High γ‐Aminobutyric Acid Content Within the Medial Prefrontal Cortex Is a Functional Signature of Somatic Symptoms Disorder in Patients With Parkinson's Disease
ABSTRACT Background The dysfunctional activity of the medial prefrontal cortex has been associated with the appearance of the somatic symptom disorder, a key feature of the Parkinson's disease (PD) psychosis complex. Objectives The objectives of this study were to investigate whether the basal...
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| Published in | Movement disorders Vol. 35; no. 12; pp. 2184 - 2192 |
|---|---|
| Main Authors | , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Hoboken, USA
John Wiley & Sons, Inc
01.12.2020
Wiley Subscription Services, Inc |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0885-3185 1531-8257 1531-8257 |
| DOI | 10.1002/mds.28221 |
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| Abstract | ABSTRACT
Background
The dysfunctional activity of the medial prefrontal cortex has been associated with the appearance of the somatic symptom disorder, a key feature of the Parkinson's disease (PD) psychosis complex.
Objectives
The objectives of this study were to investigate whether the basal contents of inhibitory γ‐aminobutyric acid and excitatory glutamate plus glutamine neurotransmitter levels are changed in the medial prefrontal cortex of patients with PD with somatic symptom disorder and whether this alteration represents a marker of susceptibility of PD to somatic symptom disorder, thus representing a signature of psychosis complex of PD.
Methods
Levels of the γ‐aminobutyric acid and glutamate plus glutamine were investigated, at rest, with proton magnetic resonance spectroscopy. Total creatine was used as an internal reference. The study cohort included 23 patients with somatic symptom disorder plus PD, 19 patients with PD without somatic symptom disorder, 19 healthy control subjects, and 14 individuals with somatic symptom disorder who did not show other psychiatric or neurological disorders.
Results
We found that, compared with patients with PD without somatic symptom disorder or healthy control individuals, patients with somatic symptom disorder, with or without PD, show increased γ‐aminobutyric acid/total creatine levels in the medial prefrontal cortex. The medial prefrontal cortex contents of glutamate plus glutamine/total creatine levels or γ‐aminobutyric acid/glutamate plus glutamine were not different among groups.
Conclusions
Our findings highlight a crucial pathophysiologic role played by high γ‐aminobutyric acid within the medial prefrontal cortex in the production of somatic symptom disorder. This phenomenon represents a signature of psychosis complex in patients with PD. © 2020 International Parkinson and Movement Disorder Society |
|---|---|
| AbstractList | ABSTRACT
Background
The dysfunctional activity of the medial prefrontal cortex has been associated with the appearance of the somatic symptom disorder, a key feature of the Parkinson's disease (PD) psychosis complex.
Objectives
The objectives of this study were to investigate whether the basal contents of inhibitory γ‐aminobutyric acid and excitatory glutamate plus glutamine neurotransmitter levels are changed in the medial prefrontal cortex of patients with PD with somatic symptom disorder and whether this alteration represents a marker of susceptibility of PD to somatic symptom disorder, thus representing a signature of psychosis complex of PD.
Methods
Levels of the γ‐aminobutyric acid and glutamate plus glutamine were investigated, at rest, with proton magnetic resonance spectroscopy. Total creatine was used as an internal reference. The study cohort included 23 patients with somatic symptom disorder plus PD, 19 patients with PD without somatic symptom disorder, 19 healthy control subjects, and 14 individuals with somatic symptom disorder who did not show other psychiatric or neurological disorders.
Results
We found that, compared with patients with PD without somatic symptom disorder or healthy control individuals, patients with somatic symptom disorder, with or without PD, show increased γ‐aminobutyric acid/total creatine levels in the medial prefrontal cortex. The medial prefrontal cortex contents of glutamate plus glutamine/total creatine levels or γ‐aminobutyric acid/glutamate plus glutamine were not different among groups.
Conclusions
Our findings highlight a crucial pathophysiologic role played by high γ‐aminobutyric acid within the medial prefrontal cortex in the production of somatic symptom disorder. This phenomenon represents a signature of psychosis complex in patients with PD. © 2020 International Parkinson and Movement Disorder Society The dysfunctional activity of the medial prefrontal cortex has been associated with the appearance of the somatic symptom disorder, a key feature of the Parkinson's disease (PD) psychosis complex.BACKGROUNDThe dysfunctional activity of the medial prefrontal cortex has been associated with the appearance of the somatic symptom disorder, a key feature of the Parkinson's disease (PD) psychosis complex.The objectives of this study were to investigate whether the basal contents of inhibitory γ-aminobutyric acid and excitatory glutamate plus glutamine neurotransmitter levels are changed in the medial prefrontal cortex of patients with PD with somatic symptom disorder and whether this alteration represents a marker of susceptibility of PD to somatic symptom disorder, thus representing a signature of psychosis complex of PD.OBJECTIVESThe objectives of this study were to investigate whether the basal contents of inhibitory γ-aminobutyric acid and excitatory glutamate plus glutamine neurotransmitter levels are changed in the medial prefrontal cortex of patients with PD with somatic symptom disorder and whether this alteration represents a marker of susceptibility of PD to somatic symptom disorder, thus representing a signature of psychosis complex of PD.Levels of the γ-aminobutyric acid and glutamate plus glutamine were investigated, at rest, with proton magnetic resonance spectroscopy. Total creatine was used as an internal reference. The study cohort included 23 patients with somatic symptom disorder plus PD, 19 patients with PD without somatic symptom disorder, 19 healthy control subjects, and 14 individuals with somatic symptom disorder who did not show other psychiatric or neurological disorders.METHODSLevels of the γ-aminobutyric acid and glutamate plus glutamine were investigated, at rest, with proton magnetic resonance spectroscopy. Total creatine was used as an internal reference. The study cohort included 23 patients with somatic symptom disorder plus PD, 19 patients with PD without somatic symptom disorder, 19 healthy control subjects, and 14 individuals with somatic symptom disorder who did not show other psychiatric or neurological disorders.We found that, compared with patients with PD without somatic symptom disorder or healthy control individuals, patients with somatic symptom disorder, with or without PD, show increased γ-aminobutyric acid/total creatine levels in the medial prefrontal cortex. The medial prefrontal cortex contents of glutamate plus glutamine/total creatine levels or γ-aminobutyric acid/glutamate plus glutamine were not different among groups.RESULTSWe found that, compared with patients with PD without somatic symptom disorder or healthy control individuals, patients with somatic symptom disorder, with or without PD, show increased γ-aminobutyric acid/total creatine levels in the medial prefrontal cortex. The medial prefrontal cortex contents of glutamate plus glutamine/total creatine levels or γ-aminobutyric acid/glutamate plus glutamine were not different among groups.Our findings highlight a crucial pathophysiologic role played by high γ-aminobutyric acid within the medial prefrontal cortex in the production of somatic symptom disorder. This phenomenon represents a signature of psychosis complex in patients with PD. © 2020 International Parkinson and Movement Disorder Society.CONCLUSIONSOur findings highlight a crucial pathophysiologic role played by high γ-aminobutyric acid within the medial prefrontal cortex in the production of somatic symptom disorder. This phenomenon represents a signature of psychosis complex in patients with PD. © 2020 International Parkinson and Movement Disorder Society. The dysfunctional activity of the medial prefrontal cortex has been associated with the appearance of the somatic symptom disorder, a key feature of the Parkinson's disease (PD) psychosis complex. The objectives of this study were to investigate whether the basal contents of inhibitory γ-aminobutyric acid and excitatory glutamate plus glutamine neurotransmitter levels are changed in the medial prefrontal cortex of patients with PD with somatic symptom disorder and whether this alteration represents a marker of susceptibility of PD to somatic symptom disorder, thus representing a signature of psychosis complex of PD. Levels of the γ-aminobutyric acid and glutamate plus glutamine were investigated, at rest, with proton magnetic resonance spectroscopy. Total creatine was used as an internal reference. The study cohort included 23 patients with somatic symptom disorder plus PD, 19 patients with PD without somatic symptom disorder, 19 healthy control subjects, and 14 individuals with somatic symptom disorder who did not show other psychiatric or neurological disorders. We found that, compared with patients with PD without somatic symptom disorder or healthy control individuals, patients with somatic symptom disorder, with or without PD, show increased γ-aminobutyric acid/total creatine levels in the medial prefrontal cortex. The medial prefrontal cortex contents of glutamate plus glutamine/total creatine levels or γ-aminobutyric acid/glutamate plus glutamine were not different among groups. Our findings highlight a crucial pathophysiologic role played by high γ-aminobutyric acid within the medial prefrontal cortex in the production of somatic symptom disorder. This phenomenon represents a signature of psychosis complex in patients with PD. © 2020 International Parkinson and Movement Disorder Society. BackgroundThe dysfunctional activity of the medial prefrontal cortex has been associated with the appearance of the somatic symptom disorder, a key feature of the Parkinson's disease (PD) psychosis complex.ObjectivesThe objectives of this study were to investigate whether the basal contents of inhibitory γ‐aminobutyric acid and excitatory glutamate plus glutamine neurotransmitter levels are changed in the medial prefrontal cortex of patients with PD with somatic symptom disorder and whether this alteration represents a marker of susceptibility of PD to somatic symptom disorder, thus representing a signature of psychosis complex of PD.MethodsLevels of the γ‐aminobutyric acid and glutamate plus glutamine were investigated, at rest, with proton magnetic resonance spectroscopy. Total creatine was used as an internal reference. The study cohort included 23 patients with somatic symptom disorder plus PD, 19 patients with PD without somatic symptom disorder, 19 healthy control subjects, and 14 individuals with somatic symptom disorder who did not show other psychiatric or neurological disorders.ResultsWe found that, compared with patients with PD without somatic symptom disorder or healthy control individuals, patients with somatic symptom disorder, with or without PD, show increased γ‐aminobutyric acid/total creatine levels in the medial prefrontal cortex. The medial prefrontal cortex contents of glutamate plus glutamine/total creatine levels or γ‐aminobutyric acid/glutamate plus glutamine were not different among groups.ConclusionsOur findings highlight a crucial pathophysiologic role played by high γ‐aminobutyric acid within the medial prefrontal cortex in the production of somatic symptom disorder. This phenomenon represents a signature of psychosis complex in patients with PD. © 2020 International Parkinson and Movement Disorder Society |
| Author | Calvanese, Francesco Bubbico, Giovanna Bonanni, Laura Ferretti, Antonio Tartaro, Armando Delli Pizzi, Stefano Esposito, Roberto Franciotti, Raffaella Zöllner, Helge J. Onofrj, Marco Sensi, Stefano L. Edden, Richard A.E. Aiello, Claudia |
| AuthorAffiliation | 6 Department of Radiology, Area Vasta 1, ASUR Marche, Pesaro, Italy 3 Center of Aging Sciences and Translational Medicine, University “G. d’Annunzio” of Chieti-Pescara, Chieti, Italy 4 Russell H. Morgan Department of Radiology, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA 1 Department of Neuroscience, Imaging and Clinical Sciences, University “G. d’Annunzio” of Chieti-Pescara, Chieti, Italy 2 Institute for Advanced Biomedical Technologies (ITAB), “G. d’Annunzio” University, Chieti-Pescara, Italy 7 Department of Medical Sciences, Oral and Biotechnology, University “G. d’Annunzio” of Chieti-Pescara, Chieti, Italy 5 F.M. Kirby Center for Functional MRI, Kennedy Krieger Institute, Baltimore, Maryland, USA |
| AuthorAffiliation_xml | – name: 7 Department of Medical Sciences, Oral and Biotechnology, University “G. d’Annunzio” of Chieti-Pescara, Chieti, Italy – name: 3 Center of Aging Sciences and Translational Medicine, University “G. d’Annunzio” of Chieti-Pescara, Chieti, Italy – name: 1 Department of Neuroscience, Imaging and Clinical Sciences, University “G. d’Annunzio” of Chieti-Pescara, Chieti, Italy – name: 6 Department of Radiology, Area Vasta 1, ASUR Marche, Pesaro, Italy – name: 5 F.M. Kirby Center for Functional MRI, Kennedy Krieger Institute, Baltimore, Maryland, USA – name: 2 Institute for Advanced Biomedical Technologies (ITAB), “G. d’Annunzio” University, Chieti-Pescara, Italy – name: 4 Russell H. Morgan Department of Radiology, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA |
| Author_xml | – sequence: 1 givenname: Stefano surname: Delli Pizzi fullname: Delli Pizzi, Stefano organization: University “G. d'Annunzio” of Chieti‐Pescara – sequence: 2 givenname: Raffaella surname: Franciotti fullname: Franciotti, Raffaella organization: University “G. d'Annunzio” of Chieti‐Pescara – sequence: 3 givenname: Antonio surname: Ferretti fullname: Ferretti, Antonio organization: Institute for Advanced Biomedical Technologies (ITAB), “G. d'Annunzio” University – sequence: 4 givenname: Richard A.E. surname: Edden fullname: Edden, Richard A.E. organization: Kennedy Krieger Institute – sequence: 5 givenname: Helge J. surname: Zöllner fullname: Zöllner, Helge J. organization: Kennedy Krieger Institute – sequence: 6 givenname: Roberto surname: Esposito fullname: Esposito, Roberto organization: Area Vasta 1, ASUR Marche – sequence: 7 givenname: Giovanna surname: Bubbico fullname: Bubbico, Giovanna organization: Institute for Advanced Biomedical Technologies (ITAB), “G. d'Annunzio” University – sequence: 8 givenname: Claudia surname: Aiello fullname: Aiello, Claudia organization: University “G. d'Annunzio” of Chieti‐Pescara – sequence: 9 givenname: Francesco surname: Calvanese fullname: Calvanese, Francesco organization: University “G. d'Annunzio” of Chieti‐Pescara – sequence: 10 givenname: Stefano L. surname: Sensi fullname: Sensi, Stefano L. organization: University “G. d'Annunzio” of Chieti‐Pescara – sequence: 11 givenname: Armando surname: Tartaro fullname: Tartaro, Armando organization: University “G. d'Annunzio” of Chieti‐Pescara – sequence: 12 givenname: Marco surname: Onofrj fullname: Onofrj, Marco organization: University “G. d'Annunzio” of Chieti‐Pescara – sequence: 13 givenname: Laura surname: Bonanni fullname: Bonanni, Laura email: l.bonanni@unich.it organization: University “G. d'Annunzio” of Chieti‐Pescara |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/32744357$$D View this record in MEDLINE/PubMed |
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| Copyright | 2020 International Parkinson and Movement Disorder Society 2020 International Parkinson and Movement Disorder Society. |
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| Keywords | Parkinson's disease medial prefrontal cortex proton magnetic resonance spectroscopy somatic symptoms disorder γ-aminobutyric acid |
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| Notes | Nothing to report. Funding agency Relevant conflicts of interests/financial disclosures This study is not industry sponsored. This work was supported by the Italian Ministry of Health (Grant GR‐2010‐2313418). This study applies tools developed under the National Institutes of Health (Grants NIH R01 EB016089 and P41 EB015909). Richard A.E. Edden also receives salary support from these grants. ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 |
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Background
The dysfunctional activity of the medial prefrontal cortex has been associated with the appearance of the somatic symptom disorder, a key... The dysfunctional activity of the medial prefrontal cortex has been associated with the appearance of the somatic symptom disorder, a key feature of the... BackgroundThe dysfunctional activity of the medial prefrontal cortex has been associated with the appearance of the somatic symptom disorder, a key feature of... |
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| SubjectTerms | Acids Creatine gamma-Aminobutyric Acid Glutamic Acid Glutamine Humans Magnetic resonance spectroscopy medial prefrontal cortex Medically Unexplained Symptoms Movement disorders Neurodegenerative diseases Neurological diseases Parkinson Disease - complications Parkinson's disease Prefrontal cortex Prefrontal Cortex - diagnostic imaging proton magnetic resonance spectroscopy Psychosis somatic symptoms disorder γ‐aminobutyric acid |
| Title | High γ‐Aminobutyric Acid Content Within the Medial Prefrontal Cortex Is a Functional Signature of Somatic Symptoms Disorder in Patients With Parkinson's Disease |
| URI | https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fmds.28221 https://www.ncbi.nlm.nih.gov/pubmed/32744357 https://www.proquest.com/docview/2470845258 https://www.proquest.com/docview/2430094208 https://pubmed.ncbi.nlm.nih.gov/PMC9652613 |
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