Cortical and amygdalar Lewy body burden in Parkinson's disease patients with visual hallucinations

Papapetropoulos, Spiridon; McCorquodale, Donald; Gonzalez, Jocely; Jean-Gilles, Lucie; Mash, Deborah C.

doi:10.1016/j.parkreldis.2005.10.005

Cited by 88 publications

(70 citation statements)

References 14 publications

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“…Progressive atrophic changes have also been observed in the bilateral superior temporal gyri and frontal areas of PD patients with VH 14 . Prior pathological studies found an association between VH and a high density of Lewy bodies in temporal areas 10,23,26 . Our findings also suggest that VH may be a prodromal symptom of CI in PD patients.…”

Section: Discussionmentioning

confidence: 93%

Visual Hallucinations and Cognitive Impairment in Parkinson's Disease

Park

Kim

et al. 2013

Can. J. Neurol. Sci.

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Visual hallucination (VH) is the most common psychosis in Parkinson's disease (PD) 1,2 , and is present in 25-50% of PD patients 1,3 . Visual hallucination in PD patients is an important risk factor in terms of nursing home placement, poor quality of life, and mortality 4 . Neuroimaging studies suggested that brain regions involved in higher-order visual processing, ventral or dorsal pathways, were associated with VH in PD patients [5][6][7][8][9] . Pathologic study in Lewy body (LB) disease reported a striking association between the distribution of temporal lobe LB and VH 10 . Visual hallucination in PD seems to be associated with dysfunction of higher-order visual pathways, specifically, the occipitotemporal pathway (the ventral visual pathway). We investigated the regional cerebral glucose metabolism related to VH in PD patients to identify brain regions, focusing on the ventral visual pathway.Previous studies excluded patients with cognitive impairment (CI), an important VH-related nonmotor symptom in PD 8 , Compared to the patients with PDNVH, PD-VHNCI patients showed glucose hypometabolism in the inferior and middle temporal cortices, fusiform gyri, and frontal areas, suggesting the involvement of the ventral visual pathway. Compared to the patients with PDNVH, PD-VHCI patients showed glucose hypometabolism in the temporoparietal association cortices with scattered frontal areas. Conclusion: Dysfunction of ventral visual pathway involving the temporal lobe may play a key role in VH development in PD patients. The evolving distribution from the ventral visual pathway to more extensive posterior cortices in PD-VHCI patients suggests that VH may be a prodromal symptom occurring prior to CI in PD patients. Résultats : Les patients atteints de MP-HVNDC avaient un hypométabolisme du glucose dans le cortex temporal inférieur et moyen, la circonvolution occipito-temporale latérale et les zones frontales par rapport aux patients atteints de MP-NHV, ce qui indique que la voie visuelle ventrale pourrait être impliquée. Les patients atteints de MP-HVDC avaient un hypométabolisme du glucose dans les cortex associatifs temporo-pariétaux ainsi que dans des zones frontales dispersées par rapport aux patients atteints de MP-NHV. Conclusion : Une dysfonction de la voie visuelle ventrale impliquant le lobe temporal pourrait jouer un rôle clé dans l'apparition des HV chez les patients atteints de la MP. La distribution évoluant de la voie visuelle ventrale à des zones plus larges du cortex postérieur chez les patients atteints de MP-HVDC indique que les HV pourraient constituer un symptôme avant-coureur d'un DC chez les patients atteints de la MP.

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Section: Discussionmentioning

confidence: 93%

Visual Hallucinations and Cognitive Impairment in Parkinson's Disease

Park

Kim

et al. 2013

Can. J. Neurol. Sci.

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“…Thus rather than a simple sequela of dopamine dysfunction alone, VH appear intrinsic to PD in itself and have significant neuropathologic basis: there is now a significant corpus of data [27][28][29][30] which indicates that the strongest predictor of VH is the presence of neocortical alpha-synuclein aggregates (Lewy Bodies or Neurites) in the brains of patients with parkinsonism [31,32]. Indeed as a consequence it has been proposed that VH as a non-motor symptom of Parkinson's should be added as a supportive criteria to the operational clinical criteria for the diagnosis of PD [31].…”

Section: Introductionmentioning

confidence: 99%

Visual Hallucinations in PD and Lewy Body Dementias: Old and New Hypotheses

Onofrj

Taylor

Monaco

et al. 2013

Behavioural Neurology

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Abstract. Visual Hallucinations (VH) are a common non-motor symptom of Parkinson's Disease (PD) and the Lewy body dementias (LBD) of Parkinson's disease with dementia (PDD) and Dementia with Lewy Bodies (DLB). The origin of VH in PD and LBD is debated: earlier studies considered a number of different possible mechanisms underlying VH including visual disorders, Rapid Eye Movement (REM) Sleep Intrusions, dysfunctions of top down or bottom up visual pathways, and neurotransmitter imbalance. More recently newer hypotheses introduce, among the possible mechanisms of VH, the role of attention networks (ventral and dorsal) and of the Default Mode Network (DMN) a network that is inhibited during attentional tasks and becomes active during rest and self referential imagery. Persistent DMN activity during active tasks with dysfunctional imbalance of dorsal and ventral attentional networks represents a new hypothesis on the mechanism of VH. We review the different methods used to classify VH and discuss reports supporting or challenging the different hypothetical mechanisms of VH.

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“…A significant proportion of elderly people with dementia have combined degenerative disorders [12], and thus, the possibility of coexistence of other neurodegenerative conditions, including CBD [11], could not be excluded. However, the episodes of transient visual hallucinations in our patient suggested the presence of cortical LB pathology [1,13]. A voxel-based morphometric study concluded in LBD with dementia patients showed cerebral cortical atrophy in the occipital, frontal, and parietal lobes [1,14].…”

Section: Discussionmentioning

confidence: 53%