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Hindawi Publishing Corporation Parkinson’s Disease Volume 2012, Article ID 908943, 2 pages doi:10.1155/2012/908943 Editorial Neuropsychiatry of Parkinson’s Disease Antonio L. Teixeira, 1 Leonardo F. Fontenelle, 2 Edward C. Lauterbach, 3 and Sergio Starkstein 4 1 Neurology Section, Department of Internal Medicine, School of Medicine, Federal University of Minas Gerais, 30130-100 Belo Horizonte, MG, Brazil 2 Department of Psychiatry and Legal Medicine, School of Medicine, Federal University of Rio de Janeiro, 22290-140 Rio de Janeiro, RG, Brazil 3 Department of Psychiatry and Behavioral Sciences and Department of Internal Medicine (Neurology Section), Mercer University School of Medicine, Macon, GA 31201, USA 4 Neuropsychiatry Unit, Fremantle Hospital, School of Psychiatry and Clinical Neurosciences, University of Western Australia, Fremantle, WA 6959, Australia Correspondence should be addressed to Antonio L. Teixeira, [email protected] Received 12 December 2011; Accepted 12 December 2011 Copyright © 2012 Antonio L. Teixeira et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Parkinson’s disease (PD) is traditionally regarded as a mo- tor or a movement disorder. In recent years, however, an increased interest has been directed to its nonmotor symp- toms as they seem to determine significant disability at all stages of the disease. Some PD patients consider their non- motor symptoms even more disabling than motor signs. Among these nonmotor symptoms, neuropsychiatric syn- dromes (or behavioral and psychological symptoms) are of paramount importance. They include a wide array of syn- dromes such as anxiety, depression, psychosis, impulse con- trol disorders, apathy, and cognitive dysfunction. Their path- ogenesis in PD is rather complex, involving neurodegen- erative, drug-related, and psychological mechanisms. Their recognition and management represent a great challenge. The paper by R. de la Fuente-Fern´ andez presents a stag- ing model named PD-related frontostriatal cognitive dys- function (PDFCD) that provides a clinical and hypothesis- testing framework for neuropsychiatric syndromes in PD. De La Fuente-Fernandez’s PDFCD model proposes three stages based on the sequential process of dopamine depletion occurring in dierent regions of the striatum (stages I and II) and the frontal cortex (stage III). Therefore, PD patients would present executive dysfunction and mental fatigue (stage I), depression/anxiety (stage IIa), apathy/pain (stage IIb), and dementia (stage III). The paper by J. Calleo et al. summarizes the current liter- ature on the cognitive rehabilitation programs in PD pa- tients. Despite limited available data and heterogeneity of motor and nonmotor symptoms in PD, cognitive rehabili- tation seems to be promising in this context. The paper by Y. Bogdanova and A. Cronin-Golomb1 pre- sents an original study that assessed cognitive correlates of anxiety and apathy in PD patients. In comparison with matched controls, PD patients exhibited higher levels of anx- iety and apathy which were correlated with disease duration. Interestingly, anxiety and apathy correlated dierently with cognitive functions. The question remains open whether the treatment of both conditions impacts on cognitive func- tioning in PD. Until recently, most studies have focused on the impact of motor disability and depressive symptoms on the quality of life of PD patients, neglecting the role of anxiety. The paper by K. K. Hanna and A. Cronin-Golomb addressed this issue, reporting that anxiety, more than depressive, cognitive, and motor symptoms, significantly aected quality of life in PD. Dopaminergic strategies remain the mainstay of PD treatment. However, they are frequently associated with neu- ropsychiatric syndromes, notably psychosis. Alternative ther- apeutic options have been searched in the last years, and adenosine A 2A receptor antagonists seem to be very promis- ing. The paper by C. J. Bleickardt et al. demonstrates that, in comparison with dopamine receptor agonists, adenosine A 2A antagonists exhibit better neuropsychiatric profiles as they do not interfere with prepulse inhibition in rodents (a model of psychosis).

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Page 1: Editorial NeuropsychiatryofParkinson’sDiseasedownloads.hindawi.com/journals/pd/2012/908943.pdftroldisorders,apathy,andcognitivedysfunction.Theirpath-ogenesis in PD is rather complex,

Hindawi Publishing CorporationParkinson’s DiseaseVolume 2012, Article ID 908943, 2 pagesdoi:10.1155/2012/908943

Editorial

Neuropsychiatry of Parkinson’s Disease

Antonio L. Teixeira,1 Leonardo F. Fontenelle,2 Edward C. Lauterbach,3 and Sergio Starkstein4

1 Neurology Section, Department of Internal Medicine, School of Medicine, Federal University of Minas Gerais,30130-100 Belo Horizonte, MG, Brazil

2 Department of Psychiatry and Legal Medicine, School of Medicine, Federal University of Rio de Janeiro,22290-140 Rio de Janeiro, RG, Brazil

3 Department of Psychiatry and Behavioral Sciences and Department of Internal Medicine (Neurology Section),Mercer University School of Medicine, Macon, GA 31201, USA

4 Neuropsychiatry Unit, Fremantle Hospital, School of Psychiatry and Clinical Neurosciences, University of Western Australia,Fremantle, WA 6959, Australia

Correspondence should be addressed to Antonio L. Teixeira, [email protected]

Received 12 December 2011; Accepted 12 December 2011

Copyright © 2012 Antonio L. Teixeira et al. This is an open access article distributed under the Creative Commons AttributionLicense, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properlycited.

Parkinson’s disease (PD) is traditionally regarded as a mo-tor or a movement disorder. In recent years, however, anincreased interest has been directed to its nonmotor symp-toms as they seem to determine significant disability at allstages of the disease. Some PD patients consider their non-motor symptoms even more disabling than motor signs.Among these nonmotor symptoms, neuropsychiatric syn-dromes (or behavioral and psychological symptoms) are ofparamount importance. They include a wide array of syn-dromes such as anxiety, depression, psychosis, impulse con-trol disorders, apathy, and cognitive dysfunction. Their path-ogenesis in PD is rather complex, involving neurodegen-erative, drug-related, and psychological mechanisms. Theirrecognition and management represent a great challenge.

The paper by R. de la Fuente-Fernandez presents a stag-ing model named PD-related frontostriatal cognitive dys-function (PDFCD) that provides a clinical and hypothesis-testing framework for neuropsychiatric syndromes in PD.De La Fuente-Fernandez’s PDFCD model proposes threestages based on the sequential process of dopamine depletionoccurring in different regions of the striatum (stages I andII) and the frontal cortex (stage III). Therefore, PD patientswould present executive dysfunction and mental fatigue(stage I), depression/anxiety (stage IIa), apathy/pain (stageIIb), and dementia (stage III).

The paper by J. Calleo et al. summarizes the current liter-ature on the cognitive rehabilitation programs in PD pa-tients. Despite limited available data and heterogeneity of

motor and nonmotor symptoms in PD, cognitive rehabili-tation seems to be promising in this context.

The paper by Y. Bogdanova and A. Cronin-Golomb1 pre-sents an original study that assessed cognitive correlates ofanxiety and apathy in PD patients. In comparison withmatched controls, PD patients exhibited higher levels of anx-iety and apathy which were correlated with disease duration.Interestingly, anxiety and apathy correlated differently withcognitive functions. The question remains open whether thetreatment of both conditions impacts on cognitive func-tioning in PD.

Until recently, most studies have focused on the impact ofmotor disability and depressive symptoms on the quality oflife of PD patients, neglecting the role of anxiety. The paperby K. K. Hanna and A. Cronin-Golomb addressed this issue,reporting that anxiety, more than depressive, cognitive, andmotor symptoms, significantly affected quality of life in PD.

Dopaminergic strategies remain the mainstay of PDtreatment. However, they are frequently associated with neu-ropsychiatric syndromes, notably psychosis. Alternative ther-apeutic options have been searched in the last years, andadenosine A2A receptor antagonists seem to be very promis-ing. The paper by C. J. Bleickardt et al. demonstrates that, incomparison with dopamine receptor agonists, adenosine A2A

antagonists exhibit better neuropsychiatric profiles as they donot interfere with prepulse inhibition in rodents (a model ofpsychosis).

Page 2: Editorial NeuropsychiatryofParkinson’sDiseasedownloads.hindawi.com/journals/pd/2012/908943.pdftroldisorders,apathy,andcognitivedysfunction.Theirpath-ogenesis in PD is rather complex,

2 Parkinson’s Disease

The paper by E. C. Lauterbach et al. presents a compre-hensive review of the neuroprotective effects of the psycho-tropic drugs used in PD.

Antonio L. TeixeiraLeonardo F. FontenelleEdward C. Lauterbach

Sergio Starkstein

Page 3: Editorial NeuropsychiatryofParkinson’sDiseasedownloads.hindawi.com/journals/pd/2012/908943.pdftroldisorders,apathy,andcognitivedysfunction.Theirpath-ogenesis in PD is rather complex,

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