Movement Disorders (revue)

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Anterior Cingulate Integrity: Executive and Neuropsychiatric Features in Parkinson's Disease

Identifieur interne : 002C23 ( PascalFrancis/Curation ); précédent : 002C22; suivant : 002C24

Anterior Cingulate Integrity: Executive and Neuropsychiatric Features in Parkinson's Disease

Auteurs : Simon J. G. Lewis [Australie] ; James M. Shine [Australie] ; Shantel Duffy [Australie] ; Glenda Halliday [Australie] ; Sharon L. Naismith [Australie]

Source :

RBID : Pascal:12-0369635

Descripteurs français

English descriptors

Abstract

Patients with advanced Parkinson's disease (PD) commonly suffer with significant executive dysfunction and concomitant visual hallucinations. Although the underlying pathophysiology remains poorly understood, numerous studies have highlighted the strong association between these neuropsychiatric features, suggesting common neural pathways. Although previous neuroimaging studies have identified widespread volume loss across a number of cortical regions, to date, no studies have utilized proton magnetic resonance spectroscopy to provide insights into how neuro-metabolic changes may relate to such symptoms. Twenty patients with PD and 20 healthy controls underwent spectroscopy to determine the N-acetyl aspartate/ creatine (NAA/Cr) ratio, which reflects the degree of neuronal integrity in neurodegenerative diseases. Voxels were obtained from the anterior cingulate cortex (ACC), an area critical for a wide range of executive mechanisms as well as from a control volume in the posterior cingulate cortex (PCC). Compared to controls, patients with PD had lower NAA/Cr ratios in the ACC. In turn, lower NAA/Cr ratios significantly correlated with poorer executive function on tasks of attentional set-shifting and response inhibition, as well as more-severe psychotic symptoms and poorer performance on the Bistable Percept Paradigm, a neuropsychological probe of visual hallucinations. NAA/Cr ratios were significantly lower in hallucinators, compared to nonhallucinators, within the ACC, but did not differ in the PCC. These results suggest that loss of neuronal integrity within the ACC plays an important role in the pathophysiology underlying executive functioning and visual hallucinations in PD.
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A11 01  1    @1 LEWIS (Simon J. G.)
A11 02  1    @1 SHINE (James M.)
A11 03  1    @1 DUFFY (Shantel)
A11 04  1    @1 HALLIDAY (Glenda)
A11 05  1    @1 NAISMITH (Sharon L.)
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C01 01    ENG  @0 Patients with advanced Parkinson's disease (PD) commonly suffer with significant executive dysfunction and concomitant visual hallucinations. Although the underlying pathophysiology remains poorly understood, numerous studies have highlighted the strong association between these neuropsychiatric features, suggesting common neural pathways. Although previous neuroimaging studies have identified widespread volume loss across a number of cortical regions, to date, no studies have utilized proton magnetic resonance spectroscopy to provide insights into how neuro-metabolic changes may relate to such symptoms. Twenty patients with PD and 20 healthy controls underwent spectroscopy to determine the N-acetyl aspartate/ creatine (NAA/Cr) ratio, which reflects the degree of neuronal integrity in neurodegenerative diseases. Voxels were obtained from the anterior cingulate cortex (ACC), an area critical for a wide range of executive mechanisms as well as from a control volume in the posterior cingulate cortex (PCC). Compared to controls, patients with PD had lower NAA/Cr ratios in the ACC. In turn, lower NAA/Cr ratios significantly correlated with poorer executive function on tasks of attentional set-shifting and response inhibition, as well as more-severe psychotic symptoms and poorer performance on the Bistable Percept Paradigm, a neuropsychological probe of visual hallucinations. NAA/Cr ratios were significantly lower in hallucinators, compared to nonhallucinators, within the ACC, but did not differ in the PCC. These results suggest that loss of neuronal integrity within the ACC plays an important role in the pathophysiology underlying executive functioning and visual hallucinations in PD.
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C07 03  X  SPA  @0 Enfermedad degenerativa @5 39
C07 04  X  FRE  @0 Pathologie du système nerveux central @5 40
C07 04  X  ENG  @0 Central nervous system disease @5 40
C07 04  X  SPA  @0 Sistema nervosio central patología @5 40
C07 05  X  FRE  @0 Aminoacide excitateur @5 42
C07 05  X  ENG  @0 Excitatory aminoacid @5 42
C07 05  X  SPA  @0 Aminoácido excitador @5 42
C07 06  X  FRE  @0 Neurotransmetteur @5 43
C07 06  X  ENG  @0 Neurotransmitter @5 43
C07 06  X  SPA  @0 Neurotransmisor @5 43
N21       @1 289
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<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA">
<s0>Enfermedad degenerativa</s0>
<s5>39</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE">
<s0>Pathologie du système nerveux central</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG">
<s0>Central nervous system disease</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA">
<s0>Sistema nervosio central patología</s0>
<s5>40</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE">
<s0>Aminoacide excitateur</s0>
<s5>42</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG">
<s0>Excitatory aminoacid</s0>
<s5>42</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA">
<s0>Aminoácido excitador</s0>
<s5>42</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE">
<s0>Neurotransmetteur</s0>
<s5>43</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG">
<s0>Neurotransmitter</s0>
<s5>43</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA">
<s0>Neurotransmisor</s0>
<s5>43</s5>
</fC07>
<fN21>
<s1>289</s1>
</fN21>
<fN44 i1="01">
<s1>OTO</s1>
</fN44>
<fN82>
<s1>OTO</s1>
</fN82>
</pA>
</standard>
</inist>
</record>

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