Neurocircuit models of obsessive-compulsive disorder: limitations and future directions for research

Abstract

Obsessive-compulsive disorder (OCD) is a common psychiatric condition classically characterized by obsessions (recurrent, intrusive and unwanted thoughts) and compulsions (excessive, repetitive and ritualistic behaviors or mental acts). OCD is heterogeneous in its clinical presentation and not all patients respond to first-line treatments. Several neurocircuit models of OCD have been proposed with the aim of providing a better understanding of the neural and cognitive mechanisms involved in the disorder. These models use advances in neuroscience and findings from neuropsychological and neuroimaging studies to suggest links between clinical profiles that reflect the symptoms and experiences of patients and dysfunctions in specific neurocircuits. Several models propose that treatments for OCD could be improved if directed to specific neurocircuit dysfunctions, thereby restoring efficient neurocognitive function and ameliorating the symptomatology of each associated clinical profile. Yet, there are several important limitations to neurocircuit models of OCD. The purpose of the current review is to highlight some of these limitations, including issues related to the complexity of brain and cognitive function, the clinical presentation and course of OCD, etiological factors, and treatment methods proposed by the models. We also provide suggestions for future research to advance neurocircuit models of OCD and facilitate translation to clinical application.

An fMRI study of cognitive planning before and after symptom provocation in pediatric obsessive–compulsive disorder

“…A recently published review highlights the importance of the PFC in the etiology of OCD symptoms. 42 One theory is that deficits in a PFC cognitive control network (such as the dorsal cognitive CSTC circuit described in previous neurocircuitbased models of OCD 4,5,43 ) could lead directly to compulsions, because hypoactivity could cause impairments in inhibitory control and automatic engagement in compulsive behaviours, particularly in stressful circumstances. Hyperactivity in PFC regions at baseline and during symptom provocation is thought to reflect compensatory responses that boost performance of critical PFC executive control functions, including decision-making and goal-directed planning.…”

“…Future studies should include ROIs related to the dorsal cognitive CSTC circuit (including the dorsal aspects of the PFC), given the current neurocircuit-based models of OCD 4,5,43 and this circuit's implication in executive function, such as working memory and planning, as well as emotion regulation. 4…”

Brain Wave Oscillations as an Objective Neurophysiological Biomarker of Homeopathic Subjective Well-Being

“…In turn, these signals of abnormal network activity normalize with usual treatment and/or predict disease progression or recovery. 17,[19][20][21][22][23] In a recent systematic review of the neural correlates of well-being, 11 studies used qEEG (measuring the EEG power) to link well-being to regional brain activation, suggesting that a larger α asymmetry (more activation on the brain's left side than on the right) is related to greater well-being, according to the neuropsychological theory of lateralized affective function. 24 With the aim of using EEG profiles as a biomarker of wellbeing, Chilver et al 25 examined the association between mental well-being and EEG power (delta, theta, α and β) in 422 healthy adults using linear mixed models.…”

“…In turn, these signals of abnormal network activity normalize with usual treatment and/or predict disease progression or recovery. 17 19 20 21 22 23…”

Differential connectivity of frontolimbic circuit induced by individualized disorder-specific stimuli in distinct symptom profiles of obsessive-compulsive disorder

“…Recent neuroimaging studies have shown that the standard cortico-striato-thalamo-cortical (CSTC) model alone may be inadequate to explain this heterogeneity (Milad and Rauch 2012) and indicated evidence for the involvement of wider cortical and subcortical structures beyond the CSTC circuit (Menzies et al 2008; van den Heuvel et al 2016). It has been postulated that the diverse clinical presentations and the associated neurocognitive deficits may be explained by the varied involvement of the dorsal cognitive, ventral cognitive, fronto-limbic, sensorimotor, and frontoparietal networks (Shephard et al 2021; 2022).…”