Serendip is an independent site partnering with faculty at multiple colleges and universities around the world. Happy exploring!

Obsessive Compulsive Disorder: A Neurobiological Model

Amelia Jordan's picture

Obsessive Compulsive Disorder (OCD) is a psychiatric disorder that is commonly characterized by obsessions and compulsions (1).  Obsessions are recurrent thoughts, images, or impulses that an individual with OCD experiences frequently.  These obsessions are unwanted and usually occur automatically.  People with OCD perform compulsive acts in order to relieve the anxiety caused by the obsessions.  Compulsions are repetitive rituals that are completed according to “rules” that may or may not be related to the obsession (2).  Although people with the disorder recognize that their actions are irrational, they feel compelled to do them out of fear that something disastrous will ensue.  Most compulsions fall into four categories: counting, checking, cleaning, and avoidance.  An example of compulsive cleaning is someone who washes her hands five hundred times a day because she is afraid of being contaminated by germs (1).  Clearly a life based around the completion of rituals is not an easy or particularly pleasant one, but people abstain from getting help because of the shameful stigma attached (to the disorder).  There are a variety of treatments available, however, and due to technological advancements there is serotonin therapy which is based on a neurobiological model of OCD.

            There is now evidence to support the idea that the symptoms of OCD are caused by a neurological imbalance.  This imbalance can be viewed using positron emission tomography (PET) scans and it manifests itself as hyperactivity in the frontal lobes (particularly orbitofrontal) and caudate nucleus of a patient with OCD.  The cerebral cortex sends information to the basal ganglia, which is a mass of gray matter located near the base of the cerebral hemisphere (it includes the caudate nucleus) (3).  For information to be processed by the basal ganglia it must flow through both the indirect and direct pathways before it is eventually sent back to the cerebral cortex.  The direct pathway is excitatory and allows learned behaviors to become automatic so that they can be carried out quickly.  The orbitofrontal cortex relates to the direct pathway because it recognizes situations that contain personal significance and can activate the direct pathway as well as the learned behaviors it controls.  Conversely, the indirect pathway is inhibitory and functions to suppress the automatic actions that are managed by the direct pathway (1).  So, if an individual’s direct pathway becomes overly active and the indirect pathway does not block messages of learned automatic behaviors accordingly, he or she will then presumably exhibit obsessive-compulsive behaviors.  

A possible cause of excessive neuronal firing in the caudate and orbitofrontal cortex is insufficient levels of serotonin (2).  Serotonin is a neurotransmitter that plays a role in the processes of sleep, memory function, the output of motor systems, and anxiety (4).  Serotonin reduces anxiety and repetition of species-typical behaviors (e.g. washing, grooming, danger avoidance) by inhibiting cellular firing in the caudate (3).  This lack of inhibition leads to hyperactivity in the caudate and the onset of obsessive-compulsive behaviors.   

            The above cause of OCD is supported by findings associated with Selective Serotonin Reuptake Inhibitors (SSRIs).  The orbitofrontal cortex and basal ganglia receive a certain amount of input from the serotonergic neurons and this input increases with the use of SSRIs (i.e. SSRIs produce more serotonin).  Thus, when SSRIs are administered to patients with OCD, hyperactivity in the caudate (seen via PET scans) diminishes (due to elevated levels of serotonin) and over time the behaviors linked with the disorder decrease as well (3).    

WWW Sources

1)      Carson, N. (2004). Physiology of Behavior: Eighth Edition. Boston: Pearson (Allyn and Bacon).




3)      Meyer, J. & Quenzer, L. (2005). Psychopharmacology: Drugs, the Brain and Behavior. Massachusetts: Sinauer Associates Inc.