Imaging: What can it tell us about parkinsonian gait?
Identifieur interne : 000726 ( PubMed/Curation ); précédent : 000725; suivant : 000727Imaging: What can it tell us about parkinsonian gait?
Auteurs : Nicolaas I. Bohnen [États-Unis] ; Klaus JahnSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2013.
English descriptors
- KwdEn :
- MESH :
- chemical , metabolism : Neurotransmitter Agents.
- complications : Parkinsonian Disorders.
- etiology : Gait Disorders, Neurologic.
- metabolism : Brain.
- pathology : Brain, Gait Disorders, Neurologic.
- physiopathology : Brain.
- Humans, Neuroimaging.
Abstract
Functional neuroimaging has provided new tools to study cerebral gait control in Parkinson's disease (PD). First, imaging of blood flow functions has identified a supraspinal locomotor network that includes the (frontal) cortex, basal ganglia, brainstem tegmentum, and cerebellum. These studies also emphasize the cognitive and attentional dependency of gait in PD. Furthermore, gait in PD and related syndromes like progressive supranuclear palsy may be associated with dysfunction of the indirect, modulatory prefrontal-subthalamic-pedunculopontine loop of locomotor control. The direct, stereotyped locomotor loop from the primary motor cortex to the spinal cord with rhythmic cerebellar input appears to be preserved and may contribute to the unflexible gait pattern in parkinsonian gait. Second, neurotransmitter and proteinopathy imaging studies are beginning to unravel novel mechanisms of parkinsonian gait and postural disturbances. Dopamine displacement imaging studies have shown evidence for a mesofrontal dopaminergic shift from a depleted striatum in parkinsonian gait. This may place additional burden on other brain systems mediating attention functions to perform previously automatic motor tasks. For example, our preliminary cholinergic imaging studies suggest significant slowing of gait speed when additional forebrain cholinergic denervation occurs in PD. Cholinergic denervation of the pedunculopontine nucleus and its thalamic projections have been associated with falls and impaired postural control. Deposition of β-amyloid may represent another non-dopaminergic correlate of gait disturbance in PD. These findings illustrate the emergence of dopamine non-responsive gait problems to reflect the transition from a predominantly hypodopaminergic disorder to a multisystem neurodegenerative disorder involving non-dopaminergic locomotor network structures and pathologies.
DOI: 10.1002/mds.25534
PubMed: 24132837
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Imaging: What can it tell us about parkinsonian gait?</title><author><name sortKey="Bohnen, Nicolaas I" sort="Bohnen, Nicolaas I" uniqKey="Bohnen N" first="Nicolaas I" last="Bohnen">Nicolaas I. Bohnen</name><affiliation wicri:level="1"><nlm:affiliation>Department of Radiology, University of Michigan, Ann Arbor, Michigan, USA; Department of Neurology, University of Michigan, Ann Arbor, Michigan, USA; Neurology Service and Geriatric Research, Education, and Clinical Center, VA Ann Arbor Healthcare System, Ann Arbor, Michigan, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Radiology, University of Michigan, Ann Arbor, Michigan, USA; Department of Neurology, University of Michigan, Ann Arbor, Michigan, USA; Neurology Service and Geriatric Research, Education, and Clinical Center, VA Ann Arbor Healthcare System, Ann Arbor, Michigan</wicri:regionArea></affiliation></author><author><name sortKey="Jahn, Klaus" sort="Jahn, Klaus" uniqKey="Jahn K" first="Klaus" last="Jahn">Klaus Jahn</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2013">2013</date><idno type="doi">10.1002/mds.25534</idno><idno type="RBID">pubmed:24132837</idno><idno type="pmid">24132837</idno><idno type="wicri:Area/PubMed/Corpus">000726</idno><idno type="wicri:Area/PubMed/Curation">000726</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Imaging: What can it tell us about parkinsonian gait?</title><author><name sortKey="Bohnen, Nicolaas I" sort="Bohnen, Nicolaas I" uniqKey="Bohnen N" first="Nicolaas I" last="Bohnen">Nicolaas I. Bohnen</name><affiliation wicri:level="1"><nlm:affiliation>Department of Radiology, University of Michigan, Ann Arbor, Michigan, USA; Department of Neurology, University of Michigan, Ann Arbor, Michigan, USA; Neurology Service and Geriatric Research, Education, and Clinical Center, VA Ann Arbor Healthcare System, Ann Arbor, Michigan, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Radiology, University of Michigan, Ann Arbor, Michigan, USA; Department of Neurology, University of Michigan, Ann Arbor, Michigan, USA; Neurology Service and Geriatric Research, Education, and Clinical Center, VA Ann Arbor Healthcare System, Ann Arbor, Michigan</wicri:regionArea></affiliation></author><author><name sortKey="Jahn, Klaus" sort="Jahn, Klaus" uniqKey="Jahn K" first="Klaus" last="Jahn">Klaus Jahn</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="2013" type="published">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Brain (metabolism)</term><term>Brain (pathology)</term><term>Brain (physiopathology)</term><term>Gait Disorders, Neurologic (etiology)</term><term>Gait Disorders, Neurologic (pathology)</term><term>Humans</term><term>Neuroimaging</term><term>Neurotransmitter Agents (metabolism)</term><term>Parkinsonian Disorders (complications)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Neurotransmitter Agents</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Parkinsonian Disorders</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Gait Disorders, Neurologic</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Brain</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Brain</term><term>Gait Disorders, Neurologic</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Brain</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Humans</term><term>Neuroimaging</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Functional neuroimaging has provided new tools to study cerebral gait control in Parkinson's disease (PD). First, imaging of blood flow functions has identified a supraspinal locomotor network that includes the (frontal) cortex, basal ganglia, brainstem tegmentum, and cerebellum. These studies also emphasize the cognitive and attentional dependency of gait in PD. Furthermore, gait in PD and related syndromes like progressive supranuclear palsy may be associated with dysfunction of the indirect, modulatory prefrontal-subthalamic-pedunculopontine loop of locomotor control. The direct, stereotyped locomotor loop from the primary motor cortex to the spinal cord with rhythmic cerebellar input appears to be preserved and may contribute to the unflexible gait pattern in parkinsonian gait. Second, neurotransmitter and proteinopathy imaging studies are beginning to unravel novel mechanisms of parkinsonian gait and postural disturbances. Dopamine displacement imaging studies have shown evidence for a mesofrontal dopaminergic shift from a depleted striatum in parkinsonian gait. This may place additional burden on other brain systems mediating attention functions to perform previously automatic motor tasks. For example, our preliminary cholinergic imaging studies suggest significant slowing of gait speed when additional forebrain cholinergic denervation occurs in PD. Cholinergic denervation of the pedunculopontine nucleus and its thalamic projections have been associated with falls and impaired postural control. Deposition of β-amyloid may represent another non-dopaminergic correlate of gait disturbance in PD. These findings illustrate the emergence of dopamine non-responsive gait problems to reflect the transition from a predominantly hypodopaminergic disorder to a multisystem neurodegenerative disorder involving non-dopaminergic locomotor network structures and pathologies.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">24132837</PMID><DateCreated><Year>2013</Year><Month>10</Month><Day>17</Day></DateCreated><DateCompleted><Year>2014</Year><Month>05</Month><Day>19</Day></DateCompleted><DateRevised><Year>2014</Year><Month>11</Month><Day>12</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>28</Volume><Issue>11</Issue><PubDate><Year>2013</Year><Month>Sep</Month><Day>15</Day></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Imaging: What can it tell us about parkinsonian gait?</ArticleTitle><Pagination><MedlinePgn>1492-500</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/mds.25534</ELocationID><Abstract><AbstractText>Functional neuroimaging has provided new tools to study cerebral gait control in Parkinson's disease (PD). First, imaging of blood flow functions has identified a supraspinal locomotor network that includes the (frontal) cortex, basal ganglia, brainstem tegmentum, and cerebellum. These studies also emphasize the cognitive and attentional dependency of gait in PD. Furthermore, gait in PD and related syndromes like progressive supranuclear palsy may be associated with dysfunction of the indirect, modulatory prefrontal-subthalamic-pedunculopontine loop of locomotor control. The direct, stereotyped locomotor loop from the primary motor cortex to the spinal cord with rhythmic cerebellar input appears to be preserved and may contribute to the unflexible gait pattern in parkinsonian gait. Second, neurotransmitter and proteinopathy imaging studies are beginning to unravel novel mechanisms of parkinsonian gait and postural disturbances. Dopamine displacement imaging studies have shown evidence for a mesofrontal dopaminergic shift from a depleted striatum in parkinsonian gait. This may place additional burden on other brain systems mediating attention functions to perform previously automatic motor tasks. For example, our preliminary cholinergic imaging studies suggest significant slowing of gait speed when additional forebrain cholinergic denervation occurs in PD. Cholinergic denervation of the pedunculopontine nucleus and its thalamic projections have been associated with falls and impaired postural control. Deposition of β-amyloid may represent another non-dopaminergic correlate of gait disturbance in PD. These findings illustrate the emergence of dopamine non-responsive gait problems to reflect the transition from a predominantly hypodopaminergic disorder to a multisystem neurodegenerative disorder involving non-dopaminergic locomotor network structures and pathologies.</AbstractText><CopyrightInformation>© 2013 Movement Disorder Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Bohnen</LastName><ForeName>Nicolaas I</ForeName><Initials>NI</Initials><AffiliationInfo><Affiliation>Department of Radiology, University of Michigan, Ann Arbor, Michigan, USA; Department of Neurology, University of Michigan, Ann Arbor, Michigan, USA; Neurology Service and Geriatric Research, Education, and Clinical Center, VA Ann Arbor Healthcare System, Ann Arbor, Michigan, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jahn</LastName><ForeName>Klaus</ForeName><Initials>K</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>P01 NS015655</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 NS070856</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018377">Neurotransmitter 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