Gliomatosis of the spinal cord in a cat: a case report

Abstract

Gliomatosis cerebri situated in the thoracolumbar and lumbosacral segments of the spinal cord was diagnosed in a Persian 10.5-year old tom cat. Clinical manifestation consisted of rump ataxy, weakened posture in the hind limbs, paraparesis, weakened spinal reflexes, no spinal hyperaesthesia or pain, and hypotonia of the urinary bladder. Magnetic resonance imaging revealed a diffuse hyperintense signal in the thoracolumbar junction and in lumbosacral segments (L6-S1) of the spinal cord. Normal size, form and colour of the spinal cord were apparent at autopsy; however, changes in grey matter shape were recorded on some transversal sections of the spinal cord. Dense, diffuse infiltration of the grey matter and surrounding white matter by glia-like neoplastic cells was histologically demonstrated. Immunohistochemical examination did not enable specification of the origin of the neoplastic cells but their neuroectodermal histogenesis can be assumed. On the basis of MRI, histological and immunohistochemical examinations gliomatosis of the spinal cord was diagnosed.Keywords: feline; medulla; neoplasia; clinic; pathology Gliomatosis cerebri is a rare neoplasia both in humans and animals. Maxie and Youssef (2007) and Vandevelde et al. (2012) have described gliomatosis as a widespread diffuse infiltrating disease of dogs, predominantly of brachycephalic breeds, characterised by an infiltrative cell type more reminiscent of astrocytes than of the formation of a distinct tumour mass. The infiltrates involve the hemispheric lobes, cerebellum and brainstem, often bilaterally but assymetrically. Discontinuous areas of gliomatosis have also been described in the spinal cord. There is no tumour mass, rather a diffuse enlargement of the affected regions; the neoplastic cells insinuate among normal structures that remain intact with only slight damage to axons and neurons. The tumour cells usually have elongated, enlarged, often twisted mildly hyperchromic nuclei without detectable cytoplasm. Case descriptionThe owner of an indoor/outdoor Persian 10.5-year old tom cat reported that his cat suddenly could not jump on the armchair and that his hind limbs appeared week. Over the next 12 days the owner observed that some attempts of similar jumps were successful and some of them not. In this period micturition habits also changed. Instead of the former two or three urinations per day, the frequency increased up to nine but the quantity of urine markedly decreased per each micturition. Seven days after the onset of the motion disorder, biochemical and haematological examinations were carried out. These examinations revealed only mild monocytosis (7%) and mild renal azotaemia (creatinine 157 µmol/l). All remaining haematological and biochemical parameters were within the physiological range. Twelve days after appearance of the first symptoms, the cat could not rise to his hind limbs and was referred to the veterinary clinic for a specialized examination.

Primary leptomeningeal gliomatosis in a domestic shorthaired cat

“…Glial tumors including astrocytomas, oligodendrogliomas, and gliomatosis cerebri (diffuse glioma) are uncommon to rare in cats compared to their canine counterparts. 4,6,7,10 The most common primary central nervous system (CNS) tumors of cats are lymphoma (either primary or part of systemic spread) and meningiomas. 4,6 Gliomatosis cerebri is characterized by diffuse infiltration of the neuroparenchyma with preservation of the CNS architecture by neoplastic glial cells that are predominantly astrocytic or oligodendrocytic in origin.…”

Gliomatosis Cerebri in the Brain of a Cat

“…GC has been reported in the feline spinal cord, with a similar hyperintense T2-weighted MRI signal as described in the brains of people and dogs. Feline brain and spinal cord GC has been characterized by neoplastic infiltrates that are GFAP-negative [ 14 , 20 , 21 ]. In feline spinal cord GC, the neoplastic cells are also reported to be negative for Ki-67, Pax5, and CD45, with strong cytoplasmic immunoreactivity for BLA.36 [ 21 ].…”