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:Can you clarify what you find offensive about the photo and how you feel it discriminates against people who have schizophrenia? [[User:TylerDurden8823|TylerDurden8823]] ([[User talk:TylerDurden8823|talk]]) 18:25, 30 August 2018 (UTC)
:Can you clarify what you find offensive about the photo and how you feel it discriminates against people who have schizophrenia? [[User:TylerDurden8823|TylerDurden8823]] ([[User talk:TylerDurden8823|talk]]) 18:25, 30 August 2018 (UTC)


:IMO, this is likely due to the [[Framing effect (psychology)]] from the first sentence discussed above. The picture is merely negative, subjective and puts emphasis, perhaps undue, on the delusion of control. [[User:Asterixf2|Asterixf2]] ([[User talk:Asterixf2|talk]]) 11:12, 16 September 2018 (UTC)
:IMO, this is likely due to the [[Framing effect (psychology)]] from the first sentence of the article discussed above in another section of the talk page. The picture is merely negative, subjective and puts emphasis, perhaps undue, on the delusion ofl control. [[User:Asterixf2|Asterixf2]] ([[User talk:Asterixf2|talk]]) 11:12, 16 September 2018 (UTC)


==Text==
==Text==

Revision as of 11:16, 16 September 2018

Featured articleSchizophrenia is a featured article; it (or a previous version of it) has been identified as one of the best articles produced by the Wikipedia community. Even so, if you can update or improve it, please do so.
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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.

You are correct. This is overly simplistic, stigmatizing and incorrect. It shouldn't be described in a simple way because this is a complex disorder that describes various clusters of psychomotor symptoms. Asterixf2 (talk) 10:06, 15 September 2018 (UTC)[reply]
The sentence People with schizophrenia often have additional mental health problems... describes another disorder -- schizoaffective -- and is also incorrect. Asterixf2 (talk) 10:12, 15 September 2018 (UTC)[reply]
  1. People with schizophrenia often have additional mental health problems... is not correct. Look at comorbidity, and then perhaps compare the diagnostic criteria for schizophrenia and schizoaffective disorder.
  2. Schizophrenia is a chronic and severe mental condition that encompasses any of a group of psychomotor symptoms that vary widely among affected individuals. Psychomotor symptoms are a subset of psychotic symptoms, and do not encompass, for example, delusions, hallucinations or though disorder.
  3. Paresthesia is not a common manifestation of schizophrenia.Petergstrom (talk) 04:51, 16 September 2018 (UTC)[reply]
    1. Thank you for the clarification. My goal here is to improve the top paragraph by making it less stigmatizing and written in a more encyclopedic, informative style.
    2. Regarding #Paresthesia is not a common manifestation of schizophrenia. -- I may remove the wikilink to paresthesia, because what I meant are "sensory hallucinations" as noted in the WHO document as one of the core symptoms of schizophrenia. However I have found it useful to link "needles" to paresthesia as these are the most common afaik "bizarre physical sensations" (original WHO wording). Please take a look at page 4: http://www.who.int/mental_health/media/en/55.pdf among others. Furthermore, please note that according to WHO auditory hallucinations (voices) occur only in 70% of patients. I insist on improving the top paragraph, please help. Thank you for your valuable input.
    3. Do you find the following wording sufficiently tolerable?:
      Schizophrenia is a chronic and severe mental condition that encompasses any of a group of symptoms that vary widely among affected individuals. Some of the following disturbances can always be observed: delusions – firmly held false beliefs that usually include ideas of reference, control or persecution; hallucinations – hearing, seeing or feeling things that are not there like voices or needles; thought disorders – as evidenced by disorganized speech, illogical associations or sensations of thought insertion; altered motor activity – reduction of spontaneous movements, prolonged bizarre positions; abnormal affect – reduction in emotional intensity or variation, lack of motivation.[1][2][3] Symptoms typically begin in early adulthood.[4][5] About 45% of patients recover after one or more episodes and 35% show a mixed pattern with varying degrees of remission and exacerbations of different length. Schizophrenia is treatable. Risk of relapse during the first year following an acute episode in patients on antipsychotic medications is reduced to about 20%, in comparison with about 60% on placebo.[6] People with schizophrenia often have additional mental health problems such as anxiety, depressive, or substance-use disorders.[7]
      Asterixf2 (talk) 05:35, 16 September 2018 (UTC)[reply]
    4. Alternatively, I propose to change the first sentence into:
      Schizophrenia is a mental disorder characterized by abnormal behavior and disturbances in the perception of reality.[8]
      Asterixf2 (talk) 06:07, 16 September 2018 (UTC)[reply]
Auditory hallucinations are by far the most common type of hallucination, although there is significant variability across time and cultures; in the end, its not worth specifying any sensory modality, as the intro is meant to be general. Furthermore, the current wording is not at all stigmatizing, and is fine the way it is. There is no reason to change that sentence, and the proposed edit just doesn't work - it doesn't flow well, is excessively convoluted, and doesn't provide a succinct overview. Lets get some other editor input on this.Petergstrom (talk) 06:07, 16 September 2018 (UTC)[reply]
Ok. Please also take into consideration another alternative that I have proposed. Asterixf2 (talk) 06:11, 16 September 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.

[9] [10] [11] [12]

References

  1. ^ "Schizophrenia Fact sheet". WHO. April 2018. Archived from the original on 15 September 2018. Retrieved 15 September 2018. {{cite web}}: Unknown parameter |deadurl= ignored (|url-status= suggested) (help)
  2. ^ "Schizophrenia". Encyclopedia Britannica. April 2018. Archived from the original on 17 June 2018. Retrieved 15 September 2018. {{cite web}}: Unknown parameter |deadurl= ignored (|url-status= suggested) (help)
  3. ^ Barbato, Angelo (1998). Schizophrenia and public health (PDF). Geneva: World Health Organization. pp. 2–5.
  4. ^ "Schizophrenia". National Institute of Mental Health. January 2016. Archived from the original on 25 November 2016. Retrieved 3 February 2016. {{cite web}}: Unknown parameter |deadurl= ignored (|url-status= suggested) (help)
  5. ^ Cite error: The named reference DSM5pg101 was invoked but never defined (see the help page).
  6. ^ Barbato, Angelo (1998). Schizophrenia and public health (PDF). Geneva: World Health Organization. pp. 8–17.
  7. ^ Buckley PF, Miller BJ, Lehrer DS, Castle DJ (March 2009). "Psychiatric comorbidities and schizophrenia". Schizophrenia Bulletin. 35 (2): 383–402. doi:10.1093/schbul/sbn135. PMC 2659306. PMID 19011234.
  8. ^ "Schizophrenia Fact sheet N°397". WHO. September 2015. Archived from the original on 18 October 2016. Retrieved 3 February 2016. {{cite web}}: Unknown parameter |deadurl= ignored (|url-status= suggested) (help)
  9. ^ https://link.springer.com/chapter/10.1007/978-1-4899-4457-3_2
  10. ^ https://www.ncbi.nlm.nih.gov/pubmed/1678937
  11. ^ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4494623/
  12. ^ http://www.emedmd.com/content/diagnosis-classification-and-differential-diagnosis-schizophrenia

Misleading and offensive quotation marks.

Please change this

  • Schizophrenia does not imply a "split personality" or "dissociative identity disorder" – conditions with which it is often confused in public perception.

to this

  • Schizophrenia does not imply a "split personality" or dissociative identity disorder – conditions with which it is often confused in public perception.

because there is nothing actually quoted, and quotation marks in absence of an actual quote signify an expression, which is colloquial (however, dissociative identity disorder is not colloquial), or signify a sentiment, which is not shared by the author (similar to: so-called, alleged, ...). Here, it reads as if dissociative identity disorder is would be some sort of parapsychological, hysterical pseudo-diagnosis, where as, in fact, the nosological entity has been validated through multiple /somatic/ studies, eg using fMRI. Hence, those quotes are misleading for the reader and offensive to those affected by the condition. --92.194.46.84 (talk) 13:23, 13 August 2018 (UTC)[reply]

Sure Doc James (talk · contribs · email) 03:14, 14 August 2018 (UTC)[reply]

Silica gel as a cure for "paranoid schizophrenia"

The DDR (socialist part of Germany up to 1989) used silica gel for people with psychosis. Nobel-laureate Julius Wagner-Jauregg from Austria treated hospitalized people bathing in horsetail-brew, coming to the conclusion that they were in a state where hospitalization wasn't necessary anymore. It was an easy step for me to find out the biological agent of the horsetail was silica-compunds. Note that healing earth, silicon dioxide (chert) or homeopathy is not meant. The both first aren't water-soluble. What's more, I know some people reacting like this - being healed - from e.g. hallucinations. However, amalgam-allergy induced dementia does exist asmuch as gluten-sensitivity up to coeliac disease. These might also cause - according to the diagnostician - schizophrenia. I want to remark here that typing with the angloamerican speakers is MUCH more fun than doing it in wikipedia.de (where you get kicked/deleted when you write some words). I want to mention here, that I was diagnosed with it; however, weeks of hallucinations or "slurred speech" was absent. Lutz Fehling — Preceding unsigned comment added by 2003:D7:BD8:8F00:5532:A673:4BB4:B92C (talk) 14:19, 20 August 2018 (UTC)[reply]

Please change the photo.

Hi. Please change the photo. Stop of discrimination of patients. — Preceding unsigned comment added by Artystka88 (talk • contribs) 16:32, 30 August 2018 (UTC)[reply]

Can you clarify what you find offensive about the photo and how you feel it discriminates against people who have schizophrenia? TylerDurden8823 (talk) 18:25, 30 August 2018 (UTC)[reply]
IMO, this is likely due to the Framing effect (psychology) from the first sentence of the article discussed above in another section of the talk page. The picture is merely negative, subjective and puts emphasis, perhaps undue, on the delusion ofl control. Asterixf2 (talk) 11:12, 16 September 2018 (UTC)[reply]

Text

This text

"Childhood trauma - particularly childhood sexual abuse - is a causal factor for schizophrenia. Some believe that Posttraumatic Stress Disorder (PTSD) is often misdiagnosed as schizophrenia. It is imperative that before a diagnosis of schizophrenia is made, a bio-psycho-social history that explicitly asks about childhood trauma is taken.[1][2] [3]"

Is not supported by the refs in question. Plus we should try to use more recent sources.

The most recent review from 2007 that was added actually says "The evidence that childhood trauma causes psychosis is controversial and contestable."

References

  1. ^ Read J, van Os J, Morrison AP, Ross CA (November 2005). "Childhood trauma, psychosis and schizophrenia: a literature review with theoretical and clinical implications". Acta Psychiatrica Scandinavica. 112 (5): 330–50. doi:10.1111/j.1600-0447.2005.00634.x. PMID 16223421.
  2. ^ Mueser KT, Goodman LB, Trumbetta SL, Rosenberg SD, Osher fC, Vidaver Rf, Auciello P, Foy DW (June 1998). "Trauma and posttraumatic stress disorder in severe mental illness". Journal of Consulting and Clinical Psychology. 66 (3): 493–9. doi:10.1037/0022-006x.66.3.493. PMID 9642887. {{cite journal}}: Vancouver style error: name in name 5 (help)
  3. ^ Morgan C, Fisher H (January 2007). "Environment and schizophrenia: environmental factors in schizophrenia: childhood trauma--a critical review". Schizophrenia Bulletin. 33 (1): 3–10. doi:10.1093/schbul/sbl053. PMC 2632300. PMID 17105965.

Doc James (talk · contribs · email) 00:11, 1 September 2018 (UTC)[reply]

Support deleting the text. Perhaps it could be replaced by this review?--Literaturegeek | T@1k? 14:01, 1 September 2018 (UTC)[reply]
User:Literaturegeek generally we try to avoid Frontier journals as they are of questionable veracity.
This would be better IMO https://www.ncbi.nlm.nih.gov/pubmed/28216171 Doc James (talk · contribs · email) 03:40, 2 September 2018 (UTC)[reply]

Changes to the "mechanism" section

I posted a potential rewrite of the mechanism section(which I don't think is up to date, and gives a bit too much weight to certain lines of research) in July, and it only got one response. I am reposting it here as it was archived, and would appreciate other editors inputs.Petergstrom (talk) 21:49, 1 September 2018 (UTC)[reply]

Overly complicated IMO and needs substantial simplification. Doc James (talk · contribs · email) 03:37, 2 September 2018 (UTC)[reply]
An improvement over the current text IMO. I personally don't understand the following words in this context: "frameworks", "consistent observation" (... in PET of elevated dopamine synthesis. <-- what is consistent, the observation or the elevated synthesis?), "Dopaminergic predictions errors" (the ending -s in both words mess with me), "putatively" could possibly be switched with a synonym, "post mortem" could be hyphenated (as it is in 2nd mention), "associativty" seems to be missing a letter i. These changes would improve readability IMO. --Treetear (talk) 22:34, 13 September 2018 (UTC)[reply]

Mechanism

The mechanism of schizophrenia is unknown. Evidence 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 antagonists, as well as the consistent observation in positron emission tomography of elevated dopamine synthesis[2] and release during acute psychosis.[3] Abnormalities in dopaminergic signalling 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, putatively reflecting the functionality of the dopaminergic system, is present in schizophrenia and correlates with delusion severity.[7] Dysfunctional prediction errors may be related to hyperactive input from the hippocampus, which has been 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 antagonists mimic both schizophrenia symptoms and the electrophysiological abnormalities associated with schizophrenia (notably 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 is 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.[16][17][18]

Multiple lines of evidence suggest that schizophrenia has a neurodevelopmental component. Schizophrenia is associated with premorbid impairments in cognition, social functioning, and motor skills.[19] Furthermore, prenatal insults such as maternal infection,[20][21] maternal malnutrition and obsteric complications all increase risk for schizophrenia.[22] 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.[23] Schizophrenia usually emerges symptomatically during late adolescence, 18-25, an age period that overlaps with certain stages of neurodevelopment that are implicated in schizophrenia.[24]

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.[25][26]. 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.[27]

Positive and negative symptoms have been linked to reduced cortical thickness in the superior temporal lobe,[28] and orbitofrontal cortex, respectively.[29] 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,[30] and that what is reported to be anhedonia is a reflection of dysfunction in other processes related to reward.[31] 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.[32]

Bayesian models of brain functioning have been utilized to link abnormalities in cellular functioning to symptoms.[33][34] 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.[35][7]

References

  1. ^ Insel TR (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 (May 2014). "Schizophrenia: an integrated sociodevelopmental-cognitive model". Lancet. 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 (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. 9 (5): 404–16. doi:10.1177/1073858403252674. PMID 14580124.
  11. ^ Maia TV, Frank MJ (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. ^ a b Marín O (January 2012). "Interneuron dysfunction in psychiatric disorders". Nature Reviews. Neuroscience. 13 (2): 107–20. doi:10.1038/nrn3155. PMID 22251963.
  17. ^ 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.
  18. ^ Senkowski D, Gallinat J (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.
  19. ^ 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.
  20. ^ 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.
  21. ^ 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.
  22. ^ 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.
  23. ^ Negrón-Oyarzo I, Lara-Vásquez A, Palacios-García I, Fuentealba P, Aboitiz F (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)
  24. ^ 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.
  25. ^ Lesh TA, Niendam TA, Minzenberg MJ, Carter CS (January 2011). "Cognitive control deficits in schizophrenia: mechanisms and meaning". Neuropsychopharmacology. 36 (1): 316–38. doi:10.1038/npp.2010.156. PMC 3052853. PMID 20844478.
  26. ^ 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.
  27. ^ Eisenberg DP, Berman KF (January 2010). "Executive function, neural circuitry, and genetic mechanisms in schizophrenia". Neuropsychopharmacology. 35 (1): 258–77. doi:10.1038/npp.2009.111. PMC 2794926. PMID 19693005.
  28. ^ Walton E, Hibar DP, van Erp TG, Potkin SG, Roiz-Santiañez R, Crespo-Facorro B, et al. (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.
  29. ^ Walton E, Hibar DP, van Erp TG, Potkin SG, Roiz-Santiañez R, Crespo-Facorro B, et al. (Karolinska Schizophrenia Project Consortium (KaSP)) (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.
  30. ^ 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.
  31. ^ 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.
  32. ^ 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) {{cite book}}: Unknown parameter |name-list-format= ignored (|name-list-style= suggested) (help)
  33. ^ 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.
  34. ^ Griffin JD, Fletcher PC (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.
  35. ^ 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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