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

Abstract

Abstract:The spatiotemporal progression of dopamine depletion in Parkinson's disease (PD) provides a special model for assessing dopaminergic effects on neural systems with differential baseline dopamine levels. This study aims at reviewing cognitive effects of dopaminergic stimulation in PD. While considering dopaminergic drugs (levodopa or dopamine agonists), temporal intervals (acute or chronic) and cognitive domains, we found that empirical evidence was almost focused on acute effects of levodopa on executive functions. The paucity of empirical evidence suggests that no meaningful conclusions can be actually drawn and further research is needed in relation to: (1) other cognitive domains; (2) the acute cognitive effects of dopamine agonists, as compared with levodopa; (3) possible differences between cognitive effects of different dopamine agonists; (4) the cognitive effects of chronic dopaminergic therapies. The latter issue is of particular clinical interest considering that many PD patients present a mild cognitive impairment: is this cognitive feature worsened or improved by the prolonged dopaminergic therapy? In addition to the potential risk of inducing dyskinesia and behavioral side effects such as impulse control disorders, also cognitive effects of prolonged dopaminergic treatments should be taken in account by clinicians in order to anticipate or to delay their prescription to PD patients.

Longitudinal brain volumetric changes and their predictive effects on cognition among cognitively asymptomatic patients with Parkinson's disease

“…Finally, all of our subjects were in the ON medication state during the study period, making it difficult to determine the medication effects on cognition and brain volume. Although cognitive deficits in PD could be a result of dopaminergic treatment (Dopamine Overdose Hypothesis) or due to dopaminergic deficiency (Dopamine Depletion Hypothesis) [31], thus far, there is a lack of sufficient evidence to conclude the effects of medication on cognition in PD [32]. Also, while previous studies have shown improved functional connectivity when PD patients were in the ON medication state (e.g.…”

Neurochemical correlation between major depressive disorder and neurodegenerative diseases

“…These alterations lead to a progressive loss of dopaminergic neurons and the clinical signs of illness [63][64][65][66][67][68]. However, these pathologic changes are not limited to the substantia nigra pars compacta.…”

Simultaneous glutamate recordings in the frontal cortex network with multisite biomorphic microelectrodes: New tools for ADHD research

“…The aberrant regulation of neurotransmitters has been implicated in numerous disease states including schizophrenia, Parkinson's disease, Alzheimer's disease, mood disorders, attention-deficit/hyperactivity disorder (ADHD), and drug addiction (Brambilla et al, 2003;Moghaddam and Javitt, 2012;Lesch et al, 2013;Paula-Lima et al, 2013;Poletti and Bonuccelli, 2013;Quintero, 2013). Of particular note, the frontal cortex is a glutamate-rich brain region and deficits in this area cause poor impulse control, distractibility, hyperactivity, forgetfulness and poor organization and planning (Stuss and Levine, 2002).The frontal cortex is organized into different cortical layers, including the cingulate cortex, prelimbic cortex, infralimbic cortex, and the dorsal peduncle.…”