From the nightclubs of Ibiza to the libraries of Cambridge, pleasure comes in a vast range of shapes and sizes but is universally appreciated as being a fundamental motive in our day-to-day behaviour. Anhedonia is the inability to experience pleasure in response to things that are typically enjoyed by other people. Anhedonic symptoms are a shared feature of both clinical depression and schizophrenia.
A group of researchers from the University of Cambridge recently published findings from a study that looked at the relationship between long-term anhedonic symptoms and task-related motivation. The study focused on exploring how differences in activations across the brain related to both anhedonic symptoms and task-related motivation. The study also looked at how these mechanisms might vary across two different clinical conditions: depression and schizophrenia. Reward processing, implicated in both motivational and anhedonic processes, is also known to be disrupted in both depression and schizophrenia. However, the extent to which the disruption is similar across the two clinical conditions is not yet comprehensively understood.
The authors highlighted how previous studies investigating reward receipt in psychiatric conditions have been somewhat limited by their use of deterministic and predictable rewards. The mechanisms of processing unexpected rewards in clinical conditions such as depression and schizophrenia are of particular interest due to the suggestions involvement of disruption of the neural mechanisms of prediction in these conditions. Therefore, the research group focused specifically on how the reward systems reacted to unexpected rewards in the present study.
The study involved the recruitment of two separate clinical groups, one made up of patients with depression and one of patients with schizophrenia, alongside a control group made up of healthy volunteers. Self-reported ratings of anhedonia were taken alongside a task-based motivational measure. Functional magnetic resonance imaging (fMRI) was used to measure brain activation during a casino-style slot machine task. The task could either produce rewards under expected or unexpected conditions, allowing the researchers to isolate patterns of activity specifically associated with the receipt of unexpected rewards. Participants were also assessed immediately after the scanning sessions to gauge both the amount of pleasure that they received from winning in the task as well as the degree to which winning encouraged them to play more. Higher levels of motivation within the task were found to be associated with increased activation to unexpected rewards across the three subject groups as a whole.
The fact that activation was linked to motivation separately from pleasure leads to a more complex picture of reward processing that makes a distinction between motivation and reward. The authors also found that brain activation in response to unexpected rewards were reduced in both depression and schizophrenia across areas of the brain associated with reward; such as the striatum, orbitofrontal cortex and medial prefrontal cortex. Specifically, they found that this reduction in activity was particularly pronounced in schizophrenic patients in contrast to healthy controls. Finally, they found that the degree of motivation reported related to severity of anhedonic symptoms in schizophrenia.
The authors conclude that the results of the study provide evidence for comparable hypofunction of the striatum and orbitofrontal cortex in these two clinical conditions. They also infer that these results might indicate that measures of motivational state are able to provide a bridge between atypical brain activation of the reward networks in the brain and long-term anhedonic symptoms. Furthering our understanding of the extent of neurobiological overlap between these conditions will provide numerous advantageous both for the treatment and classification of these disorders. While schizophrenia and depression still show numerous behavioural and neural differences, the present findings provide further support for some degree of shared pathophysiology between the two conditions.
We asked the principle investigator Dr Graham Murray to summarise the significance of the study: “Patients with depression and schizophrenia both report anhedonia (the medical term for having problems with being motivated and enjoying life), but it is not known whether this symptom has the same brain basis in these two illnesses. If the symptom has a shared brain basis across illnesses, this has implication for treatment, as it suggests that the same treatments might work in different conditions. […] The results shed new light on the brain basis of anhedonia, suggesting some common neural underpinnings in both depression and schizophrenia, with additional abnormalities distinct to schizophrenia.”
Written by Owen Parsons.