The interplay of cholinergic function, attention, and falls in Parkinson's disease
Identifieur interne : 000318 ( Main/Corpus ); précédent : 000317; suivant : 000319The interplay of cholinergic function, attention, and falls in Parkinson's disease
Auteurs : Alison Yarnall ; Lynn Rochester ; David J. BurnSource :
- Movement Disorders [ 0885-3185 ] ; 2011-12.
English descriptors
- KwdEn :
Abstract
Dopamine loss in the substantia nigra causes several of the motor signs seen in Parkinson's disease, but there is now increasing evidence highlighting the importance of cholinergic loss in the pathophysiology of nonmotor symptoms. The nucleus basalis of Meynert supplies the majority of the cholinergic input to the cerebral cortex, with the pedunculopontine nucleus providing many subcortical structures with acetylcholine. Both these structures undergo degeneration in Parkinson's disease (PD), with more severe loss associated with cognitive impairment. The risk of dementia in PD is greater than that in control subjects, with impairments in attention, visuospatial function, and executive control dominating. Imaging studies have demonstrated degeneration of the cholinergic system in PD, Parkinson's disease dementia, and dementia with Lewy bodies, with improvements in attention seen following the introduction of cholinesterase inhibitors. Conversely, anticholinergic drugs are associated with cognitive decline, with neuropathology studies indicating the presence of increased neurofibrillary tangles and senile plaque formation. In addition, these drugs are also known to precipitate visual hallucinations, lending support to a cholinergic basis for visual hallucinations in PD. Gait, falls, and cognition may also be related, as evidenced by the findings that fallers perform less well on test of attention than nonfallers and that greater postural instability is associated with worse scores on attention and executive function. It is therefore feasible that cognition (namely, attention), visual hallucinations, falls, and gait are subserved by acetylcholine, and this is further explored in this clinically orientated review. © 2011 Movement Disorder Society
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DOI: 10.1002/mds.23932
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ISTEX:6BC03334B6665EDFA036B10C276E747DE2CAB136Le document en format XML
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In addition, these drugs are also known to precipitate visual hallucinations, lending support to a cholinergic basis for visual hallucinations in PD. Gait, falls, and cognition may also be related, as evidenced by the findings that fallers perform less well on test of attention than nonfallers and that greater postural instability is associated with worse scores on attention and executive function. 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The nucleus basalis of Meynert supplies the majority of the cholinergic input to the cerebral cortex, with the pedunculopontine nucleus providing many subcortical structures with acetylcholine. Both these structures undergo degeneration in Parkinson's disease (PD), with more severe loss associated with cognitive impairment. The risk of dementia in PD is greater than that in control subjects, with impairments in attention, visuospatial function, and executive control dominating. Imaging studies have demonstrated degeneration of the cholinergic system in PD, Parkinson's disease dementia, and dementia with Lewy bodies, with improvements in attention seen following the introduction of cholinesterase inhibitors. Conversely, anticholinergic drugs are associated with cognitive decline, with neuropathology studies indicating the presence of increased neurofibrillary tangles and senile plaque formation. In addition, these drugs are also known to precipitate visual hallucinations, lending support to a cholinergic basis for visual hallucinations in PD. Gait, falls, and cognition may also be related, as evidenced by the findings that fallers perform less well on test of attention than nonfallers and that greater postural instability is associated with worse scores on attention and executive function. It is therefore feasible that cognition (namely, attention), visual hallucinations, falls, and gait are subserved by acetylcholine, and this is further explored in this clinically orientated review. © 2011 Movement Disorder Society</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p><b>Relevant conflicts of interest/financial disclosures:</b> Nothing to report.</p></note><note xml:id="fn2"><p>Full financial disclosures and author roles may be found in the online version of this article.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>The interplay of cholinergic function, attention, and falls in Parkinson's disease</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Cholinergic Function, Attention, Falls in PD</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>The interplay of cholinergic function, attention, and falls in Parkinson's disease</title></titleInfo><name type="personal"><namePart type="given">Alison</namePart><namePart type="family">Yarnall</namePart><namePart type="termsOfAddress">MRCP</namePart><affiliation>Institute for Ageing and Health, Newcastle University, Newcastle upon Tyne, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Lynn</namePart><namePart type="family">Rochester</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Institute for Ageing and Health, Newcastle University, Newcastle upon Tyne, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">David J.</namePart><namePart type="family">Burn</namePart><namePart type="termsOfAddress">FRCP, MD, MA</namePart><affiliation>Institute for Ageing and Health, Newcastle University, Newcastle upon Tyne, United Kingdom</affiliation><description>Correspondence: Clinical Ageing Research Unit, Newcastle University, Campus for Ageing and Vitality, Newcastle upon Tyne NE4 5PL, UK</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="review-article" displayLabel="reviewArticle"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2011-12</dateIssued><dateCaptured encoding="w3cdtf">2011-06-01</dateCaptured><dateValid encoding="w3cdtf">2011-08-02</dateValid><copyrightDate encoding="w3cdtf">2011</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">1</extent><extent unit="tables">1</extent><extent unit="references">91</extent><extent unit="words">7039</extent></physicalDescription><abstract lang="en">Dopamine loss in the substantia nigra causes several of the motor signs seen in Parkinson's disease, but there is now increasing evidence highlighting the importance of cholinergic loss in the pathophysiology of nonmotor symptoms. The nucleus basalis of Meynert supplies the majority of the cholinergic input to the cerebral cortex, with the pedunculopontine nucleus providing many subcortical structures with acetylcholine. Both these structures undergo degeneration in Parkinson's disease (PD), with more severe loss associated with cognitive impairment. The risk of dementia in PD is greater than that in control subjects, with impairments in attention, visuospatial function, and executive control dominating. Imaging studies have demonstrated degeneration of the cholinergic system in PD, Parkinson's disease dementia, and dementia with Lewy bodies, with improvements in attention seen following the introduction of cholinesterase inhibitors. Conversely, anticholinergic drugs are associated with cognitive decline, with neuropathology studies indicating the presence of increased neurofibrillary tangles and senile plaque formation. In addition, these drugs are also known to precipitate visual hallucinations, lending support to a cholinergic basis for visual hallucinations in PD. Gait, falls, and cognition may also be related, as evidenced by the findings that fallers perform less well on test of attention than nonfallers and that greater postural instability is associated with worse scores on attention and executive function. It is therefore feasible that cognition (namely, attention), visual hallucinations, falls, and gait are subserved by acetylcholine, and this is further explored in this clinically orientated review. © 2011 Movement Disorder Society</abstract><note type="content">*Relevant conflicts of interest/financial disclosures: Nothing to report.</note><note type="content">*Full financial disclosures and author roles may be found in the online version of this article.</note><subject lang="en"><genre>Keywords</genre><topic>Parkinson's disease</topic><topic>cholinergic</topic><topic>dementia</topic><topic>falls</topic><topic>attention</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. 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