Cerebral Hemispheres 2
NEUROSCIENTIFICALLY CHALLENGED

NEUROSCIENCE MADE SIMPLER

Know Your Brain: Obsessive-Compulsive Disorder (OCD)


Every night, Steven spends over an hour preparing for bed. For many of us, preparing for bed involves routines like putting on pajamas, going to the bathroom, and brushing our teeth. But for Steven, his preparation doesn’t truly begin until after he has already done these things.

Once Steven is ready to get into bed, he goes downstairs. He turns out the lights, locks the door, and checks to make sure the stove hasn’t been left on. But he does more than just look at the stove; he also gently touches the dials to confirm they are in the “off” position. Then, he stares at the dials for 30 seconds to convince himself that touching them didn’t accidentally move them into the “on” position—even though this seems like it would be impossible with such a light touch.

Finally, he goes upstairs to get into bed. But he is stopped by the thought that maybe he forgot to make sure the door was locked.

He thinks he remembers doing this, but the memory isn’t as clear as he would like it to be. Regardless, there’s always the chance he might not have turned the lock completely. So, he goes back to check the lock again. The short amount of time that has passed suggests maybe he should check the stove one more time, too. So he does.

Once he gets into bed, he immediately begins to question if he turned off the lights. Or, maybe he brushed up against the dials of the stove on his way back upstairs, unintentionally turning it back on. The uncertainty is almost unbearable, and it would only take a short walk downstairs to relieve his anxiety. Thus, he goes through the whole process again. He’ll repeat these steps about 15-20 times before finally feeling like he’s able to stay in bed and go to sleep.


OCD symptoms

Steven has obsessive-compulsive disorder (OCD), a surprisingly common condition that affects up to 3% of the general population. People with OCD are plagued by persistent, intrusive thoughts called obsessions. The obsessions are typically linked to compulsions, which are acts a patient feels compelled to do in order to mitigate the distress caused by obsessive thoughts. For some, compulsions involve observable behaviors (like Steven’s stove-checking), but for others they might consist of mental acts like praying, reviewing past events, counting, etc.

OCD obsessions often follow common themes like: fears of contamination (e.g., by germs), a preoccupation with symmetry, taboo thoughts (e.g., pedophilia, incest), and concerns about harming oneself or others.

It’s important to note that people with OCD are very unlikely to actually have taboo desires, or to intentionally hurt someone. Instead, they’re tortured by the fact that these types of thoughts can even appear in their consciousness. They go to great lengths, represented by their compulsions, to try to keep the thoughts from becoming reality.

OCD symptoms occur on a spectrum, and the disorder can look quite different from case to case. One patient may seem to be outwardly healthy but suffer from obsessive thinking that disrupts her ability to concentrate, sleep, and maintain relationships. Another patient may be clearly debilitated by the disorder. One teenage girl, for example, was afraid that pinworms might enter her mouth. To ward off the danger, she stopped speaking for 10 months and shunned eating until she needed to be hospitalized.

 

OCD and the brain

Neuroscientists are still uncertain about what happens in the brain to cause OCD, but one popular hypothesis suggests it involves brain circuits that connect the frontal cortex with a collection of structures called the basal ganglia.

The basal ganglia (within red square). Note that the basal ganglia are not actually seen on the surface of the brain.

According to this perspective, OCD symptoms begin with activity in a part of the frontal cortex called the orbitofrontal cortex, or OFC. The OFC sits just above the eye sockets (aka the orbits), and has diverse functions—most of which are still poorly understood. Research, however, suggests that areas of the OFC are highly active when we notice something dangerous or threatening in the environment.

After we recognize that a threat is present, pathways that connect the OFC to the basal ganglia are activated. The basal ganglia are best known for their role in movement, but they are also involved in a variety of cognitive and emotional functions. They are especially important to: facilitation of goal-directed actions, development of habitual responses, and switching to a new behavior when it’s deemed necessary. The circuitry of the basal ganglia can be divided into two opposing pathways: the direct pathway, which facilitates action, and the indirect pathway, which inhibits it. (See this article if you want more details on how these basal ganglia circuits work.)

Let’s look at how a simplified version of this OFC-basal ganglia circuit might work in a healthy individual. First, they notice something in the environment that could be identified as dangerous, and the OFC is involved in recognizing it as a potential threat. Let’s say they touch a door handle in a public restroom, which of course carries a risk of exposure to germs. The OFC interacts with the basal ganglia via the direct pathway to initiate an action to mitigate the threat. This leads to the person using a few squirts of hand sanitizer. At this point, the indirect pathway kicks in and inhibits further action.

In someone with OCD, the pathway from the OFC to the basal ganglia tends to be overly excitable. OCD patients are hyper-aware of things in the environment that might pose a threat, and that level of awareness is linked to high levels of OFC activity. Thus, in the OCD patient, a threat might be detected not only when they touch the door handle in a public restroom, but also when they brush up against any surface that hasn’t recently been sanitized—even if it’s a countertop in their own home.

This extreme vigilance is associated with over-excitation of the direct pathway. When the direct pathway is activated, the individual is prompted to clean their hands. But the high level of activity in the direct pathway drowns out the inhibitory action of the indirect pathway, and the patient has a difficult time switching to a different behavior. Additionally, each time the threat is temporarily alleviated, the individual feels a transient sense of relief—which reinforces the response. All of this leads to compulsive behavior, and the hand-washing must be repeated a number of times before the patient is satisfied.

 

Not the whole story

This model of OCD is supported by a wealth of studies. Some have found increased activity among the circuits mentioned above in OCD patients, and others have found a reduction in that activity in response to the most common treatments for OCD (which include cognitive behavioral therapy and selective serotonin reuptake inhibitors).

More recent research, however, suggests that this model is too simplistic (a common refrain in neuroscience). For example, one problem is that the OFC is not a homogenous brain area, and while some OFC regions are hyperactive in OCD, others appear to be hypoactive. Additionally, research indicates that other parts of the brain (like the amygdala, hippocampus, and other regions) also play important roles in the manifestation of OCD symptoms, suggesting the model outlined above is incomplete.

Thus, although the OFC and basal ganglia seem to play important roles in OCD, the original model describing their interaction to produce OCD symptoms is likely only part of the story. Neuroscientists hope that further research will elucidate the neural circuitry behind OCD, and lead to better ways to help patients like Steven manage a disorder that can completely upend someone’s life.

 

References (in addition to linked text above):

Menzies L, Chamberlain SR, Laird AR, Thelen SM, Sahakian BJ, Bullmore ET. Integrating evidence from neuroimaging and neuropsychological studies of obsessive-compulsive disorder: the orbitofronto-striatal model revisited. Neurosci Biobehav Rev. 2008;32(3):525-49. doi: 10.1016/j.neubiorev.2007.09.005. Epub 2007 Oct 17. PMID: 18061263; PMCID: PMC2889493.

Milad MR, Rauch SL. Obsessive-compulsive disorder: beyond segregated cortico-striatal pathways. Trends Cogn Sci. 2012 Jan;16(1):43-51. doi: 10.1016/j.tics.2011.11.003. Epub 2011 Dec 2. PMID: 22138231; PMCID: PMC4955838.

Pauls DL, Abramovitch A, Rauch SL, Geller DA. Obsessive-compulsive disorder: an integrative genetic and neurobiological perspective. Nat Rev Neurosci. 2014 Jun;15(6):410-24. doi: 10.1038/nrn3746. PMID: 24840803.

Saxena S, Brody AL, Schwartz JM, Baxter LR. Neuroimaging and frontal-subcortical circuitry in obsessive-compulsive disorder. Br J Psychiatry Suppl. 1998;(35):26-37. PMID: 9829024.

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