Causes of the disorder: cortico–striato–thalamo–cortical circuit, genes that affect serotonergic, dopaminergic and glutaminergic system, environmental factors

 In a study that evaluated two rodent models of OCD, a disruption of the dopaminergic system, more specifically a decrease in the dopamine signaling mediated by dopamine neurons reflected and supported the theory that OCD affects dopaminergic systems. In this experiment, investigators repeated injection of dopamine D2 agonist quinpirole and injection of the tricyclic antidepressant agent clomipramine in combination with a behavioral paradigm designed to

produce compulsive lever pressing. The results were then compared with their relative impact on the state of activity of the mesolimbic dopaminergic system in the ventral tegmental area. The clomipramine model did not caused an increase in compulsive level pressing. In contrast, quinpirole treated animals did in fact showed significant increases in compulsive level pressing. Therefore, it was concluded that VTA dopamine activity correlated with the behavioral responses in these models and confirmed other experiments that concluded that the disorder impacted the dopaminergic system.

Obsessive compulsive disorder is a multifactorial condition that, as demonstrated in twin studies, it’s related to polygenetic and environmental factors. It has been observed in neuroimaging studies with patients that have the condition that the cortico-striato-thalamo- cortical circuit or corticostriatal system plays a role in OCD. This circuit is part of one of the feedback loops between the basal ganglia and the motor cortex/ premotor cortex. In OCD, genes affecting the dopaminergic, serotonergic and glutaminergic systems as well as the interaction within them have been identified as causes of the disorder. Also, external circumstances like prenatal events, psychological and neurological trauma may modify the expression of risk genes and, hence, trigger the manifestation of obsessive–compulsive behaviors. Since the late 1980s, a rapid growth in the number of imaging studies of individuals with OCD and improve­ments in imaging technology and methods have led to considerable advancement in the understanding of the neural indicators of OCD pathophysiology. As said earlier, the corticostriatal system has been the prevailing model regarding the neural and pathophysiological foundations of OCD. It has been explained that the corticostriatal system performs an excitatory and inhibitory pathway. In healthy individuals, the excitatory pathway is modulated by the inhibitory function and based on convergent findings from animal and human research, the prevailing model postulates that a lower threshold for activation of this system results in excessive activity in the excitatory pathway over the inhibitory one. This leads to hyperactivation of the orbitofrontal–subcortical pathway. As a result, exaggerated concerns about danger, hygiene or harm may result in persistent conscious attention to the per­ceived threat (obsessions) and, subsequently, to compulsions aimed at neutralizing the perceived threat. The temporary relief that results from performing compul­sions leads to reinforcement and repetitive or ritualistic behavior when obsessions reappear.

Finally, it’s important to mention that some functional imaging stud­ies have found distinct neural correlates of specific OCD symptom dimensions. In other words, variations in neuronal systems may be partially different depending of the kind of symptom that the person has like washing, hoarding and checking.