A 6-week-old female Simmental calf was evaluated for acute non-ambulatory tetraparesis. Physical and laboratory examinations revealed no clinically relevant abnormalities. Neurological findings were consistent with acute, progressive and painful cervical myelopathy. Radiographs displayed a fractured odontoid process (dens axis) and vertebral step misalignment at the fracture site. A traumatic origin was suspected. Advanced diagnostic imaging was considered to allow better planning of potential surgical stabilisation and to exclude any additional lesions of the cervical vertebral column. However, during trailer transportation to the advanced diagnostic imaging and surgery site, the calf deteriorated neurologically and was humanely euthanised. Magnetic resonance imaging (MRI) and computed tomography (CT) were performed immediately post-mortem for scientific reasons. The MRI examination reflected the radiographic findings and confirmed severe spinal cord compression at the fracture site. In addition, a T2W-hyperintense signal change within the paravertebral soft tissue dorsal to the fracture site was indicative of a traumatic event. CT identified the fracture site at the synchondrosis between the odontoid process and the body of the axis, and this finding was confirmed by post-mortem examination. Advanced diagnostic imaging and post-mortem examination did not identify any other cervical lesion. In summary, this calf was diagnosed with a traumatic odontoid process synchondrosis fracture, which has not been reported previously in calves but presents a challenging and well-known fracture type in young children. This case report indicates that the odontoid process synchondrosis is a potential predisposed injury site and that traumatic odontoid process synchondrosis fractures should be considered as a potential differential in calves with acute cervical pain and/or signs of a cervical myelopathy.

Drug-resistant epilepsy is a common complaint in dogs and affects up to 30% of dogs with idiopathic epilepsy. Experimental data suggest that targeting cyclooxygenase-2 (COX-2) mediated signaling might limit excessive excitability and prevent ictogenesis. Moreover, the role of COX-2 signaling in the seizure-associated induction of P-glycoprotein has been described. Thus, targeting this pathway may improve seizure control based on disease-modifying effects as well as enhancement of brain access and efficacy of the co-administered antiseizure medication. The present open-label non-controlled pilot study investigated the efficacy and tolerability of a COX-2 inhibitor (firocoxib) add-on therapy in a translational natural occurring chronic epilepsy animal model (client-owned dogs with phenobarbital-resistant idiopathic epilepsy). The study cohort was characterized by frequent tonic–clonic seizures and cluster seizures despite adequate phenobarbital treatment. Enrolled dogs (n = 17) received a firocoxib add-on therapy for 6 months. Tonic–clonic seizure and cluster seizure frequencies were analyzed at baseline (6 months) months during the study (6 months). The responders were defined by a substantial reduction of tonic–clonic seizure and cluster seizure frequency (≥50%). In total, eleven dogs completed the study and were considered for the statistical analysis. Two dogs (18%, 2/11) were classified as responders based on their change in seizure frequency. Interestingly, those two dogs had the highest baseline seizure frequency. The overall tolerability was good. However, given the low percentage of responders, the present data do not support an overall considerable efficacy of COX-2 inhibitor add-on therapy to overcome naturally occurring phenobarbital-resistant epilepsy in dogs. Further translational evaluation should only be considered in the canine patients with a very high baseline seizure density.