All of us sometimes go back to check whether we really locked the front door, or imagine giving a punch in the nose to somebody at work whom we really can't stand. But when someone goes back to check the door 20 or 30 times, or keeps thinking so much about punching that person in the nose that they can't concentrate on their work, then they may be suffering from the strange condition known as obsessive-compulsive disorder (commonly known as “OCD”).

But unlike bulimics or compulsive gamblers, who also have an irrepressible desire to keep repeating the same behaviours, victims of OCD do not get anypleasure from it. They recognize the irrational, ridiculous nature of their compulsions and suffer from them tremendously. For this reason, many compulsive behaviours are carried out in secret, which only reinforces the stressassociated with this affliction.

In talking about OCD, a distinction is made between the obsessions, which are the undesired thoughts, and the compulsions, which are the uncontrollable behaviours designed to calm the obsessions. For example, to calm an obsession with cleanliness, a person may follow a compulsion to keep washing his hands repeatedly until his skin is raw. Or someone may be obsessed by the thought that she may have hit someone with her car, and keep driving around the neighbourhood compulsively looking for a body until she has quelled her doubts. Some people compare compulsions with “mental hiccups” that can't be stopped, because even though they are very disturbing, they temporarily dispell the even greater anxiety caused by obsessions.

Obsessive-compulsive disorder involves thoughts and/or behaviours that are invasive, persistent, and repetitive. These behaviours are carried out in a very precise way that is meant to neutralize anxiety, but they constitute such excessive responses to the situations that they are meant to neutralize that they can actually become quite a handicap.

The exact causes of obsessive-compulsive disorder (OCD) are not yet well understood. It was once thought that a very strict upbringing, emotional deprivation, or an excessive emphasis on cleanliness in childhood might contribute to the development of OCD later in life. But these explanations were soon found inadequate. In other words, you do not have to have monsters for parents in order to develop OCD.

As with many other anxiety disorders, certain genes may be involved in OCD. Cases of OCD that develop in childhood tend to be hereditary. When a parent has OCD, there is a slightly higher probability that his or her child will do so as well. When OCD is inherited, it is the general nature of the disorder that seems to be transmitted, and not the specific symptoms (for example, a mother may have a handwashing compulsion, while her child engages in compulsive checking rituals).

More recent studies also seem to indicate that streptococcal infections in young children may damage the part of the brain responsible for repetitive behaviour and thus predispose these children to develop OCD. Other preliminary studies have found that the brains of people who had OCD contained less white matter than those of people who did not.

Brain-imaging studies have also revealed differences between the brain-activity patterns of OCD sufferers and those of normal subjects. For example, people with OCD seem to show a problem in communication between the frontal cortex and the deeper structures of the central grey nuclei. Positron-emission tomography (PET) scans have also shown that after treatments that produced notable improvements in the condition of OCD patients, the activity patterns in these parts of the brain became more normal.

Researchers have also found lower levels of serotonin in these parts of the brain in OCD patients, which helps to explain why treatment with selective serotonin reuptake inhibitors (SSRIs) produces positive effects.

OCD is diagnosed when such ritualized behaviours are causing the person significant distress and taking up so much time (in general, more than one hour per day) that they are interfering with his or her normal daily activities.

Conditioned fear (follow the Experiment module link to the left) is regarded as the primary mechanism underlying many anxiety disorders, such as phobias and post-traumatic stress disorder. A conditioned fear exists when a neutral stimulus is strongly associated with an aversive one in a person's mind. After a while, the neutral stimulus alone suffices to produce anxiety—for example, when the low rumble of thunder suddenly plunges a former soldier back into all the horrors of the battlefield.

Anxiety disorders can be treated successfully with behavioural therapies (see sidebar) that extinguish the underlying conditioned fears. This process ofextinctioninvolves gradually weakening the conditioned fear until the conditioned stimulus (in the preceding example, the sound of thunder) is no longer associated with the aversive stimulus (the horrors of battle). In other words, over time, the patient learns how to overcome the association that he or she had formed between a neutral stimulus and a fear. In addition to the passage of time, a change in context can also facilitate the extinction of a conditioned fear.

Extinction is thus an adaptive phenomenon: if the actual threatening situation is not recurring, no purpose is served by continuing to experience fear simply because its context has recurred. Researchers have therefore proposed that certain anxiety disorders may be due to a malfunction in the mechanism by which conditioned fears are extinguished.

Also, a number of studies have shown that deconditioning through extinction does not involve actually erasing the conditioning, but rather learning something new in addition to it. Extinction is thus different from forgetting. The original fear is still there; it is simply masked and is no longer expressed.

Other experimental data support the idea that fear conditioning and fear extinction are carried out by different parts of the brain. The role of the amygdala in fear conditioning is well established. The role of the prefrontal cortex in fear extinction is less well established, but the ventromedial portion of this cortex definitely plays a role in this process, just as it does in depression. This makes sense, because the prefrontal cortex has long been known to play a role in inhibiting inappropriate behavioural responses. In experimental studies, when lesions were made in an animal's ventromedial prefrontal cortex, they did not prevent it from learning new conditioned fears. But when the researchers then attempted to extinguish a conditioned fear (for example, by subjecting the animal to a sound without the accompanying electric shock that it had previously been taught to expect), the process of extinction took much longer.

The precise role of the ventromedial prefrontal cortex remains ambiguous, however, because it does not seem to be needed to achieve the extinction itself, but only to recall the newly learned information some time after extinction has been achieved. These observations would therefore suggest that this structure's role is more to consolidate the extinction or to recall the context in which the extinction took place.