Metabolic Alterations in Patients With Parkinson Disease and Visual Hallucinations

Boecker, Henning; Ceballos-Baumann, Andrés; Volk, Dominik; Conrad, Bastian; Förstl, Hans; Häussermann, Peter

doi:10.1001/archneur.64.7.984

Cited by 116 publications

(99 citation statements)

References 33 publications

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“…Visual association cortex hypometabolism as a herald of dementia is interesting in view of the prominence of visual hallucinations in more advanced PD and PDD. Prior metabolic imaging studies suggest that visual hallucinations are associated with hypometabolism of visual association cortices (24). Visual hallucinations are by far the most common form of hallucination in PD, and incidence of visual hallucinations in PD may herald progression of dementia (25).…”

Section: Discussionmentioning

confidence: 99%

Cerebral Glucose Metabolic Features of Parkinson Disease and Incident Dementia: Longitudinal Study

et al. 2011

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Longitudinal studies in nondemented Parkinson disease (PD) subjects offer an opportunity to study the earliest regional cerebral subcortical and cortical metabolic changes underlying incident dementia in this disorder. Methods: Twenty-three PD subjects without dementia (Hoehn and Yahr stages I-III; age, 61.8 6 9.7 y; Mini-Mental State Examination, 28.0 6 1.4) and 27 controls (age, 59.8 6 11.5 y) underwent 18 F-FDG PET at study entry. PD subjects underwent yearly clinical assessment to determine conversion to dementia. The mean duration of follow-up was 3.9 6 1.2 y (range, 2.0-6.8 y). Follow-up 18 F-FDG PET was available in a subset of subjects at 2 or more years. Both volume-of-interest and 3-dimensional stereotactic surface projection (3D-SSP) analyses were performed. Results: Six subjects became demented (PDD), with a mean time of 3.8 6 1.7 y (range, 1.9-6.0 y) to development of dementia. Mean duration of disease before onset of dementia was 9.7 6 4.2 y (range, 3.1-14 y). There were significant metabolic reductions in the occipital (211.8% vs. controls, F (2,22) 5 7.0, P 5 0.002) and posterior cingulate (212.1% vs. controls, F (2,22) 5 5.2, P 5 0.009) cortices in PDD subjects at baseline, before diagnosis of dementia, compared with controls. Metabolism was most diminished in the visual association cortex (Brodmann area [BA] 18; 220.0% vs. control, F (2,22) 5 8.45, P 5 0.0007) of PDD subjects. There was mild hypometabolism in the caudate nucleus (28.4% vs. control, F (2,22) 5 3.2, P , 0.05). There was no significant hypometabolism in the temporal or frontal lobes. PD subjects who did not become demented (non-PDD), compared with controls, had reduced cerebral metabolism in the primary occipital cortex (BA 17) that was revealed only by 3D-SSP analysis. Follow-up scans in 5 PDD subjects at 2 y after study entry demonstrated a significant interval within-subject change in the thalamus (211.4%), posterior cingulate (29%), occipital (27%), parietal (27%), and frontal cortices (27%) and mild reductions in the temporal cortex (25%) and hippocampus (23%), compared with study entry scans. Conclusion: Incident dementia in idiopathic PD is heralded by decreased metabolism in the visual association (BA 18) and posterior cingulate cortices, with mild involvement also of the caudate nucleus. Two-year follow-up data from 5 PDD converters show that progression to dementia is associated with mixed subcortical and cortical changes that involve the mesiofrontal lobes also. These findings provide insights into early metabolic features of parkinsonian dementia.

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Section: Discussionmentioning

confidence: 99%

Cerebral Glucose Metabolic Features of Parkinson Disease and Incident Dementia: Longitudinal Study

et al. 2011

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“…Pathological studies have reported increased Lewy bodies within visual areas of the temporal cortex in PD patients with visual hallucinations compared with nonhallucinators [56,57]. Imaging studies have also shown selective changes within these regions [58,59]. There is some evidence that dysfunction of 5HT2A receptors within the visual pathways may be associated with the development of visual hallucinations in PD patients [60].…”

Section: Psychosis In Pdmentioning

confidence: 99%

Treatment of Cognitive, Psychiatric, and Affective Disorders Associated with Parkinson's Disease

Connolly

Fox

2014

Neurotherapeutics

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Neuropsychiatric symptoms are common in Parkinson's disease (PD) and add significantly to the burden of disease. These symptoms are most commonly part of the disease spectrum owing to pathological changes within relevant brain regions. Neuropsychiatric problems include disorders of cognition, ranging from mild cognitive impairment to dementia, psychotic symptoms, including, most commonly, well-formed visual hallucinations and paranoid delusions, and mood disorders, such as depression and anxiety. The other common cause of neuropsychiatric problem is secondary to use of dopaminergic drugs. Some PD patients may develop behavioral disorders, including impulse control disorders (ICDs) and addictive symptoms. Psychosis can be due to a mixture of underlying pathology, with triggering or worsening of symptoms with changes to PD medications. Currently, management of these disorders primarily uses therapies developed for general psychiatry and cognitive neurology, rather than specifically for PD. However, significant adverse effects, such as worsening of the motor symptoms of PD, can limit use of some drug therapies. Identification of drug-induced symptoms, such as ICDs, enables withdrawal of the offending drug as the principal management strategy. Research is ongoing in an effort to develop more specific therapies for PD-related neuropsychiatric symptoms.

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“…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 .…”

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confidence: 99%

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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Metabolic Alterations in Patients With Parkinson Disease and Visual Hallucinations

Cited by 116 publications

References 33 publications

Cerebral Glucose Metabolic Features of Parkinson Disease and Incident Dementia: Longitudinal Study

Cerebral Glucose Metabolic Features of Parkinson Disease and Incident Dementia: Longitudinal Study

Treatment of Cognitive, Psychiatric, and Affective Disorders Associated with Parkinson's Disease

Visual Hallucinations and Cognitive Impairment in Parkinson's Disease

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