- Research article
- Open Access
- Open Peer Review
Incentive motivation in first-episode psychosis: A behavioural study
© Murray et al; licensee BioMed Central Ltd. 2008
- Received: 11 September 2007
- Accepted: 08 May 2008
- Published: 08 May 2008
It has been proposed that there are abnormalities in incentive motivational processing in psychosis, possibly secondary to subcortical dopamine abnormalities, but few empirical studies have addressed this issue.
We studied incentive motivation in 18 first-episode psychosis patients from the Cambridge early psychosis service CAMEO and 19 control participants using the Cued Reinforcement Reaction Time Task, which measures motivationally driven behaviour. We also gathered information on participants' attentional, executive and spatial working memory function in order to determine whether any incentive motivation deficits were secondary to generalised cognitive impairment.
We demonstrated the anticipated "reinforcement-related speeding" effect in controls (17 out of 19 control participants responded faster during an "odd-one-out" task in response to a cue that indicated a high likelihood of a large points reward). Only 4 out of 18 patients showed this effect and there was a significant interaction effect between reinforcement probability and diagnosis on reaction time (F1,35 = 14.2, p = 0.001). This deficit was present in spite of preserved executive and attentional function in patients, and persisted even in antipsychotic medication free patients.
There are incentive motivation processing abnormalities in first-episode psychosis; these may be secondary to dopamine dysfunction and are not attributable to generalised cognitive impairment.
- Probability Trial
- Brief Psychiatric Rate Scale
- Spatial Working Memory
- Reinforcement Probability
- Incentive Motivation
Motivational problems such as avolition have been noted in schizophrenia since the initial descriptions of the illness . Proposed neurological models of psychosis have linked schizophrenic motivational deficits to hypofrontality, but an alternative hypothesis is that motivational dysfunction in schizophrenia and other psychoses is underpinned by abnormal activity of subcortical monoamine systems [2–4]. In particular, ascending midbrain dopamine neurons are known to play a key role in incentive motivation [5, 6] and to signal unexpected reward and errors in reward prediction . Reward system dysfunction may underlie not only avolition but also, or alternatively, other psychotic symptoms including stereotyped patterns of thought and behaviour  and delusional beliefs [8–13]. For example, it has been argued that dysregulated midbrain dopamine neuron firing could result in an individual maladaptively attributing motivational importance to innocuous stimuli or events, i.e. experiencing abnormal referential ideas [10, 11]. An affected individual, having experienced abnormally salient phenomena secondary to dysregulated dopamine, may then impose a "top-down" cognitive explanation onto such experiences in order to make sense of them, potentially culminating in a delusion . Alternatively, dysregulated dopamine neuron firing could result in an amplification of the salience of an internally generated voice, which could in turn lead to an abnormal perception .
In spite of such speculations that disrupted reward and motivational processing may underpin positive and/or negative psychotic symptoms, it has yet to be clearly demonstrated whether such disruptions are present in psychosis or not, let alone whether such disruptions relate to symptom expression. A major challenge in evaluating the hypothesis that reward processing is abnormal in psychosis is the lack of available behavioural measures to assess reward processing and incentive motivational processes in humans; the consequence has been that, to date, such processes have only been addressed indirectly in behavioural studies. Patients with schizophrenia display a range of abnormalities of classic associative learning phenomena including Kamin blocking and latent inhibition [15, 16], and these abnormalities are responsive to short-term antipsychotic treatment, consistent with a dopaminergic mechanism. In addition, reward-based decision-making on the Iowa Gambling Test (IGT) has been shown to be impaired in psychosis  and these effects are also sensitive to medication status , although there have been some failures to replicate the case-control difference , and the IGT requires several cognitive processes in addition to reward sensitivity.
In the present study, we sought to examine incentive motivation in psychosis, using a simple choice reaction time task (the Cued Reinforcement Reaction Time Task, or CRRT ) in which healthy participants have previously shown speeding of responses after presentation of coloured cues signalling higher probability of reward: 'reinforcement-related speeding'. Thus a particular cue (an initially and objectively neutral piece of information) becomes associated with enhanced likelihood of reinforcement, and so stimulates more effortful (i.e. rapid) responding in an adaptive performance of the task. We administered the CRRT to a group of patients with first-episode psychosis, in addition to a number of neuropsychological tests of attentional and executive function. By studying first-episode cases, we were able to explore motivational processes in the absence of substantial global cognitive impairment. We hypothesised that patients with psychosis would be less sensitive than healthy participants to the motivational manipulation, and would therefore show attenuated or absent 'reinforcement-related speeding' on the task.
18 individuals (mean age 23; 9 men) with first-episode psychosis were recruited from the Cambridge first episode psychosis service, CAMEO for the study. Inclusion criteria for CAMEO is age between 17 and 35, suffering from a first episode of psychosis as defined by the Melbourne criteria of the presence of psychotic symptoms for at least one week , and duration of antipsychotic treatment of under 6 months at the time of initial assessment. Nineteen healthy volunteers (mean age 25; 9 men) were recruited from the general population by advertisement to act as a control group. Eleven of the 18 patients were taking antipsychotic medication; all of these 11 were taking "atypical" antipsychotic agents with a mean chlorpromazine equivalent dose of 264 mg. Of these, 3 were taking olanzapine (10 mg daily), 2 risperidone (1 mg daily and 3 mg daily), 2 quetiapine (500 mg daily and 400 mg daily), 1 clozapine (400 mg daily), 2 aripiprazole (10 mg daily and 15 mg daily), and 1 amisulpride (200 mg daily). Of the 7 antipsychotic-free patients, 5 were taking no medication, 1 was taking sertraline and 1 sodium valproate. Only 1 of the antipsychotic free patients had previously briefly taken antipsychotics, but was antipsychotic free for 2 weeks prior to assessment. After referral to the service, we waited until clinical presentation at least partially stabilised before commencing the study (over 75% studied within 5 months of referral, all assessed within a year of referral). As a consequence most patients in this study had mild symptoms at the time of the experiment: mean Brief Psychiatric Rating Scale (BPRS) positive symptom score 1.8 (very mild) and mean BPRS negative symptom score 1.8 (very mild). BPRS scores were unavailable on two patients. Twelve months after the experiment, a psychiatrist (GM) assigned DSM-IV diagnoses to patients using all available clinical information; 9 patients met criteria for schizophrenia, 2 for schizoaffective disorder, 5 for bipolar disorder, 1 for delusional disorder and 1 for psychosis not otherwise specified. This range of diagnoses is broadly representative of outcomes in first episode psychosis services . The research was approved by the local Research Ethics Committee; all participants provided informed consent.
The Cued Reinforcement Reaction Time Task 
Additional Neuropsychological Measures
Three further tests (described in Additional file 1: information on additional neuropsychological measures) from the Cambridge Neuropsychological Test Automated Battery (CANTAB) were administered to assess attentional and executive function: the Intra-Dimensional/Extra-Dimensional (ID/ED) Shift test [derived from the Wisconsin Card Sort Test, see 23], the Rapid Visual Information Processing (RVIP) test [derived from the Continuous Performance Test, see 24], and the Spatial Working Memory (SWM) test .
Demographic characteristics of the two groups were compared using independent-samples t-tests and chi-squared tests. Incorrect trials were excluded from the CRRT reaction time analysis. CRRT performance was assessed using mixed-model ANOVA with group (patients, controls) as a between-subjects factor, and probability of reinforcement (10%, 50%, 90%) as a within-subjects factor. A linear contrast was used to test for reaction time trend across the reinforcement contingencies [26, 27]. Debriefing data were analysed with chi-squared tests. In order to attempt to rule the possibility that differences between groups were attributable to the effects of dopamine antagonist medication, we repeated the mixed-model ANOVA having excluded the participants who were taking antipsychotic drugs. The proportion of participants in each group who showed reinforcement-related speeding (responding faster on trials with a high probability of reinforcement than on trials with a low probability of reinforcement) was compared using a Chi-Squared Test when all patients were included and Fisher's exact test when antipsychotic treated patients were excluded.
Skewed data were transformed where possible to enable the use of parametric tests. A logarithmic transformation was used for ID/ED extra-dimensional shift errors and total errors, and for RVIP latency data. A square root transformation was used for SWM between errors and within errors. Fisher's Exact Test was used to compare the number of participants from each group who completed the ID/ED test. The Mann Whitney U-Test was used to compare RVIP response bias data groups. All tests were two-tailed with alpha set at 0.05.
Cued Reinforcement Reaction Time Task
We then examined the correlation between symptoms and reinforcement-related speeding, but there was no significant relationship (r = 0.3, p = 0.3, negative symptoms; r = 0.03, p = 0.9, positive symptoms).
Other cognitive test scores (Table 1)
Cognitive Test Scores
ID/ED (Proportion completing)*
ID/ED EDS errors
ID/ED Pre-EDS errors
ID/ED Total errors
SWM Between Errors
SWM Within Errors
RVIP Target Detection
RVIP Response Bias$
there were no significant differences between groups on set-shifting or attentional function. 15 out of 18 patients passed all stages of the ID/ED Test, compared to 18 out of 19 control volunteers (p = 0.3). There was no significant difference between groups on number of extra-dimensional shift errors (t = 1.4, p = 0.2), or on pre-extradimensional shift errors (t = 0.4, p = 0.7) or on total errors (t = 1.4, p = 0.2). In the RVIP, there was no difference between groups in terms of response bias (U = 109, p = 0.2), target detection (t = 1.6, p = 0.13) or latency (t = 0.5, p = 0.6). Patients showed impairment in spatial working memory on strategy score (t = 2.7, p = 0.01) and on between-stage errors (t = 2.5, p = 0.02). Spatial working memory scores were unavailable for 4 control participants due to technical problems. There was no difference between groups on the subsidiary measure of within stage-errors (t = 1, p = 0.3).
We then examined the relationship between incentive motivation and spatial working memory. We performed a logistic regression analysis in patients to test whether the presence of reinforcement-related speeding can be predicted by spatial working memory performance. Neither spatial working memory strategy score (p = 0.3) nor between search error score (p = 0.2) predicted the presence of reinforcement-related speeding. We further examined whether the degree of reinforcement-related speeding (mean reaction time on 90% probability of reinforcement trials – mean reaction time of 10% probability trials, and mean RT on 90% probability trials – mean RT on 50% probability trials) correlated with spatial working memory performance in patients. These correlations were not significant: r = 0.35, p = 0.2 (mean RT 90-50 vs strategy); r = 0.02, p = 0.9 (mean RT 90-10 v strategy); r = 0.1, p = 0.7 (mean RT 90-50 vs between search errors); r = 0.3, p = 0.2 (mean RT 90-10 vs between search errors).
Finally we tested whether patients who ultimately were diagnosed with schizophrenia performed differently on cognitive tests from those ultimately diagnosed with bipolar disorder, but there was no significant difference on any test.
Control participants demonstrated an adaptive behavioural response to cues of varying degree of motivational salience (acquired through association with reward). Whilst the majority of patients were able to report correctly the cue most associated with reward, they did not show the adaptive behavioural reinforcement-related speeding effect of controls. As such, there was a disconnection between their awareness of the environment, and their ability to modulate their behaviour in accordance with that knowledge. This supports the theory that patients with early psychosis show deficits in incentive motivation.
Whilst we follow other authors in arguing that incentive motivation plays a key role in response speeds and latencies during reinforcement tasks in general [28, 29] and the CRRT in particular [20, 30], we do acknowledge that other cognitive processes also contribute to the CRRT, including attentional and learning processes. We note that these first-episode psychosis patients did form a fairly cognitive intact group, given their good performance on attentional set shifting and rapid information processing. The use of these comparison cognitive assessments shows that the patients' abnormal performance in the CRRT was not purely secondary to generalised cognitive deficits and is likely to truly reflect abnormalities in motivational processing. Patients did show impaired spatial working memory, in accordance with previous evidence documenting spatial working deficits early in the course of psychotic illness . However, patients' spatial working memory deficits did not relate to their performance on the CRRT, indicating that the incentive motivation abnormalities we observed were not confounded by the patients' cognitive deficits. We note that there was a moderate, but non-significant, correlation between spatial working memory strategy and performance on the CRRT. A recent study  that investigated motivation processing in chronic medicated schizophrenia also showed a moderate correlation between motivated responding and working memory. It is possible that if we had used a larger sample size we might have seen a significant relationship between CRRT performance and working memory, and this area warrants further study in larger samples.
Some limitations should be noted. The sample size is small, and some of the patients were taking atypical antipsychotic medication, which may have affected the results. However there is evidence that atypical antipsychotic agents do not impair motivational processing in patients with psychosis, but rather such medications may ameliorate underlying abnormalities in reward expectation in the ventral striatum . Furthermore, when we excluded patients who were taking antipsychotic medication from the analysis, a statistically significant difference between groups in incentive motivation remained, which suggests that the abnormality in patients is not solely attributable to dopamine antagonist effects of treatment.
A variety of evidence from studies in both humans and experimental animals indicates that subcortical dopamine systems play a critical role in reward and motivational processing [34, 35]. Dopamine may be more critical in motivation, anticipation of rewards and prediction error signalling than in consummatory processing, which has been linked to opioid receptor activation [7, 36]. Despite extensive previous theorising attempting to link dopamine dysfunction, abnormalities in reward processing, and psychosis [8, 10, 14], few experimental behavioural or physiological studies have investigated such theories in patients. In a recent functional MRI study of reward learning, Murray et al  showed that brain responses correlating with reward prediction error in the dopaminergic midbrain and associated dopamine neuron striatal and limbic target regions were abnormal in patients with active psychotic symptoms. Juckel and colleagues  demonstrated that expectation of reward, when compared with expectation of neutral feedback, is associated with reduced ventral striatal activity in schizophrenia when compared to controls. Taken together, these studies provide preliminary evidence for physiological abnormalities in psychotic illness in learning about and anticipating rewards, combined with an impaired ability to modulate behaviour in response to incentives. We suggest that this impairment may be secondary to dopamine dysfunction, though we acknowledge that, as yet, no direct evidence has proved that performance on the CRRT is dopamine dependent. In contrast to demonstrated anticipatory and motivational deficits, consummatory reward processing in psychosis may be intact [32, 39, 40].
This study reports deficits in incentive motivation processing in first episode psychosis. Future studies should examine whether incentive motivation deficits in psychosis are sensitive to pharmacological, especially dopaminergic, modulation.
This research was supported by a UK Department of Health, National Institute of Health Research, Research Capacity Development Award to Graham Murray. The work was completed within the University of Cambridge Behavioural and Clinical Neuroscience Institute, supported by a joint award from the Wellcome Trust and Medical Research Council. CAMEO received pump priming funding from the Stanley Medical Research Institute and GlaxoSmithKline, and now receives support from the UK National Health Service. We are grateful to staff from CAMEO for help with recruitment and data collection, to Dr Paul Fletcher for helping write the original grant proposal, and to the participants. The funding bodies played no role in study design or in the collection, analysis or interpretation of the data, or in the decision to submit the manuscript for publication.
- Bleuler E: Dementia Praecox or the group of schizophrenias. New York , International University Press, 1911/1950Google Scholar
- Krystal JH, D'Souza DC, Gallinat J, Driesen N, Abi-Dargham A, Petrakis I, Heinz A, Pearlson G: The vulnerability to alcohol and substance abuse in individuals diagnosed with schizophrenia. Neurotox Res. 2006, 10 (3-4): 235-252.View ArticlePubMedGoogle Scholar
- Stein L, Wise CD: Possible etiology of schizophrenia: progressive damage to the noradrenergic reward system by 6-hydroxydopamine. Science. 1971, 171 (975): 1032-1036. 10.1126/science.171.3975.1032.View ArticlePubMedGoogle Scholar
- Drew MR, Simpson EH, Kellendonk C, Herzberg WG, Lipatova O, Fairhurst S, Kandel ER, Malapani C, Balsam PD: Transient overexpression of striatal D2 receptors impairs operant motivation and interval timing. J Neurosci. 2007, 27 (29): 7731-7739. 10.1523/JNEUROSCI.1736-07.2007.View ArticlePubMedGoogle Scholar
- Crow TJ: Catecholamine-containing neurones and electrical self-stimulation. 2. A theoretical interpretation and some psychiatric implications. Psychol Med. 1973, 3 (1): 66-73.View ArticlePubMedGoogle Scholar
- Berridge KC, Robinson TE: What is the role of dopamine in reward: hedonic impact, reward learning, or incentive salience?. Brain Res Brain Res Rev. 1998, 28 (3): 309-369. 10.1016/S0165-0173(98)00019-8.View ArticlePubMedGoogle Scholar
- Schultz W, Dayan P, Montague PR: A neural substrate of prediction and reward. Science. 1997, 275 (5306): 1593-1599. 10.1126/science.275.5306.1593.View ArticlePubMedGoogle Scholar
- Robbins TW: Relationship between reward-enhancing and stereotypical effects of psychomotor stimulant drugs. Nature. 1976, 264 (5581): 57-59. 10.1038/264057a0.View ArticlePubMedGoogle Scholar
- Beninger RJ: The slow therapeutic action of antipsychotic drugs. A possible mechanism involving the role of dopamine in incentive learning. Selected Models of Anxiety, Depression and Psychosis. Edited by: Simon P, Soubrie P, Widlocher D. 1988, Basel , Karger, 36-51.Google Scholar
- Kapur S: Psychosis as a state of aberrant salience: a framework linking biology, phenomenology, and pharmacology in schizophrenia. Am J Psychiatry. 2003, 160 (1): 13-23. 10.1176/appi.ajp.160.1.13.View ArticlePubMedGoogle Scholar
- Miller R: Schizophrenic psychology, associative learning and the role of forebrain dopamine. Med Hypotheses. 1976, 2 (5): 203-211. 10.1016/0306-9877(76)90040-2.View ArticlePubMedGoogle Scholar
- McKenna PJ: Pathology, phenomenology and the dopamine hypothesis of schizophrenia. Br J Psychiatry. 1987, 151: 288-301.View ArticlePubMedGoogle Scholar
- Crow TJ: Catecholamine reward pathways and schizophrenia: the mechanism of the antipsychotic effect and the site of the primary disturbance. Fed Proc. 1979, 38: 2462-2467.PubMedGoogle Scholar
- Miller R: Striatal dopamine in reward and attention: a system for understanding the symptomatology of acute schizophrenia and mania. Int Rev Neurobiol. 1993, 35: 161-278.View ArticlePubMedGoogle Scholar
- Gray JA: Integrating schizophrenia. Schizophr Bull. 1998, 24 (2): 249-266.View ArticlePubMedGoogle Scholar
- Corlett PR, Murray GK, Honey GD, Aitken MR, Shanks DR, Robbins TW, Bullmore ET, Dickinson A, Fletcher PC: Disrupted prediction-error signal in psychosis: evidence for an associative account of delusions. Brain. 2007, 130 (Pt 9): 2387-2400. 10.1093/brain/awm173.View ArticlePubMedGoogle Scholar
- Ritter LM, Meador-Woodruff JH, Dalack GW: Neurocognitive measures of prefrontal cortical dysfunction in schizophrenia. Schizophr Res. 2004, 68 (1): 65-73. 10.1016/S0920-9964(03)00086-0.View ArticlePubMedGoogle Scholar
- Beninger RJ, Wasserman J, Zanibbi K, Charbonneau D, Mangels J, Beninger BV: Typical and atypical antipsychotic medications differentially affect two nondeclarative memory tasks in schizophrenic patients: a double dissociation. Schizophr Res. 2003, 61 (2-3): 281-292. 10.1016/S0920-9964(02)00315-8.View ArticlePubMedGoogle Scholar
- Cavallaro R, Cavedini P, Mistretta P, Bassi T, Angelone SM, Ubbiali A, Bellodi L: Basal-corticofrontal circuits in schizophrenia and obsessive-compulsive disorder: a controlled, double dissociation study. Biol Psychiatry. 2003, 54 (4): 437-443. 10.1016/S0006-3223(02)01814-0.View ArticlePubMedGoogle Scholar
- Cools R, Blackwell A, Clark L, Menzies L, Cox S, Robbins TW: Tryptophan depletion disrupts the motivational guidance of goal-directed behavior as a function of trait impulsivity. Neuropsychopharmacology. 2005, 30 (7): 1362-1373.PubMedGoogle Scholar
- McGorry PD, Edwards J, Mihalopoulos C, Harrigan SM, Jackson HJ: EPPIC: an evolving system of early detection and optimal management. Schizophr Bull. 1996, 22 (2): 305-326.View ArticlePubMedGoogle Scholar
- Schimmelmann BG, Conus P, Cotton S, McGorry PD, Lambert M: Pre-treatment, baseline, and outcome differences between early-onset and adult-onset psychosis in an epidemiological cohort of 636 first-episode patients. Schizophr Res. 2007, 95 (1-3): 1-8. 10.1016/j.schres.2007.06.004.View ArticlePubMedGoogle Scholar
- Downes JJ, Roberts AC, Sahakian BJ, Evenden JL, Morris RG, Robbins TW: Impaired extra-dimensional shift performance in medicated and unmedicated Parkinson's disease: evidence for a specific attentional dysfunction. Neuropsychologia. 1989, 27 (11-12): 1329-1343. 10.1016/0028-3932(89)90128-0.View ArticlePubMedGoogle Scholar
- Park SB, Coull JT, McShane RH, Young AH, Sahakian BJ, Robbins TW, Cowen PJ: Tryptophan depletion in normal volunteers produces selective impairments in learning and memory. Neuropharmacology. 1994, 33 (3-4): 575-588. 10.1016/0028-3908(94)90089-2.View ArticlePubMedGoogle Scholar
- Owen AM, Downes JJ, Sahakian BJ, Polkey CE, Robbins TW: Planning and spatial working memory following frontal lobe lesions in man. Neuropsychologia. 1990, 28 (10): 1021-1034. 10.1016/0028-3932(90)90137-D.View ArticlePubMedGoogle Scholar
- Altman DG: Practical Statistics for Medical Research. 1990, London , Chapman and HallGoogle Scholar
- Rosenthal R, Rosnow RL, Rubin DB: Contrasts and Effect Sizes in Behavioral Research: A Correlational Approach. 2000, Cambridge , Cambridge University PressGoogle Scholar
- Niv Y: Cost, benefit, tonic, phasic: what do response rates tell us about dopamine and motivation?. Ann N Y Acad Sci. 2007, 1104: 357-376. 10.1196/annals.1390.018.View ArticlePubMedGoogle Scholar
- Crespi LP: Quantatative variation of incentive and performance in the white rat. American Journal of Psychology. 1942, 55: 467-517. 10.2307/1417120.View ArticleGoogle Scholar
- Roiser JP, Blackwell AD, Cools R, Clark L, Rubinsztein DC, Robbins TW, Sahakian BJ: Serotonin transporter polymorphism mediates vulnerability to loss of incentive motivation following acute tryptophan depletion. Neuropsychopharmacology. 2006, 31 (10): 2264-2272. 10.1038/sj.npp.1301084.View ArticlePubMedPubMed CentralGoogle Scholar
- Wood SJ, Pantelis C, Proffitt T, Phillips LJ, Stuart GW, Buchanan JA, Mahony K, Brewer W, Smith DJ, McGorry PD: Spatial working memory ability is a marker of risk-for-psychosis. Psychol Med. 2003, 33 (7): 1239-1247. 10.1017/S0033291703008067.View ArticlePubMedGoogle Scholar
- Heerey EA, Gold JM: Patients with schizophrenia demonstrate dissociation between affective experience and motivated behavior. J Abnorm Psychol. 2007, 116 (2): 268-278. 10.1037/0021-843X.116.2.268.View ArticlePubMedGoogle Scholar
- Juckel G, Schlagenhauf F, Koslowski M, Filonov D, Wustenberg T, Villringer A, Knutson B, Kienast T, Gallinat J, Wrase J, Heinz A: Dysfunction of ventral striatal reward prediction in schizophrenic patients treated with typical, not atypical, neuroleptics. Psychopharmacology (Berl). 2006, 187 (2): 222-228. 10.1007/s00213-006-0405-4.View ArticleGoogle Scholar
- Pessiglione M, Seymour B, Flandin G, Dolan RJ, Frith CD: Dopamine-dependent prediction errors underpin reward-seeking behaviour in humans. Nature. 2006, 442 (7106): 1042-1045. 10.1038/nature05051.View ArticlePubMedPubMed CentralGoogle Scholar
- Robbins TW, Everitt BJ: Neurobehavioural mechanisms of reward and motivation. Curr Opin Neurobiol. 1996, 6 (2): 228-236. 10.1016/S0959-4388(96)80077-8.View ArticlePubMedGoogle Scholar
- Berridge KC: The debate over dopamine's role in reward: the case for incentive salience. Psychopharmacology (Berl). 2007, 191 (3): 391-431. 10.1007/s00213-006-0578-x.View ArticleGoogle Scholar
- Murray GK, Corlett PR, Clark L, Pessiglione M, Blackwell AD, Honey G, Jones PB, Bullmore ET, Robbins TW, Fletcher PC: Substantia nigra/ventral tegmental reward prediction error disruption in psychosis. Mol Psychiatry. 2008, 13 (3): 239-276. 10.1038/sj.mp.4002157.View ArticlePubMedGoogle Scholar
- Juckel G, Schlagenhauf F, Koslowski M, Wustenberg T, Villringer A, Knutson B, Wrase J, Heinz A: Dysfunction of ventral striatal reward prediction in schizophrenia. Neuroimage. 2006, 29 (2): 409-416. 10.1016/j.neuroimage.2005.07.051.View ArticlePubMedGoogle Scholar
- Gard DE, Kring AM, Gard MG, Horan WP, Green MF: Anhedonia in schizophrenia: distinctions between anticipatory and consummatory pleasure. Schizophr Res. 2007, 93 (1-3): 253-260. 10.1016/j.schres.2007.03.008.View ArticlePubMedPubMed CentralGoogle Scholar
- Barch DM: The relationships among cognition, motivation, and emotion in schizophrenia: how much and how little we know. Schizophr Bull. 2005, 31 (4): 875-881. 10.1093/schbul/sbi040.View ArticlePubMedGoogle Scholar
- The pre-publication history for this paper can be accessed here:http://www.biomedcentral.com/1471-244X/8/34/prepub
This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.