Obsessive-compulsive disorder (OCD) is primarily conceived as an anxiety disorder but has features resembling addictive behavior. Patients with OCD may develop dependency upon compulsive behaviors because of the rewarding effects following reduction of obsession-induced anxiety.
Reward processing is critically dependent on ventral striatal-orbitofrontal circuitry and brain imaging studies in OCD have consistently shown abnormal activation within this circuitry. This study (1) is the first functional imaging study to investigate explicitly reward circuitry in OCD.
This study’s methods looked at brain activity during reward anticipation and receipt, and compared 18 OCD patients and 19 healthy control subjects, using a monetary incentive delay task and functional magnetic resonance imaging. Reward processing was compared between OCD patients with predominantly contamination fear and patients with predominantly high-risk assessment.
Results showed that obsessive-compulsive disorder patients showed attenuated reward anticipation activity in the nucleus accumbens compared with healthy control subjects. Reduced activity of the nucleus accumbens was more pronounced in OCD patients with contamination fear than in patients with high-risk assessment.
The authors concluded that the results pointed to obsessive-compulsive disorder patients being less able to make beneficial choices because of altered nucleus accumbens activation when anticipating rewards. This finding supports the conceptualization of OCD as a disorder of reward processing and behavioral addiction.
“Obsessive-compulsive disorder is characterized by the presence of recurrent and anxiety-provoking thoughts, images, or impulses (obsessions), typically followed by repetitive ritualistic behaviors (compulsions) to relieve anxiety.
The anxiety symptoms and inadequate fear responses pathognomonic for OCD may result from inadequate dorsal prefrontalstriatal control of the amygdala (3). However, obsessive-compulsive symptoms are not always anxiety-driven and may also be related to cognitive and behavioral inflexibility, reflected by impairments in response inhibition and attentional set shifting (4) because of dysfunctional frontal-striatal circuitry (5,6).
Alternatively, OCD has been conceptualized as a disorder of behavioral addiction, with obsessions and compulsions being related to loss of voluntary control and a dependency on repetitious, self-defeating behavior (7–9). Compulsions could be viewed as addictive because of their rewarding effects following reduction of obsession-induced anxiety.
Addictive behavior is associated with defective processing of natural rewards. Likewise, OCD patients were found to be impaired in adjusting their behavior following monetary incentives (10). Reward processing is critically dependent on ventral striatal-orbitofrontal circuitry (11), and resting-state imaging studies have consistently shown abnormal metabolism in striatum and orbitofrontal cortex (OFC) in OCD (12). Moreover, recent studies have shown that the nucleus accumbens (NAcc), as part of the ventral striatum, is a successful target for deep brain stimulation in OCD treatment (13– 15).
In OCD patients, obsessive-compulsive behaviors are likely to be associated with reward circuitry hyperactivity, reflected by findings of increased OFC-striatal activity at rest and in symptom provocation studies (12,18), at the expense of its responsiveness to natural rewards.
Therefore, we expect to find decreased OFC-striatal activity during reward processing, more specifically, decreased reward anticipatory activation in the nucleus accumbens and decreased activation of the OFC related to reward feedback.
Discussion – OCD patients reacted significantly slower than matched healthy control subjects in anticipation of rewards. Compared with healthy control subjects, OCD patients showed greatly attenuated reward anticipation activity in the bilateral NAcc. Reduced brain activity of the NAcc was more pronounced in OCD patients with contamination fear, compared with patients with high-risk assessment symptoms. The difference between both patient groups in the absence of differences in performance speed indicates that blunted NAcc activity is primarily accounted for by defective reward anticipation and not by motor impairments.
Obsessive-compulsive disorder patients who suffered predominantly from contamination fear showed reduced ventral striatal activation when compared with patients with predominantly high-risk assessment and checking symptoms.
This is in agreement with Rauch et al. (34), who reported an inverse relationship between striatal activation and washing but not checking symptoms during implicit learning. Also, a study by Mataix-Cols et al. (35) suggests that OCD with contamination fear may be characterized by dysfunctional brain circuits involved in emotion processing, whereas OCD with checking symptoms might be associated with regions that are important for motor and attentional functions.
The reward network, which is linked to limbic regions for emotion processing, may thus be more compromised in OCD with predominant contamination fear symptoms. Furthermore, patients with contamination fear showed reduced reward anticipation activity of the left insula, a region that is implicated in emotion perception and processing of personally rewarding stimuli (21) but also in the integration of gustatory and olfactory inputs.
Previous functional magnetic resonance imaging studies found increased activation of the left insula in OCD patients when viewing aversive pictures (35) and in OCD patients with contamination fear when viewing pictures depicting washing or contamination (20). The insula may thus be excessively activated during obsessive-compulsive symptoms, particularly in association to disgust-related symptoms, compromising its recruitment for normal reward processing.
Our results match up remarkably with the findings of functional imaging studies in addiction disorders. Blunted reactivity of the ventral striatum during anticipation of monetary gain was found in detoxified alcoholics (36), nicotine smokers (27,37,38), and cannabis smokers (27,37,38).
Drug-related stimuli, however, increase activity of the reward circuitry in drug addicts (39). Likewise, blunted responsiveness of the reward circuitry in our study is paralleled by increased activity in response to OCD-provoking stimuli in previous studies (reviewed by ).
Therefore, the NAcc may be less responsive when recruited during conventional reward processing due to its bias toward drugs of abuse in addiction, as well as toward obsessions and compulsions in OCD, supporting the conceptualization of OCD as a disorder of behavioral addiction (8).
Although population studies show relatively little comorbidity between OCD and substance abuse, dysfunctional brain reward circuitry underlying both disorders may explain some shared phenomena, such as a dependency on repetitious, self-defeating behavior that becomes more difficult to control over time. Because OCD patients are already fully engaged in reinforcing compulsive behaviors, they may be less prone to develop substance abuse.”
Two major points of interest here in terms of our general theories of addiction.
1. OCD can be conceptulised as a behvioural addiction as the altered reward and anxiety reliving properties of OCD behaviour point to the stress and reward dysregulation commonly seen in other addictive behaviours.
2. An impaired insular-related emotion processing deficit also, as with other addictive behaviours, points to a maladaptive decision making mechanism in which emotion does not recruit the goal directed adaptive decision making of the prefrontal cortex but instead recruits less “thinking” more reacting subcortical compulsive response.
In line with what we are hoping to achieve in this blog, OCD may be considered an addictive behaviour or alternatively addictive behaviours may be seem as obsessive compulsive behaviours.
1. Figee, M., Vink, M., de Geus, F., Vulink, N., Veltman, D. J., Westenberg, H., & Denys, D. (2011). Dysfunctional reward circuitry in obsessive-compulsive disorder. Biological psychiatry, 69(9), 867-874.