Lesions in different prefrontal sectors are associated with different types of acquired personality disturbances

Barrash, Joseph; Bruss, Joel; Anderson, Steven W.; Kuceyeski, Amy; Manzel, Kenneth; Tranel, Daniel; Boes, Aaron D.

doi:10.1016/j.cortex.2021.12.004

“… 129 , 149 Apathy has been attributed to lesions in the medial prefrontal cortex in humans, further highlighting the ACC’s role in regulating goal-directed behaviour. 130 …”

Section: The Prefrontal Cortex: Social Controlmentioning

confidence: 99%

A neuroanatomical and cognitive model of impaired social behaviour in frontotemporal dementia

Rouse,

Binney,

Patterson

et al. 2024

Brain

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Impaired social cognition is a core deficit in frontotemporal dementia (FTD). It is most commonly associated with the behavioural-variant of FTD, with atrophy of the orbitofrontal and ventromedial prefrontal cortex. Social cognitive changes are also common in semantic dementia, with atrophy centred on the anterior temporal lobes. The impairment of social behaviour in FTD has typically been attributed to damage to the orbitofrontal cortex and/or temporal poles and/or the uncinate fasciculus that connects them. However, the relative contributions of each region are unresolved. In this Review, we present a unified neurocognitive model of controlled social behaviour that not only explains the observed impairment of social behaviours in FTD, but also assimilates both consistent and potentially contradictory findings from other patient groups, comparative neurology and normative cognitive neuroscience. We propose that impaired social behaviour results from damage to two cognitively- and anatomically-distinct components. The first component is social-semantic knowledge, a part of the general semantic-conceptual system supported by the anterior temporal lobes bilaterally. The second component is social control, supported by the orbitofrontal cortex, medial frontal cortex and ventrolateral frontal cortex, which interacts with social-semantic knowledge to guide and shape social behaviour.

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“…131,132 Apathy has been attributed to lesions in the medial prefrontal cortex in humans, further highlighting the ACC's role in regulating goal-directed behaviour. 133 In contrast, circumscribed lesions to the dorsolateral prefrontal cortex do not cause the severe social disturbances associated with orbitofrontal/ventromedial damage but instead have been linked to problems with executive function. [133][134][135][136] Likewise, patients with post-stroke semantic aphasia following lateral prefrontal lesions have problems with controlling and regulating semantic knowledge, 21,[109][110][111][112]137 including semantic tasks involving emotion and abstract concepts.…”

Section: Comparative Neurology and Other Patient Groupsmentioning

confidence: 99%

“…133 In contrast, circumscribed lesions to the dorsolateral prefrontal cortex do not cause the severe social disturbances associated with orbitofrontal/ventromedial damage but instead have been linked to problems with executive function. [133][134][135][136] Likewise, patients with post-stroke semantic aphasia following lateral prefrontal lesions have problems with controlling and regulating semantic knowledge, 21,[109][110][111][112]137 including semantic tasks involving emotion and abstract concepts. In formal metaanalyses of healthy participant fMRI studies, these same semantic control regions are engaged by social control tasks.…”

Section: Comparative Neurology and Other Patient Groupsmentioning

confidence: 99%

A neuroanatomical and cognitive model of impaired social behaviour in frontotemporal dementia

Rouse¹,

Binney²,

Patterson³

et al. 2023

Preprint

View full text Add to dashboard Cite

Impaired social cognition is a core deficit of frontotemporal dementia (FTD). It is most commonly associated with the behavioural-variant of FTD, with atrophy of the orbitofrontal and ventromedial prefrontal cortex. However, social cognitive changes are also common in semantic dementia, with atrophy centred on the anterior temporal lobes. The impairment of social behaviour in FTD has typically been attributed to damage to the orbitofrontal cortex and/or temporal poles and/or the uncinate fasciculus that connects them. However, the relative contribution of each region is unresolved. In this review, we present a unified neurocognitive model of controlled social behaviour that not only explains the observed impairment of social behaviours in FTD, but also assimilates findings from other patient groups, comparative neurology, and normative cognitive neuroscience. We propose that impaired social behaviour results from damage to two cognitively- and anatomically-distinct components. The first component is social-semantic knowledge, supported by the anterior temporal lobes bilaterally. The second component is social control, supported by the orbitofrontal cortex, medial frontal cortex and ventrolateral frontal cortex, which interact with social-semantic knowledge to guide and shape social behaviour.

show abstract

“…131,132 Apathy has been attributed to lesions in the medial prefrontal cortex in humans, further highlighting the ACC's role in regulating goal-directed behaviour. 133 In contrast, circumscribed lesions to the dorsolateral prefrontal cortex do not cause the severe social disturbances associated with orbitofrontal/ventromedial damage but instead have been linked to problems with executive function. [133][134][135][136] Likewise, patients with post-stroke semantic aphasia following lateral prefrontal lesions have problems with controlling and regulating semantic knowledge, 21,[109][110][111][112]137 including semantic tasks involving emotion and abstract concepts.…”

Section: Comparative Neurology and Other Patient Groupsmentioning

confidence: 99%

“…133 In contrast, circumscribed lesions to the dorsolateral prefrontal cortex do not cause the severe social disturbances associated with orbitofrontal/ventromedial damage but instead have been linked to problems with executive function. [133][134][135][136] Likewise, patients with post-stroke semantic aphasia following lateral prefrontal lesions have problems with controlling and regulating semantic knowledge, 21,[109][110][111][112]137 including semantic tasks involving emotion and abstract concepts. In formal metaanalyses of healthy participant fMRI studies, these same semantic control regions are engaged by social control tasks.…”

Section: Comparative Neurology and Other Patient Groupsmentioning

confidence: 99%

A neuroanatomical and cognitive model of impaired social behaviour in frontotemporal dementia

Rouse¹,

Binney²,

Patterson³

et al. 2023

Preprint

View full text Add to dashboard Cite

Impaired social cognition is a core deficit of frontotemporal dementia (FTD). It is most commonly associated with the behavioural-variant of FTD, with atrophy of the orbitofrontal and ventromedial prefrontal cortex. However, social cognitive changes are also common in semantic dementia, with atrophy centred on the anterior temporal lobes. The impairment of social behaviour in FTD has typically been attributed to damage to the orbitofrontal cortex and/or temporal poles and/or the uncinate fasciculus that connects them. However, the relative contribution of each region is unresolved. In this review, we present a unified neurocognitive model of controlled social behaviour that not only explains the observed impairment of social behaviours in FTD, but also assimilates findings from other patient groups, comparative neurology, and normative cognitive neuroscience. We propose that impaired social behaviour results from damage to two cognitively- and anatomically-distinct components. The first component is social-semantic knowledge, supported by the anterior temporal lobes bilaterally. The second component is social control, supported by the orbitofrontal cortex, medial frontal cortex and ventrolateral frontal cortex, which interact with social-semantic knowledge to guide and shape social behaviour.

show abstract

Lesions in different prefrontal sectors are associated with different types of acquired personality disturbances

Cited by 9 publications

References 101 publications

A neuroanatomical and cognitive model of impaired social behaviour in frontotemporal dementia

A neuroanatomical and cognitive model of impaired social behaviour in frontotemporal dementia

A neuroanatomical and cognitive model of impaired social behaviour in frontotemporal dementia

A neuroanatomical and cognitive model of impaired social behaviour in frontotemporal dementia

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