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      Frontostriatal Cognitive Staging in Parkinson's Disease

      review-article
      Author(s): *
      Publication date (Electronic):
      Journal: Parkinson's Disease
      Publisher: Hindawi Publishing Corporation

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          Abstract

          Cognitive impairment and behavioural disorders are often encountered in subjects with Parkinson's disease (PD). A simple PD-related frontostriatal cognitive dysfunction (PDFCD) staging is proposed. Executive dysfunction and mental fatigue (stage I), depression/anxiety (stage IIa), apathy/pain (stage IIb), and dementia (stage III) reflect a sequential process of dopamine depletion occurring in different regions of the striatum (stages I and II) and the frontal cortex (stage III). In addition to these nonmotor manifestations present in the unmedicated (OFF) state, the PDFCD model also predicts a number of complications related to dopaminergic treatment (ON state), from impulse control disorders (stages I and IIa) to hallucinations (stage IIb) and psychosis (stage III). Although the model admittedly needs further refinements, it provides a framework for hypothesis testing and may help clinicians optimize therapeutic strategies.

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          Getting formal with dopamine and reward.

          Wolfram Schultz (2002)
          Recent neurophysiological studies reveal that neurons in certain brain structures carry specific signals about past and future rewards. Dopamine neurons display a short-latency, phasic reward signal indicating the difference between actual and predicted rewards. The signal is useful for enhancing neuronal processing and learning behavioral reactions. It is distinctly different from dopamine's tonic enabling of numerous behavioral processes. Neurons in the striatum, frontal cortex, and amygdala also process reward information but provide more differentiated information for identifying and anticipating rewards and organizing goal-directed behavior. The different reward signals have complementary functions, and the optimal use of rewards in voluntary behavior would benefit from interactions between the signals. Addictive psychostimulant drugs may exert their action by amplifying the dopamine reward signal.
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            Uneven pattern of dopamine loss in the striatum of patients with idiopathic Parkinson's disease. Pathophysiologic and clinical implications.

            S J Kish, K Shannak, O Hornykiewicz (1988)
            Autografting of dopamine-producing adrenal medullary tissue to the striatal region of the brain is now being attempted in patients with Parkinson's disease. Since the success of this neurosurgical approach to dopamine-replacement therapy may depend on the selection of the most appropriate subregion of the striatum for implantation, we examined the pattern and degree of dopamine loss in striatum obtained at autopsy from eight patients with idiopathic Parkinson's disease. We found that in the putamen there was a nearly complete depletion of dopamine in all subdivisions, with the greatest reduction in the caudal portions (less than 1 percent of the dopamine remaining). In the caudate nucleus, the only subdivision with severe dopamine reduction was the most dorsal rostral part (4 percent of the dopamine remaining); the other subdivisions still had substantial levels of dopamine (up to approximately 40 percent of control levels). We propose that the motor deficits that are a constant and characteristic feature of idiopathic Parkinson's disease are for the most part a consequence of dopamine loss in the putamen, and that the dopamine-related caudate deficits (in "higher" cognitive functions) are, if present, less marked or restricted to discrete functions only. We conclude that the putamen--particularly its caudal portions--may be the most appropriate site for intrastriatal application of dopamine-producing autografts in patients with idiopathic Parkinson's disease.
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              Reciprocal limbic-cortical function and negative mood: converging PET findings in depression and normal sadness.

              H Mayberg, M Liotti, S Brannan … (1999)
              Theories of human behavior from Plato to Freud have repeatedly emphasized links between emotion and reason, a relationship now commonly attributed to pathways connecting phylogenetically "old" and "new" brain regions. Expanding on this theory, this study examined functional interactions between specific limbic and neocortical regions accompanying normal and disease-associated shifts in negative mood state. Regions of concordant functional change accompanying provocation of transient sadness in healthy volunteers and resolution of chronic dysphoric symptoms in depressed patients were examined with two positron emission tomography techniques: [15O]water and [18F]fluorodeoxyglucose, respectively. With sadness, increases in limbic-paralimbic blood flow (subgenual cingulate, anterior insula) and decreases in neocortical regions (right dorsolateral prefrontal, inferior parietal) were identified. With recovery from depression, the reverse pattern, involving the same regions, was seen--limbic metabolic decreases and neocortical increases. A significant inverse correlation between subgenual cingulate and right dorsolateral prefrontal activity was also demonstrated in both conditions. Reciprocal changes involving subgenual cingulate and right prefrontal cortex occur with both transient and chronic changes in negative mood. The presence and maintenance of functional reciprocity between these regions with shifts in mood in either direction suggests that these regional interactions are obligatory and probably mediate the well-recognized relationships between mood and attention seen in both normal and pathological conditions. The bidirectional nature of this limbic-cortical reciprocity provides additional evidence of potential mechanisms mediating cognitive ("top-down"), pharmacological (mixed), and surgical ("bottom-up") treatments of mood disorders such as depression.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Parkinsons Dis
                Journal ID (publisher-id): PD
                Title: Parkinson's Disease
                Publisher: Hindawi Publishing Corporation
                ISSN (Print): 2090-8083
                ISSN (Electronic): 2042-0080
                Publication date (Print): 2012
                Publication date (Electronic): 6 December 2011
                Volume: 2012
                Electronic Location Identifier: 561046
                Affiliations
                Section of Neurology, Hospital A. Marcide, 15405 Ferrol, Spain
                Author notes
                *Raúl de la Fuente-Fernández: rfuente@ 123456medynet.com

                Academic Editor: Leonardo F. Fontenelle

                Article
                DOI: 10.1155/2012/561046
                PMC ID: 3236592
                PubMed ID: 22191070
                SO-VID: 65d0bbdd-55e7-4c59-b784-9f9fe999d6f8
                Copyright © Copyright © 2012 Raúl de la Fuente-Fernández.
                License:

                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.

                History
                Date received : 20 July 2011
                Date accepted : 16 September 2011
                Categories
                Subject: Review Article

                ScienceOpen disciplines: Neurology
                Data availability:
                ScienceOpen disciplines: Neurology

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