bs_bs_banner
34
EQUINE VETERINARY EDUCATION Equine vet. Educ. (2015) 27 (1) 34-38 doi: 10.1111/eve.12272
Case Report
Cerebral malacia in a mule with ependymoma F. Mendes de Cordova*, L. Vaz Burns, A. Tony Ramos†, S. Estevan Moron‡, C. A. Silva de Cordova and G. M. da Luz Silva Escola de Medicina Veterinária e Zootecnia, Universidade Federal do Tocantins (UFT), Araguaína, Brazil; †Campus Curitibanos, Universidade Federal de Santa Catarina (UFSC), Curitibanos, Brazil; and ‡Unidade CIMBA, Universidade Federal do Tocantins (UFT), Araguaína, Brazil. *Corresponding author email:
[email protected] Keywords: horse; cerebral malacia; tumour; ependymoma; mule; post mortem diagnosis
Summary Ependymoma is a rare tumour of the central nervous system that can vary in anatomical location and produce a broad range of clinical signs. Sporadically described in dogs, cats, cattle and horses, this disease has never previously been reported in a mule. This report describes a case of a 12-year-old mule showing neurological signs, including blindness, dysphagia, incoordination, sternal recumbency, depression, apathy and emaciation. Because of the worsening health conditions, the animal was subjected to euthanasia for humane reasons. At necropsy, an area of malacia in the right subcortical region of the frontoparietal area of the cerebrum and an ovoid, firm, grey, 2.4 × 1.0 × 0.7 cm nodule in the right lateral ventricle was observed. Histopathology revealed that the nodule was a densely cellular mass with cells arranged in nests and cords, formations of pseudorosettes with perivascular deposition of fibrillar eosinophilic material and the presence of a few lymphocytes. The cells had rounded and moderately hyperchromatic nuclei, punctate chromatin, distinct nucleoli, and indistinct cytoplasmic margins. Based on the histopathological features, the nodule was diagnosed as an ependymoma, a tumour considered rare, but that may be included in the differential diagnosis for diseases with neurological signs.
Introduction Many types of neoplasms can occur in the central nervous system (CNS), and these can be benign or malignant, primary or secondary (metastatic) (Fankhauser et al. 1974; Graça et al. 2010). However, except for in dogs and cats, primary CNS tumours are considered rare in domestic species (Fankhauser et al. 1974; Maxie and Youssef 2007). For dogs, the frequency and variety of CNS neoplasms are similar to those of human patients (Fankhauser et al. 1974; Baba and Câtoi 2007; Zachary 2009). Regardless of the biological behaviour of the neoplasm, the physical presence of the tumour can cause significant neurological disorders, due to cranium and spinal canal volume limitations. However, many neoplasms can acquire large proportions before inducing neurological signs and symptoms (Graça et al. 2010). Causal factors for CNS tumours of animals are essentially unknown, but multiple environmental and/or genetic factors are considered predisposing conditions (Maxie and Youssef 2007; Graça et al. 2010). Ependymoma is a tumour of neuroepithelial tissue (Fankhauser et al. 1974; Johnson 1990; Maxie and Youssef 2007) originating from the cells lining the ventricles and central canal of the spinal cord (ependyma or ependymal
© 2014 EVJ Ltd
epithelium) (Maxie and Youssef 2007; Graça et al. 2010). Ependymomas are rare in all animal species (Fankhauser et al. 1974; Sanches et al. 2000; Troxel et al. 2003; Snyder et al. 2006; Sfacteria et al. 2010), but are relatively more common in cattle, dogs and cats (McGill and Wells 1993; Koestner and Jones 1997; Sanches et al. 2000; Maxie and Youssef 2007). Although uncommon, the tumour has also been described in horses (Heath et al. 1995; Carrigan et al. 1996; Huxtable et al. 2000; Leser et al. 2013), sheep (Bosschere et al. 2003) and rodents (Lo et al. 1974; Corallini et al. 1978; Dagle et al. 1979). In man, ependymoma comprises 6–9% of all intracranial tumours, typically involving children or young adults (Andrade et al. 2009). Clinical signs associated with ependymoma are variable and depend on both CNS location and compression of adjacent tissue (Heath et al. 1995; Andrade et al. 2009), but may include weight loss, neuroendocrine disorders, anorexia, progressive visual impairment, behavioural changes, ataxia, paresis, seizures, circling, disorders of the cranial nerves and reduced proprioceptive reflexes (Heath et al. 1995; Sanches et al. 2000; Zachary 2009; Leser et al. 2013; Woolford et al. 2013). Ependymomas are typically benign, but can also be large, infiltrative and destructive (Graça et al. 2010). In the histological classification of tumours of animals by the World Health Organization (WHO), there are 2 main subtypes of neoplasms originating from the ependyma: ependymomas and anaplastic ependymomas (Koestner and Higgins 2002). Anaplastic ependymomas are extremely rare and have only been described in 3 dogs (Savage et al. 1962; Teuscher and Cherrstrom 1974; Michimae et al. 2004). In man, histological subclassification includes cellular, papillary, myxopapillary, subependymoma, tanycytic and clear cell variants (Friede and Pollak 1978). Although there are a few reports of occurrence of ependymomas in horses (Equus caballus) (Heath et al. 1995; Carrigan et al. 1996; Huxtable et al. 2000; Leser et al. 2013), this paper represents the first time this tumour has been described in a mule (Equus asininus × Equus caballus) with concomitant cerebral malacia.
Case presentation An approximately 12-year-old mule was taken to the Veterinary Teaching Hospital of Universidade Federal do Tocantins, Brazil, with a history of progressive clinical signs indicating neurological disease over a course of 3 months, including dysphagia, incoordination and blindness. At clinical evaluation, the mule showed blindness, sternal recumbency, severe depression and apathy. After clinical examination,
F. Mendes de Cordova et al.
35
Fig 1: Anatomopathological examination of the mule cerebrum with a brain tumour. a) Right cerebral hemisphere gross examination cross-section showing an area of subcortical malacia. b) Right cerebral hemisphere submicroscopic image showing the area of cavitation in the brain parenchyma. c) Photomicrograph of malacia, showing the border of the cavity; haematoxylin and eosin, 100× magnification. d) Border of the central region of the malacia, containing cellular debris, blood vessels and gitter cells; haematoxylin and eosin, 200× magnification. The inset shows a macrophage (blue arrow) and a blood vessel (red arrow).
Fig 2: Morphological aspects of ependymoma found in the right lateral ventricle of a mule brain. a) Gross pathology of ependymoma, with an undulating surface and solid cut surface (arrow); formalin fixed tissue. Note the fibrovascular filament attached to the tumour (arrowhead). b) Submicroscopic image of ependymoma revealing the high cell density of the tissue. c) Ependymoma with well vascularised stroma and tumour cells arranged in nests and cords; haematoxylin and eosin, 200× magnification. d) Ependymoma showing pseudorosette formation (green arrow) surrounded by tumour cells with rounded nuclei and indistinct cytoplasmic margins; haematoxylin and eosin, 400× magnification.
euthanasia was chosen for humane reasons. The animal was submitted for gross post mortem examination and sample collection for microscopic analysis. Samples of several tissues were fixed in 10% buffered formalin and sent to the Laboratory of Veterinary Pathology of the university. Samples were submitted for routine histological processing (embedding in paraffin, sectioning at 3 μm in thickness and staining with haematoxylin and eosin). Histopathological analysis and image capture was performed using a microscope coupled to a camera. The relevant macroscopic changes were restricted to the CNS. No external changes were detected on the surface of the brain. However, cross-sectioning of the cerebrum revealed
a soft, dark yellow, well-defined area located in the subcortical region of the right frontoparietal lobe (unilateral lesion; Fig 1). Histologically, this area was characterised by parenchymal cavitation filled by cellular debris, activated microglia (gitter cells) and remaining blood vessels, typical of malacia (Fig 1b–d). In addition, an ovoid nodular mass (Fig 2) was present freely moveable within the cavity of the right lateral ventricle, attached to the choroid plexus by a fibrovascular strand, with an undulating surface, firm to palpation, grey and approximately 2.4 × 1.0 × 0.7 cm (Fig 2a). Microscopically, the nodule was characterised by high cell density and well vascularised tissue (Fig 2b), with cells arranged in nests, sometimes in cords, with formations of
© 2014 EVJ Ltd
36
pseudorosettes with perivascular deposits of eosinophilic fibrillar material (Fig 2c). Additionally, a few lymphocytes in the mass were observed, mainly around the vessels. The tumour cells had round and moderately hyperchromatic nuclei, punctate chromatin and detectable nucleoli, with indistinct cytoplasmic margins, which was sometimes vacuolated (Fig 2d). The histopathological findings of the nodule were characteristic of an ependymoma.
Discussion Pathological evaluation of the nodule found in the lateral ventricle of the mule’s brain in this case resulted in the diagnosis of ependymoma. Characteristically, the literature describes ependymoma as a solid, well-defined mass that protrudes into the ventricles or central canal of the spinal cord, has good vascularity and hypercellularity, few mitotic figures, with neoplastic cells with round, uniform and hyperchromatic nuclei, indistinct cytoplasmic margins, and an arrangement that results in rosettes or pseudorosette formation (Fankhauser et al. 1974; Baba and Câtoi 2007; Maxie and Youssef 2007; Zachary 2009; Graça et al. 2010; Woolford et al. 2013). In animals, the most common location of ependymoma is in the lateral ventricles (Fankhauser et al. 1974; Koestner and Higgins 2002; Zachary 2009; Graça et al. 2010), but it may also be located in the third or fourth ventricles and least commonly identified in the spinal cord (Fankhauser et al. 1974; Zachary et al. 1981; Koestner and Higgins 2002; Bosschere et al. 2003; Maxie and Youssef 2007; Graça et al. 2010; Sfacteria et al. 2010). Extraventricular ependymal neoplasms have been reported outside the ventricles and central canal in man (Molina et al. 1999; Moritani et al. 2003; Shuangshoti et al. 2005). Despite ependymal morphology, their histogenesis remains uncertain. Ependymal cell rests in the white matter at the angle of the ventricles (foramen of Luschka) have been proposed as the cell of origin (Furie and Provenzale 1995; Schwartz et al. 1999). Carrigan et al. (1996) described a papillary ependymoma in a horse as an ovoid nodule of 2.5 × 1.0 cm, dark red, linked to the hypothalamus through the ventral surface, to the optic chiasm by the rostral surface, and to the pituitary gland through the caudal surface. Histologically, the mass showed pseudorosettes, cells with oval and elongated nuclei of different sizes, and eosinophilic intracytoplasmic inclusions. In another case report, Huxtable et al. (2000) found a large soft red mass approximately 5 × 3 × 2.5 cm in size on the left side of the cerebellopontine angle, classified histologically as a myxopapillary ependymoma in a horse. Cytological features of papillary ependymomas have been described in 2 dogs and one cat, characterised by prominent blood vessels, thickened by deposits of ependymal tumour cells forming pseudorosettes (Vernau et al. 2001). A 5 mm soft, grey, well-defined and nonencapsulated mass was found in the third ventricle of a sheep, histologically characterised by clusters of rounded or cuboidal cells forming tubules, cords and rosettes, with sparse and well-vascularised stroma, abundant eosinophilic granular cytoplasm and hyperchromatic nuclei (Bosschere et al. 2003). Because of the morphological variability of ependymomas, it is necessary to differentiate them from other possible CNS neoplastic diseases. The first differential diagnosis for this case is a choroid plexus tumour (Vernau et al. 2001; Bosschere et al. 2003). Choroid plexus tumours are papillomas or carcinomas that frequently arise in the fourth ventricle
© 2014 EVJ Ltd
Ependymoma in a mule
(Koestner and Higgins 2002; Zachary 2009), have coral or cauliflower aspect, are friable (Baba and Câtoi 2007), and are vascular papillary growths that implant widely on the meninges (Maxie and Youssef 2007). In the present case, the tumour was located in the lateral ventricle, a common site for ependymomas. Furthermore, ependymoma is histologically characterised by ependymal rosettes and vascular pseudorosette formation, while choroid plexus tumours do not have these characteristics (Koestner and Higgins 2002), but share a similar appearance with normal plexus with stroma of arboriform vascularised connective tissue covered with a cuboid to columnar epithelial layer (Vernau et al. 2001; Baba and Câtoi 2007; Zachary 2009). The second differential diagnosis is the primitive neuroectodermal tumour (Bosschere et al. 2003) from embryonic origin, which may possibly also exhibit pseudorosette formation, but can be excluded by cerebellar location and occurrence in young animals (Maxie and Youssef 2007; Zachary 2009). The tumour found in the mule was freely movable in the right lateral ventricle, but attached to the choroid plexus by a fibrovascular strand. Although this finding might suggest a choroid plexus tumour, the histological features are sufficiently typical to allow the diagnosis of ependymoma. Several studies have used immunohistochemical methods to differentiate between these tumours (Carrigan et al. 1996; Huxtable et al. 2000; Michimae et al. 2004; Sfacteria et al. 2010; Woolford et al. 2013); however, there are currently no trusted markers for ependymomas and choroid plexus tumours (Zachary 2009). This difficulty is evidenced by the great variability in results obtained in these studies (Hamaya et al. 1985; Vandevelde et al. 1985; Baumgärtner and Peixoto 1987; Ang et al. 1990; Carrigan et al. 1996; Park et al. 1996; Huxtable et al. 2000; Michimae et al. 2004; Grajkowska et al. 2009; Sfacteria et al. 2010; Woolford et al. 2013). The most used immunohistochemical markers are glial fibrillary acidic protein (GFAP), cytokeratin and vimentin (Koestner and Higgins 2002). For GFAP, immunostaining is highly variable. Some studies showed strong staining for GFAP in ependymomas (Carrigan et al. 1996; Huxtable et al. 2000; Grajkowska et al. 2009; Sfacteria et al. 2010), while for others the staining was weak (Hamaya et al. 1985), inconsistent (Hamaya et al. 1985; Vandevelde et al. 1985; Woolford et al. 2013) or absent (Baumgärtner and Peixoto 1987; Michimae et al. 2004) in both ependymomas and choroid plexus tumours. Immunostaining for cytokeratin in ependymomas is considered essentially negative in the literature (Koestner and Higgins 2002), but studies have also shown its occurrence in ependymomas and in choroid plexus tumours (Michimae et al. 2004; Woolford et al. 2013). Vimentin immunostaining is also variable, ranging from strong (Huxtable et al. 2000; Grajkowska et al. 2009; Sfacteria et al. 2010) to weak (Carrigan et al. 1996; Michimae et al. 2004). As well as the possible neoplastic differential diagnoses, cholesteatoma (cholesterol granuloma) should also be a consideration in equids (Leser et al. 2013). This lesion is characterised by the development of a tumour-like mass, located in brain ventricles, found in 15–20% of older horses, and can be associated with neurological clinical signs (Jackson et al. 1994; Vink-Nooteboom et al. 1998; Maxie and Youssef 2007; Vanschandevijl et al. 2008). Despite the description of the most common sites for the development of ependymomas, the possible anatomical variations among affected individuals and the occurrence of secondary lesions probably reflects the significant
F. Mendes de Cordova et al.
unpredictability of clinical signs (Troxel et al. 2003; Snyder et al. 2006; Graça et al. 2010). As with all brain lesions, the clinical signs associated with brain neoplasia vary depending on the area of the brain involved. Neurological deficits resulting from tumours usually progress insidiously over a period of several weeks. However, affected animals may deteriorate acutely if there is haemorrhage, herniation or obstructive hydrocephalus (Koestner and Jones 1997; Jones and Shiel 2009). In our case report, the mule presented with a history of blindness, dysphagia and incoordination, progressing over a period of 3 months to sternal recumbency, severe depression and apathy. The animal had a significant area of malacia in the right frontoparietal region of the telencephalon, ipsilateral to the tumour location. This area was characterised by parenchymal cavitation filled by cellular debris, macrophages and remaining blood vessels. In this lesion, many capillary vessels survive, partly because of their relative insensitivity to anoxia and partly because they benefit first from the collateral circulation that develops. In addition, the necrotic tissues are removed by liquefaction and microglial phagocytosis, and a residual cyst remains (Maxie and Youssef 2007). Although the origin and causal factors associated with malacia were not evident, it is possibly due to a compressive effect on the tissues and blood vessels by the tumour or increased intraventricular pressure. Some studies show that expansion of lesions within the lateral ventricles is associated with increased mortality rate and aggravated neurological dysfunctions (Liliang et al. 2001; Matsushita et al. 2013), related to exacerbation of pathological changes such as hypoperfusion and oedema, rather than structural disturbances such as damage to axonal projections (Matsushita et al. 2013). The presence of these telencephalic lesions may have contributed to the clinical signs manifest in this case (Vink-Nooteboom et al. 1998). Malacia can be caused by a broad range of conditions, such as vascular occlusion (thrombosis and embolism), trauma, toxic or metabolic disorders, and encephalomyelitis. However, no significant lesions were observed to indicate the pathogenesis in this case. Obstructive lesions of cerebrospinal vessels are not commonly observed in animals. Lesions that are regarded as being of ischaemic type are quite commonly observed in the absence of demonstrable vascular occlusion (Maxie and Youssef 2007). Because of the variability in clinical signs associated with CNS tumours, diagnosis determination requires careful investigation (Fankhauser et al. 1974; Bosschere et al. 2003). Many brain tumours in subclinical stages are only identified incidentally at post mortem examination (Graça et al. 2010). When clinical signs are evident, the diagnosis requires detailed neurological examination and support of advanced image analysis methods (such as computed tomography and magnetic resonance imaging) that permit early detection, treatment, and a better prognosis (Vink-Nooteboom et al. 1998; Maxie and Youssef 2007; Vanschandevijl et al. 2008; Graça et al. 2010; Leser et al. 2013). As we suspect has probably occurred in this case, secondary pathology may develop and result in significant neurological signs. Although rare in all species, ependymoma should be considered as a differential in equids with neurological signs.
Authors’ declaration of interests No conflicts of interest have been declared.
37
References Andrade, F.G. de, Aguiar, P.H.P. de, Matushita, H., Taricco, M.A., Oba-Shinjo, S.M., Marie, S.K.N. and Teixeira, M.J. (2009) Intracranial and spinal ependymoma. Arq. Neuropsiquiatr. 67, 626-632. Ang, L.C., Taylor, A.R., Bergin, D. and Kaufman, J.C. (1990) An immunohistchemical study of papillary tumors in the central nervous system. Cancer 65, 2712-2719. Baba, A.I. and Câtoi, C. (2007) Nervous system tumors. In: Comparative Oncology, The Publishing House of the Romanian Academy, Bucharest. Available from: http://www.ncbi.nlm.nih.gov/books/ NBK9547/ Baumgärtner, W. and Peixoto, P.V. (1987) Immunohistochemical demonstration of keratin in canine neuroepithelioma. Vet. Pathol. 24, 500-503. Bosschere, H., Roels, S. and Vanopdenbosch, E. (2003) Ependymoma in a sheep. Vlaams Diergeneeskundig Tijdschrift 72, 364-365. Carrigan, M.J., Higgins, R.J., Carlson, G.P. and Naydan, D.K. (1996) Equine papillary ependymoma. Vet. Pathol. 33, 77-80. Corallini, A., Altavilla, G., Cecchetti, M.G., Fabris, G., Grossi, M.P., Balboni, P.G., Lanza, G. and Barbanti-Brodano, G. (1978) Ependymomas, malignant tumors of pancreatic islets, and osteosarcomas induced in hamsters by BK virus, a human papovavirus. J. Natl Cancer Inst. 61, 875-883. Dagle, G.E., Zwicker, G.M. and Renne, R.A. (1979) Morphology of spontaneous brain tumors in the rat. Vet. Pathol. 16, 318-324. Fankhauser, R., Luginbühl, H. and McGrath, J.T. (1974) Tumours of the nervous system. Bull. World Health Organ. 50, 53-69. Friede, R.L. and Pollak, A. (1978) The cytogenetic basis for classifying ependymomas. J. Neuropathol. Exp. Neurol. 37, 103-118. Furie, D.M. and Provenzale, M.J. (1995) Supratentorial ependymomas and subependymomas: CT and MR appearance. J. Comput. Assist. Tomogr. 19, 518-526. Graça, D.L., Alessi, A.C., Ecco, R. and Viott, A. de M. (2010) Patologia do Sistema Nervoso. In: Patologia Veterinária, Eds: R. de L. Santos and A.C. Alessi, Roca, São Paulo. pp 525-610. Grajkowska, W., Matyja, E., Pronicki, M., Daszkiewicz, P., Roszkowski, M., Perek, D. and Drogosiewicz, M. (2009) Papillary ependymoma with unique superficial cortical location: immunohistochemical and ultrastructural studies. A case report. Folia Neuropathol. 47, 354-361. Hamaya, K., Tanaka, T., Doi, K. and Nishimoto, A. (1985) The determination of glial fibrillary acidic protein for the diagnosis and histogenetic study of central nervous system tumors: a study of 152 cases. Acta Med. Okayama 39, 453-462. Heath, S.E., Peter, A.T., Janovitz, E.B., Selvakumar, R. and Sandusky, G.E. (1995) Ependymoma of the neurohypophysis and hypernatremia in a horse. J. Am. Vet. Med. Ass. 207, 738-741. Huxtable, C.R., Lahunta, A., Summers, B.A. and Divers, T. (2000) Marginal siderosis and degenerative myelopathy: a manifestation of chronic subarachnoid hemorrhage in a horse with a myxopapillary ependymoma. Vet. Pathol. 37, 483-485. Jackson, C.A., Lahunta, A., Dykes, N.L. and Divers, T.J. (1994) Neurological manifestation of cholesterinic granulomas in three horses. Vet. Rec. 135, 228-230. Johnson, G.C. (1990) Genesis and pathology of tumors of the nervous system. Semin. Vet. Med. Surg. (Small Anim.) 5, 210-222. Jones, B.R. and Shiel, R. (2009) Neurologic disorders. In: Clinical Medicine of the Dog and Cat, Ed: M. Schaer, Manson Publishing, London. pp 631-672. Koestner, A. and Higgins, R.J. (2002) Tumors of the nervous system. In: Tumors in Domestic Animals, Ed: D.J. Meuten, Iowa State Press, Ames. pp 707-716. Koestner, A. and Jones, T.C. (1997) The nervous system. In: Veterinary Pathology, Eds: T.C. Jones, R.D. Hunt and N.W. King, Williams & Wilkins, Baltimore. pp 1259-1297. Leser, S., Flatz, K., Brühschwein, A., May, A., Janik, D. and Matiasek, K. (2013) Magnetic resonance imaging of an equine ependymoma. Pferdeheilkunde 29, 467-470. Liliang, P.-C., Liang, C.-L., Lu, C.-H., Chang, H.-W., Cheng, C.-H., Lee, T.-C. and Chen, H.-J. (2001) Hypertensive caudate hemorrhage prognostic predictor, outcome, and role of external ventricular drainage. Stroke 32, 1195-1200.
© 2014 EVJ Ltd
38
Ependymoma in a mule
Lo, J.S., Mirakian, A. and Kellen, J.A. (1974) Suppression of mouse ependymoma growth after immunization with tumor ribosomal complexes. Oncology 30, 467-474. Matsushita, H., Hijioka, M., Hisatsune, A., Isohama, Y., Iwamoto, S., Terasawa, H. and Katsuki, H. (2013) MRI-based analysis of intracerebral hemorrhage in mice reveals relationship between hematoma expansion and the severity of symptoms. PLoS ONE 8, e67691. Maxie, M.G. and Youssef, S. (2007) Nervous system. In: Jubb, Kennedy & Palmer’s Pathology of Domestic Animals, Ed: M.G. Maxie, W.B. Saunders, Philadelphia. pp 281-457. McGill, I.S. and Wells, G.A. (1993) Neuropathological findings in cattle with clinically suspect but histologically unconfirmed bovine spongiform encephalopathy (BSE). J. Comp. Pathol. 108, 241-260. Michimae, Y., Morita, T., Sunagawa, Y., Sawada, M., Okamoto, Y. and Shimada, A. (2004) Anaplastic ependymoma in the cervical spinal cord of a Maltese dog. J. Vet. Med. Sci. 66, 1155-1158. Molina, O.M., Colina, J.L., Luzardo, G.D., Mendez, O.E., Cardozo, D., Velasquez, H.S. and Cardozo, J.J. (1999) Extraventricular cerebral anaplastic ependymomas. Surg. Neurol. 51, 630-635. Moritani, S., Kushima, R., Bamba, M., Kobayashi, T.K., Oka, H., Fujimoto, M., Hattori, T. and Okabe, H. (2003) Highly anaplastic extraventricular ependymoma arising in an adult, mimicking metastatic adenocarcinoma with heavy stromal inflammation and emperiporesis. Pathol. Int. 53, 539-546. Park, S.H., Park, H.H. and Chi, J.G. (1996) Papillary ependymoma - Its differential diagnosis from choroid plexus papilloma. J. Korean Med. Sci. 11, 415-421. Sanches, A.W.D., Langohr, I.M., Stigger, A.L. and Barros, C.S.L. (2000) Doenças do sistema nervoso central em bovinos no Sul do Brasil. Pesqui. Vet. Bras. 20, 113-118. Savage, A., Isa, J.M. and Fischer, W. (1962) Malignant ependymoma in a dog. Cornell Vet. 52, 68-70. Schwartz, T.H., Kim, S., Glick, R.S., Bagiella, E., Balmaceda, C., Fetell, M.R., Stein, B.M., Sisti, M.B. and Bruce, J.N. (1999) Supratentorial ependymomas in adult patients. Neurosurgery 44, 721-731.
Sfacteria, A., Macrì, F., Perillo, L., Rapisarda, G., Lanteri, G. and Mazzullo, G. (2010) Cytologic and histologic features of spinal cord ependymoma in a young dog: a case report. Vet. Med. (Praha) 55, 35-38. Shuangshoti, S., Rushing, E.J., Mena, H., Olsen, C. and Sandberg, G.D. (2005) Supratentorial extraventricular ependymal neoplasms: a clinicopathologic study of 32 patients. Cancer 103, 2598-2605. Snyder, J.M., Shofer, F.S., Van Winkle, T.J. and Massicotte, C. (2006) Canine intracranial primary neoplasia: 173 cases (1986-2003). J. Vet. Intern. Med. 20, 669-675. Teuscher, E. and Cherrstrom, E.C. (1974) Ependymoma of the spinal cord in a young dog. Schweiz. Arch. Tierheilkd. 116, 461-466. Troxel, M.T., Vite, C.H., Winkle, T.J., Van Newton, A.L., Tiches, D., Dayrell-Hart, B., Kapatkin, A.S., Shofer, F.S. and Steinberg, S.A. (2003) Feline intracranial neoplasia: retrospective review of 160 cases (1985-2001). J. Vet. Intern. Med. 17, 850-859. Vandevelde, M., Fankhauser, R. and Luginbühl, H. (1985) Immunocytochemical studies in canine neuroectodermal brain tumors. Acta Neuropathol. 66, 111-116. Vanschandevijl, K., Gielen, I., Nollet, H., Vlaminck, L., Deprez, P. and van Bree, H. (2008) Computed tomography-guided brain biopsy for in vivo diagnosis of a cholesterinic granuloma in a horse. J. Am. Vet. Med. Ass. 233, 950-954. Vernau, K.M., Higgins, R.J., Bollen, A.W., Jimenez, D.F., Anderson, J.V., Koblik, P.D. and LeCouteur, R.A. (2001) Primary canine and feline nervous system tumors: intraoperative diagnosis using the smear technique. Vet. Pathol. 38, 47-57. Vink-Nooteboom, M., Junker, K., van den Ingh, T.S. and Dik, K.J. (1998) Computed tomography of cholesterinic granulomas in the choroid plexus of horses. Vet. Radiol. Ultrasound 39, 512-516. Woolford, L., Lahunta, A., Baiker, K., Dobson, E. and Summers, B.A. (2013) Ventricular and extraventricular ependymal tumors in 18 cats. Vet. Pathol. 50, 243-251. Zachary, J.F. (2009) Sistema nervoso. In: Bases da Patologia em Veterinária, Eds: M.D. McGavin and J.F. Zachary, Elsevier, Rio de Janeiro. pp 833-972. Zachary, J.F., O’Brien, D.P. and Ely, R.W. (1981) Intramedullary spinal ependymoma in a dog. Vet. Pathol. 18, 697-700.
Robinson’s Current Therapy in Equine Medicine 7th edition Editors: Kim A. Sprayberry and N. Edward Robinson Publisher: Elsevier, September 2014 • Hardback, 1104 pages Stay uptodate on the latest advances and current issues in equine medicine! With coverage of current issues and emerging trends, this allnew reference helps you recognise, diagnose and treat equine disorders and conditions. The Current Therapy format focuses on treatment protocols and diagnostic updates in areas that have seen significant advances in the last 5 years. Features of this new edition: • 212 concise, NEW chapters include both a succinct guide to diagnosis of disorders and a detailed discussion of therapy. • Cutting edge topics include new sections on trauma, pain management, and the sport horse; and chapters on hoof lameness in foals, upper airway diseases, and colic diagnosis that describe use of new imaging, endoscopy, and other diagnostic prcedures. • A body systems organisation makes it easy to find solutions for specific conditions and disorders. • Updated Table of Common Drugs and Approximate Dosages in the appendix provides a handy quick reference and adds allnew coverage of drug dosages for donkeys and mules. • Nearly 200 expert contributors represent private equine practices, referral hospitals and academia, providing perspectives from around the world.
EVJ price:
£102.60 plus p&p BEVA member price: £92.34 plus p&p
EVJ Bookshop, Mulberry House, 31 Market Street, Fordham, Ely, Cambs. CB7 5LQ, UK Tel: 01638 723555 ! Fax: 01638 724043 ! Email:
[email protected] ! www.beva.org.uk © 2014 EVJ Ltd
