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      Meningeal carcinomatosis and spinal cord infiltration caused by a locally invasive pulmonary adenocarcinoma in a cat

      case-report

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          Abstract

          Case summary

          A 12-year-old domestic shorthair cat was presented with acute non-painful hindlimb proprioceptive ataxia localising to T3–L3 spinal cord segments. MRI revealed paravertebral muscular hyperintensity on T2-weighted images at the level of T7–T8 vertebrae. The cat improved on conservative management but deteriorated 3 months later. Repeated MRI showed meningeal enhancement at the same level and hyperintensity of the paravertebral musculature extending to the right thoracic wall and pleural space on short tau inversion recovery images. Thoracic CT showed mineralised lesions of the right lung, restricted pleural effusion and expansile bone lesions affecting multiple ribs. The cat had been treated for pyothorax 5 years earlier but manifested no current respiratory signs. Cerebrospinal fluid (CSF) examination showed lymphocytic pleocytosis but no neoplastic cells. Biopsy of the affected muscles and cytology of the lung and pleural lesions suggested a malignant epithelial cell tumour. Post-mortem examination confirmed a pulmonary adenocarcinoma locally infiltrating the thoracic wall, T7–T8 vertebrae and the spinal cord white matter. Meningeal carcinomatosis was detected with neoplastic cells invading the ventral median fissure of the spinal cord. No metastases were observed in other organs, indicating that neoplastic cells reached the spinal cord by direct extension.

          Relevance and novel information

          Spinal meningeal carcinomatosis has not been reported in dogs or cats with extraneural tumours but is a well-recognised condition in humans. A metastatic cause of meningeal enhancement should be considered in patients with neurological signs of unknown origin. Imaging findings and CSF results can be non-specific.

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          Most cited references26

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          Leptomeningeal carcinomatosis.

          Leptomeningeal carcinomatosis occurs in approximately 5% of patients with cancer. This disorder is being diagnosed with increasing frequency as patients live longer and as neuro-imaging studies improve. The most common cancers to involve the leptomeninges are breast cancer, lung cancer, and melanomas. Tumour cells reach the leptominges by hematogenous spread or by direct extension from pre-existing lesions and are then disseminated throughout the neuroaxis by the flow of the cerebrospinal fluid. Patients present with signs and symptoms from injury to nerves that traverse the subarachnoid space, direct tumour invasion into the brain or spinal cord, alterations in blood supply to the nervous system, obstruction of normal cerebrospinal fluid (CSF) flow pathways, or general interference with brain function. The diagnosis is most commonly made by lumbar puncture although the CSF cytology is persistently negative in about 10% of patients with leptomeningeal carcinomatosis. Radiologic studies may reveal subarachnoid masses, diffuse contrast enhancement of the meninges, or hydrocephalus without a mass lesion. Without treatment, the median survival of patients with this disorder is 4-6 weeks and death occurs from progressive neurologic dysfunction. Early diagnosis and therapy is critical to preserving neurologic function. Radiation therapy to symptomatic sites and disease visible on neuroimaging studies and intrathecal chemotherapy increases the median survival to 3-6 months. The major favorable prognostic factors include excellent performance status, absence of serious fixed neurologic deficits, normal CSF flow scans, and absent or responsive systemic tumour. Aggressive therapy for this disorder is often accompanied by a necrotizing leukoencephalopathy which becomes symptomatic months after treatment with radiation and intrathecal methotrexate. As currently available therapies are toxic and provide limited benefits, novel approaches are being studied. Further information on the mechanisms of neurotoxicity from antineoplastic agents is critical to providing better outcomes for this increasing common complication of cancer. Copyright 1999 W.B. Saunders Company Ltd.
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            Clinical, cerebrospinal fluid, and histological data from twenty-seven cats with primary inflammatory disease of the central nervous system.

            The purpose of this report is to present the clinical, cerebrospinal fluid (CSF) and histological data from 27 cats with inflammatory disease of the central nervous system (CNS). The cats were part of a study of 61 cats admitted to two university clinics over an eight-year period because of signs of CNS disease. The most frequent diseases were feline infectious peritonitis (FIP) (12/27) and suspected viral disease other than FIP (10/27). Typical CSF findings in cats with FIP were a protein concentration of greater than 2 g/L (200 mg/dL) and a white cell count of over 100 cells/microL, which consisted predominantly of neutrophils. In contrast, the CSF of cats with suspected viral disease had a protein concentration of less than 1 g/L (100 mg/dL) and a total white cell count of less than 50 cells/microL. In general, cats with FIP or suspected viral disease were less than four years of age. Neurological signs were usually multifocal in cats with FIP, but focal in cats with suspected viral disease. The CSF findings were variable in five other inflammatory diseases represented. Two cats with protozoan infection had normal CSF total cell counts but abnormal differential counts. The CSF findings were invaluable in differentiating FIP from other causes of inflammatory CNS disease.
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              Inflammatory cerebrospinal fluid analysis in cats: clinical diagnosis and outcome

              The medical records of 62 cats with clinical signs of central nervous system disease and accompanying inflammatory cerebrospinal fluid (CSF) analysis were examined retrospectively to determine if signalment, clinical signs, CSF analysis and ancillary testing could accurately predict the type of central nervous system disease that was present. An inflammatory CSF was defined as one in which a total nucleated cell count was greater than 5 cells/μl or one in which the total nucleated cell count was normal but the nucleated cell differential count was abnormal. Sex, degree of CSF inflammation, neuroanatomical location and systemic signs provided little contributory information to the final diagnosis. In 63% of the cases a presumptive diagnosis could be made based on a combination of clinical signs, clinicopathological data and ancillary diagnostic tests. CSF analysis alone was useful only in the diagnosis of cats with feline infectious peritonitis, Cryptococcus species infection, lymphoma and trauma. Overall, despite extensive diagnostic evaluation, a specific diagnosis could not be made in 37% of cats. The prognosis for cats with inflammatory CSF was poor with 77% of cats surviving less than 1 year.
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                Author and article information

                Journal
                JFMS Open Rep
                JFMS Open Rep
                JOR
                spjor
                JFMS Open Reports
                SAGE Publications (Sage UK: London, England )
                2055-1169
                23 November 2017
                Jul-Dec 2017
                : 3
                : 2
                : 2055116917742812
                Affiliations
                [1 ]Department of Neurology / Neurosurgery, Pride Veterinary Centre, Derby, UK
                [2 ]School of Veterinary Medicine and Science, University of Nottingham, UK
                [3 ]Department of Radiology, Pride Veterinary Centre, Derby, UK
                Author notes
                [*]Annette Wessmann DrMedVet, DipECVN, MRCVS, Department of Neurology/Neurosurgery, Pride Veterinary Centre, Riverside Road, Derby DE24 8HX, UK Email: annette.wessmann@ 123456scarsdalevets.com
                Article
                10.1177_2055116917742812
                10.1177/2055116917742812
                5703112
                8641753f-0392-4646-a63e-861343209064
                © The Author(s) 2017

                This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License ( http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access page( https://us.sagepub.com/en-us/nam/open-access-at-sage).

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                July-December 2017

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