PURPOSE: To determine the prognostic significance of pretreatment edema, lesion size and location on morbidity following stereotactic radiosurgery (SRS). METHODS AND MATERIALS: Forty-seven evaluable patients with 63 lesions were treated on a 6-MV linear accelerator radiosurgery system at Memorial Sloan Kettering Cancer Center. All patients received a 10-mg intravenous bolus of dexamethasone sodium phosphate (Decadron) prior to SRS. Thirteen patients were treated for asymptomatic lesions while 34 were treated because of neurologic symptoms. The median dose delivered was 1800 cGy and the median prescription isodose curve was 85%. Pretreatment edema was measured on a transaxial T2-weighted MR image acquired within 1 month of the SRS. RESULTS: Ten patients experienced morbidity as a result of their treatment. The complication rate was measured by neurologic events following SRS and was not significantly influenced by the extent of peritumoral edema. Lesion size was also unrelated to the development of post-treatment symptoms as assessed by the ease of tapering steroids. The only parameter found to influence post-SRS complications was lesion location. Four of six (66%) patients treated to lesions in the motor cortex suffered post-SRS seizure activity, whereas only 6 of 37 (16%) patients treated to lesions elsewhere in the brain parenchyma experienced seizure activity. CONCLUSION: The presence of pretreatment edema and lesion size are not predictors of post-SRS complication rates or the ability to taper Decadron. Lesion location is predictive of post-SRS seizure activity.
PURPOSE: To determine the prognostic significance of pretreatment edema, lesion size and location on morbidity following stereotactic radiosurgery (SRS). METHODS AND MATERIALS: Forty-seven evaluable patients with 63 lesions were treated on a 6-MV linear accelerator radiosurgery system at Memorial Sloan Kettering Cancer Center. All patients received a 10-mg intravenous bolus of dexamethasone sodium phosphate (Decadron) prior to SRS. Thirteen patients were treated for asymptomatic lesions while 34 were treated because of neurologic symptoms. The median dose delivered was 1800 cGy and the median prescription isodose curve was 85%. Pretreatment edema was measured on a transaxial T2-weighted MR image acquired within 1 month of the SRS. RESULTS: Ten patients experienced morbidity as a result of their treatment. The complication rate was measured by neurologic events following SRS and was not significantly influenced by the extent of peritumoral edema. Lesion size was also unrelated to the development of post-treatment symptoms as assessed by the ease of tapering steroids. The only parameter found to influence post-SRS complications was lesion location. Four of six (66%) patients treated to lesions in the motor cortex suffered post-SRS seizure activity, whereas only 6 of 37 (16%) patients treated to lesions elsewhere in the brain parenchyma experienced seizure activity. CONCLUSION: The presence of pretreatment edema and lesion size are not predictors of post-SRS complication rates or the ability to taper Decadron. Lesion location is predictive of post-SRS seizure activity.