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Aberrations in reward and penalty processing are implicated in depression and putatively reflect altered dopamine signalling. This study exploits the advantages of a placebo-controlled design to examine how a novel D2 antagonist with adjunctive antidepressant properties modifies activity in the brain's reward network in depression.
We recruited 43 medication-naïve subjects across the range of depression severity (Beck's Depression Inventory-II score range: 0–43), including healthy volunteers, as well as people meeting full-criteria for major depressive disorder. In a double-blind placebo-controlled cross-over design, all subjects received either placebo or lurasidone (20 mg) across two visits separated by 1 week. Functional magnetic resonance imaging with the Monetary Incentive Delay (MID) task assessed reward functions via neural responses during anticipation and receipt of gains and losses. Arterial spin labelling measured cerebral blood flow (CBF) at rest.
Lurasidone altered fronto-striatal activity during anticipation and outcome phases of the MID task. A significant three-way Medication-by-Depression severity-by-Outcome interaction emerged in the anterior cingulate cortex (ACC) after correction for multiple comparisons. Follow-up analyses revealed significantly higher ACC activation to losses in high- v. low depression participants in the placebo condition, with a normalisation by lurasidone. This effect could not be accounted for by shifts in resting CBF.
Lurasidone acutely normalises reward processing signals in individuals with depressive symptoms. Lurasidone's antidepressant effects may arise from reducing responses to penalty outcomes in individuals with depressive symptoms.
Ethnic minority individuals have an increased risk of developing a psychotic disorder, particularly if they live in areas of ethnic segregation, or low own group ethnic density. The neurobiological mechanisms underlying this ethnic minority associated risk are unknown. We used functional MRI to investigate neural responses to faces of different ethnicity, in individuals of black ethnicity, and a control group of white British ethnicity individuals.
In total 20 individuals of black ethnicity, and 22 individuals of white British ethnicity underwent a 3T MRI scan while viewing faces of black and white ethnicity. Own group ethnic density was calculated from the 2011 census. Neighbourhood segregation was quantified using the Index of Dissimilarity method.
At the within-group level, both groups showed greater right amygdala activation to outgroup faces. Between groups, the black ethnicity group showed greater right amygdala activation to white faces, compared to the white ethnicity group. Within the black ethnicity group, individuals living in areas of lower own group ethnic density showed greater right amygdala reactivity to white faces (r = −0.61, p = 0.01).
This is the first time an increased amygdala response to white faces has been demonstrated in individuals of black ethnicity. In the black ethnicity group, correlations were observed between amygdala response and neighbourhood variables associated with increased psychosis risk. These results may have relevance for our understanding of the increased rates of paranoia and psychotic disorders in ethnic minority individuals.
Neurotransmitters are the means by which one neuron influences the action of another. Abnormalities in neurotransmitter function are implicated in a variety of neurological and neuropsychiatric disorders and drugs that influence the neurotransmitter systems are often used in treating the symptoms of such disorders. The effects of these drugs can be paradoxical. A small dose of a pharmacological agent might have entirely the opposite effect to a large dose, a drug may improve one ability whilst impairing another, a drug may have opposite effects in different populations or opposite effects in the same individual at different times. In this chapter, we illustrate these effects using clinical data and data from healthy volunteers in experimental studies. With one of the best studied neuromodulators – dopamine – as our focus, we introduce key principles that can help to explain these apparent paradoxes. First, the effect of a drug depends on baseline levels of the neurotransmitter already in the system. When baseline levels are low, a given pharmacological dose can increase function closer to an optimal level. When baseline levels are high, the same dose can over-stimulate the system and trigger compensatory mechanisms that reduce performance on a given task. Second, a drug could have quite different effects in different brain regions. Accordingly, a function that is predominantly influenced by one region may be enhanced, whilst another function, more dependent on another region, may be impaired. In the final section of the chapter, we turn to attention deficit hyperactivity disorder (ADHD).
The adequacy of pharmacotherapy received in practice by patients after an acute episode of depression has been little studied.
To describe and assess adequacy of drug continuation and maintenance in patients with depression.
Patients with depression were interviewed 18 months after discharge from hospital. Quantitative assessments of drug treatment doses and compliance were made monthly over this period, and qualitative ratings in continuation and maintenance phases.
About 20% of patients were prescribed low drug doses after discharge and 10% were prescribed no drugs at all. Reported compliance was around 70%. About 30% failed to receive adequate longer-term treatment, mostly due to the continuation phase being too short. Deficiencies of dosage and compliance were greater in patients who never achieved full recovery. Patient refusal was the most common reason for not using antidepressants. Further episodes of depression were not particularly associated with inadequate treatment.
There were deficiencies in drug treatment that did not appear to be the principal cause of further episodes but may be important in non-recovery. Patient fears require discussion.
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