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Background: Brain tumors present unique challenges to patient and family quality of life (QOL). Cognitive dysfunction is common and functionally limiting, with no established treatments. These studies evaluate feasibility and preliminary efficacy of behavioral interventions developed for neuro-oncology patients. Study 1: A randomized controlled trial (N=25 primary brain tumor patients) compared an adapted version of Goal Management Training (GMT, a neuroscience-based integration of mindfulness and strategy training) and a newly-designed supportive psychoeducational intervention (Brain Health Program, BHP) to standard of care. Each intervention comprised 8 individual sessions and at-home practice between sessions. GMT patients’ executive functions improved immediately (p=.077, d=1.13), with maintenance at 4-month follow-up (p=.046, d=1.09). Both intervention groups reported improvements in everyday cognitive functioning immediately (p=.049; d’s GMT=0.43, BHP=0.79) and at follow-up (p=.001; d’s GMT=0.22, BHP=1.01). BHP patients also reported improved mood (p’s=.026 & .012, d’s=0.61 & 0.62). Study 2: Following a needs assessment about cognitive concerns and QOL in brain metastases patients (N=109) and caregivers (N=31), we developed a novel, brief (3 sessions + homework) Cognitive Support Program to provide education and strategy-training in key areas of concern: executive functions, memory, and communication. Options include caregiver co-training, and in-person or web-based delivery. Preliminary data from a pilot trial in progress demonstrate objective and subjective improvements. Conclusions: Cognitive rehabilitation may be a feasible and effective option for primary or metastatic brain tumor patients, addressing a need that is largely unmet in standard cancer care. Further development and larger trials appear warranted, with capacity for remote delivery recommended.

Improving neurocognitive outcomes following treatment for brain metastases have become increasingly important. We propose that a brief telephone-based neurocognitive assessment may improve follow-up cognitive assessments in this palliative population. Aim: To prospectively assess the feasibility and reliability of a telephone based brief neurocognitive assessment compared to the same tests delivered face-to-face. Methods: Brain metastases patients to be treated with whole brain radiotherapy (WBRT) were assessed using a brief validated neurocognitive battery at baseline, at 1 month and 3 months following WBRT (in person and over the phone). The primary outcome was feasibility and inter-procedural (in person versus telephone) reliability. The secondary objective was to evaluate the change in neurocognitive function before and after WBRT. Results: Out of 39 patients enrolled, 82% of patients completed the baseline in-person and telephone neurocognitive assessments. However, at 1 month, only 41% of enrolled patients completed the in-person and telephone cognitive assessments and at 3 months, only 10% of patients completed them. Results pertaining to reliability and change in neurocognitive function will be updated. Conclusion: The pre-defined definition of feasibility (at least 80% completion for face to face and telephone neurocognitive assessments) was met at baseline. However, a large proportion of participants did not complete either telephone or in person neurocognitive follow-up at 1 month and at 3 months post-WBRT. Attrition remained a challenge for neurocognitive testing in this population even when a telephone-based brief assessment was used.

metastases and suggests practical solutions to mitigate their undesired effects. Materials/Methods: Serial patients treated with radiosurgery with hemorrhagic brain metastases well-defined on CT were included in this study. For each patient, CT and corresponding Gd-enhanced T1-weighted FSPGR, acquired on a 3T MRI, were co-registered using a commercial rigid mutual information algorithm. Subsequently, the target lesions were manually segmented on the MR images. The scanner-related distortions (i.e., B0 inhomogeneity and gradient non-linearities) were measured by using a dedicated phantom. The susceptibility geometric distortions (Dx) were modeled by numerically solving the Maxwell equations for a static magnetic field, i.e., div[(1+ChiM)grad(PhiM)] Z 0, where PhiM is the magnetic scalar potential and ChiM is the magnetic susceptibility constant. The input data required by the simulations consisted of the spatial distribution of susceptibility values in the patient anatomy (i.e., soft-tissue, air, bone, hemorrhagic mets) derived from CT and PhiM boundary values. The simulations were performed for B0 of 0.2T to 5T and GE of 2 to 20 mT/m. The CT contours were modified to include the simulated susceptibility distortions and then compared to the MR contours. Results: The magnitude of the susceptibility effects for hemorrhagic metastases depends on several parameters including the size, shape and iron content of the metastasis. There is a strong dependence on the strength of B0 and encoding gradient (GE) (i.e., Dx w B0/GE), and a weak influence due to the relative orientation of B0 with regard to the volume shape. The geometric distortions amounted to about 1.5 mm for B0 and GE values of 3T and 4 mT/m, respectively. The MR acquisition may be optimized by increasing GE strength (for a given B0) to reduce the distortions affecting the target volumes such that residual distortions are not clinically significant. However, the increase of GE introduces an image quality penalty due to the decrease in the signal to noise ratio. Conclusions: The susceptibility effects were investigated and quantified for several parameters. The correction of only the system-related distortions may not be enough for an accurate MR-based target definition. The susceptibility effects need to be carefully investigated and their impact quantified. Author Disclosure: T. Stanescu: None. C. Chung: None. A. Simeonov: None. M. van Prooijen: None. B. Millar: None. C. Menard: None.

task and left HC, -0.81 for the faces task and the right HC. These correlations were non-significant (p>.10) at the three month test. Conclusion: Preliminary results point to a mild and transient decline in memory after SRS, which is associated with low dose delivered to the HC in the range of 1-2 Gy. The pattern is similar to non-human studies suggesting disruption of neurogenesis as a possible mechanism. Further investigations in a larger cohort of patients is necessary to better characterize the severity, dose thresholds and time course of these effects following therapeutic radiation.

10064 Background: The purpose of this study is to determine the frequency of late endocrine complications following radiation therapy (RT) in children treated for medulloblastomas or ependymomas. Methods: Seventy children with medulloblastoma or ependymoma were treated using RT from June 2000 to June 2005 at our institute. Median age at diagnosis was 6 years (range 1–17), and 52 (74%) were boys. Forty-eight patients (69%) had medulloblastomas and 22 (31%) had ependymomas. Twenty-two received highly conformal RT to the tumor bed alone (focal RT: median dose 54 Gy, range 54–59.4), 24 received low dose cranio-spinal RT (CSI: median dose 23.4 Gy) followed by a boost to the post fossa/tumor bed (median 30.6 Gy), and 24 patients received high dose CSI (median 36 Gy) followed by a boost (median 18 Gy). Only two of the 22 children with ependymomas received CSI. All patients underwent CT-based planning and were treated using conventional fractionation; 58 (83%) also received chemotherapy. None of the children had documented endocrinopathy prior to diagnosis. Results: After a median follow-up of 65.3 months, the 5-yr PFS and OS was 70% and 75% for children with medulloblastomas, and 54% and 84% for patients with ependymomas, respectively. Thirty-five children developed evidence of endocrinopathy (Growth hormone deficiency (GHD): 31, hypothyroidism (HPT): 23, precocious puberty (PP): 6, gonadotropin deficiency: 3, ACTH deficiency: 2, and diabetes insipidus: 2). The 5-yr cumulative incidence (CI) of endocrinopathy was 71% for the children treated with CSI vs. 18% for those treated with focal RT (Gray's test p-value = 0.004). The median time to development of endocrinopathy was 38 months for the patients who had CSI. For these children the 5-yr CI was 68% for GHD, 52% for HPT, and 16% for PP. There was no significant difference in the incidence of endocrinopathy for patients treated with low dose vs. high dose CSI. Conclusions: The 5-yr CI of endocrine toxicity in children treated with cranio-spinal RT is 71% (median time to development: 38 months), which is significantly higher than in children treated with focal RT. All children treated for medulloblastomas or ependymomas require long-term surveillance and close monitoring for the development of endocrinopathies. No significant financial relationships to disclose.