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The First Sentence

May I suggest that characterizing schizophrenia as a "failure to understand reality" is unnecessarily stigmatic? The cited source says nothing about "failure" or "reality." I think the words "failure to understand reality" represent an unneccessary extrapolation on the part of the author(s) of this page. I'm not saying it is an inaccurate description, but I am saying that such an assertion is definitely not directly supported by the cited source. The source says that schizophrenia is characterized by "distortions in thinking, perception, emotions, language, sense of self and behaviour." I see no reason to characterize schizophrenia as a "failure" when there are much more precise ways to describe the disease (i.e., the disease constitutes a distortion, not a failure). Moreover, I fail to see any reason to extrapolate "failure" from a cluster of symptoms described on a WHO page. "Failure" connotes judgment. I suggest that someone in control of this article revise this wording. Even though it might seem trivial, when the very first sentence of the article describes schizophrenia as a "failure" it certainly contributes to the stigma surrounding the disease. I submit my comment very humbly, and without any intention to be inflammatory -- I'm just saying that if I were a schizophrenic I would feel bad if I went to Wikipedia to learn about my disease and found it characterized as a "failure." I would be further distressed if I went to the cited source and found the word "failure" did not appear anywhere in the source. Nor did the word "reality." Using words like these seem to lay bare the judgment of their author. Not very informative.

Prevalence

The prevalence is not 0.5% as indicated but would be rather around 0.4-0.46% according to better sources than the one mentioned in this article. [1]

The lancet source form 2009 looks perfectly fine.http://xa.yimg.com/kq/groups/19525360/611943554/name/Schizophrenia+-+The+Lancet.pdf
And yes 0,46 is about 0.5% as we say. Doc James (talk · contribs · email) 19:54, 2 June 2018 (UTC)[reply]

0.46 is close to 0.5 but it would be at that time more appropriate to the round up to 0.45%. Moreover, the prevalence seems more oriented around 0.4%. Your article seems more include schizophreniform disorder (duration less than 6 months).

— Preceding unsigned comment added by 176.166.234.116 (talk) 13:13, 18 June 2018 (UTC)[reply]

Round up 6 to 5? [citation needed] ... ;^]   - Mark D Worthen PsyD (talk) 19:00, 22 June 2018 (UTC)[reply]

Differential diagnosis

There are, I think, more differential diagnoses than those reported here, including: (M) TBI and PSTBI (psychosis secondary to traumatic brain injury), catatonia, stroke, delusion and psychosis (due to drug abuse or others) and (psychotic) depression.

[2] [3] [4] [5]

References

  1. ^ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1140960/
  2. ^ https://link.springer.com/chapter/10.1007/978-1-4899-4457-3_2
  3. ^ https://www.ncbi.nlm.nih.gov/pubmed/1678937
  4. ^ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4494623/
  5. ^ http://www.emedmd.com/content/diagnosis-classification-and-differential-diagnosis-schizophrenia

Text

Neither one of these appear to be pubmed indexed?

"Twin and adoption studies of schizophrenia yield inflated estimates of the role that genetics plays in its etiology. More recent molecular genetics studies indicate that genetic factors play a minor role in causing schizophrenia relative to environmental influences.[1][2]"

Doc James (talk · contribs · email) 17:24, 18 June 2018 (UTC)[reply]

References

  1. ^ Fosse, Roar; Joseph, Jay; Jones, Mike (2015-09-14). "Schizophrenia: A critical view on genetic effects". Psychosis. 8 (1): 72–84. doi:10.1080/17522439.2015.1081269. ((cite journal)): Unknown parameter |name-list-format= ignored (|name-list-style= suggested) (help)
  2. ^ Leo, Jonathan (Winter 2016). "The Search for Schizophrenia Genes". Issues in Science and Technology. ((cite journal)): Unknown parameter |name-list-format= ignored (|name-list-style= suggested) (help)
I have read a lot of mainstream reviews of causes of schizophrenia and genetics is nearly always the main cause mentioned. In the Behavior Genetics 6th ed. (leading textbook for the field, I don't have a copy of 7th ed.), the authors cite (p. 234) a heritability of about 80% based on the Sullivan et al 2003 meta-analysis (exact reported value = 81% [73%-90%], k = 12). The entire chapter 14 is dedicated to discussion of this trait. Some researchers think otherwise (as always), but it is a minority view from my reading. Deleet (talk) 17:58, 22 June 2018 (UTC)[reply]
I agree. This minority opinion should not be in the lead. If for some strange reason we do include it in the lead, then we should also include a sentence or two about how schizophrenogenic mothers cause the illness.... ;^)   - Mark D Worthen PsyD (talk) 19:10, 22 June 2018 (UTC)[reply]

Semi-protected edit request on 19 June 2018

The sentence "Evidence for metacognitive training is mixed with one 2016 review finding benefit and another not.[151][152]" needs to be updated, as there is a more recent meta-analysis suggesting evidence in favor of MCT (-> 10.1111/wvn.12282). I suggest to change the sentence as follows: "A recent meta-analysis (10.1111/wvn.12282) shows that MCT exerts a significant effect on delusions relative to control conditions at post and follow-up." Perhaps add that the effect is small to medium to clarify that its effect is lower than that found for antipsychotics Wiki psych21 (talk) 19:36, 19 June 2018 (UTC)[reply]

2016 is not that old. New paper is in a journal with an unclear impact factor. Have added it as a ref. Doc James (talk · contribs · email) 08:59, 21 June 2018 (UTC)[reply]
Dear Doc James, I agree. 2016 is not that old but the meta-analysis from van Oosterhout only covers 3-9 studies (depending on outcome) and perhaps more importantly considers far less patients (N(max) = 438) in comparison to the more recent two meta-analyses (e.g., Eichner & Berna: 15 studies for positive symptoms, N(max)=807 patients!). So, the van Oosterhout et al. meta-analysis might be worth reporting but may not receive the same weight. Worldviews on Evidence-Based Nursing is a journal published by Wiley, a publisher with a good reputation. The most recent impact factor is 2.143.
--Wiki psych21 (talk) 11:31, 30 June 2018 (UTC)[reply]
"Psychol Med" has an impact factor of 6.2. Per pt numbers I see "(three studies; 219 participants), delusions (seven studies; 500 participants) and positive symptoms (nine studies; 436 participants)" Doc James (talk · contribs · email) 14:50, 2 July 2018 (UTC)[reply]
Thanks a lot. Psychol Med has a lower impact (5.475) but I am not sure this is a good index for the quality of an individual study - Schizo Bull (Eichner & Berna) has even a larger impact factor (currently 6.94). I am sorry that my numbers on sample size were inaccurate. Still, the new meta-analyses have a much larger base than the older by van Oosterhout et al. (in their reply letter van Oosterhout et al. even acknowledge that with newer studies their results become significant) and this deserves to be acknowledged I think. Also, the Australian & New Zealand Psychiatrist Association (already in 2016) and the German Psychologists (DGPs, upcoming guidelines) recommend the program for the treatment of positive symptoms which also deserves to be mentioned I think. Again, I am sorry about the false numbers, should not have happened --Wiki psych21 (talk) 08:33, 8 July 2018 (UTC)[reply]

Mechanism

The mechanism section doesn't flow very well, is somewhat outdated, and focuses a bit too much on DA. I threw together a rough draft in my sandbox, and am looking for input from other editors as to whether or not it would be a good idea to replace the old section.Petergstrom (talk) 23:44, 24 July 2018 (UTC)[reply]

Mechanism

The cause and mechanism of schizophrenia is unknown. Evidence from phenomenology, pharmacology, neuroimaging, post mortem studies, genetics, and animal models implicate a number of possible mechanisms, such as abnormalities in dopaminergic signalling, glutaminergic neurotransmission, and neurodevelopment. Many frameworks have been hypothesized to link these biological abnormalities to symptoms, including psychological and computational mechanisms.[1]

Abnormal dopamine signalling has been implicated in schizophrenia by the efficacy of D2 receptor agonists, as well as the consistent observation in positron emission tomography of elevated dopamine synthesis[2] and release during acute psychosis.[3] Abnormalities in dopaminergic symptoms have been hypothesized to underlie delusions via dysfunctional signalling of salience.[4][5][6] Dopaminergic predictions errors, which mediate learning when expectancies are violated, are abnormal in schizophrenia, and these abnormalities correlate with the severity of delusions. Furthermore, impaired learning, punitively reflecting the functionality of the dopaminergic system, is present in schizophrenia and correlated with delusion severity as well.[7] Dysfunctional prediction errors may be related to hyperactive input from the hippocampus, which is observed to be metabolically overactive in schizophrenia.[4] Hypoactivation of D1 receptors in the prefrontal cortex may also be responsible for deficits in working memory.[8][9][10][11]

Reduced NMDA receptor signalling is suggested by multiple lines of evidence. Post-mortem studies demonstrate reduced NMDA receptor expression and NMDA receptor agonists mimic both schizophrenia symptoms and the electrophysiological abnormalities associated with schizophrenia (notable reduced mismatch negativity and P300).[12][13][14] This deficit in NMDA signalling may be related to the abnormalities observed in parvalbumin interneurons that express NMDA receptors.[15] Post mortem studies consistently find that a subset of these neurons fail to express GAD67,[16] in addition to abnormalities in morphology. The subsets of interneurons that are abnormal in schizophrenia are responsible for the synchronizing of neural ensembles that is necessary during working memory tasks, a process that electrophysiologically reflected in gamma frequency (30-80 Hz) oscillations. Both working memory tasks and gamma oscillations are impaired in schizophrenia, which may reflect abnormal interneuron functionality.[17][18][19]

Multiple lines of evidence suggest that schizophrenia has a neurodevelopmental component. Schizophrenia is associated with premorbid impairments in cognition, social functioning, and motor skills.[20] Furthermore, prenatal insults such as maternal infection,[21][22] maternal malnutrition and obsteric complications all increase risk for schizophrenia.[23] Animal models of these insults demonstrate patterns of cellular and molecular abnormalities similar to those in schizophrenia, such as increased RELN methylation and abnormal GABAergic cell development.[24] Schizophrenia usually emerges symptomatically during late adolescence, 18-25, an age period that overlaps with certain stages of neurodevelopment that are implicated in schizophrenia.[25]

Deficits in executive functions, such as planning, inhibition, and working memory, are pervasive in schizophrenia. Although these functions are dissociable, their dysfunction in schizophrenia may reflect an underlying deficit in the ability to represent goal related information in working memory, and to utilize this to direct cognition and behavior.[26][27]. These impairments have been linked to a number of neuroimaging and neuropathological abnormalities. For example, functional neuroimaging studies report evidence of reduced neural processing efficiency, whereby the dorsolateral prefrontal cortex is activated to a greater degree to achieve a certain level of performance relative to controls on working memory tasks. These abnormalities may be linked to the consistent post-mortem finding of reduced neuropil, evidenced by increased pyramidal cell density and reduced dentritic spin density. These cellular and functional abnormalities may also be reflected in structural neuroimaging studies that find reduced grey matter volume in association with deficits in working memory tasks.[28]

Positive and negative symptoms have been linked to reduced cortical thickness in the superior temporal lobe,[29] and orbitofrontal cortex, respectively.[30] Anhedonia, traditionally defined as a reduced capacity to experience pleasure, is frequently reported in schizophrenia. However, a large body of evidence suggests that hedonic responses are intact in schizophrenia,[31] and that what is reported to be anhedonia is a reflection of dysfunction in other processes related to reward.[32] Overall, a failure of online maintence and reward associativty is thought to lead to impairment in the generation of cognition and behavior required to obtain rewards, despite normal hedonic responses.[33]

Bayesian models of brain functioning have been utilized to link abnormalities in cellular functioning to symptoms.[34][35] Both hallucinations and delusions have been suggested to reflect improper encoding of prior expectations, thereby causing expectation to excessively influence sensory perception and the formation of beliefs. In canonical models of circuits that mediate predictive coding, hypoactive NMDA receptor activation, similar to that seen in schizophrenia, could theoretically result in classic symptoms of schizophrenia such as delusions and hallucinations.[36][7]

Well, it violates Wikipedia Rule #347: Do not utilize the word "utilize". No, but seriously, it looks pretty good, except that the last paragraph may go a bit deeper than a top-level Wikipedia article ought to. Looie496 (talk) 15:40, 25 July 2018 (UTC)[reply]

References

  1. ^ Insel, TR (11 November 2010). "Rethinking schizophrenia". Nature. 468 (7321): 187–93. doi:10.1038/nature09552. PMID 21068826.
  2. ^ Fusar-Poli, P; Meyer-Lindenberg, A (January 2013). "Striatal presynaptic dopamine in schizophrenia, part II: meta-analysis of [(18)F/(11)C]-DOPA PET studies". Schizophrenia bulletin. 39 (1): 33–42. doi:10.1093/schbul/sbr180. PMC 3523905. PMID 22282454.
  3. ^ Howes, OD; Kambeitz, J; Kim, E; Stahl, D; Slifstein, M; Abi-Dargham, A; Kapur, S (August 2012). "The nature of dopamine dysfunction in schizophrenia and what this means for treatment". Archives of general psychiatry. 69 (8): 776–86. doi:10.1001/archgenpsychiatry.2012.169. PMC 3730746. PMID 22474070.
  4. ^ a b Broyd, A; Balzan, RP; Woodward, TS; Allen, P (June 2017). "Dopamine, cognitive biases and assessment of certainty: A neurocognitive model of delusions". Clinical psychology review. 54: 96–106. doi:10.1016/j.cpr.2017.04.006. PMID 28448827.
  5. ^ Howes, OD; Murray, RM (10 May 2014). "Schizophrenia: an integrated sociodevelopmental-cognitive model". Lancet (London, England). 383 (9929): 1677–1687. doi:10.1016/S0140-6736(13)62036-X. PMC 4127444. PMID 24315522.
  6. ^ Grace, AA (August 2016). "Dysregulation of the dopamine system in the pathophysiology of schizophrenia and depression". Nature reviews. Neuroscience. 17 (8): 524–32. doi:10.1038/nrn.2016.57. PMC 5166560. PMID 27256556.
  7. ^ a b Corlett, PR; Taylor, JR; Wang, XJ; Fletcher, PC; Krystal, JH (November 2010). "Toward a neurobiology of delusions". Progress in neurobiology. 92 (3): 345–69. doi:10.1016/j.pneurobio.2010.06.007. PMC 3676875. PMID 20558235.
  8. ^ Goldman-Rakic, PS; Castner, SA; Svensson, TH; Siever, LJ; Williams, GV (June 2004). "Targeting the dopamine D1 receptor in schizophrenia: insights for cognitive dysfunction". Psychopharmacology. 174 (1): 3–16. doi:10.1007/s00213-004-1793-y. PMID 15118803.
  9. ^ Arnsten, AF; Girgis, RR; Gray, DL; Mailman, RB (1 January 2017). "Novel Dopamine Therapeutics for Cognitive Deficits in Schizophrenia". Biological psychiatry. 81 (1): 67–77. doi:10.1016/j.biopsych.2015.12.028. PMC 4949134. PMID 26946382.
  10. ^ Abi-Dargham, A; Moore, H (October 2003). "Prefrontal DA transmission at D1 receptors and the pathology of schizophrenia". The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry. 9 (5): 404–16. doi:10.1177/1073858403252674. PMID 14580124.
  11. ^ Maia, TV; Frank, MJ (1 January 2017). "An Integrative Perspective on the Role of Dopamine in Schizophrenia". Biological psychiatry. 81 (1): 52–66. doi:10.1016/j.biopsych.2016.05.021. PMC 5486232. PMID 27452791.
  12. ^ Catts, VS; Lai, YL; Weickert, CS; Weickert, TW; Catts, SV (April 2016). "A quantitative review of the postmortem evidence for decreased cortical N-methyl-D-aspartate receptor expression levels in schizophrenia: How can we link molecular abnormalities to mismatch negativity deficits?". Biological psychology. 116: 57–67. doi:10.1016/j.biopsycho.2015.10.013. PMID 26549579.
  13. ^ Michie, PT; Malmierca, MS; Harms, L; Todd, J (April 2016). "The neurobiology of MMN and implications for schizophrenia". Biological psychology. 116: 90–7. doi:10.1016/j.biopsycho.2016.01.011. PMID 26826620.
  14. ^ Pratt, J; Dawson, N; Morris, BJ; Grent-'t-Jong, T; Roux, F; Uhlhaas, PJ (February 2017). "Thalamo-cortical communication, glutamatergic neurotransmission and neural oscillations: A unique window into the origins of ScZ?". Schizophrenia research. 180: 4–12. doi:10.1016/j.schres.2016.05.013. PMID 27317361.
  15. ^ Cohen, SM; Tsien, RW; Goff, DC; Halassa, MM (September 2015). "The impact of NMDA receptor hypofunction on GABAergic neurons in the pathophysiology of schizophrenia". Schizophrenia research. 167 (1–3): 98–107. doi:10.1016/j.schres.2014.12.026. PMC 4724170. PMID 25583246.
  16. ^ Marín, O (18 January 2012). "Interneuron dysfunction in psychiatric disorders". Nature reviews. Neuroscience. 13 (2): 107–20. doi:10.1038/nrn3155. PMID 22251963.
  17. ^ Marín, O (18 January 2012). "Interneuron dysfunction in psychiatric disorders". Nature reviews. Neuroscience. 13 (2): 107–20. doi:10.1038/nrn3155. PMID 22251963.
  18. ^ Lewis, DA; Hashimoto, T; Volk, DW (April 2005). "Cortical inhibitory neurons and schizophrenia". Nature reviews. Neuroscience. 6 (4): 312–24. doi:10.1038/nrn1648. PMID 15803162.
  19. ^ Senkowski, D; Gallinat, J (15 June 2015). "Dysfunctional prefrontal gamma-band oscillations reflect working memory and other cognitive deficits in schizophrenia". Biological psychiatry. 77 (12): 1010–9. doi:10.1016/j.biopsych.2015.02.034. PMID 25847179.
  20. ^ Birnbaum, R; Weinberger, DR (December 2017). "Genetic insights into the neurodevelopmental origins of schizophrenia". Nature reviews. Neuroscience. 18 (12): 727–740. doi:10.1038/nrn.2017.125. PMID 29070826.
  21. ^ Khandaker, GM; Zimbron, J; Lewis, G; Jones, PB (February 2013). "Prenatal maternal infection, neurodevelopment and adult schizophrenia: a systematic review of population-based studies". Psychological medicine. 43 (2): 239–57. doi:10.1017/S0033291712000736. PMC 3479084. PMID 22717193.
  22. ^ Brown, AS; Derkits, EJ (March 2010). "Prenatal infection and schizophrenia: a review of epidemiologic and translational studies". The American journal of psychiatry. 167 (3): 261–80. doi:10.1176/appi.ajp.2009.09030361. PMC 3652286. PMID 20123911.
  23. ^ Brown, AS (January 2011). "The environment and susceptibility to schizophrenia". Progress in neurobiology. 93 (1): 23–58. doi:10.1016/j.pneurobio.2010.09.003. PMC 3521525. PMID 20955757.
  24. ^ Negrón-Oyarzo, I; Lara-Vásquez, A; Palacios-García, I; Fuentealba, P; Aboitiz, F (11 March 2016). "Schizophrenia and reelin: a model based on prenatal stress to study epigenetics, brain development and behavior". Biological research. 49: 16. doi:10.1186/s40659-016-0076-5. PMC 4787713. PMID 26968981.((cite journal)): CS1 maint: unflagged free DOI (link)
  25. ^ Cannon, TD (December 2015). "How Schizophrenia Develops: Cognitive and Brain Mechanisms Underlying Onset of Psychosis". Trends in cognitive sciences. 19 (12): 744–756. doi:10.1016/j.tics.2015.09.009. PMC 4673025. PMID 26493362.
  26. ^ Lesh, TA; Niendam, TA; Minzenberg, MJ; Carter, CS (January 2011). "Cognitive control deficits in schizophrenia: mechanisms and meaning". Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology. 36 (1): 316–38. doi:10.1038/npp.2010.156. PMC 3052853. PMID 20844478.
  27. ^ Barch, DM; Ceaser, A (January 2012). "Cognition in schizophrenia: core psychological and neural mechanisms". Trends in cognitive sciences. 16 (1): 27–34. doi:10.1016/j.tics.2011.11.015. PMC 3860986. PMID 22169777.
  28. ^ Eisenberg, DP; Berman, KF (January 2010). "Executive function, neural circuitry, and genetic mechanisms in schizophrenia". Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology. 35 (1): 258–77. doi:10.1038/npp.2009.111. PMC 2794926. PMID 19693005.
  29. ^ Walton, E; Hibar, DP; van Erp, TG; Potkin, SG; Roiz-Santiañez, R; Crespo-Facorro, B; Suarez-Pinilla, P; Van Haren, NE; de Zwarte, SM; Kahn, RS; Cahn, W; Doan, NT; Jørgensen, KN; Gurholt, TP; Agartz, I; Andreassen, OA; Westlye, LT; Melle, I; Berg, AO; Mørch-Johnsen, L; Faerden, A; Flyckt, L; Fatouros-Bergman, H; Karolinska Schizophrenia Project Consortium, (KaSP).; Jönsson, EG; Hashimoto, R; Yamamori, H; Fukunaga, M; Preda, A; De Rossi, P; Piras, F; Banaj, N; Ciullo, V; Spalletta, G; Gur, RE; Gur, RC; Wolf, DH; Satterthwaite, TD; Beard, LM; Sommer, IE; Koops, S; Gruber, O; Richter, A; Krämer, B; Kelly, S; Donohoe, G; McDonald, C; Cannon, DM; Corvin, A; Gill, M; Di Giorgio, A; Bertolino, A; Lawrie, S; Nickson, T; Whalley, HC; Neilson, E; Calhoun, VD; Thompson, PM; Turner, JA; Ehrlich, S (May 2017). "Positive symptoms associate with cortical thinning in the superior temporal gyrus via the ENIGMA Schizophrenia consortium". Acta psychiatrica Scandinavica. 135 (5): 439–447. doi:10.1111/acps.12718. PMC 5399182. PMID 28369804.
  30. ^ Walton, E; Hibar, DP; van Erp, TGM; Potkin, SG; Roiz-Santiañez, R; Crespo-Facorro, B; Suarez-Pinilla, P; van Haren, NEM; de Zwarte, SMC; Kahn, RS; Cahn, W; Doan, NT; Jørgensen, KN; Gurholt, TP; Agartz, I; Andreassen, OA; Westlye, LT; Melle, I; Berg, AO; Morch-Johnsen, L; Færden, A; Flyckt, L; Fatouros-Bergman, H; Karolinska Schizophrenia Project Consortium, (KaSP).; Jönsson, EG; Hashimoto, R; Yamamori, H; Fukunaga, M; Jahanshad, N; De Rossi, P; Piras, F; Banaj, N; Spalletta, G; Gur, RE; Gur, RC; Wolf, DH; Satterthwaite, TD; Beard, LM; Sommer, IE; Koops, S; Gruber, O; Richter, A; Krämer, B; Kelly, S; Donohoe, G; McDonald, C; Cannon, DM; Corvin, A; Gill, M; Di Giorgio, A; Bertolino, A; Lawrie, S; Nickson, T; Whalley, HC; Neilson, E; Calhoun, VD; Thompson, PM; Turner, JA; Ehrlich, S (January 2018). "Prefrontal cortical thinning links to negative symptoms in schizophrenia via the ENIGMA consortium". Psychological medicine. 48 (1): 82–94. doi:10.1017/S0033291717001283. PMC 5826665. PMID 28545597.
  31. ^ Cohen, AS; Minor, KS (January 2010). "Emotional experience in patients with schizophrenia revisited: meta-analysis of laboratory studies". Schizophrenia bulletin. 36 (1): 143–50. doi:10.1093/schbul/sbn061. PMC 2800132. PMID 18562345.
  32. ^ Strauss, GP; Gold, JM (April 2012). "A new perspective on anhedonia in schizophrenia". The American journal of psychiatry. 169 (4): 364–73. doi:10.1176/appi.ajp.2011.11030447. PMC 3732829. PMID 22407079.
  33. ^ Young, Jared; Anticevic, Alan; Barch, Deanna (2018). "Cognitive and Motivational Neuroscience of Psychotic Disorders". In Charney, Dennis; Buxbaum, Joseph; Sklar, Pamela; Nestler, Eric (eds.). Charney & Nestler's Neurobiology of Mental Illness (5th ed.). New York: Oxford University Press. pp. 215, 217. ISBN 9780190681425. Several recent reviews (e.g., Cohen and Minor, 2010) have found that individuals with schizophrenia show relatively intact self-reported emotional responses to affect-eliciting stimuli as well as other indicators of intact response(215)...Taken together, the literature increasingly suggests that there may be a deficit in putatively DA-mediated reward learning and/ or reward prediction functions in schizophrenia. Such findings suggest that impairment in striatal reward prediction mechanisms may influence "wanting" in schizophrenia in a way that reduces the ability of individuals with schizophrenia to use anticipated rewards to drive motivated behavior.(217)
  34. ^ Friston, KJ; Stephan, KE; Montague, R; Dolan, RJ (July 2014). "Computational psychiatry: the brain as a phantastic organ". The lancet. Psychiatry. 1 (2): 148–58. doi:10.1016/S2215-0366(14)70275-5. PMID 26360579.
  35. ^ Griffin, JD; Fletcher, PC (8 May 2017). "Predictive Processing, Source Monitoring, and Psychosis". Annual review of clinical psychology. 13: 265–289. doi:10.1146/annurev-clinpsy-032816-045145. PMC 5424073. PMID 28375719.
  36. ^ Fletcher, PC; Frith, CD (January 2009). "Perceiving is believing: a Bayesian approach to explaining the positive symptoms of schizophrenia". Nature reviews. Neuroscience. 10 (1): 48–58. doi:10.1038/nrn2536. PMID 19050712.
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