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Glioblastoma Multiforme and Ascending Weakness

Published online by Cambridge University Press:  02 December 2014

L.J. Cooke
Affiliation:
Department of Clinical Neurosciences, University of Calgary, Foothills Hospital, Calgary, AB, Canada
William Morrish
Affiliation:
Department of Clinical Neurosciences, University of Calgary, Foothills Hospital, Calgary, AB, Canada
W.J. Becker
Affiliation:
Department of Clinical Neurosciences, University of Calgary, Foothills Hospital, Calgary, AB, Canada
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An 18-year-old man with a known glioblastoma multiforme, previously treated with de-bulking, chemotherapy, radiation and steroids, underwent a repeat craniotomy after presenting with several days of intractable vomiting and headache. Postoperatively, he developed progressive delirium, bilateral sixth and seventh nerve palsies, dysphagia and ascending weakness of the upper and lower limbs. Within five postoperative days, he was quadraparetic, areflexic and had marked extraocular muscle and facial weakness, dysphagia, dysphonia and respiratory muscle weakness. The patient was started empirically on intravenous immunoglobulin for suspected Guillain-Barré syndrome (GBS). The following day, lumbar puncture demonstrated elevated protein (1.96g/l; normal <0.45), and a reduced glucose (0.5 mmol/l) and elevated red (4125x106 per litre) and white cell (214x106 per litre) counts in the cerebrospinal fluid (the red cells were felt to be related to surgery). The cell differential included 69% neutrophils, 3% lymphocytes, 15% monocytes and 13% blast-like cells. Gram stains and cultures of the cerebrospinal fluid were negative.

Type
Research Article
Copyright
Copyright © The Canadian Journal of Neurological 2002

References

1. Yung, WA, Horten, BC, Shapiro, WR. Meningeal gliomatosis: a review of 12 cases. Ann Neurol 1980;8(6):605608.Google Scholar
2. Erlich, SS, Davis, RL. Spinal subarachnoid metastasis from primary intracranial glioblastoma multiforme. Cancer 1978;42(6):28542864.Google Scholar
3. Moonis, M, Smith, TW. Meningeal gliomatosis presenting as multiple cerebral infarcts: a case report. Neurology 1996;46(6):17601764.Google Scholar
4. Grant, R, Naylor, B, Junck, L, Greenberg, HS. Clinical outcome in aggressively treated meningeal gliomatosis. Neurology 1992;42(1):252254.CrossRefGoogle ScholarPubMed
5. DeMarcaida, JA, Reik, L. Disorders that mimic central nervous system infections. Neurol Clin 1999;17(4):901941.Google Scholar
6. Minami, T, Kai, T, Hirabaru, C, et al. A case of cerebral glioblastoma with extensive cerebrospinal fluid dissemination: diagnostic value of immunohistochemical examination and MR imaging. Childs Nerv Syst 1993;9(8):478480.Google Scholar
7. Wison, EO. Consilience. New York: Alfred A. Knopf 2000:53.Google Scholar
8. Lam, CH, Cosgrove, RG, Drislane, FW, Sotrel, A. Spinal leptomeningeal metastasis from cerebral glioblastoma. Appearance on magnetic resonance imaging. Surg Neurol 1991;35:377380.Google Scholar
9. Matsushima, K, Kocha, H, Watanabe, R, Honda, M, Nakamura, N. Diffuse cerebrospinal gliomatosis mimicking amyotrophic lateral sclerosis. Internal Medicine 1993;32(6):476479.CrossRefGoogle ScholarPubMed
10. Izumoto, S, Ohnishi, T, Kanemura, H, et al. PTEN mutations in malignant gliomas and their relation with meningeal gliomatosis. J Neuro-Onc 2001;53(1):2126.Google Scholar
11. Witham, TF, Fukui, MB, Meltzer, CC, et al. Survival of patients with high grade glioma treated with intrathecal thiotriethylenephos-phoramide for ependymal or leptomeningeal gliomatosis. Cancer 1999;86:13471353.3.0.CO;2-M>CrossRefGoogle ScholarPubMed