It has been theorized that a miscommunication between the orbital-frontal cortex, the
caudate nucleus, and the
thalamus may be a factor in the explanation of OCD. The
orbitofrontal cortex (OFC) is the first part of the brain to notice whether or not something is wrong. When the OFC notices that something is wrong, it sends an initial “worry signal” to the thalamus. When the thalamus receives this signal, it in turn sends signals back to the OFC to interpret the worrying event. The caudate nucleus lies between the OFC and the thalamus and it prevents the initial worry signal from being sent back to the thalamus after it has already been received. However, it is suggested that in those with OCD, the caudate nucleus does not function properly, and therefore does not prevent this initial signal from recurring. This causes the thalamus to become hyperactive and creates a virtually never-ending loop of worry signals being sent back and forth between the OFC and the thalamus. The OFC responds by increasing anxiety and engaging in compulsive behaviors in an attempt to relieve this apprehension.
[4] This over activity of the OFC is shown to be attenuated in patients who have successfully responded to
SSRI medication. The increased stimulation of the serotonin receptors
5-HT2A and
5-HT2C in the OFC is believed to cause this inhibition.
[citation needed]