The functional anatomy of impulse control disorders

Abstract

Impulsive-compulsive disorders such as pathological gambling, hypersexuality, compulsive eating, and shopping are side effects of the dopaminergic therapy for Parkinson's disease. With a lower prevalence, these disorders also appear in the general population. Research in the last few years has discovered that these pathological behaviors share features similar to those of substance use disorders (SUD), which has led to the term "behavioral addictions". As in SUDs, the behaviors are marked by a compulsive drive toward and impaired control over the behavior. Furthermore, animal and medication studies, research in the Parkinson's disease population, and neuroimaging findings indicate a common neurobiology of addictive behaviors. Changes associated with addictions are mainly seen in the dopaminergic system of a mesocorticolimbic circuit, the so-called reward system. Here we outline neurobiological findings regarding behavioral addictions with a focus on dopaminergic systems, relate them to SUD theories, and try to build a tentative concept integrating genetics, neuroimaging, and behavioral results.

Fig. 1

Heightened striatal dopamine release during gambling in Parkinson’s disease (PD) with pathological gambling (a) [35] and reduced activation of the orbitofrontal cortex (OFC) and rostral cingulate zone (RCZ) in pathological gambling after dopamine (DA) administration (b) [•]. a Ventral striatal DA release (indexed by a reduction of [¹¹C]raclopride binding potential) during gambling as compared with that in a control task in PD patients with (top) and without (bottom) pathological gambling. b Differential effect of medication on brain activity in PD gamblers compared to controls. Gamblers showed a significant dopamine-induced reduction in the left lateral OFC (top) and right RCZ (bottom). (a With permission from: Steeves et al. [35]; b with permission from van Eimeren et al. [•])

Fig. 2

Interacting factors associated with the development of behavioral addictions. AHDH attention deficit–hyperactivity disorder, OCD obsessive–compulsive disorders, SUD substance use disorders

Fig. 3

A model of striatal DA level and subsequent influence of appetitive and inhibitory areas on executive control. Right panel, dotted line normal tonic and phasic DA release from the ventral tegmental area (VTA) to the nucleus accumbens (Nacc). Left panel, bottom the influences of inhibitory and appetitive areas are well balanced and adequately regulated. Right panel, solid line 1 vulnerable individuals have an increased tonic DA level, leading to reduced influence of inhibitory control areas via increased D₂ receptor activation (left panel, middle) [, –, •]; 2 increased D₂ receptor activation interferes with the dip following punishments [55]; 3 adequate reinforcing stimuli now lead to suprathreshold D₁ receptor stimulation, which drives the formation of pathological habits [••]