Radiation-Induced Meningioma

Felix Umansky, M.D.; Yigal Shoshan, M.D.; Guy Rosenthal, M.D.; Shifra Fraifeld, M.B.A.; Sergey Spektor, M.D., PH.D.

Disclosures

Neurosurg Focus. 2008;24(5):E7 

In This Article

Radiation-Induced Meningioma

Radiation-induced meningioma is the most common brain neoplasm known to be caused by ionizing radiation.[3,28] Harrison et al.[24] grouped RIMs into 3 categories: those due to high-dose (> 20 Gy), intermediate-dose (10-20 Gy), and low-dose (< 10 Gy) radiation. Other authors define doses > 10 Gy as high.[42,78]

In 1953, Mann et al.[33] described a meningioma in a 4-year-old girl who had undergone radiation treatment for optic nerve glioma. The child's meningioma eventually became malignant. Several authors have summarized up to 126 cases of high-dose RIMs reported in the literature between 1953 and 2002.[4,17,42,66,67,78,81] The radiation doses ranged from 22 to 87 Gy, and the majority of patients had undergone radiotherapy as children. The mean latency from irradiation to diagnosis of the meningioma was ~ 19 years,[42,67] with a tendency for shorter latency in patients treated with higher doses and those who had undergone radiotherapy at younger ages.[2,17,24,32,42,78]

The increased incidence of meningiomas following exposure to low-dose radiation has been reported in patients who, as children, had undergone radiation treatment for tinea capitis, those whose heads and necks were exposed to medical and dental x-rays at a young age, and survivors of the atomic explosions in Hiroshima and Nagasaki.

Prior to the introduction of griseofulvin in 1960,[18,27,60,82] the world standard for treatment of tinea capitis was scalp irradiation.[5,7,22,59] Treatment for tinea capitis was administered using the Adamson-Keinbock technique, which was designed to irradiate the entire scalp as uniformly as possible through exposure to 5 overlapping treatment areas.[1] Phantom studies using this technique showed that the radiation dose to the scalp was 5-8 Gy, the surface dose to the scalp was 5-8 Gy, the surface dose to the brain was 1.4-1.5 Gy, and the skull base received an average of 0.7 Gy.[5] In 1966, Albert et al.[5] reported a substantial increase in cancer, mental disease, and permanent damage to scalp hair in 1908 patients in whom radiotherapy was performed for tinea capitis at the New York University Medical Center between 1940 and 1958, compared with 1801 patients treated for tinea capitis without radiotherapy during the same years. Other reports followed.[7,20,24,41,59,76]

In 1974, Modan and colleagues[37] at the Sheba Medical Center in Tel Aviv published a retrospective cohort study showing a significantly higher risk of malignant and benign head and neck tumors among ~ 11,000 Israeli adults treated for tinea capitis as children. This major epidemiological work is widely credited as proving the causal role of radiation in the development of meningiomas in some patients. Follow-up studies of the Israeli cohort showed that a radiation dose of only 1-2 Gy administered during childhood led to a 9.5-fold increase in meningioma incidence.[57] Continuing follow-up[63,64,65] shows that elevated risk of brain tumor, including meningioma, is positively associated with dose, with excess relative risk for benign meningioma rising to 18.82 for doses > 2.6 Gy.[63] These studies showed a higher prevalence of calvarial tumors and multiple meningiomas, and higher recurrence rates in RIMs than SMs. The mean latency was ~ 36 years.

In 1953, Nolan alone[50] and with Patterson[51] published studies in which significant blood changes occurred in patients exposed to 1.15-2.8 Gy during full-mouth radiographic examinations. Nolan observed that full-mouth series delivered converging lines of radiation, with high points near the meninges. In 1980, nearly 30 years later, Preston-Martin et al.[54] noted a higher incidence of meningioma in women with a history of full-mouth dental x-rays. The risk in this cohort study was higher in patients who had undergone radiographic examinations as children or teenagers and in those in whom radiographic examinations were conducted before 1945, when doses were higher. The majority of tumors were located in the tentorial or subtentorial region. The authors of more recent case-control studies in Sweden[56] and the US[29] have found that dental radiographic examinations performed during the adult years may also increase the risk of meningioma.

The increased incidence of meningiomas among survivors of the 1945 atomic explosions in Japan was shown only in 1994, when Shibata et al.[70] demonstrated a higher incidence of meningiomas in survivors of the bombing in Nagasaki. In 1997 Shintani et al.[71,72] published similar findings after studying data obtained in Hiroshima survivors. Due to the relatively low-dose exposure to ionizing radiation among these survivors compared with those undergoing radiotherapy for tinea capitis, the average latency was greater in the Japanese studies. The risk of meningioma induction was shown to increase with closer proximity to the bombs' epicenters and in those exposed during childhood.[53]

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