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Background <p>Repetitive head impacts (RHI) are associated with an increased risk of neurodegenerative disease, most notably chronic traumatic encephalopathy (CTE). This study characterized neuropsychological profiles of RHI-exposed individuals compared to unexposed controls. To investigate whether cognitive dysfunction is linked to behavioural symptoms in RHI, we examined associations between executive functioning, social cognition and behavioural disinhibition.</p> Methods <p>We included RHI-exposed individuals (<i>N</i> = 72, 90.4% male, mean age 53.84 ± 12.45) and unexposed, cognitively healthy controls (<i>N</i> = 40, 82.5% male, mean age 54.55 ± 12.12) from the “Neurodegeneration: Traumatic brain injury as the Origin of Neuropathology” (NEwTON) study from Amsterdam UMC. Neurocognitive functioning was assessed through a comprehensive test battery covering episodic memory, attention and processing speed, executive functioning, visuospatial abilities, language and semantic memory, and social cognition. Behavioural disinhibition was measured in the RHI group using informant-based questionnaires (the positive items of the Frontal Behavioural Inventory (FBI) and the Neuropsychiatric Inventory (NPI)). Group differences in cognitive domains were assessed with analysis of covariance (ANCOVA) corrected for age, sex and education. The RHI-exposed group was evaluated for Traumatic Encephalopathy Syndrome (TES) criteria (No TES, Suggestive of CTE, Possible CTE, Probable CTE), TES subgroups were exploratively compared on cognitive performance. Associations between behavioural disinhibition and executive functioning or social cognition were assessed with regression analyses.</p> Results <p>RHI-exposed individuals performed worse on episodic memory (η<sup>2</sup> = 0.12, <i>p</i><sub><i>FDR</i></sub> ≤ .001), language and semantic memory (η<sup>2</sup> = 0.10, <i>p</i><sub><i>FDR</i></sub> = .001), executive functioning (η<sup>2</sup> = 0.04, <i>p</i><sub><i>FDR</i></sub> = .046), and social cognition (η<sup>2</sup> = 0.04, <i>p</i><sub><i>FDR</i></sub> = .040). No differences were found for visuospatial abilities (η<sup>2</sup> = 0.01, <i>p</i><sub><i>FDR</i></sub> = .221) and, although borderline significant, attention and processing speed (η<sup>2</sup> = 0.03, <i>p</i><sub><i>FDR</i></sub> = .074). Greater TES severity was associated with poorer performance on all cognitive domains. No significant associations were found between executive function or social cognition and behavioural disinhibition, as measured with the NPI and the FBI positive subscale (all <i>p</i> &gt; .05).</p> Conclusions <p>RHI-exposed individuals showed poorer cognitive performance across several domains (episodic memory, executive functioning, social cognition and language and semantic memory). We found no association between cognitive function and behavioural disinhibition. Further longitudinal studies employing neuroimaging and biomarker data are needed to disentangle the underlying pathology in populations at risk for CTE.</p>

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Neuropsychological profiles and behavioural correlates in individuals exposed to repetitive head impacts: findings from the NEwTON study

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  • 发表日期：

    2026年7月29日

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  • Suzie Kamps,
  • Esmé H. J. Habraken,
  • Suzan van Amerongen,
  • Dirk N. van Paassen,
  • Sterre C. M. de Boer,
  • Emma M. Coomans,
  • Sietske A. M. Sikkes,
  • Philip Scheltens,
  • Rik Ossenkoppele,
  • Everard G. B. Vijverberg

摘要

Background

Repetitive head impacts (RHI) are associated with an increased risk of neurodegenerative disease, most notably chronic traumatic encephalopathy (CTE). This study characterized neuropsychological profiles of RHI-exposed individuals compared to unexposed controls. To investigate whether cognitive dysfunction is linked to behavioural symptoms in RHI, we examined associations between executive functioning, social cognition and behavioural disinhibition.

Methods

We included RHI-exposed individuals (N = 72, 90.4% male, mean age 53.84 ± 12.45) and unexposed, cognitively healthy controls (N = 40, 82.5% male, mean age 54.55 ± 12.12) from the “Neurodegeneration: Traumatic brain injury as the Origin of Neuropathology” (NEwTON) study from Amsterdam UMC. Neurocognitive functioning was assessed through a comprehensive test battery covering episodic memory, attention and processing speed, executive functioning, visuospatial abilities, language and semantic memory, and social cognition. Behavioural disinhibition was measured in the RHI group using informant-based questionnaires (the positive items of the Frontal Behavioural Inventory (FBI) and the Neuropsychiatric Inventory (NPI)). Group differences in cognitive domains were assessed with analysis of covariance (ANCOVA) corrected for age, sex and education. The RHI-exposed group was evaluated for Traumatic Encephalopathy Syndrome (TES) criteria (No TES, Suggestive of CTE, Possible CTE, Probable CTE), TES subgroups were exploratively compared on cognitive performance. Associations between behavioural disinhibition and executive functioning or social cognition were assessed with regression analyses.

Results

RHI-exposed individuals performed worse on episodic memory (η2 = 0.12, pFDR ≤ .001), language and semantic memory (η2 = 0.10, pFDR = .001), executive functioning (η2 = 0.04, pFDR = .046), and social cognition (η2 = 0.04, pFDR = .040). No differences were found for visuospatial abilities (η2 = 0.01, pFDR = .221) and, although borderline significant, attention and processing speed (η2 = 0.03, pFDR = .074). Greater TES severity was associated with poorer performance on all cognitive domains. No significant associations were found between executive function or social cognition and behavioural disinhibition, as measured with the NPI and the FBI positive subscale (all p > .05).

Conclusions

RHI-exposed individuals showed poorer cognitive performance across several domains (episodic memory, executive functioning, social cognition and language and semantic memory). We found no association between cognitive function and behavioural disinhibition. Further longitudinal studies employing neuroimaging and biomarker data are needed to disentangle the underlying pathology in populations at risk for CTE.