Correlation of visual hallucinations with occipital rCBF changes by donepezil in DLB

Mori, Takaaki; Ikeda, Manabu; Fukuhara, Ryuji; Nestor, Peter J.; Tanabe, Hirotaka

doi:10.1212/01.wnl.0000203114.03976.b0

Cited by 67 publications

(64 citation statements)

References 12 publications

(9 reference statements)

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“…The metabolic or perfusion pattern in response to ChEI therapy seems to be different between PDD and DLB. Mori et al (30) found that increased perfusion after ChEI treatment in patients with DLB was localized in the occipital area, whereas a previous study by Ceravolo et al (13) and our current data showed that increased perfusion or metabolism in patients with PDD was observed in the frontal or parietal areas. Controversy still exists as to whether PDD and DLB are indeed the same disease entities.…”

Section: Discussioncontrasting

confidence: 78%

Changes in Cerebral Glucose Metabolism in Patients with Parkinson Disease with Dementia After Cholinesterase Inhibitor Therapy

Lee¹,

Yong²,

An³

2008

J Nucl Med

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We investigated changes in cerebral glucose metabolism after cholinesterase inhibitor (ChEI) therapy in patients with Parkinson disease dementia (PDD) to determine whether cognitive improvements would be reflected in changes of cerebral metabolic patterns, thus offering insight into the neural substrate of cognitive dysfunction in patients with PDD. Methods: We performed a serial PET study before (baseline) and after ChEI therapy on 10 patients with PDD, using statistical parametric mapping. Additionally, covariance analysis was performed to extract regions in which increased change in regional cerebral metabolism correlated significantly with increased Mini-Mental State Examination scores. Results: The statistical parametric mapping analysis indicated that significantly increased cerebral metabolism after ChEI therapy, compared with at baseline, was most evident in the left angular gyrus extending to the supramarginal area and left superior and middle frontal gyri. Additionally, cerebral metabolism was significantly increased in the right superior frontal and left middle orbitofrontal gyri. In contrast, the right fusiform gyrus showed significantly decreased metabolism after ChEI, compared with at baseline. In the correlation analysis, improvements in Mini-Mental State Examination scores after ChEI treatment were significantly associated with increased cerebral metabolism in the left supramarginal, orbitofrontal, and cingulate areas. Conclusion: Our data suggest that prefrontal and parietal association areas may be relevant structures for the pharmacologic response to ChEI in patients with PDD. Cogni tive dysfunction occurs in 25%230% of patients with Parkinson disease (PD); this prevalence is 6 times greater than that among the population in general (1-3). The key feature of dementia in PD is executive dysfunction; thus, patients with PD dementia (PDD) have difficulty in tasks that require generation of mental sets, planning, and cognitive sequencing. Additionally, patients with PDD often exhibited worse performance in visuospatial tasks and memory impairment in free recalls, which improved significantly with external cues, suggesting that these patients still had the ability to store new information (3,4).Although the exact pathophysiologic substrate in PDD is still controversial, progressive involvement of subcortical and cortical structures, by Lewy-type pathology or Alzheimer disease-like histologic changes, has been suggested (5,6). Regarding neurochemical substrates in PDD, recent pathologic and functional studies have suggested that cholinergic deficits were significantly correlated with cognitive dysfunction in patients with PD (7-9). Various kinds of cholinesterase inhibitors (ChEIs), including rivastigmine (10), donepezil (11), and galantamine (12), have proven to be effective in improving cognitive function in patients with PDD, supporting this theory.Only 1 study, which used SPECT, reported that ChEIs significantly increased cerebral perfusion in frontal and cingulate areas (13). However, images ob...

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Section: Discussioncontrasting

confidence: 78%

Changes in Cerebral Glucose Metabolism in Patients with Parkinson Disease with Dementia After Cholinesterase Inhibitor Therapy

Lee¹,

Yong²,

An³

2008

J Nucl Med

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“…Improved ways of measuring hallucinations will make it easier to track treatment response, while better understandings of the mechanisms which underlie hallucinations may open up new treatment avenues. In this regard, neuroimaging, neurophysiological and neuropathological/neurochemical studies have begun to provide powerful insights in the etiology of visual hallucinations [67][68][69][70][71]. For example, postmortem and neuroimaging studies in LBD patients have found that alterations in both nicotinic and muscarinic receptors are associated with visual hallucinations [45,71].…”

Section: Future Perspectivementioning

confidence: 99%

Advances In the Treatment of Visual Hallucinations In Neurodegenerative Diseases

Collerton

2013

Future Neurol.

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Treatment of visual hallucinations in neurodegenerative disorders is not well advanced. The complexity of underlying mechanisms presents a number of potential avenues for developing treatments, but also suggests that any single one may be of limited efficacy. Reducing medication, with the careful introduction of antidementia medication if needed, is the mainstay of current management. Antipsychotic medication leads to excessive morbidity and mortality and should only be used in cases of high distress that do not otherwise respond. Education, reduction of risk factors and psychological treatments have limited evidence of efficacy, but are unlikely to cause harm.

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“…Treatment with a cholinesterase inhibitor reduces the severity of hallucinations and improves general cognitive function [4,5,6]. Using technetium-99m hexamethyl-propyleneamine oxine ( 99m Tc-HMPAO) single photon emission tomography (SPECT), some authors have shown a relationship between the improvement of VHs and increased occipital perfusion [4,7]. Mori et al [7] reported serial cerebral blood flow (CBF) in DLB by 99m Tc- HMPAO SPECT before and after donepezil treatment.…”

Section: Introductionmentioning

confidence: 99%

Improved Visual Hallucination by Donepezil and Occipital Glucose Metabolism in Dementia with Lewy Bodies: The Osaki-Tajiri Project

et al. 2010

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Deficits in the cholinergic system are pronounced in dementia with Lewy bodies (DLB) and are more severe in patients with visual hallucinations (VHs). The aim is to identify the occipital glucose metabolism patterns by positron emission tomography (PET) and the changes following donepezil treatment. 13 DLB patients with VHs were enrolled in the study. After the first FDG-PET study, 5 mg/day donepezil was administered orally, and a second PET study was performed 3 months later. After donepezil administration, VHs disappeared completely in 6 patients, and the PET studies revealed significantly decreased glucose metabolism in the medial occipital cortex. These results suggest that VHs in DLB were associated with impaired glucose metabolism in the medial occipital cortex. Donepezil treatment may modify regional glucose metabolism.

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Correlation of visual hallucinations with occipital rCBF changes by donepezil in DLB

Cited by 67 publications

References 12 publications

Changes in Cerebral Glucose Metabolism in Patients with Parkinson Disease with Dementia After Cholinesterase Inhibitor Therapy

Changes in Cerebral Glucose Metabolism in Patients with Parkinson Disease with Dementia After Cholinesterase Inhibitor Therapy

Advances In the Treatment of Visual Hallucinations In Neurodegenerative Diseases

Improved Visual Hallucination by Donepezil and Occipital Glucose Metabolism in Dementia with Lewy Bodies: The Osaki-Tajiri Project

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