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Show J. Clin. Neuro-ophthalmoI. 4: 137-138, 1984. Editorial Comment Spontaneous Reduction of Growth Rate of a Large Intracranial Meningioma The case presented by Drs. Saul and King in this issue is instructive, for it emphasizes the fact that meningiomas do not progress inexorably to blindness. Although it is impossible to cull from the literature a picture of the natural history of untreated meningiomas, it is interesting that Wood et al.I report finding 100 cases of incidental astymptomatic meningiomas over a IS-year period. Although the majority of their tumors are small (as Drs. Saul and King emphasize), two are extraordinary-one being 7.5 x 5.5 cm and the other 7.5 x 6 x 5 cm. Tumor distribution in their cases is 30.5% parasagittal, 24.6% free convexity, 16.2% sphenoid ridge, 12.7% sellar or parasellar region, 9.2% posterior fossa, and 6.8% basofrontal region. Using data derived from 217 operative patients, Earle and Richany" conclude that histological subclassification is neither reliable nor useful in predicting the biologic behavior of meningiomas. Chan and Thompson3 review 237 patients who underwent craniotomies for meningiomas. With the exception of the so-called malignant meningiomas classified according to Burger and VogeL4 Chan and Thompson concur that histologic type does not seem to have an effect on survival. Of interest is the fact that no malignant meningiomas are present in the 100 cases of incidental meningiomas reported by Wood et al.I Although many questions remain unanswered, we address two of them. If histologic type (other than that classified malignant by pleomorphism) is an unreliable prognosticator of biologic behavior, then what makes some tumors remain static, grow slowly, or grow rapidly? What approach should the clinician taken when dealing with a patient who appears with a deficit fixed for a period of time, and who is found to have a mass radiologically compatible with a diagnosis of meningioma? The first question may be answered only hypothetically. There is a burgeoning literature on the presence of steroid receptor proteins in human meningiomas."-7 The presence of such receptors suggests that the biologic behavior of a given June 1984 meningioma is determined by the presence or absence of cellular surface receptors which modulate growth in response to circulating hormones. In a study of 16 patients with meningiomas, Yu et al. 7 report finding estrogen receptors in 15 of 16 tumors and progestin receptors in nine of 11 tumors assayed. They further state that both estrogen and progestin concentrations were higher in women. Findings such as these explain why: 1) approximately two-thirds of all intracranial meningiomas and 80% of all spinal meningiomas occur in women,"·4.H." and 2) meningiomas often appear to grow rapidll and become symptomatic during pregnancy. Ill-I. Wood et al. I report finding an equal sex distribution in their series of incidental meningiomas found at autopsy (suggesting benignity and nongrowth), adding credence to the argument that many symptomatic tumors are probably hormonally sensitive. In those patients with symptomatic meningiomas demonstrating estrogen receptors, in whom excision is incomplete, tamoxifen (a potent antiestrogenic agent) may be of value. One of us (RMB) observed the use of tamoxifen in a young woman whose meningioma, which involved the right sphenoid wing, became clinically apparent during the initial phase of her pregnancy, producing proptosis and visual loss. After the successful delivery of a normal child, the patient underwent a transfrontal craniotomy, at which time it was discovered that the tumor was invading bone and was not resectable. An assay for estrogen receptors was positive, and the patient was treated with external beam irradiation and continuous oral tamoxifen, 10 mg daily since 1977, without evidence of recurrence. Whether hormonal receptors other than estrogen and progestin ultimately will be identified on all actively growing, so-called "benign" meningiomas is highly unlikely, but at least from this approach we have a beginning. The answer to the second question is one of personal bias rather than hypothesis. If a presumed meningioma is found incidentally as part of a neurologic evaluation for some other problem, it should be left alone. Similarly, if a patient 137 Editorial Comment: Intracranial Meningioma presents with a fixed deficit that is static by history, and a presumed meningioma is identified during an appropriate workup, this patient should also be followed clinically and radiologically for signs of further functional compromise before neurosurgical intervention is contemplated. Ronald M. Burde, M.D. Washington University School of Medicine St. Louis, Missouri J. Lawton Smith, M.D. Bascom Palmer Eye Institute Miami, Florida References 1. Wood, M.W., White, RJ., and Kernohan, J.W.: One hundred intracranial meningiomas found incidentally at necropsy. J. Neuropathol. Exp. Neurol. 16: 337-340,1957. 2. Earle, K.M., and Richany, S.F.: Meningiomas. A study of the histology, incidence, and biologic behavior of 243 cases from the Frazier-Grant collection of brain tumors. Med. Ann. D.C 38: 353-358, 1979. 3. Chan, R.C., and Thompson, G.B.: Morbidity, mortality, and quality of life following surgery for intracranial meningiomas. A retrospective study in 257 cases. J. Neurosurg. 60: 52-60, 1984. 4. Burger, P.c., and Vogel, F.S.: Surgical Pathology of the Nervous System and its Coverings (2nd ed.). John Wiley & Sons, New York, 1982, pp. 83-170. 5. Tilzer, L.L., Plapp, F.V., Evans, J.P., Stone, D., and Alward K.: Steroid receptor proteins in human meningiomas. Cancer 49: 633-636, 1982. 6. Donnell, MS., Meyer, G.A, and Donegan, W.L.: Estrogen-receptor protein in intracranial meningioma. J. Neurosurg. 50: 499-502,1979. 7. Yu, Z.-Y., Wrange, Q., Haglund, B., Granholm, L., and Gustafsson, J.-A: Estrogen and progestin receptors in intracranial meningomas. J. Steroid Biochem. 16: 451-456, 1982. 8. Rausing, A, Ybo, W., and Stenflo, I.: Intracranial meningioma-a population study of ten years. Acta Neurol. Scand. 46: 102-110, 1970. 9. Lombardi, G., and Passerini, A: Spinal cord tumors. Radiology 76: 381-390, 1961. 10. Rand, C.W., and Andler, M.: Tumors in the brain complicating pregnancy. Arch. Neurol. Psychiatry 63: 1-14, 1950. 11. Kempers, RD., and Miller, R.H.: Management of pregnancy associated with brain tumors. Am. J. Obstet. Gynecol. 87: 858-864, 1963. 12. Bickerstaff, E. R, Small, I.J., and Guest, LA: The relapsing course of certain meningiomas in relation to pregnancy and menstruation. J. Neurol. Neurosurg. Psychiatry 21: 89-91, 1958. 13. Goldstein, P.I., Rosenberg, S., and Smith, RW.: Maternal death and brain tumors: Case report. Am. J. Obstet. Gynecol. 112: 297-298, 1972. Journal of Clinical Neuro-ophthalmology |
