Most of us think that Obsessive Compulsive Disorder (OCD) is just about fussy tidying. But it’s actually much more serious and it causes sufferers to be locked into obsessions – intrusive, unwanted, thoughts – as well as repetitive, compulsive actions. Sometimes, patients engage in patterns of thinking or behaviour which might seem completely irrational.
This might lead some of us to believe that patients simply don’t have sufficient will power to stop performing them. Over the course of history, patients with OCD and other mental illnesses have been stigmatised, with such disorders being perceived as an indulgence or sign of weakness. The reason behind this perception, which is still common, is partly rooted in the fact that some of these disorders are not associated with any clear lesion of the brain. This distinguishes psychiatric conditions from neurological disorders such as Parkinson’s disease, where damage is visible (i.e., degeneration of dopaminergic cells).
Importantly, the introduction of Magnetic Resonance Imaging (MRI) has allowed scientists to scrutinise the brain and, by doing so, find evidence of functional and structural abnormalities in patients affected by OCD. Therefore, while our understanding of OCD is still incomplete, this and other ‘mental’ disorders clearly do have a biological underpinning.
The new study from our team at the University of Cambridge, published in Biological Psychiatry, made a step forward in understanding the relationship between such brain abnormalities and cognitive traits characterising patients with OCD.
In our study, 43 OCD patients and 44 controls (people without OCD) were asked to perform an experiment with a particular type of MRI method. Participants had to lie still in the scanner and look at a cross for a short period of time. Data from their brains was being acquired while they were at rest. However, the brain is never really at rest and by means of sophisticated analysis it is possible to investigate how information flows within brain circuits, connecting different parts of the brain. Because the participants were not involved in any particular task, such analyses identified the underlying, baseline connectivity of specific circuits.
The first finding was that the flow of information between specific brain areas is disrupted in OCD. Abnormalities have been found specifically in the neural pathways connecting the frontal cortex – the conductor of the brain – with the basal ganglia (nuclei located deep in the brain). In particular, communication within the dorsal frontostriatal pathways was shown to be disrupted with a lack of ‘chatter’ between these brain areas. In contrast, a complementary circuit, involving the ventral frontostriatal pathways, was overloaded, or over-connected in the brains of OCD patients.
In the same study, we have linked such specific patterns of alteration with performance on cognitive tasks. These behavioural measures were collected outside the scanner, and generally aimed at measuring abilities in cognitive control. Cognitive control is relevant to most thoughts and behaviour, such as problem solving, attention, decision making and habit formation.
One of the tasks measured cognitive flexibility, which can be defined as the ability to disengage attention from a previously relevant stimulus to then turn attention to a new one. Even if OCD patients were able to tune their attention to a stimulus, they showed specific difficulties in the ability to disengage their attention away from that stimulus to then flexibly turn to a different one. A separate task showed difficulties in OCD patients in the ability of planning ahead and organising the best course of action in order to reach a specific goal.
Importantly, our study revealed the potential of a rapid brain scan, such as resting state, in order to define patterns of nerve cell connectivity which relate to objective cognitive measures. Thus, resting state connectivity might serve as a biomarker and, together with behavioural measures of cognitive traits, it might allow a better characterisation of patients who might have different cognitive and connectivity profiles. Resting state represents a promising tool with possible clinical implications in the future, especially in light of its relative ease and simplicity of data collection and its potential for providing reliable brain mapping from relatively short duration of scanning. In a final step, we related the brain connectivity at rest with the performance obtained outside the scanner on those cognitive tasks. We found that reduced connectivity within specific, separate frontostriatal circuits was able to predict cognitive performance on these tasks. Therefore, OCD patients who were particularly rigid also had reduced cross talk within the frontostriatal circuit responsible for the ability of flexibly adapt to stimuli. Reduced connectivity in another frontostriatal circuit accounted for reduced ability to plan in a goal-directed manner.
Interestingly, inabilities to learn in “cold” unemotional situations – such as the one described above and measuring cognitive flexibility and the ability of planning ahead in a goal-directed manner – relate to abnormalities within the dorsal frontostriatal circuits. In contrast, another recent study published in the Proceedings of the National Academy of Sciences, found that learning in “hot” emotional situations in OCD patients was linked to abnormalities in areas located within the ventral frontostriatal circuits. Altered activity in this circuit was implicated with difficulties in OCD patients to learn when a stimulus was safe, i.e., not associated with a mild electric shock.
Together these studies, suggest that imbalanced activity within separate frontostriatal circuits contribute to the multifaceted nature of OCD. This suggests that specific brain abnormalities are linked to specific cognitive functions that might underlie some of the rigid, inflexible behaviour that we see in patients affected by OCD. For example, inability to flexibly regulate which stimulus to attend to or which stimulus is safe might be related to intrusive patterns of thinking which stay focused over on over on the same dysfunctional thought in OCD patients. Difficulties to plan ahead in a goal-directed manner might contribute to repetitive and habitual patterns of behaviours. However, further studies are needed in order to understand how altered cognitive traits contribute to symptomatology.
By obtaining a better understanding of the biological circuits involved in the disorder, we hope to develop measures that will objectively inform on the severity of illness for each patient. These studies are also aimed at identifying specific neural correlates that can be targeted by specific behavioural and pharmacological therapies.