*A. Lujan, A. Philbey, S.N. Long, T.J. Anderson
*University of Glasgow Veterinary School, Division of Small Animal Clinical Studies
Glasgow, Scotland, UK
A 2.5-year-old female neutered, indoor Burmese cat was presented to the University of Glasgow Veterinary School Hospital with a 2-day progressive history of right hemiparesis. Physical examination was unremarkable. Neurological findings included conscious and unconscious proprioceptive deficits in all four limbs, particularly affecting the right side. No pain could be elicited upon palpation of the spine. Neurological examination located the lesion to the C6-T2 spinal cord segments. Initial investigation included routine haematology, biochemistry and serology (Toxoplasma, Feline Immunodeficiency Virus, Feline Coronavirus, Feline Leukaemia Virus). Hyperglobulinemia and increased Toxoplasma and FCoV titres, both consistent with active infection in an indoor cat, where found. An MRI study of the brain, cervical and cranial thoracic spine was undertaken using a Phillips Gyroscan (1.5 Tesla). This demonstrated a circumscribed 7x6x10 mm right-sided lesion in the C6-C7 region, with ventrolateral compression of the spinal cord. This structure was hypointense on T1-weighted scans and hyperintense on T2-weighted scans, suggesting a high water content. A provisional diagnosis of a subarachnoid cyst was reached based on the MRI images, however, neoplasia, abscess, focal malacia and vascular malformations were also considered. Initial treatment, targeted to the concurrent diseases, was associated with marked improvement of the clinical signs, thus, surgical decompression was postponed. The patient was treated with anti-inflammatory doses of prednisolone and trimethoprim-sulphonamide. A second MRI scan performed 9 weeks later, at the time when the patient was in remission, revealed that the lesion persisted. Toxoplasma and Neospora titres remained high. A sudden deterioration of the patient's clinical signs 12 weeks after the initial presentation precipitated interventional surgery. The approach to the spinal cord was via right C6-C7 hemilaminectomy. Once the dorsal lamina was removed, a well circumscribed expansion of the dura could be seen. CSF-like fluid was aspirated from the structure, however further analysis was inconclusive due to blood contamination. A 2x2 mm durectomy was performed. Closure of the laminectomy site consisted of muscle layer apposition. Recovery after surgery was uneventful. The patient was ambulatory and comfortable 3 days post-op. Histopathologic examination of the resected dura suggested this was a benign cystic lesion. Clinical signs recurred acutely 3 weeks after surgery and persisted for 7 days. A course of a prednisolone (0.5mg/kg BID) was instigated. The patient remains unremarkable at 6 weeks following surgery.
To the authors' knowledge this is the first described case of a ventral subarachnoid cyst in a cat. Three other cases have been reported of such structures, but these are confined to the dorsal aspect of the spinal cord. Proposed aetiologies for such structures in man include trauma, chronic arachnoiditis, spina bifida, dysraphism, hygroma and congenital dural diverticula. No evidence of anomalous vertebra was observed on plain radiographs of this patient, though there was some evidence of a chronic compressive lesion at the C6/C7 intervertebral space. The significance of persistent Toxoplasma and FCoV titres remains uncertain since no evidence of clinical deterioration related to this findings has been reported to this date. Interestingly, the clinical deficits in this patient appeared to wax and wane independently of treatment. It is possible that the observation of a cystic structure compressing the cord is important in rendering the cord with less reserve but not responsible for the observed neurological deficits.