Brain Signatures of Obsessive-Compulsive Disorder
Research in neuroanatomy suggests what OCD "looks" like in the brain.
Posted January 13, 2018
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.
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.
"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 has been considered to be a hallmark of OCD (Chamberlain et al., 2007) and various other inhibitory control disorders. Using Stop Signal Reaction Time (SSRT) and Go/No-Go (GNG) tasks with magnetic resonance imaging (together, fMRI), researchers have been able to create controlled experiments which measure both time for correctly withholding responses, average time for response errors (due to lack of inhibiting a response), and are able to evaluate brain activation and deactivation in specific regions during these tasks. In OCD samples, participants with successful inhibition had greater activation in the supplementary motor area compared to controls, although impaired performance on response inhibition tasks like the SSRT was found to be more likely in individuals with OCD (Abramovitch, 2013). Related studies have also found reduced grey matter size in the OFC and in right inferior frontal areas, a region related to inhibition and attentional control (Menzies et al., 2008).
Perhaps most interesting, both mental health professionals and scientists alike have proposed that a critical impairment in OCD may be the ability to flexibly and intentionally shift attention adaptively for some desired goal. It has thus been suggested that cognitive flexibility may also play a role in the symptomology and severity of OCD. Intradimensional-Extradimensional set shifting paradigms, designed after the Cambridge Neuropsychological Test Battery, have been used to elucidate information on OCD patients’ ability for reversal learning, set formation, and the ability to shift attention to relevant stimuli or inhibit attention from irrelevant stimuli. On these types of attention shifting tasks, OCD patients are able to direct their attention intentionally but have difficulty shifting attention to new, relevant stimuli and away from an extraneous stimuli (Chamberlain et al., 2006) and this impairment has been found to be significant in first-degree relatives of OCD patients compared to healthy controls as well.
Neuroimaging studies have extended this behavioral work on cognitive flexibility since there may be ceiling effects with behavioral studies specifically for reversal learning. The OFC appears to be significantly less activated in OCD patients than in controls in fMRI reversal learning-based tasks (Remijnse et al., 2006). The lateral OFC, lateral PFC, and parietal cortex regions were also found to be less activated in reversal learning tasks with OCD patients compared to controls. Importantly, patients with OCD make more mistakes when switching between tasks than non-OCD individuals, which has been tied to reduced activation of the dPFC, lateral OFC, ACC, and caudate (Gu et al., 2008).
Another key higher order function implicated in OCD is that of planning, which is the process of getting to a goal by following small, sequential steps that in and of themselves do not produce the desired end result. Using the Tower of London, a classic neuropsychological test, with both behavioral and modified fMRI versions, studies have found that patients with OCD and their even unaffected relatives have longer response times and impaired performance as the difficulty of the task increases (Delorme et al., 2007). In imaging an imaging study, these problems with planning have been linked to decreased activation of the dPFC and the dorsal striatum (caudate and putamen) in medication-free patients with OCD compared to a non-clinical sample (van den Heuvel et al., 2005). Interestingly, possible compensatory mechanisms existed for the patients with OCD which normal subjects did not display. These compensations included increased activation of areas related to performance monitoring and the processing of short-term memories, including the ACC, ventrolateral PFC, and parahippocampal cortex. While memory anomalies have typically been thought of as peripheral in OCD, this study indicates along with a growing body of evidence that hyperactivation of short-term memory processing circuits may be more central than previously thought in the disorder. Additionally, this type of study gives further credence to the hypothesis that OCD is more than “just anxiety” related and is an interplay of emotional dysregulation with executive impairments, since the CSTS circuitry which is disrupted is independent of anxiety.
Goal Direction and Habit Learning
Concurrently to research on response inhibition, cognitive flexibility, and planning, other scientists have focused their attention on the possible interplay of goal directed behavior and automatic, habitual behaviors served by the CSTC system. Many researchers have suggested that perhaps “maladaptive habit learning” may be at play, meaning that when habits become aversive or unneeded after being learned, they continue to be relied upon rather than learning a new, relevant habit in the service of some goal. As in other studies, researchers with new paradigms targeting goal direction and habit learning have continued to find increased activation of the caudate nucleus and putamen (Gillan et al.,, 2015; Yin & Knowlton, 2006). This underscores the importance of the dorsal striatum not only in goal directed and habitual motor behaviors but also in the domains of response inhibition and planning, both of which can be viewed as integral to performing goal directed behaviors and creating adaptive habits.
A Social Constructivist Approach to OCD
Although the above models of OCD etiology and treatment attempt to “discover” from where OCD stems, the social constructivist approach from postmodern theories of a linguistic paradigm suggest that human beings actually “create” OCD by naming it as such. From this lens, OCD has utility only because society has mutually agreed to label these cluster of experiences known as “obsessions” and “compulsions” and treat people with this label in a specific way. Walker (2006) argues that disorders are just abstractions defined by clusters of what individuals have termed as “symptoms.” While the rationale for diagnosing can serve as a shorthand for communicating between professionals, an OCD diagnosis also communicates a hierarchical role relationship, serves to pathologize an experience which may be acceptable in some cultures, and highlights a deficit-focused context through which to understand an individual. Thus, through a social constructivist lens, OCD only exists through consensus and persists by convention. To further turn the etiology debate on its head, Harrop et al. (1996) stated of the disease model addressed above:
“[It] is possible for physiological differences associated with the condition to be the result of the condition and not the cause. . . . [The] relationship between the psychological problems and the physiology should be viewed not as a simple cause-and effect relationship, but more as a reciprocal and iterative relationship where psychological effects can affect the physiology that can in turn affect the psychology.”
In this way, perhaps even the physiological proofs to which the medical models cling so strongly are perhaps not necessarily proofs of OCD at all, but rather, the consequences of labeling one with OCD and treating one as if he or she is OCD.