Obsessive-Compulsive Disorder (OCD) is a chronic neuropsychiatric condition affecting 1-2% of the population globally. OCD is regarded as an archetypal disorder of compulsivity–a tendency toward repetitive habitual actions with heavy urges to perform them–and obsessions. The disorder may express itself as primarily cognitive-affective, primarily executive-behavioral, or both. OCD patients typically suffer from anxiety disorders and major depressive disorders with a prevalence of 60-70%. Some cases of OCD can be traced back to specific neurological etiologies or structural and functional changes in the brain implicating its pathophysiology. Common neurobiological processes may contribute to OCD vulnerability and persistence.
While there is no known overt locus on neuronal degeneration of OCD, there is an indication of dysfunction within networks of brain regions and anatomical disparate brain structures. Neural circuits can trigger repetitive behaviors and thoughts that coexist with conscious awareness, all of which can be set off by innocuous events. OCD is particularly associated with the dysfunction of the basal ganglia and cortico-basal ganglia circuits as well as frontostriatal loop circuits. Neuroimaging has identified structural and functional abnormalities involving the orbitofrontal cortices and basal ganglia. These cortical and subcortical brain regions and circuits play a key role in thought and behavior. This indicates that OCD may be a disorder of maladaptive habit circuitry which has evolved into conceptualizations focusing on habit and loss of control by cortically mediated inhibitory mechanisms. Cortical thickness reductions are also observed in the frontal, parietal, and temporal regions of the brain while gray matter volume increases in subcortical structures and decreases in the cortex. OCD is associated with abnormal metabolic activity in the orbitofrontal cortex, the anterior cingulate/caudal medial prefrontal cortex, and the caudate nucleus. Activity in the cortico-basal ganglia network, known as the “OCD circuit,” is accentuated during the provocation of symptoms.
The neurobiological underpinnings of OCD have a significant effect on the function of distributed brain networks in both resting states and during cognitive tasks. OCD has impaired domains such as motor inhibitory control, cognitive flexibility, and executive planning through reduced functional connectivity between anterior and posterior cortical regions during a motor inhibition task. Reduced resting state functional connectivity between the cortex and dorsal caudate nucleus as well as the cortex and basal ganglia is linked with worse cognitive flexibility in OCD. Basal ganglia influences motor pattern generators in the brainstem and spinal cord as well as cognitive pattern generators in the cerebral cortex. The development of motor habits is influenced by loops that run from the neocortex to the basal ganglia to the thalamus and back again. The basal ganglia help in the recording of cortical behavioral sequences that are crucial for creating coordinated, sequential motor activities and streams of thought. The architecture of cortico-basal ganglia circuitry provides smooth progression from the cognitive framework. However, cortico-basal ganglia loop dysfunction in OCD brings about compulsions and obsessions. The dysfunction of the cortico-basal ganglia system contributes to the symptoms of OCD as it prevents the conceptual framework from switching from one priority to another. Symptoms remain locked on a specific behavioral output with a lack of loop closure.
There is a general understanding that in OCD, functional connectivity is compromised and critical areas are hypoactivated during tasks requiring inhibitory control. Although multivariate pattern analysis has been used to create predictive models that can classify scans, there is currently no sufficiently proven method that can diagnose OCD based on a brain scan. It is crucial to keep developing a more thorough understanding of the neurobiology of OCD in order to enhance neurosurgical interventions and predict future treatments in clinical practices.
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