Decision making in de novo Parkinson's disease

Abstract

The aim is to study decision making in patients with de novo Parkinson's disease (PD). Recent studies reported that medicated patients with PD have poor performances compared with age-matched healthy controls in decision making tasks, specially in the Iowa Gambling Task. Two principal causal hypotheses have been proposed to explain this phenomenon: the overdosing effects of dopaminergic therapy on the orbital frontostriatal circuit that is involved in reward processing, or an amygdala dysfunction, as suggested by similar Skin Conductance Responses of patients with PD and amygdala-damaged patients while performing this task. The assessment of decision making with the Iowa Gambling Task was conducted in 30 nondemented and nondepressed patients with de novo PD and in 25 age-matched healthy controls. No statistically significant difference emerged between performances of de novo PD patients and performances of healthy controls. De novo PD patients have performances in the Iowa Gambling Task similar to those of age-matched healthy controls, suggesting that difficulties in decision making emerge, at least in de novo PD patients, by dopaminergic overstimulation of the orbital frontostriatal circuits.

Impulsivity and Parkinson's disease: More than just disinhibition

“…Regarding decision-making, only few studies have compared de-novo drug-naïve PD patients with HS. These revealed no differences in cognitive performance between PD patients and HS [56]. The majority of studies investigated decision-making in non-demented medicated PD patients, showing in some cases poorer IGT performance in PD patients compared to HS [57,58].…”

Acute and chronic cognitive effects of levodopa and dopamine agonists on patients with Parkinson’s disease: a review

“…Executive functions related to this frontostriatal circuit include functions of attentional control, such as working memory, setswitching and planning, and are usually impaired from the early stages of PD [Sawamoto et al 2008;Rowe et al 2008]. In the early clinical stages of PD the orbital frontostriatal circuit and the related executive functions, providing a reward-based control of behavior, are mostly preserved [Poletti et al 2010]. With the progression of disease, the dopamine depletion impairs also the orbital-frontostriatal circuit, probably resulting in an impairment of related executive functions, although these stages of PD have been scarcely investigated by the neuropsychological point of view [Poletti and Bonuccelli, 2012].…”

Neuropsychological and Radiological Assessments of Two Cases with Apparent Idiopathic Rapid Eye Movement Sleep Behaviour Disorder

“…However, this impairment can be attributed to his preference for risky choices, as reported previously [13]. The preference of PD patients for risky choices in the IGT was explained either by amygdala dysfunction [13] or the overdosing effects of dopaminergic drugs [33]. Our case was better explained by amygdala dysfunction because our patient did not take dopaminergic drugs, just like the de novo PD patients in the study by Poletti et al [33].…”