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Materials/Methods: Between 2008 and 2011, 53 patients with primary brain malignancies were treated with conventionally fractionated RT on a prospectively accrued clinical trial performed at our institution (WFU97100/91105). Tumor types included glioblastoma (13%), primitive neuroectodermal tumors (21%), and low grade/benign tumors (66%).Ten patients received whole brain RT with region boost, all other patients received partial brain RT. The median radiation dose was 54.0 Gy (range Z 40.0-60.6 Gy) delivered in 1.8 Gy/fraction (range Z 1.5-2.5 Gy/fraction). Dose-volume histogram analysis was performed for the hippocampus, parahippocampus, amygdala, and fusiform gyrus. Hopkins Verbal Learning Test-Revised (HVLT-R) scores were obtained at least 6 months after RT. Impairment was defined as a HVLT-R immediate recall score 15, based upon studies reporting optimal sensitivity and specificity for detecting impairment using HVLT-R cut-off scores of 14.5-15.5. For each anatomic region, serial regression was performed to correlate volume receiving a given dose (V D(Gy) ) with memory impairment. Results: Hippocampal V 53.4Gy -V 60.9Gy significantly predicted post-RT memory impairment (P < 0.05). Within this range, the hippocampal V 55Gy was the most significant predictor (P Z 0.004). Hippocampal V 55Gy of 0%, 25%, and 50% were associated with post-RT impairment rates of 14.9% (95% CI Z 7.2% -28.7%), 45.9% (95% CI Z 24.7% -68.6%), and 80.6% (95% CI Z 39.2% -96.4%), respectively. Dose received by the fusiform gyrus was a significant predictor of impairment, with the most significant relationship at V 46.5Gy (P Z 0.003). No statistically significant relationship was observed for the amygdala or parahippocampus. Conclusion: Injury to the hippocampus plays a fundamental role in CRCI. This analysis provides dosimetric guidelines to limit cognitive decline after cranial RT. The hippocampal V 55Gy is a significant predictor for impairment and limiting dose below 55 Gy may minimize treatment related neuro-cognitive toxicity.

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