Giant rabbit (Lepus curpaeums) was referred for evaluation of a 7-day history of acute-onset, progressive, symmetric paraparesis.
CLINICAL FINDINGS On initial examination, the rabbit was nonambulatory, and results of neurologic examination were consistent with a lesion affecting the T3-L3 spinal cord segments. Thoracic radiography showed irregular widening of the left T11–12 articular process joint. Marked dorsolateral and lateral extradural spinal cord compression with contrast enhancement of the adjacent epaxial muscles was evident on MRI images of the spine.
TREATMENT AND OUTCOME A left-sided T11–T12 hemilaminectomy was performed, which revealed an abnormal and hypertrophic T11–12 articular process joint and an osteolytic lesion communicating with the vertebral canal. Copious purulent material causing marked spinal cord compression was evident, and the surgical site was lavaged extensively with sterile (0.9% NaCl) saline solution. Results of aerobic, anaerobic, and enriched bacteriologic cultures of swab specimens obtained from the surgical site were negative. Histologic analysis of biopsy samples revealed chronic purulent osteomyelitis, myositis, and fasciitis with necrosis, fibrosis, and dystrophic mineralization. The rabbit was discharged 48 hours after surgery. Ten weeks after surgery, the rabbit was ambulatory with mild paraparesis. On telephone follow-up 21 months after surgery, the owners indicated that the rabbit was healthy and expressed satisfaction with the treatment and outcome.
CLINICAL RELEVANCE Paraspinal abscess with vertebral canal involvement should be considered as a differential diagnosis for rabbits with clinical signs of progressive T3-L3 myelopathy. Outcome for the patient of the present report suggested that surgical treatment including decompression and debridement can result in a favorable long-term outcome.
Treatment options for human dementia remain limited, and additional research is needed to develop and validate translational models. Canine cognitive decline (CCD) is common in older dogs and a major source of morbidity. The decline includes physiological and behavioral changes comparable to those in humans diagnosed with dementia. There are also corresponding changes in plasma neurodegenerative biomarkers and neuropathology. Biomarkers for both human and canine cognitive decline can be used to identify and quantify the onset of behavioral data suggestive of CCD. Successful correlations would provide reference values for the early identification of neurodegeneration in canine patients. This could allow for the subsequent testing of interventions directed at ameliorating CCD and offer translational value leading to safe and effective treatment of dementia in people. Research can help exploit, track, and provide benefits from the rapid progression of spontaneous naturally occurring CCD in a large heterogenous community of companion dogs. Research efforts should work to deliver information using blood biomarkers, comorbidities, and wearable technologies to track and evaluate biometric data associated with neurodegeneration and cognitive decline that can be used by both human and companion animal researchers. The synergistic approach between human and veterinary medicine epitomized in one health underscores the interconnectedness of the well-being of both species. Leveraging the insights gained from studying CCD can not only lead to innovative interventions for pets but will also shed light on the complex mechanisms of human dementia.