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.
A 4-year-old female spayed domestic shorthair cat weighing 6.9 kg was presented with a 2-week history of intermittent bilateral exophthalmos, facial swelling and serous ocular discharge. Food prehension, the ability to open the mouth and pre-referral intraoral radiographs were unremarkable. Owing to a lack of visible clinical improvement following clindamycin (Zodon; Ceva) treatment, amoxicillin–clavulanic acid (Noroclav; Norbrook) and meloxicam (Metacam; Boehringer Ingelheim), the cat was referred to the neurology and neurosurgery service at the Animal Health Trust.\nAt presentation, generalised facial swelling, extending to the neck and cheeks, mild exophthalmos, third eyelid protrusion, chemosis and bulbar conjunctival hyperaemia were detected bilaterally (). The left eye was more severely affected than the right. Aqueous flare was absent and intraocular pressure, menace response and pupillary light and dazzle reflexes were unremarkable. Fluorescein staining was negative bilaterally and the Jones test was positive in the right eye only. Performing complete physical and neurological examinations was not possible given the uncooperative nature of the cat; however, the remainder of the physical examination under general anaesthesia was unremarkable. A disease affecting the retrobulbar area or the masticatory muscles, including masticatory myositis (MM), was suspected.\nHaematology and serum biochemistry revealed mild eosinophilia (3.38 × 109/l; reference interval [RI] 0.10–2.00) and a markedly elevated creatine kinase (CK) activity (5959 IU/l; RI 70–190). Serological titres against Toxoplasma gondii were consistent with previous exposure.\nMRI of the head was conducted with a 1.5 T scanner (Signa EchoSpeed; GE Healthcare). Transverse, dorsal and sagittal T2-weighted (T2W) (repetition time [TR] 3975–6221 ms/echo time [TE] 84–87 ms; field of view 140 mm, matrix 512 × 512) sequences, transverse precontrast T1-weighted (T1W) (TR 521 ms/TE 6.6 ms) images, and transverse and dorsal postcontrast T1W sequences – after the administration of an intravenous gadolinium-based agent (Gadovist; Bayer) – were obtained. Additionally, transverse short tau inversion recovery (STIR) (TR 8344 ms/TE 39 ms/TI 150 ms) and transverse postcontrast T1W images with fat saturation (TR 732 ms/TE 6.6 ms) were acquired. Slice thickness was 3 mm.\nThe temporal, masseter and medial pterygoid muscles were diffusely thickened bilaterally and showed multifocal-to-coalescing areas of marked hyperintensity on T2W and STIR images relative to normal muscle (). There were subtle hyper- and hypointensities on T1W images, producing an ill-defined striated appearance. The affected muscles showed strong and heterogenous contrast enhancement, with multiple embedded, non-contrast-enhancing areas (consistent with fluid or necrosis) within the abnormal muscles (,). The digastricus, extraocular and cervical muscles appeared to be unaffected. Significant mandibular and medial retropharyngeal lymphadenopathy was detected. The MRI was suggestive of severe infectious or immune-mediated MM.\nAs a feline-specific assay has not been established, a canine ELISA was used to detect serological titres against type IIM muscle fibre proteins and was positive at a dilution of 1:4000 (RI <1:100 in dogs). Cytological analysis of ultrasound-guided fine-needle aspirates of the left temporal and masseter muscles, including the suspected necrotic regions on MRI, revealed eosinophilic and macrophagic inflammation. Bacterial and fungal cultures were negative. Lack of evidence supporting active infection coupled with positive serological titres against type IIM muscle fibres supported the diagnosis of immune-mediated MM.\nElectromyography (EMG) was performed using digital electrodiagnostic equipment (Medelec Synergy; Oxford Instruments). The temporal, masseter, epaxial and pelvic and thoracic limb appendicular muscles were assessed. Normal insertional activity was recorded and no electrical activity abnormalities were identified.\nOpen muscle biopsy samples were obtained from the left temporal muscle. Both fresh refrigerated and formalin fixed samples were sent to the Comparative Neuromuscular Laboratory at the University of California, San Diego, by a courier service, for complete histopathological examination. The biopsies showed a moderate variability in type IIM myofibre size with scattered atrophic fibres having a round shape. Fibre type grouping was not observed and intramuscular nerve branches appeared normal. Multifocal areas of mononuclear cell infiltrations (lymphocytes and acid phosphatase/esterase reactive macrophages) had an endo- and perimysial distribution. Peroxidase reactive eosinophils were not identified. Scattered necrotic fibres were undergoing phagocytosis. Moderate perimysial fibrosis was observed. No fibre loss, organisms or cytoarchitectural abnormalities were identified. A multifocal inflammatory myopathy (myositis) with mild perimysial fibrosis and no obvious myofibre loss was diagnosed ().\nConsequently, the diagnosis of immune-mediated MM was established. The cat was started on an immunosuppressive dose of prednisolone (30 mg; 4.4 mg/kg q24h [Prednidale; Dechra]). The dose was decreased every 6 weeks with the aim of discontinuing administration 36 weeks after the initiation of treatment. Repeating the measurement of serum CK activity and serological titres for type IIM myofibres prior to decreasing the dose of prednisolone was recommended on each occasion. However, owing to the cat’s non-compliant behaviour, this was not achieved. Frequent email and telephone communications were maintained with the cat’s owner and photographs of the cat’s face were regularly checked.\nThree months after starting treatment (prior to decreasing the prednisolone dose from 2 mg/kg q24h to 1 mg/kg q24h), the serum CK activity and type IIM myofibre titres were 387 IU/l and negative at <1:100, respectively. Ten months after initial presentation, while receiving prednisolone at 1.5 mg (0.2 mg/kg) q48h for 6 weeks, the cat showed mild lethargy and an episode of unprovoked aggression to a family member. No changes in facial expression were noticed. At this point, the serum CK activity was within the RI and type IIM myofibre titres were positive at 1:500. Repeating muscle biopsies was recommended by the authors but declined by the owner. The prednisolone dose was therefore increased to 15 mg (2.1 mg/kg) q24h. Type IIM myofibre titres returned to within the RI (<1:100) and the prednisolone dose was halved after 2 months. Titres remained negative 6 weeks later inciting a further decrease in prednisolone dose to 5 mg (0.7 mg/kg) q24h. Following unremarkable blood tests 2 months after the prednisolone dose reduction, a further decrease in dose to 2.5 mg (0.35 mg/kg) q24h was implemented. Five months later, despite the cat appearing clinically normal, type IIM myofibre titres became positive at 1:500. Until this time, no significant side effects of prednisolone had been observed. The prednisolone dose was increased to 5 mg (0.7 mg/kg) q24h and ciclosporin (Atopica oral solution; Elanco) was started at 4 mg/kg q12h and continued to date. Three months later, negative type IIM myofibre titre tests were achieved. Ensuing polyphagia and weight loss prompted the performance of blood analyses, and the cat was diagnosed with diabetes mellitus. Appropriate treatment was started by the primary care veterinary surgeon; the prednisolone dose was halved (2.5 mg; 0.35 mg/kg q24h) and gradually discontinued. Immunosuppressive treatment was continued with ciclosporin alone (for 60 days at the time of writing). No reoccurrence of neurological clinical signs has been reported to date, with a follow-up of 27 months after initial diagnosis.