Home > Publications database > Hallucinations in neurodegenerative diseases > print

001     21473
005     20210129210801.0
024 7 _ |2 pmid
|a pmid:21592320
024 7 _ |2 DOI
|a 10.1111/j.1755-5949.2011.00247.x
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037 _ _ |a PreJuSER-21473
041 _ _ |a eng
082 _ _ |a 610
084 _ _ |2 WoS
|a Neurosciences
084 _ _ |2 WoS
|a Pharmacology & Pharmacy
100 1 _ |a Burghaus, L.
|b 0
|0 P:(DE-HGF)0
245 _ _ |a Hallucinations in neurodegenerative diseases
260 _ _ |a Oxford
|b Wiley-Blackwell
|c 2012
300 _ _ |a 149 - 159
336 7 _ |a Journal Article
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336 7 _ |a article
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440 _ 0 |a Neurosciences and Therapeutics
|0 26564
|y 2
|v 18
500 _ _ |a Record converted from VDB: 12.11.2012
520 _ _ |a Patients with neurodegenerative disease frequently experience hallucinations and illusionary perceptions. As early symptoms, hallucinations may even have diagnostic relevance (i.e., for the diagnosis of Lewy Body Dementia). In the later course of the disease, hallucinations may appear as characteristic symptoms and often constitute a particular challenge for therapeutic endeavors. Here, the distinction of disease-inherent hallucinations from medication-associated perceptual disturbances is particularly relevant. Synucleinopathies and tauopathies have different risk profiles for hallucinations. In synucleinopathies hallucinations are much more frequent and phenomenology is characterized by visual, short-lived hallucinations, with insight preserved for a long time. A “double hit” theory proposes that dysfunctionality of both associative visual areas and changes of limbic areas or the ventral striatum are required. In contrast, in tauopathies the hallucinations are more rare and mostly embedded in confusional states with agitation and with poorly defined or rapidly changing paranoia. The occurrence of hallucinations has even been proposed as an exclusion criterion for tauopathies with Parkinsonian features such as progressive supranuclear palsy. To date, treatment remains largely empirical, except the use of clozapine and cholinesterase inhibitors in synucleinopathies, which is evidence-based. The risk of increased neuroleptic sensitivity further restricts the treatment options in patients with Lewy Body Dementia. Coping Strategies and improvement of visual acuity and sleep quality may be useful therapeutic complements.
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588 _ _ |a Dataset connected to Web of Science, Pubmed
650 _ 2 |2 MeSH
|a Adaptation, Psychological
650 _ 2 |2 MeSH
|a Animals
650 _ 2 |2 MeSH
|a Hallucinations: epidemiology
650 _ 2 |2 MeSH
|a Hallucinations: psychology
650 _ 2 |2 MeSH
|a Hallucinations: therapy
650 _ 2 |2 MeSH
|a Humans
650 _ 2 |2 MeSH
|a Neurodegenerative Diseases: epidemiology
650 _ 2 |2 MeSH
|a Neurodegenerative Diseases: psychology
650 _ 2 |2 MeSH
|a Neurodegenerative Diseases: therapy
650 _ 2 |2 MeSH
|a Parkinson Disease: epidemiology
650 _ 2 |2 MeSH
|a Parkinson Disease: psychology
650 _ 2 |2 MeSH
|a Parkinson Disease: therapy
650 _ 2 |2 MeSH
|a Sleep Disorders: epidemiology
650 _ 2 |2 MeSH
|a Sleep Disorders: psychology
650 _ 2 |2 MeSH
|a Sleep Disorders: therapy
650 _ 7 |a J
|2 WoSType
653 2 0 |2 Author
|a Alzheimer's disease
653 2 0 |2 Author
|a Corticobasal degeneration
653 2 0 |2 Author
|a Dementia with Lewy bodies
653 2 0 |2 Author
|a Frontotemporal dementia
653 2 0 |2 Author
|a Hallucinations
653 2 0 |2 Author
|a Multiple system atrophy
653 2 0 |2 Author
|a Neurodegenerative diseases
653 2 0 |2 Author
|a Parkinson's disease
653 2 0 |2 Author
|a Progressive supranuclear palsy
653 2 0 |2 Author
|a Synucleinopathy
653 2 0 |2 Author
|a Tauopathy
700 1 _ |a Eggers, C.
|b 1
|0 P:(DE-HGF)0
700 1 _ |a Timmermann, L.
|b 2
|0 P:(DE-HGF)0
700 1 _ |a Fink, G.R.
|b 3
|u FZJ
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773 _ _ |a 10.1111/j.1755-5949.2011.00247.x
|g Vol. 18, p. 149 - 159
|p 149 - 159
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|0 PERI:(DE-600)2423467-9
|t CNS neuroscience & therapeutics
|v 18
|y 2012
|x 1755-5949
856 7 _ |u http://dx.doi.org/10.1111/j.1755-5949.2011.00247.x
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