Obsessive-Compulsive Disorder

Obsessive-Compulsive Disorder

People with OCD experience thoughts and urges that are intrusive and unwanted (obsessions) and/or the need to engage in repetitive behaviors or mental acts (compulsions). A person with this disorder might, for example, spend hours each day washing their hands or constantly checking and rechecking to make sure that a stove, faucet, or light has been turned off.

Obsessions are more than just unwanted thoughts that seem to randomly jump into our head from time to time, such as recalling an insensitive remark a coworker made recently, and they are more significant than day-to-day worries we might have, such as justifiable concerns about being laid off from a job. Rather, obsessions are characterized as persistent, unintentional, and unwanted thoughts and urges that are highly intrusive, unpleasant, and distressing (APA, 2013). Common obsessions include concerns about germs and contamination, doubts (“Did I turn the water off?”), order and symmetry (“I need all the spoons in the tray to be arranged a certain way”), and urges that are aggressive or lustful. Usually, the person knows that such thoughts and urges are irrational and thus tries to suppress or ignore them, but has an extremely difficult time doing so. These obsessive symptoms sometimes overlap, such that someone might have both contamination and aggressive obsessions (Abramowitz & Siqueland, 2013).

Compulsions are repetitive and ritualistic acts that are typically carried out primarily as a means to minimize the distress that obsessions trigger or to reduce the likelihood of a feared event (APA, 2013). Compulsions often include such behaviors as repeated and extensive hand washing, cleaning, checking (e.g., that a door is locked) and ordering (e.g., lining up all the pencils in a particular way), and they also include mental acts such as counting, praying, or reciting something to oneself (Figure 1). Compulsions characteristic of OCD are not performed out of pleasure nor are they connected in a realistic way to the source of the distress or feared event. Approximately 2.3% of the U.S. population will experience OCD in their lifetime (Ruscio, Stein, Chiu, & Kessler, 2010) and, if left untreated, OCD tends to be a chronic condition creating lifelong interpersonal and psychological problems (Norberg, Calamari, Cohen, & Riemann, 2008).

Causes of OCD

The results of family and twin studies suggest that OCD has a moderate genetic component. OCD is five times more frequent in the first-degree relatives of people with OCD than in people without the disorder (Nestadt et al., 2000). Additionally, the concordance rate (the probability that a person, usually a twin or family member, will show symptoms if another has the disorder) of OCD among identical twins is around 57%; however, the concordance rate for fraternal twins is 22% (Bolton, Rijsdijk, O’Connor, Perrin, & Eley, 2007). Studies have implicated about two dozen potential genes that may be involved in OCD. These genes regulate the function of three neurotransmitters: serotonin, dopamine, and glutamate (Pauls, 2010). Many of these studies included small sample sizes and have yet to be replicated, thus additional research needs to be done in this area.

A brain region that is believed to play a critical role in OCD is the orbitofrontal cortex (Kopell & Greenberg, 2008), an area of the frontal lobe involved in learning and decision-making (Rushworth, Noonan, Boorman, Walton, & Behrens, 2011) (Figure 2). In people with OCD, the orbitofrontal cortex becomes especially hyperactive when they are provoked with tasks in which, for example, they are asked to look at a photo of a toilet or of pictures hanging crookedly on a wall (Simon, Kaufmann, Müsch, Kischkel, & Kathmann, 2010). The orbitofrontal cortex is part of a series of brain regions that, collectively, is called the OCD circuit; this circuit consists of several interconnected regions that influence the perceived emotional value of stimuli and the selection of both behavioral and cognitive responses (Graybiel & Rauch, 2000). As with the orbitofrontal cortex, other regions of the OCD circuit show heightened activity during symptom provocation (Rotge et al., 2008), which suggests that abnormalities in these regions may produce the symptoms of OCD (Saxena, Bota, & Brody, 2001). Consistent with this explanation, people with OCD show a substantially higher degree of connectivity of the orbitofrontal cortex and other regions of the OCD circuit than do those without OCD (Beucke et al., 2013). Additionally, researchers have discovered that people diagnosed with OCD actually show under-activation of brain areas responsible for stopping habitual behavior.^[1]

Past research discussed above was based on imaging studies, which highlight the potential importance of brain dysfunction in OCD. However, one important limitation of these findings is the inability to explain differences in obsessions and compulsions. Another limitation is that the correlational relationship between neurological abnormalities and OCD symptoms cannot imply causation (Abramowitz & Siqueland, 2013).

Another cause for OCD, specifically in children and adolescents, is PANDAS (short for pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections). This diagnosis occurs when strep triggers a misdirected immune response and results in inflammation on a child’s brain. Usually, children with PANDAS have a very sudden onset or worsening of their symptoms, followed by slow, gradual improvement. If children with PANDAS get another strep infection, their symptoms suddenly worsen again. The increased symptom severity usually persists for at least several weeks but may last for several months or longer.^[2]

Though the actual prevalence of PANDAS is not known, a conservative estimate from the PANDAS Research Network suggests that 1 in 200 children are affected by this condition in the United States alone.^[3] Though symptoms often fade over time, low-level anxiety and OCD/TIC issues may remain permanently, and there are times where the exacerbation can take four to six months to remit. Treatment for this diagnosis includes antibiotics, IVIG (an intravenous pooled blood product comprising immunoglobulins that is used in treating immune deficiencies), plasmapheresis or plasma exchange (PEX) (a process during which the harmful auto-antibodies are removed from the blood system), and others such as cognitive-behavioral therapy (CBT), tonsillectomy, and probiotics. Generally, the best treatment for acute symptoms is antibiotics, and CBT to help manage neuropsychiatric symptoms.