Neurocognitive Impairment in Non-Central Nervous System Cancer Survivors: Exploratory Study of Attention and Executive Functioning Assessments Using Event-Related Potentials

Cancer and its treatments entail a profound inflammatory response of the central nervous system (CNS). This intense neurotoxic process can lead to significant neurocognitive impairment even in non-CNS cancers. Few studies have examined this domain, and data available is based on limited designs using neuropsychological assessments comprising self-report or traditional testing batteries that capture basic response data. Here, we leverage cognitive electrophysiology, specifically Event-Related Potentials (ERPs), to examine and delineate neurocognitive impairments in non-CNS cancer survivors. Eleven survivors, who were on average 4.6 years in remission from head and neck cancer and 10 matched healthy controls underwent standardized cognitive and emotional "Go-Nogo" paradigms concomitant to EEG recording. Significant differences in amplitude morphology in the very early ERP components (C1, N1, P1) and middle ERP component (N2), were apparent between non-CNS cancer survivors and controls. Later ERP components (P3, N4) did not show amplitude differences. Non-CNS cancer survivors yielded faster latencies in the early components for pain-related stimuli during the emotional paradigm, albeit tended to yield slower ERP latencies overall across both experiments. These findings suggest that early gating and inhibitory control are dysregulated in non-CNS cancer survivors, which can impact executive functioning and cognitive processing involved in everyday activities for many years post-treatment. The findings do not fully align with ERP morphologies associated with neurocognitive impairment in degenerative conditions (such as dementia and Alzheimer's disease), affecting later-stage ERP components. Our initial results suggest that (1) cognitive impairments in cancer survivors do not follow a degenerative trajectory, (2) rather are in line with "lesion" related damage (such as stroke, epilepsy), and as such, (3) have the potential for treatments involving neurocognitive plasticity.