Radiation-induced temporal lobe necrosis.

Because nasopharyngeal carcinoma has a high frequency of intracranial spread, adequate radiation treatment inevitably results in irradiation of the temporal lobes. A 38-year-old woman who was treated for nasopharyn-geal carcinoma 30 months previously and had been given radiation therapy (70 Gy to the primary site) presented with headaches. Computed tomography (CT) showed an enhancing lesion in the right temporal lobe, with edema extending superiorly into the parietal lobe. Biopsy revealed brain necrosis and a course of corticosteroid therapy was started. Five months later, magnetic resonance (MR) showed less edema in the right temporal lobe but an extensive lesion on the contralateral side, not seen before (Fig 1A–C). Corticosteroid therapy was again given and 9 months later, the nasopharynx was reevaluated but no tumor recurrence was seen. MR showed dilatation of the temporal horns indicating cerebral atrophy (Fig 1D). Enhancing lesions in both temporal lobes were still evident, though less extensive than before. Doses below 60 Gy at conventional 2 Gy daily appear inadequate for tumor control (1). Unfortunately, the effective dose for nasopharyngeal carcinoma (65 to 70 Gy) exceeds the quoted tolerance limits for the adjacent neural structures (2). There is, therefore, a substantial risk of radiation damage to the brain. Temporal lobe necrosis (TLN) is the most dreaded complication of radiation therapy and accounts for 65% of treatment mortality. Lee et al (1) reported a 3% cumulative incidence of TLN in a series of 4527 patients. The latent interval ranged from 1.5 to 13 years (median, 5 years). TLN is probably underdiagnosed, because in Lee et al's study 39% of patients had only vague symptoms, whereas 16% had no symptoms (3). Although the radiation dose to the brain is approximately equal on both sides, changes in the brain are often asymmetric. Half the patients with TLN will present with unilateral abnormalities; in only 10% of these patients will bilateral lesions subsequently develop (3). The earliest sign of TLN is cerebral edema, which can be extensive. Enhancing lesions can be located in the gray or white matter. On CT, TLN appears patchy but delayed scans often show less inhomogeneity and better-defined margins. On MR, the necrotic foci show patchy enhancement but demarcation from the adjacent brain is better seen. Necrotic foci within the gray matter are often associated with minimal edema. These lesions at the skull base can be difficult to detect on CT and hence are better seen with …