Visual hallucinations and altered visual information processing in Parkinson disease and dementia with Lewy bodies

Kurita, Akira; Murakami, Maiko; Takagi, Satoshi; Matsushima, Masato; Suzuki, Masahiko

doi:10.1002/mds.22919

Cited by 57 publications

(31 citation statements)

References 17 publications

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“…Delays in visual evoked responses and disturbances of visuospatial processing, suggesting involvement of the visual pathway beyond the retina, have also been demonstrated in PD 40. Visual event related potentials are slower in patients with PD who have reported VH, consistent with a role for visual processing pathways in their onset 41. Interestingly, visuospatial functions appear to be relatively spared in MSA and PSP, where hallucinations are rare 42…”

Section: Does the Appearance Of Visual Hallucinations Suggest Anatomimentioning

confidence: 95%

Visual hallucinations in the differential diagnosis of parkinsonism: Table 1

Bertram

Williams

2012

J Neurol Neurosurg Psychiatry

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Visual hallucinations (VH) occur commonly in Parkinson's disease (PD) and dementia with Lewy bodies (DLB) but are reported much less frequently in other neurodegenerative causes of parkinsonism, such as progressive supranuclear palsy, multiple system atrophy and corticobasal degeneration syndrome. This clinical sign may be helpful when considering the differential diagnosis of patients with parkinsonism. The observation that VH may be specific to Lewy body pathology probably reflects a greater vulnerability of the visual systems to PD and DLB neurodegeneration compared with other diseases. Topographic differences in pathology are probably the major factor producing VH in Lewy body diseases, rather than neurophysiological changes that are specific to α-synuclein protein accumulation. VH correlate with pathology in the limbic system and more specifically the amygdale that is frequently affected in PD and DLB but relatively preserved in other forms of parkinsonism often misdiagnosed as PD. In this review, the published frequencies of VH in these different conditions are compared to put into context the notion of VH as a clinical clue to underlying Lewy body pathology.

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Section: Does the Appearance Of Visual Hallucinations Suggest Anatomimentioning

confidence: 95%

Visual hallucinations in the differential diagnosis of parkinsonism: Table 1

Bertram

Williams

2012

J Neurol Neurosurg Psychiatry

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“…It is also believed that P300 is an indication of the level of cognitive resources used for processing a stimulus. 136 Using a facial discrimination task, 137 mean latency of the visual P3 response was greater in PDD with visual hallucinations (n = 11) and DLB (n = 24) compared to AD (n = 21) subjects. Furthermore, mean latency of the P2 response was greater in PDD with and without VH and in DLB subjects, but not in AD, compared with controls.…”

Section: Visual Evoked Potentialsmentioning

confidence: 99%

“…Controversial in AD but flash response could be delayed and pattern response normal 126,[131][132][133][134][135] Visual event EP Greater response in DLB than AD but greater in AD than FTD 137,138 Complex functions Defects in reading, 139 visuospatial function, 48,140,141 and object identification in AD. 47 refraction has been used or if an ocular pathology was present.…”

Section: Vepmentioning

confidence: 99%

Oculo‐visual changes and clinical considerations affecting older patients with dementia

Armstrong

Kergoat

2015

Ophthalmic Physiologic Optic

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Purpose Dementia is associated with various alterations of the eye and visual function. Over 60% of cases are attributable to Alzheimer's disease, a significant proportion of the remainder to vascular dementia or dementia with Lewy bodies, while frontotemporal dementia, and Parkinson's disease dementia are less common. This review describes the oculo‐visual problems of these five dementias and the pathological changes which may explain these symptoms. It further discusses clinical considerations to help the clinician care for older patients affected by dementia. Recent findings Visual problems in dementia include loss of visual acuity, defects in colour vision and visual masking tests, changes in pupillary response to mydriatics, defects in fixation and smooth and saccadic eye movements, changes in contrast sensitivity function and visual evoked potentials, and disturbance of complex visual functions such as in reading ability, visuospatial function, and the naming and identification of objects. Pathological changes have also been reported affecting the crystalline lens, retina, optic nerve, and visual cortex. Clinically, issues such as cataract surgery, correcting the refractive error, quality of life, falls, visual impairment and eye care for dementia have been addressed. Summary Many visual changes occur across dementias, are controversial, often based on limited patient numbers, and no single feature can be regarded as diagnostic of any specific dementia. Nevertheless, visual hallucinations may be more characteristic of dementia with Lewy bodies and Parkinson's disease dementia than Alzheimer's disease or frontotemporal dementia. Differences in saccadic eye movement dysfunction may also help to distinguish Alzheimer's disease from frontotemporal dementia and Parkinson's disease dementia from dementia with Lewy bodies. Eye care professionals need to keep informed of the growing literature in vision/dementia, be attentive to signs and symptoms suggestive of cognitive impairment, and be able to adapt their practice and clinical interventions to best serve patients with dementia.

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“…Although the major clinical manifestations of PD involve the motor systems and the responsible pathology is located in the basal ganglia, there is evidence of more widespread disease, both pathologically, electrophysiologically and clinically. Only two studies explored the possible use of VEPs for the assessment of DLB [20,21] yet no comparison were presented with other forms of dementia. In MSA the visual system is believed to be spared and dopamine deficiency has been hypothesized to be less pronounced than in PD [22], even though the data in the literature are scarce and not unanimous and nothing on retinal dopamine content has been reported.…”

Section: Synucleinopathies: Dementia With Lewy Bodiesmentioning

confidence: 99%

Is There a Place for Clinical Neurophysiology Assessments in Synucleinopathies?

Onofrj¹,

Bonanni²,

Thomas³

et al. 2011

Neuroimaging for Clinicians - Combining Research and Practice

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IntroductionParkinson Disease (PD), Dementia with Lewy Bodies (DLB) and Multiple System Atrophy (MSA) are characterized by deposition of Lewy Bodies (LB), consisting of eosinophilic intracellular (intraneural in PD and DLB and intraglial in MSA) inclusions of -synuclein and allowing the three disorders to be categorized as synucleinopathies. The identification in the last two decades of specific clinical features of synucleinopathies has been a major breakthrough in Neurology, as it prompted a reconsideration of diagnostic and therapeutic approaches to dementia and parkinsonism. The recognition of synuclein and ubiquitin markers in dementia resulted in the reclassification of patients previously considered as affected by Alzheimer Disease (AD) and Vascular Dementia (VaD), and there is now agreement that DLB is the second most common cause of dementia in elderly population: its prevalence is reported to be in the 25-43% range in different studies. DLB is clinically characterized by the presence of prominently dysexecutive dementia (frontal lobe or subcortical dementia according to earlier classification [1]), cognitive fluctuations, consisting of remitting-relapsing episodes of blunted conscience reaching levels of stupor, by the occurrence of visual hallucinations and delusions, by parkinsonian motor signs and hypersensitivity to neuroleptic treatment, ranging from worsening of parkinsonism to the possible lethal neuroleptic-malignant syndromes [2]. Yet, variances of presentation and overlapping symptoms with AD and Fronto-Temporal lobe Degeneration (FTD), could be misleading in the process of addressing a clinical diagnosis with consequent therapeutic risks(e.g. introducing neuroleptic treatments in patient with DLB), or economic costs (e.g. addressing patients with DLB to treatment protocols dedicated to AD patients, based on vaccines or antibodies against amyloid proteins, a neuropathological feature of AD). It is evident the stringent need for improvement of reliable diagnostic tools (u.e. biomarkers) to differentiate the diseases associated with dementia. In 2010 the National Institute of Health, NIH, held a symposium focused on the development of possible biomarkers for DLB. Among the different suggested biomarkers, neurophysiological assessments were reconsidered, as a large amount of neurophysiological studies had been devoted to AD and PD, whose characteristics are shared by DLB. www.intechopen.com Neuroimaging for Clinicians -Combining Research and Practice 300We contributed to several studies on this argument along the years, and in the present chapter we discuss the role of clinical neurophysiological studies in DLB in comparison with other disorders. The essential background of our original studies laid in the fact that most historical studies were performed when the DLB clinical entity was unknown and therefore some of the past results were marred by absent recognition of this clinical entity. Synucleinopathies: Dementia with lewy bodiesSynucleinopathies comprise a diverse groups of neurodegenerati...

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Visual hallucinations and altered visual information processing in Parkinson disease and dementia with Lewy bodies

Cited by 57 publications

References 17 publications

Visual hallucinations in the differential diagnosis of parkinsonism: Table 1

Visual hallucinations in the differential diagnosis of parkinsonism: Table 1

Oculo‐visual changes and clinical considerations affecting older patients with dementia

Is There a Place for Clinical Neurophysiology Assessments in Synucleinopathies?

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