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Background The numbers of pediatric brain tumor survivors are increasing due to improved treatment protocols and multimodal treatments. Many survivors have neurocognitive sequelae, especially after radiotherapy. Neuropsychologic assessment is therefore essential to interpret clinical outcome, evaluate treatments protocol, and implement rehabilitation interventions. The overall aim of this study was to describe neurocognitive functions before and after radiotherapy. We also aimed to explore potential confounding risk factors that could affect the interpretation of radiotherapy-induced neurocognitive decline. Methods Fifty pediatric brain tumor survivors who had received radiotherapy (five years or more ago) were included. Clinical characteristics, potential confounding risk factors, radiotherapy plans, and neurocognitive functions on intelligence quotient (IQ) and neuropsychologic measurements were analyzed before and after radiotherapy. Results Neurocognitive functions were affected before radiotherapy and were progressively aggravated thereafter. The last neuropsychologic assessment after radiotherapy varied between two and 139 months. Nineteen patients were tested five years after radiotherapy, and 90% of them performed ≥1 S.D. below the normative mean on IQ measurements. Several potential confounding risk factors including those induced by radiotherapy were associated with lower performance on perceptual function, working memory, and processing speed. Longer time after radiotherapy was particularly associated with lower performance on working memory and processing speed. Importantly, the neuropsychologic assessments revealed more comprehensive problems than could be inferred from IQ measurements alone. Conclusions Our study underpins the importance of systematic and structured neuropsychologic assessment before and after radiotherapy. The timing of the assessment is important, and potential confounding risk factors need to be identified to better evaluate radiotherapy-induced neurocognitive decline.

Background: Children with brain tumors are at high risk of neurocognitive decline after radiotherapy (RT). However, there is a lack of studies on how RT doses to organs at risk (OARs) impacts neurocognition. The aim of this study was to examine dose-risk relationships for mean RT dose to different brain structures important for neurocognitive networks. We explored previously established OARs and potentially new OARs.

Methods: A sample of 44 pediatric brain tumor survivors who had received proton and/or photon RT were included. Correlations between mean RT doses to OARs and IQ were analyzed. Previously established OARs were cochleae, optic chiasm, optic nerve, pituitary gland, hypothalamus, hippocampus and pons. Potential new OARs for RT-induced neurocognitive decline were cerebellum, vermis and thalamus.

Results: Mean RT dose to different OARs correlated with several IQ subtests. Higher mean RT dose to cochleae, optic nerve, cerebellum, vermis and pons was correlated with lower performance on particularly full-scale IQ (FIQ), Perceptual Reasoning (PRI), Working Memory (WMI) and Processing Speed Index (PSI). Higher mean RT dose to hippocampus correlated with lower performance on processing speed and working memory. For those receiving whole brain RT (WBRT), higher mean RT dose to the pituitary gland correlated with lower performance on working memory.

Conclusion: A high dose-risk correlation was found between IQ subtests and mean RT dose in established and potential new OARs. Thus, in the lack of validated dose constraints for vulnerable brain structures, a parsimonious approach in RT planning should be considered to preserve neurocognitive networks.

Background: Long-term follow up of neurocognitive late effects in paediatric brain tumour survivors (PBTS) is essential, particularly after radiotherapy (RT). Processing speed impairments are among the most prevalent late effects, yet their relation to underlying oculomotor control and visual attention remains unclear. Eye movement metrics reflect the integrity of neural systems supporting attention, visual processing, and executive control, and may serve as sensitive potential biomarkers of neurocognitive impairment, complementing neuropsychological assessment. To explore this, we employed a pro–antisaccade task to examine fundamental oculomotor and executive control processes. The primary aim was to assess whether PBTS showed impaired pro-antisaccade performance compared with age-matched controls. Within the PBTS group, we also examined associations between saccadic latency, processing speed, and RT doses to brain structures important for visual and neurocognitive networks.

Methods: This long-term case-control study included 21 PBTS treated with proton and/or photon RT 8-20 years earlier and 50 age-matched controls. PBTS were aged 15-34 years (mean 23; 12 males and 9 females), and controls were aged 18-34 years (mean 26; 25 males, 24 females, and one non-binary participant). Eye movements were measured with an eye-tracker, and participants were instructed to look either towards an upcoming target (pro-saccades) or away from it (anti-saccades). Between-group differences were analysed using independent t-tests (Cohen´s d effect sizes) and modified t-tests for single samples to identify individual impairments. Within the PBTS group, we further explored associations between saccadic latency, processing speed, and mean RT doses to established and potential new organs at risk.

Results: PBTS demonstrated significantly longer pro- and antisaccade latencies than controls, with effect sizes ranging from small to large and the greatest impairments in those who received whole-brain RT. Modified t-tests revealed that nearly half of the PBTS performed in the impaired range on the anti-saccade task relative to the control reference group. Within the PBTS group, longer saccadic latency correlated with slower processing speed and with higher mean RT doses to the optic nerves and pons.

Conclusion: PBTS demonstrated long-term impairments in pro- and antisaccade performance many years after RT, with longer saccadic latencies linked to higher RT doses and slower processing speed. These patterns suggest lasting disruptions in visual attention, oculomotor, and executive networks. Eye-tracking offers a sensitive measure for detecting subtle neurocognitive late effects that can complement neuropsychological assessment and may help inform targeted rehabilitation strategies. 

Background: Pediatric brain tumor survivors (PBTS) often experience fatigue and slowed processing speed after radiotherapy (RT). White matter loss and network alterations have been reported, but associations between pupil dilation, fatigue, processing speed and RT doses to organs at risk (OARs) remain unclear. Pupillometry reflects autonomic nervous system activity and may serve as a biomarker of arousal and cognitive control. This study assessed pupil dilation and fatigue in PBTS, and associations with processing speed and RT doses to OARs in PBTS. 

Methods: Twenty-one PBTS (mean age = 23 y), assessed 8–20 y after RT, and 50 age-matched controls (mean age = 26 y) completed a visual attention task with eye tracking. Pupil dilation was measured in response to unexpected auditory cues and during an anti-saccade task. Group differences were analyzed with independent t-tests (Cohen´s d). Associations between RT doses, pupil dilation, fatigue and processing speed were examined within the PBTS group. 

Results: PBTS showed greater pupil dilation to auditory cues and higher fatigue than controls (medium to large effects). Within PBTS, altered pupil dilation during anti-saccades correlated with higher fatigue and higher RT doses to the cerebellum and vermis. Fatigue was associated with slower processing speed and higher RT doses to the frontal lobes and optic nerves. Processing speed was strongly associated with higher RT doses to several OARs.

Conclusion: PBTS showed altered arousal regulation, fatigue, and slower processing speed associated with RT dose. Pupillometry and fatigue measures can complement neuropsychological assessment and may guide targeted rehabilitation.