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Classic theories posit that depression is driven by a negative learning bias. Most studies supporting this proposition used small and selected samples, excluding patients with comorbidities. However, comorbidity between psychiatric disorders occurs in up to 70% of the population. Therefore, the generalizability of the negative bias hypothesis to a naturalistic psychiatric sample as well as the specificity of the bias to depression, remain unclear. In the present study, we tested the negative learning bias hypothesis in a large naturalistic sample of psychiatric patients, including depression, anxiety, addiction, attention-deficit/hyperactivity disorder, and/or autism. First, we assessed whether the negative bias hypothesis of depression generalized to a heterogeneous (and hence more naturalistic) depression sample compared with controls. Second, we assessed whether negative bias extends to other psychiatric disorders. Third, we adopted a dimensional approach, by using symptom severity as a way to assess associations across the sample.
We administered a probabilistic reversal learning task to 217 patients and 81 healthy controls. According to the negative bias hypothesis, participants with depression should exhibit enhanced learning and flexibility based on punishment v. reward. We combined analyses of traditional measures with more sensitive computational modeling.
In contrast to previous findings, this sample of depressed patients with psychiatric comorbidities did not show a negative learning bias.
These results speak against the generalizability of the negative learning bias hypothesis to depressed patients with comorbidities. This study highlights the importance of investigating unselected samples of psychiatric patients, which represent the vast majority of the psychiatric population.
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).