A 1-year-old male neutered mixed breed cat (4.6 kg) was presented for difficulty prehending hard food. The cat was housed strictly indoors. About 2 months prior to presentation, the owner noticed the cat was not fully opening its mouth when yawning but had been able to eat slowly, managing soft food and pieces of hard food. No other behavioral or clinical signs of disease were reported. On physical examination the cat was very bright, alert, appropriate and clinically well hydrated with a body condition score of 6/9. Owing to the long haircoat palpation was necessary to appreciate the severe bilaterally symmetrical atrophy of the masticatory musculature (). Ocular retropulsion and palpation of the mandibular lymph nodes were normal.\nAn intraoral examination was impossible owing to the decreased vertical mandibular range of motion (vmROM) of 11–12 mm as measured with a metric ruler between the upper and lower incisor tips (). Visible teeth were age appropriate and normal in appearance. Occlusion was symmetrical. Limited vmROM was smooth and without discernible crepitus, but had a firm endpoint at 12 mm. The remainder of the physical and neurological examinations was unremarkable. Owing to financial constraints and anesthetic risks associated with the restricted vmROM, CT to rule out osseous abnormalities and biopsy of a masticatory muscle were declined. Blood tests and skull radiography were approved.\nComplete blood count (CBC) values were unremarkable. Serum biochemistry values, including creatine kinase activity, were within normal limits, except for an elevation of alanine transferase (214 U/l; reference interval [RI] 10–100 U/l) and aspartate aminotransferase (176 U/l; RI 10–100 U/l) activities. Dorsoventral skull radiography showed no bony abnormalities associated with the temporomandibular joints or elsewhere in the skull. Since a feline-specific assay has not yet been established for the detection of antibodies against masticatory muscle type 2M fiber proteins, an established canine ELISA system was used to detect cross-reacting antibodies against canine type 2M fiber antigens. The serum 2M antibody titer was positive at a dilution of 1:1000 (RI <1:100 in dogs, and also <1:100 using serum from five archived normal cats). Circulating antibodies against type 2M fibers are diagnostic of MM in dogs.\nMethylprednisolone (Depo-Medrol; Zoetis) was administered intramuscularly (24 mg; 5.2 mg/kg). Forced jaw opening to improve vmROM was not performed owing to the risk of iatrogenic osseous fracture or soft tissue damage. Two weeks after the initial treatment, further examination revealed no change in the extent or character of vmROM. Appetite and activity remained good. Repeat CBC and serum biochemistry values were unremarkable. Oral prednisolone (Lloyd [5 mg; 1 mg/kg q12h]) was prescribed. One month later, in a follow-up telephone conversation with the owner, it was determined the oral prednisolone prescription had not been filled. The oral prednisolone prescription was subsequently filled and administered crushed in soft food. The cat was again evaluated almost 2 months after the initial presentation. Body weight was slightly increased (4.7 kg). The vmROM, as determined with a millimeter ruler in the relaxed conscious cat, remained restricted at 11–12 mm. Severe bilaterally symmetrical masticatory muscle atrophy persisted, suggesting end-stage disease and a poor prognosis. Biopsy from a masticatory muscle would be required to determine the degree of fibrosis, population of remaining type 2M fibers, and subsequent prognosis, but this was declined.\nThe cat was lost to follow-up until 1 year after initial presentation. At this time the cat was presented to the emergency service with a recent history of vomiting, anorexia and nasal discharge. Corticosteroid therapy had been discontinued 10 months previously. The cat was alert with appropriate behavior. Body condition score was 5/9 (4.3 kg). Body temperature was 40.3°C (104.6°F) and a bilateral purulent nasal discharge was evident. vmROM remained restricted at 11–12 mm. Thoracic radiography was unremarkable. A SNAP FeLV/FIV ELISA assay (IDEXX) was negative. After 18 h of supportive treatment, body temperature remained elevated at 40.7°C (105.3°F), and severe nasal discharge and anorexia persisted. The owners elected euthanasia on welfare grounds and approved post-mortem examination to further investigate MM.\nHead CT was performed post mortem using contiguous 2.0 slice thickness with 0.1 incremental helical slides using an ultra sharp bone algorithm (Somatom, 16 slice; Siemens). It revealed pronounced bilaterally symmetrical atrophy of the masticatory muscles with no radiographic abnormalities of the temporomandibular joints or other bony structures that would restrict mouth opening ().\nSpecimens were collected from the right and left temporalis and masseter muscles, and the biceps femoris muscle, fixed in 10% neutral buffered formalin, then evaluated at the Comparative Neuromuscular Laboratory (CNL), University of California San Diego. All of the temporalis and masseter muscles exhibited similar pathological changes (). Myofiber loss and fibrosis was marked with multifocal areas of lymphocytic infiltration having an endomysial and perimysial distribution. Large nodules of lymphocytic infiltration were focally present. The biopsy from the biceps femoris muscle was normal in appearance, without obvious cellular infiltration or fibrosis, supporting the focal nature of this inflammatory myopathy and making a generalized disorder such as polymyositis unlikely. The pathologic diagnosis was severe and end-stage inflammatory myopathy myositis with extensive fibrosis in all masticatory muscles evaluated. As in dogs, inflammation restricted to the masticatory muscles and the positive serum 2M antibody titer confirmed the diagnosis of MM in this cat.
An 11-year-old, neutered male mixed breed dog was presented for evaluation of an acute onset of severe neck pain and left forelimb lameness that worsened the week prior to presentation. He had received no treatment prior to presentation. Physical and neurological examinations identified mild tetraparesis and ataxia with left thoracic root-signature signs. Left forelimb lameness was noted with mild proprioceptive deficits in the left thoracic and pelvic limbs. The right forelimb was normal. Pain was apparent on cervical but not thoracolumbar manipulation. Orthopedic examination was normal. Findings were consistent with a lesion affecting the C6–T2 spinal nerves or spinal cord segments and T3–L3 spinal cord segments.\nMagnetic resonance imaging of the cervical spine revealed that the nucleus of the intervertebral disk at C6–C7 was hypointense on all sequences, and there was mild broad-based dorsolateral protrusion of the C6–C7 intervertebral disk toward the left intervertebral foramen, compressing the left sixth nerve root. No spinal cord compression was noted.\nTreatment options were discussed with the client. The client elected fluoroscopically guided perineural injection of methylprednisolone (1 mg/kg) into the area of the intervertebral foramen of C6–C7. Anesthetic recovery was uneventful.\nIncreased willingness to ambulate and improved voluntary range of motion of the head and neck were noted on exam the following morning; lameness was still present. The patient was subsequently discharged with gabapentin (5.9–11.8 mg/kg PO BID), prednisone on a tapering dose beginning at 1.2 mg/kg q12 h and tramadol (3–4.4 mg/kg PO q8 h). At the 2-week follow-up evaluation, the patient showed only mild pain during range of motion. Forelimb weakness and lameness were no longer evident. Prioprioception was improved in the left forelimb. T3–L3 signs were unchanged. Prednisone and tramadol were discontinued at this visit. Further telephone follow-up with the owner revealed that gabapentin was continued as needed for pain for 2–3 months then discontinued. The patient remained free from clinical signs of radicular pain but had succumbed to lymphoma 18 months later.