A 10-year-old, neutered male Dachshund was presented for evaluation of severe neck pain that began 1 month earlier. Treatment prior to referral included deracoxib, tramadol, and cage rest. On presentation, physical and neurological examinations identified cervical pain and lameness of the left forelimb. Orthopedic examination was normal.\nComputed tomography of the cervical spine was performed. At C3–C4, the intervertebral disk space was collapsed and a large amount of mineral-attenuating material was present in the left intervertebral foramen, displacing the perineural fat (Figure ). Incidentally, in situ mineralization of the intervertebral disks was noted throughout the remainder of the cervical vertebral column.\nThe lateralized material at C3–C4 was thought to contribute to clinical signs due to compression of the left third spinal nerve, and its location suggested that it would not be accessible through a ventral slot approach. Interventional options included cervical hemilaminectomy or fluoroscopically guided perineural injection of local anesthetic (bupivacaine) and methylprednisolone. The client elected the latter.\nTwenty milligrams of methylprednisolone (2.1 mg/kg) and 9.4 mg of bupivacaine (1 mg/kg) were injected into the left C3–C4 foramen. The patient was moved to the ICU after the procedure for recovery. Although the patient became increasingly alert, he initially failed to regain voluntary respiration. Mechanical ventilatory support was required for 30 min; later, the patient began breathing on his own, was weaned off the ventilator, and was extubated.\nImmediate improvement in lameness was apparent while in the hospital. The patient was discharged with tramadol PO (1.4 mg/kg q8 h) and gabapentin PO (5.5 mg/kg q12 h) to be combined with cage rest and physical therapy. Fourteen days later at follow-up, the patient was doing well and was pain free. Tramadol was discontinued at that time, and the dose of gabapentin was reduced by half. By 3 months after surgery, all medications had been discontinued. Follow-up was obtained 4 years later when the patient was presented to the teaching hospital ophthalmology service for cataract evaluation. No recurrence of neck pain was reported by the client, and none was found on neurological examination.
An 8-year-old tortoiseshell spayed female domestic shorthair cat was referred for anorexia, weight loss and progressive trismus of at least 1 month duration. A history of chronic rhinitis since the age of 4 months was reported. A PCR test for calicivirus was negative. Previous antibiotic therapies (doxycyline 10 mg/kg PO q24h for 10 days; benzylpenicillin procaine 7 mg/kg [dihydrostreptomycin 10 mg/kg long-acting formulation] IM; and clindamycin hydrochloride 11 mg/kg PO q24h for 10 days) did not result in any clinical improvement. The cat was exclusively fed veterinary dry food and no history of trauma was reported.\nUpon presentation, the cat had generalised weakness, bilateral purulent nasal discharge, with concurrent reduced nasal airflow, right epiphora with chemosis and third eyelid protrusion, and concurrent mild bilateral mandibular lymph node enlargement. Body condition score was 3/9 (weight 2.9 kg [6.4 lb]). Neurological examination revealed decreased bilateral palpebral reflexes on the ophthalmic branch territories of the trigeminal nerves, and an absence of pupillary light reflexes. Vision testing revealed complete visual deficits, previously unnoticed by the owners, absent menace response in both eyes, and the patient bumping into objects. Spinal reflexes were normal and no gait abnormality was present. Oral examination showed painful mouth opening with a restricted vertical mandibular range of motion (vmROM), and an inability to close the mouth (). The rest of the physical examination was within normal limits.\nSerum biochemistry and electrolytes were unremarkable. Serological screening for infectious agents (Toxoplasma species, Ehrlichia species, Cryptococcus species, Anaplasma species) was negative. A complete blood count and blood smear examination revealed a mild microcytic non-regenerative normochromic anaemia with concurrent moderate neutrophilia and monocytosis. Antinuclear antibody testing was negative, and creatine kinase activity, activated partial thromboplastin time, activated clotting time, thrombin clotting times and D-dimers were within the normal limits. The restriction of vmROM persisted under general anaesthesia (22 mm). Intra-oral examination and dental charting revealed oropharyngeal swelling, with haematomas involving the retromolar areas, ulceration of the dorsal aspect of the tongue and mild generalised periodontitis.\nIn order to explore the cause of reduced mouth opening, CT of the head was performed. Selected reconstructed images are provided (). CT images showed bilateral, asymmetrical, non-enhancing (49 Hounsfield units in the pre- and post-contrast images), ill-defined hypodense areas within the masticatory muscles, mostly the temporalis and masseter muscles. Irregular periosteal reaction was noted on the ramus of the mandible and on the parietal and temporal bones bilaterally. Some new bone foci extended into the temporalis and medial pterygoid muscles away from the bone surfaces, indicating an ectopic mineralisation disorder. CT findings suggested bilateral chronic masticatory myositis.\nSix ultrasound-guided needle-core biopsies from the right and left masticatory muscles were collected and submitted to two different laboratories for comparative anatomopathological analysis. Biopsied material was submitted fresh and fixed in 10% neutral buffered formalin and decalcified as required. Fresh biopsies were isopentane pre-cooled in liquid nitrogen for cryohistology. Cryosections were stained with haematoxylin and eosin, Engel’s modified Gömöri trichrome stain, oil red O and periodic acid–Schiff reaction. Fixed biopsies were embedded in paraffin, sectioned at 3–5 µm thickness, mounted on glass slides and stained with haematoxylin and eosin before light microscopy evaluation. The samples showed extensive replacement of the myofibers with a dense vascularised mesenchymal tissue exhibiting progressive ossification. The mesenchymal tissue was composed of peripheral fascicles of activated fibroblasts and intermediate osteoblasts depositing woven bone and gradually forming trabeculae of lamellar bone (). Rare atypia and mitoses were present in the fibroblastic population. Residual muscle fibres embedded in the lesions were atrophic and degenerated. Some samples revealed striated muscle containing occasional inflammatory infiltrates. No infectious agent was observed within the samples. A FOP-like disease was considered the most likely diagnosis by both laboratories.\nSupportive treatment during hospitalisation consisted of fluid therapy (3 ml/kg/h), nutrition through an oesophagostomy tube, antibiotic therapy (clindamycin hydrochloride 11 mg/kg PO q24h for 7 days, then doxycycline 10 mg/kg PO q24h), pain management (buprenorphine 20 µg/kg IV q6h), a muscle relaxant (dantrolene-sulfate 1 mg/kg PO q8h) and immunosuppressive doses of methylprednisolone (3.3 mg/kg PO q24h) in case of an immune-mediated process. The latter was subsequently replaced with robenacoxib (1 mg/kg PO q24h) 4 weeks after initial presentation.\nDespite weight stabilisation, and improved willingness to move, allowing transient home care, the cat failed to recover the ability to eat spontaneously. A full-body CT scan was eventually performed 4 weeks after initial presentation and excluded additional areas of soft tissue calcification, pulmonary lesions and lymph node enlargement. Five weeks after initial presentation there had been a rapid decrease of vmROM leading to a total inability to open and close the mouth (13 mm open bite). A persistent bilateral purulent nasal discharge with almost total blockage of the nares led to the decision to perform a tracheostomy and nasal cavity lavage under general anaesthesia. During induction of anaesthesia, an emergency endotracheal intubation by tracheotomy, followed by cardiac resuscitation, had to be carried out. Because of the worsening prognosis, the owners elected humane euthanasia and rejected post-mortem investigations.\nTwo remaining samples of fresh biopsied material, kept at –80°C, were ultimately sent in dry-ice medium to a specialised laboratory for molecular analysis. Genomic DNA was extracted from the muscle samples, using sodium dodecyl sulfate/proteinase K lysis followed by purification on silica columns. The primers were synthesised at a 25 nmol scale, desalted and designed on the reference sequence of Genbank NC_018730, with the use of a software. After PCR amplification and product purification Sanger sequencing was performed for the whole nine coding exons of Felis catus ACVR1 (total linear DNA length 222,790,142 bp), located on the C1 chromosome, and purified. DNA sequencing products were analysed on a 96 capillary DNA analyser. Two deletions were highlighted in the exon 8 and exon 9 PCR products, and were further amplified and sequenced. Both of them were characterised in intron 8, upstream of the last coding exon 9 of ACVR1. Four bases (TTGA) were deleted around –123 bases of the exon 9 start (position 139,512 of the total gene sequence), and five bases (CCCAT) were deleted around –225 bases upstream of the exon 9 start (position 139,410 of the total gene sequence).