Brain Signatures of Obsessive-Compulsive Disorder

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Obsessive-Compulsive Disorder is a mental disorder situated in the “Anxiety Spectrum Disorders” chapter of the Diagnostic and Statistical Manual of Mental Disorders, 5th Edition (American Psychiatric Association, 2013). According to the mental health profession’s “Bible” of diagnosable psychiatric conditions, both obsessions and compulsions must be present in order to diagnose OCD. Obsessions are defined most simply as frequent and intense unwanted thoughts which a person experiences, causing them marked distress and anxiety. Compulsions are the response to obsessions, in which a person naturally attempts to reduce their subjective experience of distress by thought suppression, repetitive behaviors, and other rigid, repetitive acts which may or may not be logically tied to the obsession itself. Additionally, the obsessions and compulsions must be time-consuming for the patient with over one hour per day spent engaging in them, they must cause clinically significant impairment in important life areas such as social, occupational, or relational functioning, they must not be due to the physiological effects of a substance, and they must not be better explained as symptoms within the context of another medical disorder. Despite these extensive criteria, it has been hypothesized that up to 3% of the world’s population is impacted by OCD (Karno, Golding, Sorenson, Burnam, 1988) and estimates of sub-clinical OCD are as high as 25% (Zucker et al., 2006). Given the prevalence of this disorder and the impairment which many diagnosed patients experience, it is pressing to explore the etiology of OCD as it is understood at the neuroanatomical level.

OCD Etiology

The proposed etiology of OCD reflects the concept of equifinality (Bertalanffy, 1968), in that the end state of OCD is achievable through many different pathways. Neurocognitive theories of OCD implicate specific brain systems involved. It has been suggested the faulty wiring of the anterior cingulate cortex (ACC) responsible for reward anticipation, decision-making, impulse control, and autonomic functions has been partially responsible for OCD development (Millad & Rauch, 2012). Additionally, the same group has found differences in the orbitofrontal cortex (OFC), a part of the brain responsible for cognitive processing and decision making, between OCD patients and healthy controls in functional and structural magnetic resonance imaging studies. Lastly, neuroscientists suggest that the striatum, deeply embedded in the limbic system and a critical part of the reward system, will be implicated in future neuroimaging studies. Genetic explanations of OCD are not yet fully developed, however there is mounting evidence that OCD is a heritable disorder since an individual is twice as likely to develop OCD if he or she has a first-degree relative who also has the disorder. This heritability is increased ten-fold if an individual has a first-degree relative who developed the disorder in adolescence or childhood (Pauls, 2010). Environmental risk factors for OCD development include traumatic events (Grisham et al., 2011), infectious agents (Singer et al., 2012), and post-infectious autoimmune syndrome (Swedo et al., 2004). Affective theories for OCD development include higher negative emotionality as a personality trait, increased internalizing symptoms in childhood, and behavioral inhibition in childhood (Coles et al., 2006). These affective theories address the problems which may stem from behaving in overly rule-bound ways and emotional reactions which accompany these behavior patterns in childhood, as well as how these habits may feed in to the OCD cycle.

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“Just” Anxiety or Inhibitory Control Issue?

New classification criteria from the DSM 5 and the 11th Edition of the International Classification of Diseases and Related Health Problems (ICD-11) mirror the neuroscientific studies of OCD which indicate that OCD may be more closely tied to inhibitory control deficits in the fronto-striatal system than to problems only with emotion regulation in the amygdala related to anxiety. This has been corroborated by dozens of studies in which OCD patients were asked to engage in cognitive tasks of response inhibition, cognitive flexibility, planning, executing goal-directed actions, and habit learning in both behavioral and neuroimaging studies (Bandelow et al., 2017). Thus, OCD can be better understood to be characterized by both intense emotional arousal and problems with executive functioning, which together contribute to maintaining the OCD cycle (Goncalves et al., 2016).

Dysfunction of the cortico-striato-thalamo-cortical (CSTC) circuitry has been a well-agreed upon area of dysfunction in the neuroanatomical model of OCD by neuroscientists (Milad & Rauch, 2012; Goncalves et al., 2017; Li & Mody, 2016). This area houses a number of feedback loops which project from the prefrontal cortex to the striatum, to the thalamus via the globus pallidus, and back to the cortex. Therefore, it is not surprising that higher order cognition such as impulse control related to physical movements and decision making are impaired in OCD.

Another new study found regions beyond the CSTC circuitry differ in OCD as well, including abnormalities in temporal-parietal areas which are closely tied to symptom severity (Goncalves, Battistuzzo, & Sato, 2017). Specifically, decreased white matter and grey matter were found in the angular and superior temporal gyri and superior parietal lobe, respectively. These morphological differences are hypothesized to play a role in the cognitive deficits present in OCD. For instance, the globus pallidus and angular gyrus are implicated in inhibitory control; the middle frontal gyrus is related to executive control; the superior temporal gyrus has been implicated in compulsive checking behaviors; and the superior parietal lobe has been found to be relevant in visual-spatial deficits in OCD.

Response Inhibition

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