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some authors have incorporated both of these monoamines into their document impairments in decision-making in relation to reward, which
theories of psychosis.
they argue is due to a failure to accurately represent reward value.
The first scientist to make the case clearly and repeatedly for One limitation of studies in patients with chronic schizophrenia is
relating the emergence of psychotic symptoms to dopamine-driven that nearly all of the patients are taking antipsychotic medication,
associative and reinforcement learning was Robert Miller.
In his and such dopamine antagonist medication has been shown to affect
1976 article he wrote: “The process of acquiring the associations reward processing in healthy volunteers.
Thus, it is important to
necessary for learning a conditioned response in an experimental study patients who are not taking antipsychotic medication
animal depends on the presence of dopamine. In human to confirm (or refute) results in medicated samples. Relevant to this
schizophrenic patients, an excessive supply of cerebral dopamine is a recent study of ours that documented a failure of patients with
may facilitate the acquisition of associations between ‘units of first-episode psychosis to modulate their behaviour by motivational
information’, to the point where unrelated features are associated manipulation;
importantly, when the analysis was restricted to
and treated as if they are meaningful combinations: this process can patients free from dopamine antagonist medication, the deficits
be terminated by administering dopamine antagonists.”
Since that persisted. In my view, Gold’s studies are consistent with the thesis
time, several other authors have expanded and developed Miller’s advanced by Kring, Green, Barch and others that patients with
ideas, most notably Shitij Kapur. schizophrenia have reasonably intact hedonic responses but
Interestingly, modern pre-clinical scientists
Behavioural Studies of Reward have indicated that the consummatory (hedonic) reward system is at
Processing in Psychotic Illness least partially separable from anticipatory and motivational reward
Is there any evidence to support these claims? Until recently, there was systems; whereas hedonics may be driven by opioid or cannabinoid
little if any evidence to demonstrate that patients with schizophrenia neurotransmission, motivation may be primarily dopaminergic.
and other psychoses have any problems learning about rewards.
Admittedly, in the 1950s and 1960s a considerable number of studies Functional Neuroimaging Studies of
(including a number by Skinner himself) examined the effects of either Reward Processing in Psychotic Illness
reward or punishment on patients with schizophrenia.
However, in Although there is a very long tradition of studying how experimental
addition to these studies being conducted without the use of diagnostic animals learn about rewards, it has proved more difficult to find
criteria, the focus of these studies was rather different from that of adequate behavioural tests with which to investigate this
studies in the modern era. In that time, the key question was whether psychological domain in humans. However, the advent of functional
cognitive deficits in schizophrenia were ‘real’ or simply secondary to neuroimaging has re-invigorated this area of research, as this
lack of effort on behalf of patients, and the results were rather mixed. technique allows the study of humans while they learn about and
receive (or miss out on) rewards, but obviates the need to design
In the following years, non-reward-related associative learning received tasks with very careful, accurate measures of behaviour, as the
prolonged and detailed study by Jeffrey Gray and his colleagues at the dependent measure of interest is brain activation. Paradigms
Institute of Psychiatry,
but with the exception of a handful of employed in healthy human fMRI have proved fairly easy to utilise in
publications, behavioural studies of reward learning in psychosis were patient studies; since 2006 there have been at least six fMRI studies
largely abandoned. The last five years have seen a resurgence of of patients with schizophrenia or other psychoses while they learn
research into reward-related processes in schizophrenia. For example, about or receive rewards or punishments. Heinz and colleagues
in one recent study Roiser and colleagues
studied 20 medicated examined 14 unmedicated schizophrenia patients as they performed
patients with schizophrenia and 17 controls on a test in which money the Monetary Incentive Delay Task, which in controls produces robust
was used as a reinforcer: adaptive responses (fast responses to a ventral striatal activation in the anticipation of reward compared with
predictive cue) resulted in a financial reward. Patients demonstrated the anticipation of neural feedback.
Patients recruited less ventral
fewer adaptive responses to cues signalling a potential for reward striatal activation than controls, and this failure correlated moderately
compared with controls, and the degree of impairment was linked to and significantly with negative symptoms and moderately but
both positive and negative symptoms. non-significantly with positive symptoms. These researchers
have gone on to show that the responses of patients are
Gold’s group at the University of Maryland has conducted extensive partially normalised after prescription of the second-generation
behavioural studies of reward processing in schizophrenia and antipsychotic olanzapine.
Perhaps this helps to understand why,
examined the relationship between behavioural deficits in reward using a different reward processing task, Abler, Walter and colleagues
processing and negative symptoms. These studies have largely showed that schizophrenia patients taking second-generation
employed studies of patients with chronic schizophrenia, almost all of antipsychotic medication had striatal activations in anticipation of
whom are taking antipsychotic medication. In a recent review of their reward that could not be differentiated from controls.
work, Gold and colleagues describe eight studies in this area and
conclude that patients show deficits in rapid learning on the basis of Following Kapur’s theoretical paper six years ago in which he set out
trial-to-trial feedback, such as reversal learning.
This is consistent an argument to relate dopamine’s role in producing psychotic
with previous studies of reversal learning in schizophrenia
and with symptoms to dysfunction of its normal role in motivational
a recent study of mine examining reversal learning in first-episode importance,
he and his colleagues have conducted a number of
psychosis. In early psychosis, deficits were subtle and significantly studies to test the theory, examining in detail the time-course of the
correlated with negative symptoms, although the strength of action of antipsychotic drugs and reporting how the delusions of
the correlation was modest.
Gold’s studies point to evidence patients change in response to this treatment.
They have also
of comparatively intact sensitivity to reward, but at the same time conducted fMRI investigation in patients,
employing an aversive
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