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Interaction between affect and executive functions in Parkinson's disease

Paolo Barone and Gabriella Santangelo

Introduction

The relationship between affect and cognition is a topic of continuing interest [1]. Affect and cognition are processes that are interconnected, related, and mediated by a circuitry that is widely distributed throughout the brain and includes subcortical areas typically considered to be ‘affective’ (e.g. the amygdala and nucleus accumbens) as well as portions of the cortex that are typically considered ‘cognitive’ (e.g. the ventromedial prefrontal cortex/anterior cingulate and orbitofrontal cortex) [2] (Fig. 6.1).

Cognitive impairment in Parkinson’s disease (PD) can be found in all stages of the disease and may precede the development of dementia. It includes impairments in attention, encoding memory, and visuospatial and executive functions, the latter being mainly attributed to the disruption of the fronto-striatal circuitry (see Chapter 4) [3]. Affective disorders in PD include depression, apathy, and anhedonia. Prevalence rates for depression in PD vary from 2.7% to more than 90% [4], whereas the prevalence rates for apathy range from 13.9 to 70%, the mean prevalence being 35% [5]. This variability may be in part due to differences in study methods, the presence of substantial overlap between symptoms of PD and symptoms of depression, and the criteria used to diagnose depression and apathy [4]. There is a particular problem when using the Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM-IV), because of the ambiguity between depression, apathy, and dementia [6]. Furthermore, apathy and anhedonia, which are both included in DSM Criterion A.2, may be independent of depression and may reflect the decreased involvement of PD patients in their usual activities rather than being the consequence of a depressive disorder.

Classically, dopamine denervation is associated with motor symptoms in PD. However, dopamine neurotransmission seems to have a relevant role in controlling both the cognitive and the emotional aspects of the disease. Depression in PD is associated with the loss of dopamine and noradrenaline innervation in the limbic system [7], and may fluctuate along with motor functions, improving during the ‘on’ state and worsening during the ‘off’ state [8]. Similar fluctuations are reported for apathy in PD, suggesting that apathy is at least partly a dopamine-dependent syndrome [9]. Finally, the neural substrate of anhedonia is suggested to be due to dysfunction of the dopaminergic-mesolimbic reward circuit involving the ventral striatum and prefrontal cortex [10]. Along with the above observations that support a role in controlling affect in PD, the dopamine system also seems to be deeply involved in controlling cognition related to frontal lobe functions. In particular, mesocortical dopamine inputs to the prefrontal cortex regulate working memory function, planning, and attention, suggesting that dopamine alterations may at least be partly responsible for executive dysfunctions in PD [11].

Circuitry interconnections between affective and cognitive functions

Fig. 6.1 Circuitry interconnections between affective and cognitive functions. GPE, external global pallidus; STN, subth- lamic nucleus; vP, ventral pallidum; AMY, amygdala; GPi-SNpr, internal globus pallidus and substantia nigra pars reticulata; DA, dopamine; CX, cortex.

This review analyses the association between affective disorders and cognitive impairment in PD, with a special focus on the relationship between executive dysfunction, depression, anhedo- nia, and apathy.

 
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