Disinhibition, Response-Inhibition and Impulse Control Disorder in Parkinson’s Disease.

Impulse Control Disorders (ICDs) are behavioral disturbances in which a person fails to resist the drive to behave in ways that result in distress or impaired social and occupational functioning (Grant et al., 2006). The incidence of ICDs in Parkinson’s disease (PD) is as high as 20%. Dopamine agonists can induce alterations in those frontostriatal networks that manage reward and mediate impulse monitoring and control. Indeed, tonic stimulation of dopamine receptors may damage inhibitory control mechanisms and reward processing, while promoting compulsive repetition of behavior (Ray & Strafella, 2010). ICDs have, in fact, been associated with depressed mood, disinhibition, irritability, and appetite disturbance (Pantone et al., 2006). Moreover, many PD patients have difficulties with mental processing speed, response-inhibition, and shifting between different conceptual sets, suggesting frontal-executive dysfunction. The neurocognitive approach considers two measurable executive functions from which ICDs can be detected: 1) response-inhibition, which neural substrate is located in the inferior portion of the prefrontal cortex; 2) integration of reward/punishment contingencies in individual choices, which neural substrate is located in the orbital-prefrontal cortex. Establishing such a relationship between disinhibition and executive functions could potentially be helpful for therapeutic research and for the efficient targeting of symptom relief in PD. For this reason, we present the preliminary results of an fMRI study with the aim of exploring response-inhibition performance and the neural correlates of inhibition that varied on self-reported trait impulsivity. This chapter will discuss the role of functional neuroimaging for research on ICDs and disinhibition in PD. Significant neuropsychological and neuroanatomical data will be highlighted and attention will be drawn to the concept of “motor impulsivity” in terms of “disinhibition of prepotent responses.