The contribution of executive control dysfunction to freezing of gait in Parkinson’s disease

Bayot, Madli; Dujardin, Kathy; Gérard, Morgane; Braquet, Aurore; Tard, Céline; Betrouni, Nacim; Defebvre, Luc; Delval, Arnaud

doi:10.1016/j.clinph.2023.05.010

Cited by 2 publications

(1 citation statement)

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“…Visual impairment in PD, along with a heterogenous profile of CI, contributed to the development of FOG that was due to impairment of executive control [ 261 ] and decreased contrast sensitivity related to volume decrease in the cuneus, the lingual and posterior cingulate gyrus, the superior parietal lobe and middle frontal gyrus, and the central areas of the dorsal and ventral visual information system [ 262 ]. FOG converters had reduced regional homogeneity in the bilateral medial superior frontal gyrus, which was negatively correlated with the postural instability and gait difficulty score [ 263 ].…”

Section: Neuroimaging Findings In CI In Pd (See Supplement ...mentioning

confidence: 99%

Pathobiology of Cognitive Impairment in Parkinson Disease: Challenges and Outlooks

Jellinger

2023

IJMS

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Cognitive impairment (CI) is a characteristic non-motor feature of Parkinson disease (PD) that poses a severe burden on the patients and caregivers, yet relatively little is known about its pathobiology. Cognitive deficits are evident throughout the course of PD, with around 25% of subtle cognitive decline and mild CI (MCI) at the time of diagnosis and up to 83% of patients developing dementia after 20 years. The heterogeneity of cognitive phenotypes suggests that a common neuropathological process, characterized by progressive degeneration of the dopaminergic striatonigral system and of many other neuronal systems, results not only in structural deficits but also extensive changes of functional neuronal network activities and neurotransmitter dysfunctions. Modern neuroimaging studies revealed multilocular cortical and subcortical atrophies and alterations in intrinsic neuronal connectivities. The decreased functional connectivity (FC) of the default mode network (DMN) in the bilateral prefrontal cortex is affected already before the development of clinical CI and in the absence of structural changes. Longitudinal cognitive decline is associated with frontostriatal and limbic affections, white matter microlesions and changes between multiple functional neuronal networks, including thalamo-insular, frontoparietal and attention networks, the cholinergic forebrain and the noradrenergic system. Superimposed Alzheimer-related (and other concomitant) pathologies due to interactions between α-synuclein, tau-protein and β-amyloid contribute to dementia pathogenesis in both PD and dementia with Lewy bodies (DLB). To further elucidate the interaction of the pathomechanisms responsible for CI in PD, well-designed longitudinal clinico-pathological studies are warranted that are supported by fluid and sophisticated imaging biomarkers as a basis for better early diagnosis and future disease-modifying therapies.

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Section: Neuroimaging Findings In CI In Pd (See Supplement ...mentioning

confidence: 99%