Obsessive-compulsive disorder, or OCD, is characterized by unwanted, recurring, intrusive thoughts that cause anxiety. The person experiencing these thoughts commonly exhibits specific behaviors in order to avoid or minimize their anxiety.[1] Examples of these types of behaviors include repetitive hand washing or checking of locks.[2] Obsessive-compulsive behaviors can negatively affect the social, academic, and occupational lives of those with OCD. In fact, according to the World Health Organization, OCD is one of the ten most disabling conditions in the world.[3] Epidemiological data suggests that OCD occurs in 1.5-3% of the population.[4] Many studies have focused on the role serotonin plays in OCD. However, nearly half of OCD patients do not respond to SSRI treatments.[5] This suggests that there are other factors that contribute to the pathophysiology of OCD.
One of these factors appears to be dysfunction of the dopaminergic system.
Dopamine is a catecholamine neurotransmitter that is important in regulating functions in the prefrontal cortex (PFC) of the brain.[6]
Dopamine in the PFC:
- Enhances memory
- Promotes focus
- Provides salience, or preferential attention to external stimuli that promise reward
Animal models have demonstrated that unnecessary, repetitive acts, such as those involved with OCD could be induced in normal animals by increasing dopamine function in the prefrontal cortex of the brain.[7]
Neuroimaging studies have shown that patients with OCD have increased activity in brain areas such as the dorsal parietal cortex, the orbitofrontal cortex, and the basal ganglia. These areas have high concentrations of both serotonergic and dopaminergic neurons.[8],[9] Single-photon emission computed tomography (SPECT) imaging has shown higher densities of the dopamine transporter (DAT) in the basal ganglia of OCD patients. The higher transporter density may be caused by overall increased dopamine activity in the brain.[10]
OCD and Genetics
There also appears to be a fairly large genetic component to OCD in relation to dopamine function. Twin studies are commonly used to differentiate between genetic and environmental causes of disease by comparing disease states in monozygotic twins who are genetically identical (by contrast fraternal twins share only 50% of their genes). Twin studies of OCD reveal that the heritability of obsessive-compulsive symptoms range from 45-65% in children and 27-47% in adults.[11] Thus, genes have a lot to do with whether someone has OCD or not. Furthermore, researchers have found genes that code for the D4 dopamine receptor to be associated with the presence of obsessive-compulsive symptoms.[12],[13]
OCD and Neurotransmitter Imbalance
Another contributor to OCD may be COMT function. Catechol-O-methyl transferase (COMT) is an enzyme that is important in the regulation of dopamine, norepinephrine, and epinephrine. Some studies have demonstrated a correlation between reduced activity of COMT, that is to say more catecholamine neurotransmitters in the brain, and the severity of obsessive-compulsive symptoms in OCD patients.[1] However, more studies are needed for COMT to be recognized conclusively as a causative agent in OCD.
Though OCD is a complicated disorder that requires more investigation to be fully understood, research seems to suggest the importance of serotonin, dopamine, and potentially other catecholamines in its pathophysiology. Clinical observations have shown dopaminergic antagonist drugs have been effective in treating OCD patients who did not respond to SSRI monotherapy.[14] Some experts also think it is possible that serotonin–norepinephrine reuptake inhibitors may be helpful in the treatment of OCD as well.[15] Neurotransmitter testing, one of the services provided by Sanesco, could prove to be helpful in identifying complex neurotransmitter imbalances in OCD patients.
References
[1] Koo M, Kim E, Roh D, et. al. (2010). Role of dopamine in the pathophysiology and treatment of obsessive-compulsive disorder. Expert Review of Neurotherapeutics, 10(2), 275-90.
[2] Grados M & Wilcox HC (2007). Genetics of obsessive-compulsive disorder: A research update. Expert Review of Neurotherapeutics, 7(8), 967-80.
[3] Ibid.
[4] Van der Wee NJ, Stevens H, Hardeman J A, et. al. (2004). Enhanced dopamine transporter density in psychotropic-naive patients with obsessive-compulsive disorder shown by ^sup 123^I]beta]-CIT SPECT. The American Journal of Psychiatry, 161(12), 2201-6.
[5] Koo op. cit.
[6] Bo Xing, Yan-Chun Li, Wen-Jun Gao. (2016). Norepinephrine versus dopamine and their interaction in modulating synaptic function in the prefrontal cortex. Brain Research, 1641, 217-233.
[7] Koo op. cit.
[8] Ibid.
[9] Van der Wee op. cit.
[10] Ibid.
[11] Grados op. cit.
[12] Koo op. cit.
[13] Grados op. cit.
[14] Koo op. cit.
[15] Grados op. cit.
Clinical Contributor
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