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© 2000 American Society for Clinical Oncology
Meningeal Carcinomatosis in Lung CancerArthur Skarin, MDConsultant Editor
Beth Israel Deaconess Medical Center, Boston, MA CASE 1. CARCINOMATOUS LEPTOMENINGEAL METASTASES A 55-year-old woman with a heavy cigarette-smoking history developed rapidly progressing truncal ataxia, headache, and disorientation. Her physical examination did not disclose any skin lesion, breast mass, or lymphadenopathy, although her neurologic examination was remarkable for poor memory, flat affect, loss of deep tendon reflexes, appendicular dysmetria, and wide-based gait. Contrast-enhanced computed tomography of the head (Fig 1) revealed diffuse basilar enhancement of the cerebellum (black arrow). The temporal horns of the lateral ventricles (white arrow) were dilated. There was mild subependymal transudation of CSF (white arrowhead). Staging computed tomography of the body revealed only a 1.5 cm x 2.0 cm left hilar mass near a cavity from prior lung surgery, representing either recurrent or new lung cancer. Her past history was significant for an adenocarcinoma of the lung without lymph node involvement for which she had undergone resection of the left upper lobe and left lingua 9 years before. She also had had another resection of an adenocarcinoma nodule from the right upper lobe 8 years before her presentation. For her obstructive hydrocephalus, a ventriculoperitoneal shunt connected to a reservoir for intrathecal chemotherapy administration was placed. The CSF contained a WBC count of 56 cells/µL and a total protein level of 96 mg/dL. Cytology was positive for malignant cells characterized by large pleomorphic cells with enlarged nuclei, occasional nucleoli, and coarse chromatin (Fig 2, Papanicolaou’s stain, x100). After placement of the ventriculoperitoneal shunt, her mental status improved and her headaches resolved. She remained ataxic. Because of subsequent deterioration of her neurologic status with the development of hearing loss, she was transferred to another facility for hospice care. No intrathecal chemotherapy was administered.
Patients with carcinomatous leptomeningeal metastases usually present with multiple cranial neuropathies, patchy radiculopathies, or mental status change. These neurologic deficits can be caused by tumor aggregates compressing penetrating arteries in the Virchow-Robin spaces of the brain,1 direct nerve root compression by tumor cells, or obstructive hydrocephalus from blockage of CSF flow. For patients with obstructive hydrocephalus, shunting of CSF can relieve neurologic deficits, as seen in our patient. However, cranial neuropathies or radiculopathies are frequently irreversible. Thus timely diagnosis and prompt intervention is important for preserving neurologic functions.2 The gold standard for diagnosing this disease is still cytologic confirmation of malignant cells in the CSF. However, up to one third of patients will have cytologically negative CSF.3 Glantz et al4 found that false-negative results could be minimized by withdrawing at least 10 mL of CSF for cytology, obtaining CSF near the site of disease, delivering the CSF for immediate processing, and performing another lumbar puncture. Although the CSF cytology is only positive 54% of the time in an initial spinal tap, the CSF protein level is frequently elevated at a rate of 81%; with a second tap, the cumulative positive rate of CSF cytology increases to 91%.5 For patients with persistently negative CSF cytologies, a reasonably accurate diagnosis can still be made under the appropriate clinical scenario, neuroimaging findings, and CSF profile.6 Although the treatment of leptomeningeal carcinomatosis is not curative and patient survival is usually less than 6 months, radiation therapy and intrathecal chemotherapy can offer palliation by arresting neurologic progression in clinically stable patients.7 Drugs used for this purpose include methotrexate, thiotepa, cytarabine, and sustained-release cytarabine. An important issue in this patient is the possibility of another lung primary tumor. Although her lung lesion was not biopsied given her neurologic deficits, her limited workup did not disclose another systemic primary elsewhere, and her lung lesion could represent a primary neoplasm. In analyzing published data on patients with resected non–small-cell lung cancer, Johnson8 reported that their risk of developing a second lung primary is approximately 1% to 2% per year. From the time of diagnosis of the secondary primary, the median survival of these patients is less than 2 years, whereas their 5-year survival rate is approximately 20%. In this patient, the potential development of three adjacent metachronous lung primaries raises an interesting possibility of a field effect phenomenon. In fact, an adenocarcinoma-specific tumor marker has been identified in histologically normal tissue surrounding lung adenocarcinomas.9 REFERENCES 1. Klein P, Haley EC, Wooten GF, et al: Focal cerebral infarctions associated with perivascular tumor infiltrates in carcinomatous leptomeningeal metastases. Arch Neurol 46:1149-1152, 1989[Abstract] 2. Balm M, Hammack J: Leptomeningeal carcinomatosis, presenting features and prognostic factors. Arch Neurol 52:626-632, 1996
3.
Chamberlain MC: Cytologically negative carcinomatous meningitis: Usefulness of CSF biochemical markers. Neurology 50:1173-1175, 1998 4. Glantz MJ, Cole BF, Glantz LK, et al: Cerebrospinal fluid cytology in patients with cancer, minimizing false-negative results. Cancer 82:733-739, 1998[Medline] 5. Posner JB : Neurologic Complications of Cancer. Philadelphia, PA,F.A. Davis Company, 1995, pp 143-168 6. Freilich RJ, Krol G, DeAngelis LM: Neuroimaging and cerebrospinal fluid cytology in the diagnosis of leptomeningeal metastasis. Ann Neurol 38:51-57, 1995[Medline]
7.
Glantz MJ, Jaeckle KA, Chamberlain MC, et al: A randomized controlled trial comparing intrathecal sustained-release cytarabine (DepoCyte) to intrathecal methotrexate in patients with neoplastic meningitis from solid tumors. Clin Cancer Res 5:3394-3402, 1999
8.
Johnson BE: Second lung cancers in patients after treatment for an initial lung cancer. J Natl Cancer Inst 90:1335-1345, 1998
9.
Shamsuddin AM, Tyner GT, Yang GY: Common expression of the tumor marker D-Galactose-beta-[1
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Copyright © 2000 by the American Society of Clinical Oncology, Online ISSN: 1527-7755. Print ISSN: 0732-183X
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3]-N-Acetyl-D-Galactosamine by different adenocarcinomas: Evidence of field effect phenomenon. Cancer Res 55:149-152, 1995
