A 4-month-old male entire indoor-only domestic shorthair cat was referred to the Royal (Dick) School of Veterinary Studies' Neurology Service for acute onset of right thoracic monoparesis following a fall from a chair. Clinical signs progressed rapidly and within 18 h the cat was unable to walk, with right hemiplegia, left hemiparesis and right Horner's syndrome. At this stage the patient was referred. On presentation the cat was quiet, alert and responsive; vitals were within normal limits; and a large, firm bladder was evident on abdominal palpation. Neurological examination revealed anisocoria with a miotic right pupil, cervical hyperaesthesia, right hemiplegia, left hemiparesis, thoracic limb hypotonia, pelvic limb hypertonia, right thoracic limb areflexia, absent deep pain in the right thoracic limb below the elbow and pelvic limb hyperreflexia. Neurolocalisation was to the C6-T2 spinal segments, with lateralisation to the right. Differential diagnoses were trauma, vascular event and infectious/inflammatory disease (feline infectious peritonitis/toxoplasmosis).
An emergency CT scan (64-row multi-slice CT scanner; Somatom Definition AS) of the head and spine was performed shortly after admission; no structural abnormalities were identified to explain the clinical signs. Serum biochemistry and haematology identified no significant findings. An echocardiogram revealed trivial tricuspid regurgitation, no left atrial enlargement, no thrombus formation and good contractility. Activated partial thromboplastin time (APTT) and prothrombin time (PT) were within their respective reference intervals (RIs), and serum fibrinogen concentration was not increased: APTT 13.4 s (RI 10-20 s); PT 10.2 s (RI 5-12 s); and fibrinogen 3.2 g/l (RI 2-4 g/l). Testing for serum feline leukaemia virus antigen and feline immunodeficiency virus antibody was negative (SNAP FIV/FeLV Combo Test; IDEXX). Serum IgG and IgM antibody titre testing for Toxoplasma gondii was negative (<50 [Biobest Laboratories, Edinburgh]). Serum analysis for feline coronavirus antibody titre by immunofluorescence assay (<10) and alpha1-acid glycoprotein by radial immunodiffusion assay (0.5 g/l; RI 0.124-0.878 g/l) were both negative (Biobest Laboratories). Analysis of the cerebrospinal fluid (CSF) showed a total cell count of 39.6/microl (RI <5/microl) and a total protein concentration of 1.28 g/l (RI <0.45 g/l). Cytology of the CSF fluid revealed increased red blood cells (RBCs) and scattered platelets. The nucleated cells were approximately 8/1000 RBCs and they comprised 30% non-degenerate neutrophils, 46% small and a few medium lymphocytes, 23% large mononuclear cells (monocytes and macrophages) and 1% eosinophils. One macrophage showed erythrophagocytosis; otherwise, cell morphology was unremarkable. No aetiological agents were seen. These findings were consistent with either local haemorrhage or blood contamination.
Based on history, neurological examination and investigations, a presumptive diagnosis of spinal cord trauma was made. Daily physiotherapy was initiated included passive range of motion (PROM) exercises. The patient was managed symptomatically with buprenorphine (20 mug/kg IV q8h), dexamethasone (0.1 mg/kg IV q24h, increased to 0.2 mg/kg on result of negative T gondii), clindamycin (25 mg/kg PO q8h, withdrawn on result of negative toxoplasma), ranitidine (2 mg/kg IV q12h) and prazocin (250 mug/kg PO q8h) to aid frequent bladder expressions. Lactulose and enemas containing sodium citrate (450 mg) and sodium alkylsulfoacetate (45 mg [Micralax; RPH Pharmaceuticals]) were used to manage faecal retention. Seven days after the initial trauma the patient failed to show significant signs of improvement and appeared to have persistent cervical hyperaesthesia, despite analgesia and physiotherapy. Pre- and post-contrast MRI (3Philips Intera 1.5-T Pulsar System; Philips Medical Systems) study of the cervical and thoracic spine and brain was performed. All visible intervertebral discs showed normal T2 fluid intensity (Figure 1a). At C6-C7 the intervertebral disc was protruding into the mid-ventral vertebral canal, causing thinning of the subarachnoid space circumferentially and mild dorsal cord deviation (Figure 1b,c). Extending from C5-C6 to cranial C7, the spinal cord contained a large area of T1, T2 and T2* hyperintensity, with only the left dorsolateral aspect of the cord unaffected. In the same area, there was marked contrast enhancement of the right lateral aspect of the spinal cord (Figure 1d). MRI findings were therefore consistent with a C6-C7 acute non-compressive nucleus pulposus extrusion with secondary C5-C7 spinal cord chronic haemorrhage. The contrast enhancement was considered to be most likely due to vascular damage, inflammation secondary to the trauma and chronic haemorrhage. CSF analysis was repeated 7 days post-trauma and was consistent with normal CSF: total cell count 0 (RI <5/microl) and total protein concentration 0.35 g/l (RI <0.45 g/l), suggesting resolution of the previously suspected subarachnoid haemorrhage.
Following MRI, a splint was applied to the right thoracic limb to prevent knuckling and abrasion of the dorsal paw, and to assist ambulation. By 10 days post-trauma the anisocoria, cervical hyperaesthesia, left-sided paresis and postural deficits, pelvic limb hypertonus, and faecal and urinary retention had resolved. The kitten was able to run, jump and climb. However, the distal right thoracic limb was still paralysed, and over the preceding 10 days progressive contracture of the right carpus developed. PROM exercises elicited pain on extension of the carpus and flexion of the elbow, preventing the physiotherapy from being performed effectively. Splints were trialled, but they also elicited discomfort. Radiographs of the thoracic limbs were taken. No soft tissue abnormalities were detected. An 18  lateral deviation of the right carpus was evident, causing narrowing of the radiocarpal joint space affecting primarily the intermedioradial carpal bone. This was consistent with suspected contracture of the triceps and flexor muscles of the carpus and digits.
The contracture resulted in the development of a non-weightbearing carpal hyperflexion (Figure 2). Amputation of the limb or a therapeutic trial with BTX were discussed; the owners elected for the latter. Under general anaesthesia, 90 units of BTX type A (BTX-A [Botox Cosmetic; Allergan]) were injected into the flexor muscles of carpus and digits, and 10 units into the triceps. The dose was similar to what has previously been shown to be safe in cats in an experimental study.   The aim of the treatment was to alleviate discomfort and reduce the muscle spasticity, allowing the use of a brace and physiotherapy to be performed. The patient was monitored in hospital for 48 h after the treatment; there were no adverse clinical reactions. The cat was discharged with a splint to aid ambulation; the owners were instructed to change the splint daily and perform daily physiotherapy.
At a re-check 8 days post-BTX-A treatment the owners perceived the cat to be pain-free and ambulating well with support from the splint. The owners were managing well with the daily splint changes and rehabilitation exercises, although they reported that the cat resented the removal of the tape that kept the splint in place. Examination showed erythema where the tape was applied. The tape was replaced with a custom-made brace made with a spoon splint and Velcro straps. Repeat neurological examination showed that in the right thoracic limb postural reactions were still absent, sensation was decreased but now present at the second and fifth digit, and the muscle contractions had resolved but muscle tone was decreased. The postural reactions and tone in the other limbs were now normal. Mild hyperaesthesia of the cervical, epaxial and shoulder muscles was present, but there was a greatly improved level of comfort on manipulation of neck, right shoulder, elbow and carpus vs before BTX-A treatment. The owners reported that the cat was very active; we suspected that the neck and shoulder muscles were subjected to an increased load secondary to the reduced tone and function of the injected muscles of the right thoracic limb.
The cat continued to make a clinical improvement. At 6 months post-BTX-A treatment, sensation was present but still decreased on the distal right thoracic limb. The right triceps brachii muscle was atrophied and a mild increase in muscle tone had returned. However, normal mobility was not impeded and the cat was pain free and able to place its right thoracic paw in a normal position when ambulating, only requiring support from the splint after prolonged periods of exercise (see the video in the supplementary material). The residual clinical signs did not appear to be affecting its quality of life.