Anatomical and neurochemical bases of theory of mind in de novo Parkinson's Disease

Orso, Beatrice; Arnaldi, Dario; Famà, Francesco; Girtler, Nicola; Brugnolo, Andrea; Doglione, Elisa; Filippi, Laura; Massa, Federico; Peira, Enrico; Bauckneht, Matteo; Morbelli, Silvia; Nobili, Flavio; Pardini, Matteo

doi:10.1016/j.cortex.2020.06.012

Cited by 24 publications

(24 citation statements)

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“…Theory of mind, for example, is considered to be mediated by a vast cortical network focused on the prefrontal cortex in different conditions including PD, and it has been shown to be also associated with SE deafferentation in drug-naive PD patients. 11,35 Moreover, the observation of the mediatory role of thalamic metabolism in the association between SE function and prefrontal cortex activity is in line with the known anatomical distribution of the raphethalamic SE fibers and with the spatial distribution of the thalamic projections to the cortex. 36 Indeed, SE afferents to the thalamus mainly target the midline and intralaminar higher-order nuclei, 37,38 which in turn are known to present with rich cortical projections, especially to the more anterior and medial cortical regions.…”

Section: Correlation Between Thalamic [ 123 I]fp-cit Sbr Thalamic Metabolism and Cortical Metabolismsupporting

confidence: 63%

Dopaminergic and Serotonergic Degeneration and Cortical [¹⁸F]Fluorodeoxyglucose Positron Emission Tomography in De Novo Parkinson's Disease

et al. 2021

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A BS TRACT: Background: Degeneration of the nigrostriatal dopaminergic (DA) and the raphe-thalamic serotonergic (SE) systems is among the earliest changes observed in Parkinson's disease (PD). The consequences of those changes on brain metabolism, especially regarding their impact on the cortex, are poorly understood. Objectives: Using multi-tracer molecular imaging, we assessed in a cohort of drug-naive PD patients the association between cortical metabolism and DA and SE system deafferentation of either striatum or thalamus, and we explored whether this association was mediated by either striatum or thalamus metabolism. Methods: We recruited 96 drug-naive PD patients (aged 71.9 AE 7.5 years) who underwent [ 123 I]ioflupane single-photon emission computed tomography ([ 123 I] FP-CIT-SPECT) and brain [ 18 F]fluorodeoxyglucose positron emission tomography ([ 18 F]FDG-PET). We used a voxel-wise analysis of [ 18 F]FDG-PET images to correlate regional metabolism with striatal DA and thalamic SE innervation as assessed using [ 123 I]FP-CIT-SPECT.Results: We found that [ 123 I]FP-CIT specific to nondisplaceable binding ratio (SBR) and glucose metabolism positively correlated with one another in the deep gray matter (thalamus: P = 0.001, r = 0.541; caudate P = 0.001, r = 0.331; putamen P = 0.001, r = 0.423). We then observed a direct correlation between temporoparietal metabolism and caudate DA innervation, as well as a direct correlation between prefrontal metabolism and thalamus SE innervation. The effect of caudate [ 123 I]FP-CIT SBR values on temporoparietal metabolism was mediated by caudate metabolic values (percentage mediated: 89%, P-value = 0.008), and the effect of thalamus [ 123 I]FP-CIT SBR values on prefrontal metabolism was fully mediated by thalamus metabolic values (P < 0.001). Conclusions: These data suggest that the impact of deep gray matter monoaminergic deafferentation on cortical function is mediated by striatal and thalamic metabolism in drug-naive PD.

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Section: Correlation Between Thalamic [ 123 I]fp-cit Sbr Thalamic Metabolism and Cortical Metabolismsupporting

confidence: 63%

Dopaminergic and Serotonergic Degeneration and Cortical [¹⁸F]Fluorodeoxyglucose Positron Emission Tomography in De Novo Parkinson's Disease

et al. 2021

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“…This technique was also used as a proxy marker of serotoninergic impairment revealing a negative correlation with thalamic specific binding ratio. Cholinergic function was indirectly measured by quantitative electroencephalography (posterior and anterior Theta/Alpha power ratio as a proxy of cholinergic tone) [51]. These findings suggest a lack of dopamine involvement in ToM.…”

Section: Anatomical and Functional Correlates Of Theory Of Mind In Parkinson's Diseasementioning

confidence: 89%

“…These findings suggest a lack of dopamine involvement in ToM. However, 123 I-FP-CIT-SPECT has limited spatial resolution and the authors only assessed affective ToM [51].…”

Section: Anatomical and Functional Correlates Of Theory Of Mind In Parkinson's Diseasementioning

confidence: 94%

“…The dopamine depletion characterizing PD impacts the basal ganglia networks involving not only the motor circuit [44] but also the associative and the limbic circuits [45] (see Figure 1). Few neuroimaging studies [49][50][51] (see Table 1) using different methodological approaches have searched for anatomical correlates of ToM performance in PD. Grey matter voxel-based morphometry analysis demonstrated a correlation between cognitive ToM performance, and left precentral and postcentral gyrus, anterior cingulate gyrus, middle In this regard, it has been hypothesized that the progressive loss of striatal denervation in PD could initially lead to dysfunction of the associative circuit and therefore of cognitive ToM, associated with other symptoms such as executive dysfunction.…”

Section: Anatomical and Functional Correlates Of Theory Of Mind In Parkinson's Diseasementioning

confidence: 99%

“…Few neuroimaging studies [49][50][51] (see Table 1) using different methodological approaches have searched for anatomical correlates of ToM performance in PD. Grey matter voxel-based morphometry analysis demonstrated a correlation between cognitive ToM performance, and left precentral and postcentral gyrus, anterior cingulate gyrus, middle frontal gyrus and inferior frontal gyrus volumes [50].…”

Section: Anatomical and Functional Correlates Of Theory Of Mind In Parkinson's Diseasementioning

confidence: 99%

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What Do We Know about Theory of Mind Impairment in Parkinson’s Disease?

Trompeta

Rodríguez

Gasca-Salas

2021

Behavioral Sciences

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Theory of mind (ToM) is a social cognitive skill that involves the ability to attribute mental states to self and others (what they think (cognitive ToM) and feel (affective ToM)). We aim to provide an overview of previous knowledge of ToM in Parkinson’s disease (PD). In the last few years more attention has been paid to the study of this construct as a non-motor manifestation of PD. In advanced stages, both components of ToM (cognitive and affective) are commonly impaired, although in early PD results remain controversial. Executive dysfunction correlates with ToM deficits and other cognitive domains such as language and visuospatial function have also been related to ToM. Recent studies have demonstrated that PD patients with mild cognitive impairment show ToM deficits more frequently in comparison with cognitively normal PD patients. In addition to the heterogeneity of ToM tests administered in different studies, depression and dopaminergic medication may also be acting as confounding factors, but there are still insufficient data to support this. Neuroimaging studies conducted to understand the underlying networks of cognitive and affective ToM deficits in PD are lacking. The study of ToM deficit in PD continues to be important, as this may worsen quality of life and favor social stigma. Future studies should be considered, including assessment of the patients’ cognitive state, associated mood disorders, and the role of dopaminergic deficit.

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Subthalamic Nucleus Stimulation Modulates Cognitive Theory of Mind in Parkinson's Disease

Xiao,

Lang,

et al. 2024

Movement Disorders

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BackgroundTheory of mind (ToM), the ability to infer others' mental state, is essential for social interaction among human beings. It has been widely reported that both cognitive (inference of knowledge) and affective (inference of emotion) components of ToM are disrupted in Parkinson's disease (PD). Previous studies usually focused on the involvement of the prefrontal cortex.ObjectiveThis study investigated the causal role of the subthalamic nucleus (STN), a key hub of the fronto‐basal ganglia loops, in ToM.MethodsThirty‐four patients with idiopathic PD (15 women, aged 62.2 ± 8.3 years) completed a Yoni task with deep brain stimulation (DBS) ON and OFF. The Yoni task was designed to separate the cognitive and affective components of ToM. Volumes of tissue activated (VTA) were computed for three subregions of the STN.ResultsDBS showed insignificant effects on ToM inference costs at the group level, which may be due to the large interindividual variability. The associative VTA correlated with the cognitive inference cost change but not the affective inference cost change. Patients with greater associative STN stimulation infer more slowly on cognitive ToM. Stimulating associative STN can adversely affect cognitive ToM in PD patients, especially in patients with a wide range of stimulation (≥0.157) or cognitive decline (Montreal Cognitive Assessment < 26).ConclusionsThe associative STN plays a causal role in cognitive ToM in patients with PD. However, stimulating the associative STN likely impairs cognitive ToM and potentially leads to social interaction deficits in PD. © 2024 International Parkinson and Movement Disorder Society.

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Anatomical and neurochemical bases of theory of mind in de novo Parkinson's Disease

Cited by 24 publications

References 71 publications

Dopaminergic and Serotonergic Degeneration and Cortical [¹⁸F]Fluorodeoxyglucose Positron Emission Tomography in De Novo Parkinson's Disease

Dopaminergic and Serotonergic Degeneration and Cortical [¹⁸F]Fluorodeoxyglucose Positron Emission Tomography in De Novo Parkinson's Disease

What Do We Know about Theory of Mind Impairment in Parkinson’s Disease?

Subthalamic Nucleus Stimulation Modulates Cognitive Theory of Mind in Parkinson's Disease

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Anatomical and neurochemical bases of theory of mind in de novo Parkinson's Disease

Cited by 24 publications

References 71 publications

Dopaminergic and Serotonergic Degeneration and Cortical [18F]Fluorodeoxyglucose Positron Emission Tomography in De Novo Parkinson's Disease

Dopaminergic and Serotonergic Degeneration and Cortical [18F]Fluorodeoxyglucose Positron Emission Tomography in De Novo Parkinson's Disease

What Do We Know about Theory of Mind Impairment in Parkinson’s Disease?

Subthalamic Nucleus Stimulation Modulates Cognitive Theory of Mind in Parkinson's Disease

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Product

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Dopaminergic and Serotonergic Degeneration and Cortical [¹⁸F]Fluorodeoxyglucose Positron Emission Tomography in De Novo Parkinson's Disease

Dopaminergic and Serotonergic Degeneration and Cortical [¹⁸F]Fluorodeoxyglucose Positron Emission Tomography in De Novo Parkinson's Disease