The pathogenesis of Pisa syndrome in Parkinson's disease.
Identifieur interne : 000029 ( France/Analysis ); précédent : 000028; suivant : 000030The pathogenesis of Pisa syndrome in Parkinson's disease.
Auteurs : Anna Castrioto [France] ; Céline Piscicelli ; Dominic Pérennou ; Paul Krack ; Bettina DebûSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2014.
English descriptors
- KwdEn :
- MESH :
- complications : Parkinson Disease.
- etiology : Parkinson Disease, Sensation Disorders.
- pathology : Basal Ganglia, Sensation Disorders.
- physiology : Postural Balance.
- physiopathology : Musculoskeletal System.
- Animals, Humans.
Abstract
Postural abnormalities such as postural deviations affect nearly all patients with advanced Parkinson's disease and represent an important source of disability. Although their existence has long been known, their management remains a challenge as they respond poorly to medication, brain surgery, or physiotherapy. Improving management strategies will require better understanding of the mechanisms underlying such postural deformities. In this review on the pathophysiology of Pisa syndrome, we examine the data supporting the central and peripheral hypotheses that attempt to explain these lateral trunk deviations. Although the pathophysiology is very probably multifactorial, the bulk of the data supports central, rather than peripheral, hypotheses. The central hypotheses that are best supported by both animal studies and clinical data include asymmetry of basal ganglia output and abnormalities in the central integration of sensory information. Further studies are needed to elucidate the pathophysiology underlying Pisa syndrome.
DOI: 10.1002/mds.25925
PubMed: 24909134
Affiliations:
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pubmed:24909134Le document en format XML
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Grenoble Institute of Neuroscience, INSERM-UJF-CEA U836, Grenoble, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Grenoble University Hospital, Psychiatry and Neurology Dept., Grenoble, France; Grenoble Institute of Neuroscience, INSERM-UJF-CEA U836, Grenoble</wicri:regionArea><placeName><settlement type="city">Grenoble</settlement></placeName></affiliation></author><author><name sortKey="Piscicelli, Celine" sort="Piscicelli, Celine" uniqKey="Piscicelli C" first="Céline" last="Piscicelli">Céline Piscicelli</name></author><author><name sortKey="Perennou, Dominic" sort="Perennou, Dominic" uniqKey="Perennou D" first="Dominic" last="Pérennou">Dominic Pérennou</name></author><author><name sortKey="Krack, Paul" sort="Krack, Paul" uniqKey="Krack P" first="Paul" last="Krack">Paul Krack</name></author><author><name sortKey="Debu, Bettina" sort="Debu, Bettina" uniqKey="Debu B" first="Bettina" last="Debû">Bettina Debû</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="eISSN">1531-8257</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Basal Ganglia (pathology)</term><term>Humans</term><term>Musculoskeletal System (physiopathology)</term><term>Parkinson Disease (complications)</term><term>Parkinson Disease (etiology)</term><term>Postural Balance (physiology)</term><term>Sensation Disorders (etiology)</term><term>Sensation Disorders (pathology)</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Parkinson Disease</term><term>Sensation Disorders</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Basal Ganglia</term><term>Sensation Disorders</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Postural Balance</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Musculoskeletal System</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Postural abnormalities such as postural deviations affect nearly all patients with advanced Parkinson's disease and represent an important source of disability. Although their existence has long been known, their management remains a challenge as they respond poorly to medication, brain surgery, or physiotherapy. Improving management strategies will require better understanding of the mechanisms underlying such postural deformities. In this review on the pathophysiology of Pisa syndrome, we examine the data supporting the central and peripheral hypotheses that attempt to explain these lateral trunk deviations. Although the pathophysiology is very probably multifactorial, the bulk of the data supports central, rather than peripheral, hypotheses. The central hypotheses that are best supported by both animal studies and clinical data include asymmetry of basal ganglia output and abnormalities in the central integration of sensory information. 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