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The gut–brain axis

I propose to add this in causes section:

The gut-brain axis

It is now increasingly recognized that several risk factors for the development of schizophrenia may be linked through a common pathway in the intestinal tract. The gut–brain axis provides a bidirectional homeostatic route of communication that uses neural, hormonal and immunological routes. In schizophrenia is seen an increased incidence of gastrointestinal barrier dysfunction, food antigen sensitivity, the metabolic syndrome and systemic inflammation, which are probably influenced by the composition of the gut microbiota.[1]

In a significant subgroup of patients with schizophrenia, coeliac disease and non-celiac gluten sensitivity may be involved in the disruption of intestinal permeability and immunologic abnormalities, leading to psychiatric and neurologic symptomatology.[2] These patients may benefit from the initiation of a gluten-free diet [3] or a gluten and casein-free diet.[1] As early as the 1950s and 60s, the link between schizophrenia and coeliac disease was observed in clinical settings, both in children and adults.[2] However, the anti-gliadin immune response in schizophrenia may have a different antigenic specificity from that in coeliac disease, and is independent of the action of tissue transglutaminase enzyme[2] and the two main celiac disease genes (HLA-DQ2 and HLA-DQ8).[4]

  1. ^ a b Nemani K, Hosseini Ghomi R, McCormick B, Fan X (Jan 2015). "Schizophrenia and the gut-brain axis". Prog Neuropsychopharmacol Biol Psychiatry. 56: 155–60. doi:10.1016/j.pnpbp.2014.08.018. PMID 25240858.
  2. ^ a b c Arroll MA, Wilder L, Neil J (Sep 2014). "Nutritional interventions for the adjunctive treatment of schizophrenia: a brief review". Nutr J. 13: 91. doi:10.1186/1475-2891-13-91. PMC 4171568. PMID 25228271.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  3. ^ Catassi C, Bai JC, Bonaz B, Bouma G, Calabrò A, Carroccio A, Castillejo G, Ciacci C, Cristofori F, Dolinsek J, Francavilla R, Elli L, Green P, Holtmeier W, Koehler P, Koletzko S, Meinhold C, Sanders D, Schumann M, Schuppan D, Ullrich R, Vécsei A, Volta U, Zevallos V, Sapone A, Fasano A (Sep 2013). "Non-Celiac Gluten sensitivity: the new frontier of gluten related disorders". Nutrients. 5 (10): 3839–53. doi:10.3390/nu5103839. PMC 3820047. PMID 24077239.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  4. ^ Samaroo D, Dickerson F, Kasarda DD, Green PH, Briani C, Yolken RH, Alaedini A (May 2010). "Novel immune response to gluten in individuals with schizophrenia". Schizophr Res. 118 (1–3): 248–55. doi:10.1016/j.schres.2009.08.009. PMC 2856786. PMID 19748229.

Regards. --BallenaBlanca (talk) 15:23, 24 October 2015 (UTC)

Extended content
The ref does not say IBS causes schizophrenia it just says it appears that a lot of people with schizophrenia may have IBS.[5] Therefore adjusted. Doc James (talk · contribs · email) 05:28, 10 November 2015 (UTC)

Gut-brain axis 2

Several risk factors for the development of schizophrenia may be linked to the intestinal tract with dysfunction of the gut–brain axis being proposed as a mechanism. This may be related changes in the intestinal flora.[1]

In some people with schizophrenia, coeliac disease and non-celiac gluten sensitivity may be involved in the disruption of intestinal permeability.[2] It has been suggested that these people may benefit from a gluten-free diet[3] or a gluten and casein-free diet.[1] As early as the 1950s and 60s, the link between schizophrenia and coeliac disease was observed, both in children and adults.[2] However, the anti-gliadin immune response in schizophrenia may have a different specificity from that in coeliac disease, and is independent of the action of tissue transglutaminase enzyme.[2]

Extended content

Gut-brain axis 3

It has been hypothesized that development of schizophrenia is related to intestinal tract dysfunction as a result of changes in the intestinal flora.[1]

In some people with schizophrenia, coeliac disease and non-celiac gluten sensitivity may be involved in the disruption of intestinal permeability, leading to psychiatric and neurologic symptomatology.[2] It has been suggested that these people may benefit from a gluten-free diet[3] or a gluten and casein-free diet.[1] As early as the 1950s and 60s, the link between schizophrenia and coeliac disease was observed, both in children and adults.[2] However, the anti-gliadin immune response in schizophrenia may have a different specificity from that in coeliac disease, and is independent of the action of tissue transglutaminase enzyme[2] and the two main celiac disease genes (HLA-DQ2 and HLA-DQ8).[4]

Have adjusted above as a little to closely paraphrased. Probably best to go at causes of schizophrenia. Others thoughts?Doc James (talk · contribs · email) 20:26, 24 October 2015 (UTC)

I agree your new text, but only two important details: not to eliminate "leading to psychiatric and neurologic symptomatology"[2] nor "and the two main celiac disease genes (HLA-DQ2 and HLA-DQ8)".[4] So, I propose the number 3 version.
This text is only a little summary. It is perfect for schizophrenia page. It is important to consider that we are talking about "a significant subgroup of patients".[1]
For the page causes of schizophrenia, it would be good to prepare an expanded text.
So, if you agree, I'll add in schizophrenia "Gut-brain axis 3". I'll wait for your answer. Thanks for your help! --BallenaBlanca (talk) 07:11, 25 October 2015 (UTC)
Best at causes of schizophrenia rather than here IMO. Maybe one or two sentence here. The conclusions of the papers you have linked are very tentative. Doc James (talk · contribs · email) 03:03, 2 November 2015 (UTC)
"leading to psychiatric and neurologic symptomatology" is redundant. If we are saying that it causes schizophrenia than those are a given and do not need to be restated. Doc James (talk · contribs · email) 03:13, 2 November 2015 (UTC)

Okay added "It has been hypothesized that development of schizophrenia is related to intestinal tract dysfunction as a result of changes in the intestinal flora.[1]" Doc James (talk · contribs · email) 03:17, 2 November 2015 (UTC)

I feel that the proposed mechanism needs to be included, like saying "resulting in activation of immune mediated inflammatory pathways in the brain." Most lay or even many professionals reading that sentence will be left wondering as almost all of our readers of this article will know nothing about the gut-brain axis and its relationship to the field of psychoneuroimmunology and advanced neuropsychiatric research.--Literaturegeek | T@1k? 21:34, 2 November 2015 (UTC)
Thanks, @Literaturegeek:.
I see no reason not to say to the reader what it is documented in multuitud of works: that there is a subgroup of patients whose disease could be linked to the consumption of gluten and that they can benefit from a gluten-free diet. The "Schizophrenia" page receives an average of 4,400 daily visits, whereas only about 100 persons read the "Causes of schizophrenia" page. People generally do not navigate to other pages and read only the main ones. It is understood that in them there is already a resument of all important points, which is what people want to read. That means that we may be depriving about 4300 people per day of the ability to find answers.
@Doc James: you say that the conclusions of the papers I have linked are very tentative. Our mission in Wikipedia is to write from a "neutral point of view (NPOV), which means representing fairly, proportionately, and, as far as possible, without bias, all of the significant views that have been published by reliable sources on a topic." Thus, if there is a controversy, let’s talk about it. It is necessary to give the reader all the positions so that he can make his own decisions. However, let's take a different approach and let's take a look at other sources, with the most recent reviews (Oct 2014 and Dec 2014):

A connection between schizophrenia and gluten began to be noticed in the 1950s. During World War II, (…) the reduced supply of cereals seemed to determine a lower incidence of schizophrenia, suggesting that they were related. Another observation was that a great number of admissions for SCZ occurred in countries like Ireland with higher availability of wheat and rye than in England and Wales [24]. Studies on the effect of elimination of gluten from the diet of SCZ patients further strengthened the existence of an association between gluten and schizophrenia. In fact, SCZ patients whose symptoms improved after introduction of a cereal- and milk-free diet showed an interruption or reversal of clinical improvement during wheat challenge [25]. At that time, the evidence pointed to a link between schizophrenia and gluten, and the authors suggested that celiac disease and SCZ had the same pathogenesis, namely the harmful effect of wheat. They hypothesized that the common clinical manifestations might signal a genetic link. This called for further studies to establish whether gluten consumption was a triggered genetic susceptibility, as suggested by Dohan [26]. Subsequent observations often provided contrasting results.(…) Regarding the association between schizophrenia and gluten sensitivity, most recent studies agree on the involvement of gluten sensitivity rather than celiac disease in a subgroup of SCZ patients [8, 9, 30, 50, 51]. As far as the association between mood disorders and gluten sensitivity is concerned, no systematic studies have been conducted.(…) In this review of the literature on the association between SCZ/MD and CD/GS, we found that for many years, studies on the association between schizophrenia and celiac disease provided contrasting results [5–7, 28, 29]. Celiac patients were thought to be at higher risk of developing SCZ than the general population [5–7] Auto Immun Highlights. 2014 Oct 16;5(2):55-61. doi: 10.1007/s13317-014-0064-0. Celiac and non-celiac gluten sensitivity: a review on the association with schizophrenia and mood disorders. Porcelli B, Verdino V, Bossini L, Terzuoli L, Fagiolini A

Varios estudios sostienen que la retirada del gluten de la dieta de ciertos individuos puede acompañarse de una reducción drástica, e incluso de la remisión completa de los síntomas esquizofrénicos. Sin embargo, insistimos, esto ocurre sólo en un subgrupo de pacientes esquizofrénicos. Nutr Hosp. 2014 Dec 1;30(6):1203-10. doi: 10.3305/nh.2014.30.6.7866. [Is gluten the great etiopathogenic agent of disease in the XXI century? [Article in Spanish] San Mauro Martín I, Garicano Vilar E, Collado Yurrutia L, Ciudad Cabañas MJ]

So, I propose this new text for Schizophrenia page:
As early as the 1950s and 60s, the link between schizophrenia and gluten in a subset of patients was observed in clinical settings, both in children and adults.[2][5] However, results of studies carried out for years about the association between coeliac disease and schizophrenia are contradictory. Currently, recent studies agree that schizophrenia is associated with non-celiac gluten sensitivity, rather than to celiac disease[5] and that in a significant subgroup of patients, the initiation of a gluten-free diet[3][6] or a gluten and casein-free diet[1] may be accompanied by a drastic reduction or even complete remission of schizophrenic symptoms.[1][3][6]
Best regards. --BallenaBlanca (talk) 09:36, 4 November 2015 (UTC)
Your proposed text addition is too definitive and wide sweeping in how it is worded. I would not use the word 'significant subgroup'. Is that wording used in the sources? Your statement about recent studies agreeing that schizophrenia is associated with gluten is too strong as it implies all or most schizophrenics have this association. It should say recent studies agree that non celiac gluten sensitivity is associated with a subgroup of schizophrenics.... From reading the references there is evidence that a gluten free diet may have a positive effect on schizophrenia in a small subgroup of patients. Your proposed text is too detailed for this page. This page is only meant to be a very brief overview. As there is still quite some controversy about the role of gluten in schizophrenia in some patients it should be given low weight in this article. If it is mentioned at all on this page, it should be a single (not overly long) sentence. Please see WP:WEIGHT. The causes of schizophrenia article as it is dedicated to the causes would be more appropriate place for your suggested paragraph. There are many many environmental, genetic and psychological contributions to this disease which interact together. Gluten may or may not be one of those environmental contributions but it is not 'the cause' on its own.--Literaturegeek | T@1k? 15:36, 7 November 2015 (UTC)

@Literaturegeek: very thanks for your replay.

First, I answer your question: "significant subgroup'. Is that wording used in the sources?" Yes:

Nemani K, Hosseini Ghomi R, McCormick B, Fan X (Jan 2015). "Schizophrenia and the gut-brain axis". Prog Neuropsychopharmacol Biol Psychiatry 56: 155–60. doi:10.1016/j.pnpbp.2014.08.018. PMID 25240858 "A significant subgroup of patients may benefit from the initiation of a gluten and casein-free diet"

After reading your comment, think about your conclusions and possible misunderstandings of wording, I agree with you. It wasn't my intention to say that the gluten is 'the cause of schizophrenia'.

Well, then let only a single sentence:

Currently, recent studies agree that non-celiac gluten sensitivity is associated with a subgroup of schizophrenic patients,[5] in which the initiation of a gluten-free diet[3][6] or a gluten and casein-free diet[1] may be accompanied by a drastic reduction or even complete remission of schizophrenic symptoms.[1][3][6]

Do you think that is now right for Schizophrenia page?

Best regards. --BallenaBlanca (talk) 17:36, 7 November 2015 (UTC)

I could not find in the sources where it says or implies drastic reduction or remission in schizophrenia. In this source it summarises results from small controlled trials which found conflicting results regarding the effect of a gluten free diet on schizophrenic symptomatology. The reviewer concluded his commentary on gluten and schizophrenia by saying:
In summary, the role of NCGS in conditions affecting the nervous system remains a highly debated and controversial topic that requires additional, well-designed studies to establish the real role of gluten as a triggering factor in these diseases.
Why the focus on gluten? The gut-brain axis is modulated by IBS and vice versa. I would support expanding the sentence Doc James added to the article to say something like this, "It has been hypothesised that in a subgroup of people, development of schizophrenia is related to immune mediated neuroinflammation caused by non-celiac gluten sensitivity or abnormalities in the intestinal flora." Referenced appropriately. What do you think of this sentence?--Literaturegeek | T@1k? 16:18, 8 November 2015 (UTC)
@Literaturegeek: I'll first answer this: "I could not find in the sources where it says or implies drastic reduction or remission in schizophrenia." Perhaps the reason is that it is in Spanish (bold and underlined text):

PMID:25433099 Nutr Hosp. 2014 Dec 1;30(6):1203-10. doi: 10.3305/nh.2014.30.6.7866. [Is gluten the great etiopathogenic agent of disease in the XXI century? [Article in Spanish] ] Varios estudios sostienen que la retirada del gluten de la dieta de ciertos individuos puede acompañarse de una reducción drástica, e incluso de la remisión completa de los síntomas esquizofrénicos. Sin embargo, insistimos, esto ocurre sólo en un subgrupo de pacientes esquizofrénicos.

The other sources say (bold text):

PMID:24077239 Nutrients. 2013 Oct; 5(10): 3839–3853. Non-Celiac Gluten Sensitivity: The New Frontier of Gluten Related Disorders Other studies confirmed the high prevalence of antibodies to AGA among people with schizophrenia [36], however the exact mechanism underlying the observed improvement of symptoms in some patients with the GFD has remained elusive. Immunological mechanisms have been proposed, including the assertion that a subgroup of schizophrenics suffer from food intolerances that benefit from the adoption of a GFD. The beneficial effect of a GFD may also be achieved via circulating food-derived peptides (exorphins) exerting an influence on physiological processes in the brain (same mechanism as described in the autism paragraph).

PMID:25240858 Prog Neuropsychopharmacol Biol Psychiatry. 2015 Jan 2 Schizophrenia and the gut-brain axis A significant subgroup of patients may benefit from the initiation of a gluten and casein-free diet.

I agree your new sentence.
Now, who must do the edition?
Very thanks for your kindness and your help!
Best regards. --BallenaBlanca (talk)

@Literaturegeek: About this: "I could not find in the sources where it says or implies drastic reduction or remission in schizophrenia.", I had the impression that I had read the same thing in another source, in addition to the other one. I found it. There are so many articles published on this topic...!

PMID:16423158 The gluten connection: the association between schizophrenia and celiac disease Acta Psychiatr Scand. 2006 Feb;113(2):82-90. Kalaydjian AE, Eaton W, Cascella N, Fasano A.

METHOD: A review of the literature relevant to the association between schizophrenia and celiac disease (gluten intolerance) was conducted.

RESULTS: A drastic reduction, if not full remission, of schizophrenic symptoms after initiation of gluten withdrawal has been noted in a variety of studies. However, this occurs only in a subset of schizophrenic patients.

Best regards. --BallenaBlanca (talk)

That source is probably too old to use in this article as it is 2006 and this is an area under active research being regularly updated and also because this is a featured article candidate. Schizophrenia remits and reduces naturally anyway so it is not proof and while interesting there are studies that found no benefit of gluten free diet. Hopefully deeper biological research and larger clinical trials will be conducted to figure out definitively what if any role gluten plays in mental health. Until then we must be cautious what and how we include information on this subject matter.--Literaturegeek | T@1k? 00:51, 9 November 2015 (UTC)

References

  1. ^ a b c d e f g h i j Nemani K, Hosseini Ghomi R, McCormick B, Fan X (Jan 2015). "Schizophrenia and the gut-brain axis". Prog Neuropsychopharmacol Biol Psychiatry. 56: 155–60. doi:10.1016/j.pnpbp.2014.08.018. PMID 25240858.
  2. ^ a b c d e f g h Arroll MA, Wilder L, Neil J (Sep 2014). "Nutritional interventions for the adjunctive treatment of schizophrenia: a brief review". Nutr J. 13: 91. doi:10.1186/1475-2891-13-91. PMC 4171568. PMID 25228271.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  3. ^ a b c d e f Catassi C, Bai JC, Bonaz B, Bouma G, Calabrò A, Carroccio A, Castillejo G, Ciacci C, Cristofori F, Dolinsek J, Francavilla R, Elli L, Green P, Holtmeier W, Koehler P, Koletzko S, Meinhold C, Sanders D, Schumann M, Schuppan D, Ullrich R, Vécsei A, Volta U, Zevallos V, Sapone A, Fasano A (Sep 2013). "Non-Celiac Gluten sensitivity: the new frontier of gluten related disorders". Nutrients. 5 (10): 3839–53. doi:10.3390/nu5103839. PMC 3820047. PMID 24077239.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  4. ^ a b Samaroo D, Dickerson F, Kasarda DD, Green PH, Briani C, Yolken RH, Alaedini A (May 2010). "Novel immune response to gluten in individuals with schizophrenia". Schizophr Res. 118 (1–3): 248–55. doi:10.1016/j.schres.2009.08.009. PMC 2856786. PMID 19748229.
  5. ^ a b c Porcelli B, Verdino V, Bossini L, Terzuoli L, Fagiolini A (Oct 2014). "Celiac and non-celiac gluten sensitivity: a review on the association with schizophrenia and mood disorders". Auto Immun Highlights. 5 (2): 55–61. doi:10.1007/s13317-014-0064-0. PMC 4389040. PMID 26000156.
  6. ^ a b c d San Mauro I, Garicano E, Collado L, Ciudad MJ (Dec 2014). "[Is gluten the great etiopathogenic agent of disease in the XXI century?] [Article in Spanish]" (PDF). Nutr Hosp. 30 (6): 1203–10. doi:10.3305/nh.2014.30.6.7866. PMID 25433099.

Is Neurotransmitter-stress syndrome really a proposed new name for Schizophrenia? If so should we merge Neurotransmitter-stress syndrome here? ~Kvng (talk) 23:22, 29 November 2015 (UTC)

People who's parent's are OCD and own cat's linked to Schizophrenia

For someone to get it from a cat I think their immune system has to drop from amphetemine use for it to occur.

http://psychcentral.com/news/2014/09/07/ocd-patients-their-kids-at-greater-risk-of-schizophrenia/74585.html http://www.huffingtonpost.com/2015/06/11/cats-schizophrenia-cat-owners-mental-illness_n_7538240.html http://www.nytimes.com/2014/02/27/health/mental-illness-risk-higher-for-children-of-older-parents-study-finds.html?_r=0 — Preceding unsigned comment added by 71.167.71.69 (talk) 10:52, 27 December 2015 (UTC)

Image

I have reservations about the main image on this page. It seems sensationalist and may contribute to misunderstanding. I would suggest that it be removed or replaced. Totorotroll (talk) 15:07, 14 January 2016 (UTC)

Environmental Causes

I see an issue in the wording of this sentence: "Parenting style seems to have no major effect, although people with supportive parents do better than those with critical or hostile parents." Upon reviewing the cited material, I assume that the above statement is an inference from the paragraph on twin studies. perhaps it would help to add the following paragraph, or some derivative:

There is scientific evidence dating back to the mid 1950's showing that emotional dynamics within the patient's family system have a significant impact on psychotic symptoms, as well as evidence suggesting causal relationship related to the nature of the "symbiotic attachment between mother and child." [1] The results of Murray Bowen's 1954 NIMH study "indicated that all kinds of symptoms, physical, emotional or social, could be produced or reduced by changes in the relationship system." [2] That is, the evidence suggests that behavior of family members over the course of multiple generations may cause schizophrenia. The family-oriented interventions that were developed in conjunction with the hypothesis were the beginning of modern "family therapy."

I think that it is crucial to acknowledge the existence of these studies because the field seems to have forgotten that they exist, as demonstrated by researchers and media touting "new" research on the effectiveness of talk therapy and family psychoeducation in the treatment of schizophrenia: [6] [7] [8] [9]

Patrickkidd (talk) 21:15, 25 January 2016 (UTC)

For references we tend to follow WP:MEDRS Best Doc James (talk · contribs · email) 09:42, 27 January 2016 (UTC)

Not sure what this means

"In Ireland, Lucia [Joyce] was analysed by Carl Jung at the time, who after reading Ulysses, is said to have concluded that her father, James Joyce, had schizophrenia.[3]"

How is Lucia able to diagnose her father with schizophrenia? Doc James (talk · contribs · email) 09:40, 27 January 2016 (UTC)

The sentence is overly complex but it is actually valid grammatically. If you strip away all the secondary clauses, the sentence says, Lucia Joyce was analysed by Carl Jung, who concluded that her father had schizophrenia. In other words, the sentence says that it was Jung who read Ulysses and then diagnosed James Joyce as schizophrenic. But I certainly agree that the sentence is too complex -- actually I think this material probably isn't notable enough to belong in this article at all. Looie496 (talk) 15:46, 27 January 2016 (UTC)
So it is saying that Carl Jung diagnosed someone by reading their book? Doc James (talk · contribs · email) 16:32, 27 January 2016 (UTC)
Basically yes, although it ambiguously leaves open the possibility that information obtained from Lucia contributed to the diagnosis. (I'm not expressing an attitude about whether this was good clinical practice.) Looie496 (talk) 15:51, 28 January 2016 (UTC)

The State of the Science

Off topic for this page

Today, I set out to try and find an outline, of a definitive, comprehensive biological basis for schizophrenia. What I find, are many different things - theories, hypothesis, conclusions based upon multiple theories, on and on; loads of this stuff - but what I also find, is nothing, in the way of actual biological basis. Sure, imaging may show enlarged ventricles and so forth, but what appears to be happening, are very funded attempts to prove this and related malady, via associating everything from varieties of probable physical damage, to combinations of other disorders, for which there is also no sound biological basis. And I'll call that the state of the science.

Troubling, is that with no sound comprehensive biological basis (in the context of fully understanding the human brain), industry continues to assert the introduction of biology-affecting/changing chemicals (or drugs), and to do this - at all - is cart-before horse on the most basic scientific levels.

Further troubling, are ways in which the schizophrenic dx is used; in documented instances of various actual conspiracies throughout history, what have often proven to be victims of conspiracies large or small, are more often than not met with "professional" assertions they are "ill", by doctors, relatives, police, etc., acting with no biological basis whatsoever. Biological basis is very different from behavioral basis, or the desire for specific situational outcome(s) the "patient" (or, "consumer" of services) may be involved in.

This is (still) not acceptable medical science or practice.

68.235.248.70 (talk) 15:48, 13 November 2015 (UTC)IrvingSombodySomething

This page is for discussions that are specifically directed toward improving the Wikipedia article. This page is not a forum for discussing the topic of schizophrenia. Looie496 (talk) 16:30, 13 November 2015 (UTC)

Improving the wiki article... about the topic of schizophrenia. No? Or did the rules of language change without telling anyone? Seems to me, a comprehensive biological definition of the malady would (eh, how do you say...) "specifically improve the article." Substantially, even. 50.240.70.229 (talk) 18:41, 17 November 2015 (UTC)FairandBalanced

<Removed. As the header for this page states, the page is for efforts to improve the Wikipedia article. It is not for general discussion of the topic. Any material added here needs to have a direct bearing on the Wikipedia article. Criticism of the concept of schizophrenia does not belong here unless it can be translated to changes to the article, which must be justified on the basis of reputable published sources.> Looie496 (talk) 20:25, 4 December 2015 (UTC)

You're on. — Preceding unsigned comment added by 198.49.31.114 (talk) 21:05, 2 February 2016 (UTC)

Where to put Schizophrenia risk from complex variation of complement component 4?

So, my edit to put this, http://www.nature.com/nature/journal/vaop/ncurrent/full/nature16549.html, in was undone, np, so where should it be put?

This is actually a second article, here is another, http://www.karger.com/Article/Abstract/153549.

The C4 appears to be full of HERV-K(C4), http://www.pnas.org/content/98/8/4634. Here's another one about it, http://www.ncbi.nlm.nih.gov/pubmed/10859342.

And then when you have family history of schizophrenia, you have double the risk of ALS, http://www.ncbi.nlm.nih.gov/pubmed/7810588. And the Herv-K is emerging as a very key player in ALS, http://www.neurology.org/content/84/14_Supplement/S37.001.short.

Maybe a new section with links between schizophrenia and ALS?

References

— Preceding unsigned comment added by Dwot (talkcontribs) 06:16, 8 February 2016 (UTC)

These are all what we call "primary sources" - in Wikipedia we source biomedical content like this to what we call "secondary sources" - reviews in the biomedical literature or statements by major medical authorities (like the NIH itself, or the PHE in England). This is explained in WP:MEDRS. So at this point in time this doesn't go anywhere in WP. Once there are such sources describing this, we can figure out where to put it.... Jytdog (talk) 06:27, 8 February 2016 (UTC)

Name change

Extended content

Proposals have been made—and, in some countries, have already been implemented—to change the name of the nosological entity now known as "schizophrenia". Jim van Os, professor of psychiatry at Maastricht University Medical Centre, and visiting professor at the Institute of Psychiatry, London, writes in The BMJ that the term "schizophrenia" is an "unhelpful description of symptoms" that should be replaced with "psychosis spectrum syndrome".[1]

Van Os explains that ICD-10 and DSM-5 use several categories to describe psychosis. These describe symptoms rather than disease diagnoses, because the diseases themselves are still unknown. The descriptive approach permits the grouping of patients with the same set of symptoms.[2]

However, writes van Os, the American Psychiatric Association and academic journals use definitions of schizophrenia that differ from this descriptive approach. "This language is highly suggestive of a distinct, genetic brain disease. Strangely, no such language is used for other categories of psychotic illness (schizophreniform disorder, schizoaffective disorder, delusional disorder, brief psychotic disorder, and so on)."[3]

The various psychoses may be part of a spectrum syndrome, with schizophrenia representing less than a third of the possible outcomes. Van Os emphasizes that persons with psychosis spectrum disorder "display extreme heterogeneity, both between and within people, in psychopathology, treatment response, and outcome."[4]

Someones view is that it should have a new name. Not looking significant enough to be due weight here IMO. Others thoughts? Doc James (talk · contribs · email) 04:58, 15 February 2016 (UTC)

According to our own "Schizophrenia" article, the former names for "schizophrenia" were changed, respectively, in 2002 in Japan, and in 2012 in South Korea.
A similar proposal has been made in the Netherlands.
Professor van Os' proposal to change the name of "schizophrenia" in the Anglophone sphere, to "psychosis spectrum syndrome", therefore does not seem to me an instance of undue weight.
Nihil novi (talk) 05:32, 15 February 2016 (UTC)
Typically we try to stick to review articles per WP:MEDRS. I have added a sentence on it. Doc James (talk · contribs · email) 07:42, 15 February 2016 (UTC)

References

  1. ^ Jim van Os, "'Schizophrenia' does not exist", The BMJ, 2 February 2016 [1]
  2. ^ Jim van Os, "'Schizophrenia' does not exist", The BMJ, 2 February 2016 [2]
  3. ^ Jim van Os, "'Schizophrenia' does not exist", The BMJ, 2 February 2016 [3]
  4. ^ Jim van Os, "'Schizophrenia' does not exist", The BMJ, 2 February 2016 [4]

Semi-protected edit request on 27 February 2016

Under the Diagnosis title (4.) & under the differential diagnosis subtitle (4.3) & after the first two paragraphs, PLEASE add this paragragh: It also may be necessary to rule out Maladaptive daydreaming, which is mistakenly & frequently diagnosed as schizophrenia due to the fact that most psychologists have never heard of maladaptive daydreaming, and it is not officially recognized as a disorder.[1] Schizophrenia is considered a psychosis[2][3][4] whereas maladaptive daydreaming is not considered psychosis because the Maladaptive Daydreaming Scale (MDS) has been shown to be poorly correlated with a psychosis measure.[5] The fundamental difference between the two is that maladaptive daydreaming patients (MDers) are aware that their daydream characters are not real & they differentiate between what is real and what is not, whereas schizophrenia patients fail to recognize what is real and what is not.[6] MDers do not hear voices or see people that are not real, they only daydream.[7][8]

Daffodil-Beryl (talk) 14:49, 27 February 2016 (UTC)

The Atalantic is not a suitable source for medical content. Doc James (talk · contribs · email) 18:07, 28 February 2016 (UTC)

Schizophrenia May be passed down from one generation to the next

http://www.schizophrenia.com/research/hereditygen.htm Family statistics As can be seen from the graph below, schizophrenia definitely has a very significant genetic component. Those who have a third degree relative with schizophrenia are twice as likely to develop schizophrenia as those in the general population. — Preceding unsigned comment added by 71.167.64.250 (talk) 23:08, 3 March 2016 (UTC)

We discuss the strong genetic component yes. Doc James (talk · contribs · email) 21:53, 5 March 2016 (UTC)

Schizophrenia linked to epilepsy

http://pamelaspirowagner.com/2009/04/12/schizophrenia-and-temporal-lobe-epilepsy/

Schizophrenia-like epileptic psychoses often emerge when anticonvulsants are normalizing or improving the seizure activity…  — Preceding unsigned comment added by 71.167.64.250 (talk) 13:50, 6 March 2016 (UTC) 

http://www.medicalnewstoday.com/articles/266102.php

"The brain scans also showed that those who suffer from schizophrenia demonstrated the highest tissue loss in the first 2 years after their first episode, after which point it slowed down significantly."

'The results showed that the higher the dosage of anti-psychotic medication in patients, the more brain tissue was lost."

"There are several studies, mine included, that show people with schizophrenia have smaller-than-average cranial size."

http://apt.rcpsych.org/content/18/2/144

Cognitive impairment has a trajectory over the course of schizophrenia that is different from that of psychotic symptoms and it may contribute to a poor functional outcome in older patients (Davidson 1995).

http://www.ncbi.nlm.nih.gov/pubmed/22716160

CBD appears to have pharmacological profile similar to that of atypical antipsychotic drugs as seem using behavioral and neurochemical techniques in animal models. Additionally, CBD prevented human experimental psychosis and was effective in open case reports and clinical trials in patients with schizophrenia with a remarkable safety profile.

— Preceding unsigned comment added by 71.167.64.250 (talk) 23:05, 3 March 2016 (UTC)

Medication

In 2014, there was a systematic review of the drug Lurasidone; a relatively new atypical antipsychotic. The review points out that Lurasidone was most effective and practical when used as an alternative to aripiprazole in adult schizophrenic patients who may face increased negative outcomes resulting from weight gain or changes in metabolic pathways. Would any editors on this page consider taking a look at the review cited below and offering their opinion. I thought it may be beneficial to add Lurasidone into the medication section or perhaps citing this review in the references section. Any feedback would be greatly appreciated!

Scottish Medicines Consortium. (2014). lurasidone, 18.5mg, 37mg, 74mg film-coated tablets (Latuda ® ) SMC No. (994/14) Sunovion 05. NHS Scotland, (October), 1–12.

      http://www.scottishmedicines.org.uk/files/advice/lurasidone__Latuda__FINAL_Sept_2014_amended_15.09.14_for_website.pdf

Zharris24 (talk) 08:23, 6 March 2016 (UTC)

Yes, this one is being marketed alot over here in Oz. Will look later. Cas Liber (talk · contribs) 20:11, 6 March 2016 (UTC)

Prognosis

Wouldn't it be better to link to the WHO study that found a better prognosis for patients who don't take any sort of medication? There was also a NYT article that found a researcher suggesting that Schizophrenia was really a cluster of different diseases rather than one disease, that could possibly be included somewhere. — Preceding unsigned comment added by 67.246.186.186 (talk) 23:01, 17 March 2016 (UTC)

Schizophrenia is a symptom of traumatic brain injury, epilepsy, genetic disposition. Schizophrenia isn't really a disease it's a symptom of something much worse if ignored. The whole term should describe a feeling and not a disease or mental illness. — Preceding unsigned comment added by 71.167.70.87 (talk) 06:10, 29 March 2016 (UTC)

We use high quality medical sources. Doc James (talk · contribs · email) 07:30, 29 March 2016 (UTC)

Basic symptoms, self-disorders, and early detection

The basic symptoms concept of schizophrenia has been developed for a while, since I think the 1980s, and it is primarily used to detect people at high risk for psychosis, particularly schizophrenia. Basic symptoms are mildly disordered subjective experiences of the patient and are assessed using the Schizophrenia Proneness Instrument (SPI), of which there are both adult and child-youth versions. Based on the research, in 2015 the European Psychiatric Association has recommended [10] that one of the basic symptoms scales, the Cognitive Disturbances scale (COGDIS), be used to determine who is at clinical high risk for psychosis, based on a meta-analysis comparing studies using the Ultra High Risk scale (UHR) and COGDIS, finding that COGDIS is able to predict psychosis earlier with higher conversion rates. COGDIS, derived from items from the SPI showing the highest conversion to psychosis rates, is rather specific to schizophrenia. [11]

There is now an article on self-disorders, which are basic symptoms that deal with the basic experience of the self, and which have been found to be rather specific to schizophrenia spectrum conditions (including schizotypal personality disorder). Both basic symptoms and self-disorders are present rather early in the course of the illness and often remain present after remission of a psychotic episode, taxing the abilities of patients to cope and causing distress. [12][13]

Because some basic symptoms and self-disorders are specific to schizophrenia, how can we incorporate this into the network of articles relating to schizophrenia? Do we create a basic symptoms article, do we try merging this information into the main schizophrenia articles, or what else can we do?

Since this is a featured article, I'm wanting to make sure to discuss any changes. I would be happy to hear feedback. --Beneficii (talk) 07:50, 31 March 2016 (UTC)

So these are viewed primarily as risk factors for not only schizophrenia but psychosis generally? Doc James (talk · contribs · email) 10:32, 31 March 2016 (UTC)
Thank you for your response. It does appear that 14 basic symptoms are predictive of schizophrenia specifically. From Schultze-Lutter, et al. (2016) in a review: "While studies in the 1980s and 1990s indicated that most BSs are indeed not specific to psychosis and may occur in other, especially non-psychotic affective disorders (4), 14 BSs were specific to the development of first-episode schizophrenia within 9.6 years (10) and employed in two clinical high risk (CHR) criteria (4, 11, 12): Cognitive Disturbances, COGDIS, Cognitive-Perceptive BSs, and COPER (Table 1)."[14] I do agree that some of the sources, which are reviews, aren't entirely clear on that, but my impression from my research. In addition to the 2016 review is that these 14 basic symptoms seem to predict schizhoprenia in particular.
On the other hand, self-disorders as measured on the EASE tend to aggregate in the schizophrenia spectrum, with much lower occurrence in psychotic bipolar disorder, and only a little bit lower occurrence in schizotypal personality disorder, compared to schizophrenia. Because of this, the basic self-disturbance represented by these self-disorders has been proposed as a core phenotype of the schizophrenia spectrum.[15]
We might also want to update the at-risk state article as well with these sources, especially considering the European Psychiatric Association's recommendation to use COGDIS to assess CHR.--Beneficii (talk) 10:48, 1 April 2016 (UTC)
So what content specifically are you interested in adding? Doc James (talk · contribs · email) 11:37, 1 April 2016 (UTC)
What content do you think would be appropriate and where should we put it?--Beneficii (talk) 18:49, 5 April 2016 (UTC)

Clarification

Currently one lead sentence says: "Social problems, such as long-term unemployment, poverty, and homelessness are common". Could someone clarify how this is related? Does it mean those problems are experienced by schizophrenics or something else? Brandmeistertalk 16:47, 8 April 2016 (UTC)

Yes exactly Doc James (talk · contribs · email) 16:09, 22 May 2016 (UTC)

Research mentioned in New Yorker article

I've not looked for the actual research they refer to in http://www.newyorker.com/magazine/2016/03/28/the-genetics-of-schizophrenia . Is it all to preliminary to mention? --Ronz (talk) 20:16, 7 April 2016 (UTC)

I've started looking into the research. This might be a serious omission. --Ronz (talk) 15:49, 8 April 2016 (UTC)
We need review articles. Not sure which part is missing. We do state genetics is important. Doc James (talk · contribs · email) 16:01, 8 April 2016 (UTC)
Of course we do. Have you looked? I haven't. --Ronz (talk) 18:14, 8 April 2016 (UTC)
Just throwing out some potential sources that I'm finding while I look: --Ronz (talk) 18:24, 8 April 2016 (UTC)
http://www.sciencedirect.com/science/article/pii/S2352154614000035 --Ronz (talk) 18:24, 8 April 2016 (UTC)
http://www.ncbi.nlm.nih.gov/pubmed/22447077 --Ronz (talk) 18:27, 8 April 2016 (UTC)
http://www.annualreviews.org/doi/abs/10.1146/annurev-genom-082410-101459?journalCode=genom --Ronz (talk) 18:28, 8 April 2016 (UTC)
http://www.nature.com/nrn/journal/v17/n4/full/nrn.2016.20.html --Ronz (talk) 18:30, 8 April 2016 (UTC)
http://www.ncbi.nlm.nih.gov/pubmed/7932285 --Ronz (talk) 18:34, 8 April 2016 (UTC)
Looks like the theory has been around for awhile, going back to 1982. --Ronz (talk) 18:34, 8 April 2016 (UTC)
http://www.nature.com/nature/journal/v530/n7589/full/nature16549.html --Ronz (talk) 18:45, 8 April 2016 (UTC)
The Sekar 2016 paper that caused all the recent interest. --Ronz (talk) 18:45, 8 April 2016 (UTC)

This is exactly the kind of work that I think should be included, but especially also the work this builds from, that I was referring to in my comment below: Talk:Schizophrenia#Add to SCZ genetics.Vrie0006 (talk) 14:49, 22 May 2016 (UTC)

Yes this looks good http://www.sciencedirect.com/science/article/pii/S2352154614000035
Some of the others are a little old
Doc James (talk · contribs · email) 16:10, 22 May 2016 (UTC)

Add to SCZ genetics

Over the next weeks or months I'd like to expand significantly on information about genetic etiology in schizophrenia. A lot has happened in only the past few years, thanks in large part to large-scale studies of common genetic variants by the Psychiatric Genomics Consortium,[9] but the section is also short and could be improved when it comes to other behavioral genetic research designs to understand SCZ risk factors.[10] (I maintain the Gottesman source is a valuable synthesis of much important work in basic genetic studies of SCZ, despite its age. Thankfully, the work in this area has been cumulative and old sources are still valuable.) The reason I wanted to bring this up on the talk page is that my very first initial attempt to edit that section by including a link to behavioral genetics, the overarching field responsible for this kind of work,[11] was reverted. Instead of walking into an edit war I thought it would be best to make sure there's no major opposition to expanding the section on genetics, before I begin adding content. Also, thank you to everyone who has made this awesome page what it is! Vrie0006 (talk) 14:24, 22 May 2016 (UTC)

Schizophrenia is a large topic.
A three paragraph summary on genetics here is long enough IMO.
We have a entire subpage on the topic here Causes of schizophrenia were this additional material could go.
Reverted your addition as we want to keep the wording easier to understand in the main article. Doc James (talk · contribs · email) 16:09, 22 May 2016 (UTC)
I think it's pretty clear that this article is missing important information. As I mention above, the Feinberg hypothesis and subsequent research should be mentioned. It all comes down to the sources in light of MEDRS and what consensus there is in the medical research for different theories.
(edit conflict with Doc James:) Good point about Causes of schizophrenia. We should probably focus there, which is missing this information, then summarize any important changes to Schizophrenia#Causes. --Ronz (talk) 16:18, 22 May 2016 (UTC)
Big topics can have big pages! The page on Thomas Cromwell is currently larger than that on scz. Totally agree about causes of schizophrenia. But on the main scz page the current wording and current description can be improved greatly. There is no context and it jumps from a brief description of heritability to esoteric (and difficult-to-understand) descriptions of a few candidate genes. I'm not suggesting 10 more paragraphs. But what is there is not informative as a general description or otherwise. Links to the larger behavioral genetics and psychiatric genetics is also needed, IMO. Vrie0006 (talk) 17:22, 22 May 2016 (UTC)
Happy to see it improved. Thomas Cromwell is at 67K, schizophrenia is at 107k Doc James (talk · contribs · email) 17:50, 22 May 2016 (UTC)
I'm not exactly sure which esoteric bits Vrie0006 is referring to, but in general, I notice evolutionary psychology gets way too much undue weight on wikipedia when you look at psychology-related articles as a whole, relative to the amount of consideration it gets in the mainstream literature. And I find it's really difficult to get that point across when I'm debating other editors about a few sentences in one article. If this main article is just supposed to be a summary of the most important points from Causes of schizophrenia, then the paragraph on evolutionary psychology, which is in the genetics section, should be deleted. That would free up some space for more up-to-date and mainstream information. PermStrump(talk) 01:38, 23 May 2016 (UTC)
Or moved to the sub article Doc James (talk · contribs · email) 01:38, 29 May 2016 (UTC)

References

  1. ^ "When Daydreaming Replaces Real Life" – The Atlantic, April 2015
  2. ^ American Psychiatric Association, 1994 The Diagnostic and Statistical Manual Revision IV (DSM-IV)
  3. ^ Gelder, Michael G; Mayou, Richard; Geddes, John (2005). Psychiatry. New York: Oxford University Press. p. 12. ISBN 978-0-19-852863-0.
  4. ^ Yuhas, Daisy. "Throughout History, Defining Schizophrenia Has Remained a Challenge (Timeline)". Scientific American Mind (March 2013). Retrieved 2 March 2013.
  5. ^ Somer, Eli. "Maladaptive Daydreaming: A Qualitative Inquiry". Elsevier. Elsevier. Retrieved 26 Feb 2016.
  6. ^ "Schizophrenia Fact sheet N°397". WHO. September 2015. Retrieved 3 February 2016.
  7. ^ Somer, Eli. "Maladaptive Daydreaming: A Qualitative Inquiry". Journal of Contemporary Psychotherapy. Journal of Contemporary Psychotherapy. Retrieved 18 May 2014.
  8. ^ Ardino, Vittoria (ed.). Post-Traumatic Syndromes in Childhood and Adolescence. Chichester, West Sussex, UK: Wiley-Blackwell. p. 162. ISBN 978-0-470-66929-7.
  9. ^ Ripke, Stephan (2014). "Biological insights from 108 schizophrenia-associated genetic loci". Nature. 511 (7510): 421–427. doi:10.1038/nature13595. ISSN 0028-0836. {{cite journal}}: Unknown parameter |author-display= ignored (help)
  10. ^ Irving I. Gottesman (1991). Schizophrenia Genesis: The Origins of Madness. Freeman. ISBN 978-0-7167-2145-1.
  11. ^ McGue, Matt; Gottesman, Irving I. (2015). "Behavior Genetics": 1–11. doi:10.1002/9781118625392.wbecp578. {{cite journal}}: Cite journal requires |journal= (help)

Delusions

A simple explanation for it is "false beliefs" or " beliefs that are not true". Not sure the issue. Doc James (talk · contribs · email) 18:54, 17 June 2016 (UTC)

Lancet Seminar

doi:10.1016/S0140-6736(15)01121-6 JFW | T@lk 13:50, 1 July 2016 (UTC)

"Shall we really say goodbye to first-rank symptoms?"

There is a new recommendation out from the European Psychiatric Association (EPA) regarding the use of first-rank symptoms (FRS) in the diagnosis of schizophrenia, that is based on a meta-analysis. In the abstract, FRS also appears to be associated with the concept of self-disorder. The meta-analysis found high specificity, but low sensitivity, for FRS in schizophrenia; they say a single FRS should not be used to diagnose schizophrenia, but the absence of FRS suggests an organic cause, at least.

http://www.ncbi.nlm.nih.gov/pubmed/27429167

I do not have a copy of the article, however. Does anyone else?--Beneficii (talk) 02:23, 5 August 2016 (UTC)

Got copy at Research Exchange. I've updated the article.--Beneficii (talk) 15:05, 5 August 2016 (UTC)

Semi-protected edit request on 25 September 2016

Please add article https://wiki.riteme.site/wiki/Social_construction_of_schizophrenia

I believe it is an article that needs to be added because Schizophrenia´s social construction is not directly mentioned and it is a very important aspect of schizophrenia. My suggestion is to add it here:

Society and culture

See also: Social construction of schizophrenia, List of people with schizophrenia and Religion and schizophrenia


Titanoom (talk) 19:18, 25 September 2016 (UTC)

Done — Andy W. (talk ·ctb) 06:18, 26 September 2016 (UTC)

Extra terms

Both professionals and nonprofessionals understand the terms "hearing voices" and "lack of motivation" and therefore IMO "avolition" and "auditory hallucinations" are not needed aswell in the lead. They can go in the body.

The argument over if "split personally" is a real condition or not belongs within that article rather than in the lead of this one. Doc James (talk · contribs · email) 22:01, 26 November 2016 (UTC)

Perhaps a couple of things to consider:
All delusions are false beliefs, but not all false beliefs are delusions.
All persons, except for the deaf, hear voices.
Thus a cursory reading only of the information summarized in this article's lead could mislead an interested but insufficiently inquiring reader.
Thanks.
Nihil novi (talk) 22:15, 26 November 2016 (UTC)
Yes agree auditory hallucinations are technically "hearing voices which others do not". Adjusted to that.
I am not convinced the term "fixed false belief" add much to "false beliefs". I guess one could have "false beliefs despite a lack evidence to support them" Doc James (talk · contribs · email) 22:33, 26 November 2016 (UTC)

Use of clozapine in patients with tardive dyskinesia as a side effect of other antipsychotics

It is generally accepted among psychiatrists that one of the prime reasons to try clozapine is the occurrence of tardive dyskinesia in a patient who has been treated with other antipsychotics. Perhaps someone could find an acceptable source supporting this view, and add this information to the "Medication" section and the lead?
Thanks.
Nihil novi (talk) 11:15, 4 December 2016 (UTC)
It's not generally accepted at all. Yes it has a lower incidence of TD but mainly used in schizophrenia with symptoms resistant to treatment Cas Liber (talk · contribs) 11:46, 4 December 2016 (UTC)
Not supported by the Lancet review from 2016. Doc James (talk · contribs · email) 23:38, 4 December 2016 (UTC)


author?

Have you got the name of the author of the first painting? This is absolutely fabulous! I have schizophrenia and it is exactly what I think. You think that the threads are intern whereas they are real : medecines, jails. It is the shoah, you make experience on geniuses and you prevent us from saving your boring world, with so many economical problems. --Nicolas Messina (talk) 13:41, 17 January 2017 (UTC) If you feel culprit don't be afraid please, it is normal to persecute scapegoats, I can understand it. I had very serious problems with psychiatrists, I was in the "salle d'isolement" in French but I managed to be a man recently so really want to save my poor friends, I know them very well whereas you don't now who they are. It is a bad and a good news... but I really would like to know the name of the author of the painting and sorry for my English. --Nicolas Messina (talk) 13:41, 17 January 2017 (UTC)

Was published here[16] Doc James (talk · contribs · email) 18:47, 17 January 2017 (UTC)

Tab placida for schizophrenia

'accepted method' It is universally acceptable,because its half life is very lengthy so ,not getting withdrawl symptoms (Tachanuistamkada (talk) 16:18, 23 February 2017 (UTC))

Cannabis and Schizophrenia

The medical literature does not agree whether cannabis is a cause or not of schizophrenia. I suggest removing cannabis as a definitive cause, mentioning this controversy and referring to this page: https://wiki.riteme.site/wiki/Cannabis_and_psychosis

— Preceding unsigned comment added by 192.34.76.226 (talk) 14:07, 31 October 2016 (UTC)

It is definately a possible cause. Doc James (talk · contribs · email) 14:16, 31 October 2016 (UTC)

Definitely possible? Nice contradiction in terms. — Preceding unsigned comment added by 92.12.216.58 (talk) 21:31, 26 January 2017 (UTC)

There is not enough evidence to tell that there is a definitive causal link between cannabis consumption and schizophrenia. There is some evidence that cannabis can result in earlier onset of the symptoms, but not that it causes it, therefore the current state of the article is incorrect according to the current scientific literature. At the very least a note about the controversial nature of this statement needs to appear. [1][2]

— Preceding unsigned comment added by 192.34.76.226 (talk) 15:18, 31 October 2016 (UTC)

In my understanding some of the recent literature suspects a causal link, some that cannabis use is just characteristic of psychosis-prone individuals. I edited one of our maze of articles on this to reflect this recently, at Cannabis and psychosis. Alexbrn (talk) 23:20, 26 November 2016 (UTC)

I agree with the concerns. A citation needed tag is clearly missing. Tkadm30 (talk) 10:36, 1 May 2017 (UTC)

Cannabis as a "risk factor" of Schizophrenia

Hello all,

This is my first time posting something like this on Wikipedia, and I am inexperienced with Schizophrenia, and am not a psychological professional. However, I noticed that cannabis is listed as a "risk factor" of Schizophrenia, and I think that this is wrong. I'm sure that everyone here knows what the DSM is, but if not, DSM stands for Diagnostic Statistical Manual of Mental Disorders and is created by the American Psychiatric Association as the guidebook for diagnosing mental disorders. The most recent version is the 5th version, or DSM-V.

So how does the DSM-V relate to Schizophrenia? Well, the DSM-5 specifically lists criteria for diagnosing someone with Schizophrenia. Criterion E asks the reader to rule out psychosis due to substance abuse, such as usage of cannabis (click here for the DSM-V)(click here for the DSM-IV)(and click here for the APA's changes to the DSM-IV's diagnosis of Schizophrenia in the DSM-V).

My question is this: should cannabis be listed as a risk factor of Schizophrenia if the American Psychiatric Association actually uses substance abuse as a disqualification for diagnosis with Schizophrenia?

Thank you! 71.126.161.75 (talk) 01:18, 19 April 2017 (UTC)

Please look at the body of the article, at the discussion cannabis there, and the sources provided there. Jytdog (talk) 03:27, 19 April 2017 (UTC)
Criterion E refers to acute drug-induced psychosis. Schizophrenia is a chronic condition that may be caused by cannabis use and therefore extends beyond the initial intoxification. I hope this helps with your confusion. PriceDL (talk) 16:45, 19 April 2017 (UTC)
Yup thanks User:PriceDL Doc James (talk · contribs · email) 22:29, 19 April 2017 (UTC)
To be pedantic, a risk factor is something statistically correlated with a condition. Correlation does not imply causation, and to my knowledge there is little high-quality evidence that cannabis use actually causes schizophrenia. Looie496 (talk) 13:31, 1 May 2017 (UTC)
Yup doing an RCT of cannabis use and schizophrenia would be hard. Doc James (talk · contribs · email) 18:02, 1 May 2017 (UTC)
Whats does that mean precisely? I'm only a human and an "RCT" is missing to my vocabulary. Tkadm30 (talk) 08:50, 7 May 2017 (UTC)
randomized clinical trial. Jytdog (talk) 18:43, 7 May 2017 (UTC)

Semi-protected edit request on 15 May 2017

In the Violence section this sentence needs to be corrected - missing words and/or poor grammar. "Schizophrenia has been associated with a higher rate of violent acts, but most of appears to related to associated substance abuse." 12.26.187.2 (talk) 15:39, 15 May 2017 (UTC)

Done --allthefoxes (Talk) 15:43, 15 May 2017 (UTC)

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Remove a hyphen

There is no hyphen between "mental" and "health" in "mental health". The article should only say "mental health", and not "mental-health". There is only one instance where it says "mental-health" and several instances where the article says "mental health". I'm striving for consistency. One-state solution (talk) 18:14, 22 May 2017 (UTC)

User talk:One-state solution done. You will be autoconfirmed soon so will be able to make the edits yourself shortly. Doc James (talk · contribs · email) 16:25, 23 May 2017 (UTC)

Why no mention of Tardive Dyskinesia?

In the section on Medication, there is zero mention of Tardive Dyskinesia for those taking antipsychotics for a long period of time. It is not a withdrawal symptom, it is permanent nervous-system damage. It is important for those considering using medication long-term to know about this potentially devastating effect that will last the rest of a person's life even after the medication is discontinued. — Preceding unsigned comment added by 129.2.106.82 (talk) 16:15, 31 May 2017 (UTC)

I don't think all antipsychotics are causing this effect. Third-generation atypical antipsychotics like aripiprazole are generally considered safer than conventional dopamine blockers. Tkadm30 (talk) 07:13, 1 June 2017 (UTC)

Editing of page

Instead of automatically deleting user contributions automatically if they are missing something, users should suggest an edit to that material or find the missing information themselves, you are stifling potentially valuable contributions from users. How would you feel as a new user if people did this to you? — Preceding unsigned comment added by Kuzad (talkcontribs) 11:09, 13 June 2017 (UTC)

That's a valid point, but experience has shown that when material is unacceptable as it stands, often the only viable solution is to delete it until it is fixed. It is not reasonable to demand that maintainers, who are just unpaid volunteers like everybody else, spend their time fixing material added by others. And the result of suggesting an edit is often that nothing happens, causing the offending material to stay in the article indefinitely. Looie496 (talk) 13:39, 13 June 2017 (UTC)
I had my first edits as a new user reverted. Advice was than provided. I read said advice and become a better editor. Cheers Doc James (talk · contribs · email) 16:01, 13 June 2017 (UTC)

Child abuse

Were does it say it in this refFryers, Tom; Brugha, Traolach (2013-02-22). "Childhood Determinants of Adult Psychiatric Disorder". Clinical Practice and Epidemiology in Mental Health : CP & EMH. 9: 1–50. doi:10.2174/1745017901309010001. ISSN 1745-0179. PMC 3606947. PMID 23539489.{{cite journal}}: CS1 maint: PMC format (link)

Not mentioned in the 2016 Lancet review https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4940219/ Doc James (talk · contribs · email) 01:47, 15 July 2017 (UTC)

The review says "As noted in the previous paragraphs, schizophrenia and closely related syndromes have not generally been much associated with previous child abuse but the picture is not simple."[17] Doc James (talk · contribs · email) 01:25, 25 July 2017 (UTC)

Article biased (totally one-sided towards pharmaco-apologetism).

The following discussion is closed. Please do not modify it. Subsequent comments should be made on the appropriate discussion page. No further edits should be made to this discussion.


The article clearly deteriorated over the years, now representing only the reductivistic materialism of eugenics and profit oriented pharmacology. Here some links, i was able to find within a few hours of research, that are nearer to the truth:

A metastudy regarding the neuro-toxicity of neuroleptica: [1]

Another negative analysis of the therapeutic value of neuroleptica: [2]

A (maybe bad) example for the non-genetical, non material properties of schizophrenia. It has been found that war veterans with PTSD suffer similar symptoms of "delusions" and often commit suicide. The interesting part is, that they were not schizophrenic before and that medicamentation does not help:

[3]

There are (or have been) better examples for the non-factuality of psychiatric reasoning, but i do not intend to disprove the whole industry today. Therefore some suggestions regarding the validity of the underlying "neuroscience", for now:

If the existence of the soul can be disproven by neuroscience, how does the brain rule and form an ego? The material (neurons and transmitters) are fairly simple but the task to form an intelligence with them eludes these geniuses. But they claim to have found it with fMRI, which only can show blops of activity and projecting their own materialistic believes on them. Therefore the finding of a material "decission making center" might be an artifact of circular reasoning. If we use Occams Razor, as the materialists like to do, we can argue that the proposed models get more complex with every function, the brain and or "magical" medicines and drugs are supposed to have. Whereas the so called dualism is quite simple, old and global. There i must say that souls can think without a brain (i guess :) ), but it cannot be experienced then. As further example i want to remind that these scientist claim to have found a material memory "chip" in the brain. Yet, all explanations how that may work lack plausibility. For learning through the connection of dendrites to neurons, each neuron would need to know what all other neurons are for. In plain every neuron would have to be all knowing. The suggestion of a biochemical memory molecule is disproven by be the action to reaction times and by the lack of molecule aggregation in the brain. A "memory chip" like computer electronics would be susceptible to electricity and wouldnt show the differences in memorisation ability that can be observated throughout society. The whole dopamin-hypthesis is illogical as there are billions of neurons in the brain, but only about a dozen transmitters aviable. Therefore dopamin is responsible for a variety of functons by spatial separated connections and a relevant dosis of neuroleptica would (and does) scramble cognitive processes.

If you think this is "original research" so be it. :) I am a real scientist and am proud to be able to do just that. Especially in a subject that is so prone to human rights violations like western psychiatry. If you want to argue that this is no place for "discussion": I am not discussing, these are scientific facts combined with the use of logic and i will not get into arguments with anyone here. I just ask for good faith, a fair and realistic article and maybe someone who is up to the revert wars and flames and edits this article according to the shown links. (I get aggravated by the revert and wikipedia rules wars) If not, i might do it myself later, thanks. :) Oh and the articles: https://wiki.riteme.site/wiki/Materialism and: https://wiki.riteme.site/wiki/Dualism_(philosophy_of_mind) combined, (still) show that the argumentative basis for modern psychiatry and neurophilosophy are just hypothesy not (yet) scientific facts.

If you want to discuss these or other matters and know an appropriate forum for it, please let me know. I decided to "Watch this page", anyway. :)

Thanks again and have fun as life is beautiful and potentially eternal. :)

Nradabhatse die Katze (talk) 15:36, 27 July 2017 (UTC)

Your post comes very close to abusing this talk page as a forum. This is not a valid use of your editing privileges. Please do not continue to offer your opinions on the topic. I have not simply closed this as you ~approach~ offering concrete suggestions for changing the article. Please propose actual changes. If you (or others) don't, I will close this. Jytdog (talk) 15:43, 27 July 2017 (UTC)

LOL, i specifically asked not discuss with me at an educational level like this: What you call "oppinions" is deduction from known scientific facts, as i stated, as it is not cited it can be called "original research", like i already did. On the top of this page it says: This is the talk page for discussing improvements to the Schizophrenia article. And thats what i tried to do. If you cannot suggest something productive, maybe you want to visit a psychiatrist and talk about anal retentivisms and the arbitrary interpretation of rules to harrass others. But let me see... "It has been proven beyond scientific doubt, that the use of neuroleptica is of no (or little) therapeutic use. Neuroleptica are also neurodegenerative in addition to the, already known, severe "side effects". [1][2] The forced or coerced medicamentation, detention and loss of rights of schizophrenics and other psychically suffering is forbidden by the UN. [3]" I hope you like it, as i am being bold now, due to a loss of faith because of insulting and unqualified remarks. :)

PS: LOLOLOL, the little nihilst big shot already locked the article, no wonder it WAS an article ten years ago, or so. I am a scientifically educated biologist. What are you Jytdog? You do not seem qualified (from your definition of "oppinion" and the scientific quality of this article, to "own a page". Thats exactly why i dont edit articles directly but make suggestions on the talk page. Get real admin! Nradabhatse die Katze (talk) 16:49, 27 July 2017 (UTC)

As with most medications, antipsychotic drugs have positive and negative effects. A detailed discussion on antipsychotic adverse effects occurs on the appropriate page, antipsychotic - where the negative effects on brain gray matter and other problems such as tardive dyskinesia are discussed. This article is about schizophrenia. Your first reference says newer antipsychotic drugs have less adverse effect on gray matter - psychiatrists tend to prescribe these safer second generation antipsychotic drugs, showing mainstream psychiatry is prescribing medications with the most benefit and least harm to their patients. Evidence seems clear that most patients benefit from antipsychotic drugs, while a small but still significant minority are harmed. Psychopharmacology is not perfect and patients vary in their responses to treatment. There is no evidence that the bad effects of antipsychotic/neuroleptic medications is being suppressed on Wikipedia, so your negative approach to other editors seems uncalled for.
Unless I am mistaken, your second reference states that antipsychotic drugs enhance cognition in mentally ill people treated with antipsychotic drugs.
The third reference is irrelevant because PTSD is completely different from schizophrenia, both in its underlying cause and neurobiology.
it is quite clear that your scientific knowledge is very limited. I suggest you reflect on this and reconsider your aggressive, hostile interactions with people who are more knowledgable in scientific matters.--Literaturegeek | T@1k? 04:36, 28 July 2017 (UTC)

Yawn, another troll comment. :) Real scientists and real MDs tend to consider negative side effects unlike mainstream psychiatrists. The article in its current state still suggests that schizophrenia is responsible for brain volume decrease and then casually refers to the fact of neurodegenerative effects of neuroleptika as being discussed. Therefore i see no reason to look up the subarticle or limit my argumentation to it. You are mistaken: Reference 2 gives a devastating lack of correlation with 0.22 (ideal 1 and sarcastically they state it is not zero, since it is a metaanalysis which has to include (false) positives, this is scientific speak for BS) And they state it quite clearly: "It is a closed book", in that neuroleptica have no beneficial effects. Also there is no need to "discuss the negative side effects", as biological research has shown the neurodegenerative qualities of both varieties and pharmacolgy recognises the other side-effects. I just didnt find it again for citation and used another metaanalysis, which again as a rule includes the ayes and nayes of the (superficial) discussion and inevitable has a proportion of positive correlation. As i stated before, i have not yet read the subsection (why subsections for the negative and cherry-picked false positives in the main?) but the side effects are frequent and severe and i do not consider good faith anymore and you two not as my scientific peers. :) The whole article is a suspression of scientific facts and what you think is called for i dont mind at all. I and my reasoning have been needlessly attacked by stating i would "abuse privileges" and my reasoning has been belittled as "oppinion" I dont see any of the talk page rules recognised by Jytdog and, as you dont seem to have the slightest grasp of statistics, dismiss your derrogative assumption of my scientific qualifications and return the favor. :) I hereby declare that conflict resolution seems necessary, as the (seeming) page admins do not allow editing of the article and do not enter into constructive discussion of proposed and cited edits. Instead they get protective and personal without any citations or scientific merrits. As instructed, i will give you geniuses some time to enter into a productive discussion regarding the proposed changes. But i hope you dont because i want you gentlemans or womans discussed in the light of "payed editing" assumptions. Have a nice day! :)

The discussion above is closed. Please do not modify it. Subsequent comments should be made on the appropriate discussion page. No further edits should be made to this discussion.

Semi-protected edit request on 2 August 2017

Link the word with the Greek word σχιζοφρένεια 143.159.31.3 (talk) 22:48, 2 August 2017 (UTC)

Not done: it's not clear what changes you want to be made. Please mention the specific changes in a "change X to Y" format. If you are referring to interlanguage links (i.e. the links to the same article in other languages), it seems as if the greek wiki link is linked and showing. —72 talk 23:02, 2 August 2017 (UTC)

Genetics

Is there proof that the behavior labeled schizophrenia has a genetic basis? According to the web site of the National Institute of Mental Health, "Research into various genes that are related to schizophrenia is ongoing, so it is not yet possible to use genetic information to predict who will develop the disease.” Theory is not evidence. Nicmart (talk) 07:44, 27 June 2017 (UTC)



There is proof that at least some cases have a strong genetic basis, but this goes into the complexity of what it means to be genetic in the first place. I think there are quite a few mistakes in the genetics section. The twin study results are not correct and only have one source, in reality, Twins have a pairwise concordance of 20-50 % depending on country and time. According to research by Robert Plomin every single human trait is genetic, but that is a somewhat meaningless statement. I think it needs a clearer discussion about what it means to be genetic, because the majority of the evidence comes from twin studies, and the interpretation of these is very divisive. Also they can't distinguish genetics and environment if there is a confounding element. Pakistani immigrants have a substantially higher rate of schizophrenia in the UK, as do Black individuals. Factors such as racial discrimination are probably somewhat accounted for in most studies, but there are a million other factors you can't control for that will look like genetics in these studies. MoreResearchNeeded (talk) 17:27, 14 August 2017 (UTC)

Semi-protected edit request on 18 September 2017

I recommend completely removing the following paragraph:

"Assuming a hereditary basis, one question from evolutionary psychology is why genes that increase the likelihood of psychosis evolved, assuming the condition would have been maladaptive from an evolutionary point of view. One idea is that genes are involved in the evolution of language and human nature, but to date such ideas remain little more than hypothetical in nature."

The first sentence does not cite outside sources and seems intended to promote skepticism about genetic factors contributing to schizophrenia, without acknowledging obvious counterarguments. The second sentence is a dismissive statement about genetic roots of language and "human nature". While it is true that the extent to which genes affect the development of language is a controversial subject, saying that the genetic roots of language are "little more than hypothetical in nature" is inaccurate. In any case this is a statement about evolutionary psychology which is tangential to a discussion about schizophrenia. Overall the purpose of this paragraph appears to be the promotion of an ideological position regarding the influence of genes on human psychology rather than providing an in-depth discussion on the genetic roots of schizophrenia. Ryanmoll (talk) 05:49, 18 September 2017 (UTC)

Agreed - sentence removed. Cas Liber (talk · contribs) 05:55, 18 September 2017 (UTC)
I think the second sentence was actually a poorly written attempt to say something quite different, namely that the genes that increase the likelihood of schizophrenia have not evolved away because they also play important roles in language and other adaptive aspects of human nature. I vaguely recall seeing discussion of that argument in the literature. Looie496 (talk) 13:13, 18 September 2017 (UTC)

Cannabis -- can or may contribute to schizophrenia?

When I followed the citations to cannabis in the Lancet article which is linked in this article, this is what I got:

Front Psychiatry. 2014; 5: 54.
Published online 2014 May 22. doi: 10.3389/fpsyt.2014.00054
PMC 4033190
Gone to Pot – A Review of the Association between Cannabis and Psychosis
Rajiv Radhakrishnan,1,† Samuel T. Wilkinson,1,† and Deepak Cyril D’Souza1,2,3,*

The relationship between cannabis and schizophrenia fulfills many but not all of the standard criteria for causality, including temporality, biological gradient, biological plausibility, experimental evidence, consistency, and coherence. At the present time, the evidence indicates that cannabis may be a component cause in the emergence of psychosis, and this warrants serious consideration from the point of view of public health policy.

This WP entry says that "cannabis can be a contributory factor in schizophrenia."

That sounds a little too strong. It sounds like it may not happen to everyone, but it does happen sometimes.

I propose that we change the wording to may, to follow the Front Psychiatry article (which is the source for the Lancet article).

I think we ought to make it clear that there is no consensus in the literature that cannabis causes schizophrenia.

--Nbauman (talk) 19:50, 25 September 2017 (UTC)

The ref says "Accumulating evidence has implicated cannabis use in adolescence, particularly misuse of compounds with high tetrahydrocannabinol content"
We do not tend to dig back through the sources high quality secondary sources use. Doc James (talk · contribs · email) 22:29, 25 September 2017 (UTC)
We have this "strong enough evidence to warrant a public health message that cannabis use can increase the risk of psychotic disorders"
With respect to potential environmental toxins one cannot do an RCT for obvious reasons. Doc James (talk · contribs · email) 22:37, 25 September 2017 (UTC)

Semi-protected edit request on 1 October 2017

Aabelov (talk) 05:18, 1 October 2017 (UTC)

Telepathy. How to turn off voices in your head Acquainted with deaths, injuries, premature births from a careless word or intention. Formulated several rules:

1. Turn off the technical means of communication (at home and near neighbors) wireless communication (GSM, 5G, Wi-Fi, walkie-talkie, at least Internet 4G), in the laptop you can turn off the microphone, so as not to be self-excited by the noise of the fan (if you need a voice-enabled Skype you can turn on - start-control panel-sound / multimedia) electronics in the washing machine, refrigerator (electric motor of the compressor), 10-50 (200) m radius, incl. base stations. Turn off one of the two mobile or routers - they amplify each other at one (main) frequency. If you can not turn off Wi-Fi, at least change the frequency to a freer one. It is better to turn off the phone in transport. 2. Switch off biological communication means To disperse, to turn the trunk in different directions, to sleep, too, is not symmetrical. 3. Eliminate self-excitation: sources of light, noise even the slightest (windows, doors,), cold, uncomfortable shoes 4. Remove your photos or put a bad site, walk quieter, make loud music barely audible, especially with words; it is better to waddle in the ears (take out, if it ceases to help). (https://vk.com/public154348757)

Not done: it's not clear what changes you want to be made. Please mention the specific changes in a "change X to Y" format. Cannolis (talk) 05:33, 1 October 2017 (UTC)

Risk factor

Am not seeing were it says NCGS is a risk factor in this ref.[18] Doc James (talk · contribs · email) 04:23, 16 August 2017 (UTC)

Sorry for the delay!
Perhaps this may not be the most appropriate reference. The issue is as follows: the association of schizophrenia with gluten consumption has been studied for decades, specifically with celiac disease. One of the first evidence of the link between gluten (celiac disease) and schizophrenia was noted in reports from the 50's. The reference in question introduces the new concept "that (a subset of) individuals with schizophrenia exhibit a novel immune response to gluten" that "differs from that found in patients with Celiac disease."
The issue is that gluten consumption is a risk factor in a subset of people with schizophrenia. What is discussed is the association with celiac disease or non-celiac gluten sensitivity. This reference further supports the second hypothesis.
These two other references might be more appropriate: Celiac and non-celiac gluten sensitivity: a review on the association with schizophrenia and mood disorders. "This is why gluten sensitivity may easily go unrecognized and untreated, representing a risk factor for neurologic and psychiatric complications even greater than CD." and Neurologic and Psychiatric Manifestations of Celiac Disease and Gluten Sensitivity.
Best regards. --BallenaBlanca (Talk) 00:28, 1 October 2017 (UTC)
Okay which ref do you want to us to say what exactly? Doc James (talk · contribs · email) 08:26, 6 October 2017 (UTC)

Genes having "unknown transmission and expression"

Some editors of this page seem very intent on stating that schizophrenia associated genes have "unknown transmission and expression". Could they please justify this with either primary or secondary references? — Preceding unsigned comment added by Andorin (talkcontribs) 09:55, 4 October 2017 (UTC)

As the reviews cited there discuss, the genes found in GWAS don't fully account for the heritability we can actually see. This could be perhaps said better, but that is the notion. Jytdog (talk) 18:28, 4 October 2017 (UTC)

My point is that this is not communicated in any sense by saying that the known genes have "unknown transmission and expression". I have replaced this sentence multiple times with "low penetrance" but have had it reverted back insistently. In modern genetic parlance, 'expression' tends to mean 'transcript expression level' and it is a nonsense to say that this is 'unknown' for any genes. While the word 'expression' does also the meaning of 'variable expressivity of phenotype' that doesn't really make any sense in the context. As for why we would want to include 'tranmission' in that sentence I have not a clue. Anyway, I'm not changing it because I've had enough of wasting my time for the other editors to revert my changes.

You need to start indenting and signing your posts. This is a fundamental norm of communication here, as basic as "please" and "thank you". I'll respond after you fix your post above. Jytdog (talk) 17:36, 6 October 2017 (UTC)

I'll start signing them around the time the other editors quit wasting my time.

Lead

Per WP:MEDMOS we generally try to write in easier to understand language. This is particularly true for the lead of our articles. Doc James (talk · contribs · email) 16:47, 22 October 2017 (UTC)

(I think we were adding sections at the same time.) As stated below, there's a subtle but important difference between using "easier to understand language" and obscuring meaning by attempting to use layman's terms which actually mean something slightly different. Since the phrases I edited are all linked the reader can simply click on them if there is any confusion. nagualdesign 16:58, 22 October 2017 (UTC)
Since the simplified language is linked to the technical term people can verify things further as they wish. Doc James (talk · contribs · email) 17:00, 22 October 2017 (UTC)

@Doc James: I just wanted to let you know why I've undone some of the changes you made. While your edit summary read "simplified" I think your edit actually obscured a few things. For example, psychology is not quite the same thing as clinical psychology and substance abuse/misuse is not the same thing as substance-induced psychosis. On the other hand, major depressive disorder is often simply called depression, and anxiety disorder might be simplified as anxiety. Also (and I realize you didn't make this particular edit), auditory hallucination doesn't really need to be worded as hearing voices others do not, since the fact that it is linked should suffice for anybody who was unsure what the term means. Regards, nagualdesign 16:52, 22 October 2017 (UTC)

Yes I agree "substance misuse" is not the same as "substance induced psychosis" so I have restored what is there to what the reference actually supports.
Clinical psychology is a type of psychology and therefore is also correct.
Yes "auditory hallucination" should be worded as "hearing voices others do not". We are writing for a general audience per WP:MEDMOS. Doc James (talk · contribs · email) 16:57, 22 October 2017 (UTC)
Psychology is an entire field of study, whereas clinical psychology is a form of practice.
Auditory hallucinations do indeed commonly include hearing voices (which others do not) but it isn't limited to hearing voices AFAIK. If this were simple prose I'd agree that writing for a general audience should be paramount but, as I said, when the term is linked to an article there should be no confusion. nagualdesign 17:05, 22 October 2017 (UTC)
..Per WP:BRD I thought we were still here engaged in the Discussion part, but I see that you've gone ahead and changed things to how you want them. Since I'm surplus to requirements I'll just leave you to it. Never mind. nagualdesign 17:13, 22 October 2017 (UTC)
The prior wording has been in the article a long time so yes per WP:BRD. I disagree with you on the importance of using easier to understand language. Doc James (talk · contribs · email) 18:14, 22 October 2017 (UTC)

Infobox "similar conditions"

Right now the infobox says "Similar conditions: Substance abuse, Huntington's disease, mood disorders, autism[6]" I would suggest that substance abuse is not similar (substance-induced psychosis is, but that's very different from substance abuse). Substance abuse should be removed. I fail to see how Huntington's is similar, unless the intent is to relate scz to dementia broadly. In any event, Huntington's should be removed as well. The most similar conditions, IMO, are bipolar and autism. Mood disorders should be replaced with bipolar. If people feel strongly, substance abuse should be replaced with substance-induced psychosis. So, ultimately, the field should just say "Substance-induced psychosis, Bipolar disorder, Autism". Vrie0006 (talk) 14:54, 22 October 2017 (UTC)

User:Vrie0006 did you read the ref provided? We do not allow editors own opinions even if the editors are experts themselves.
The source lists:
"substance of abuse"
"Huntington's as it can initially present with psychosis
"mood disorders" (you can get depression with psychosis aswell)
"Autism
Also with respect to caps, only the first term should have one unless it is a proper name.Doc James (talk · contribs · email) 15:49, 22 October 2017 (UTC)
Vrie0006, it looks like the problem is that the parameter claims to be about "Similar conditions", but links to "Differential diagnosis". These aren't the same things. In terms of etiology and pathophysiology, schizophrenia is similar to bipolar and dissimilar to overactive thyroid. However, all three of these conditions can have a similar appearance. Whether overactive thyroid belongs in the infobox as a "similar condition" depends on whether you think that means "something biologically related to" or "unrelated things that might mimic the appearance of". It looks like you and Doc James have opposite beliefs about what "similar condition" means. WhatamIdoing (talk) 19:18, 23 October 2017 (UTC)
Probably the best place to discussion what the "differential diagnosis" tag should link to is at here.
One of our collaborators at the NIH recommended we use this term for DD. Doc James (talk · contribs · email) 19:33, 23 October 2017 (UTC)

Comorbidity

Schizophrenia is often comorbid with other disorders. Green, Canuso, Brenner, and Wojcik (2003)[1] state, “approximately half of patients with schizophrenia have at least one comorbid psychiatric or medical condition”. These additional disorders often worsen prognosis and contribute to Schizophrenia’s high suicide rate. Depression, obsessive-compulsive disorder, and alcohol and substance abuse are all associated with schizophrenia [2]. These conditions may also lead to more dysfunction in social and occupational settings. “Functional consequences include an inadequate or incomplete education, which may affect the patient’s ability to obtain and hold a stable job”[3]. Patients also often form few social and romantic relationships[4]. This inability or disinterest in relationships with others can also contribute to comorbidity of disorders such as depression.

References

  1. ^ Green, A. I. (2003). "Detection and management of comorbidity in patients with schizophrenia". Psychiatric Clinics of North America. 26 (1): 115–139. doi:10.1016/s0193-953x(02)00014-x. Retrieved 2 November 2017.
  2. ^ Green, A. I. (2003). "Detection and management of comorbidity in patients with schizophrenia". Psychiatric Clinics of North America. 26 (1): 115–139. doi:10.1016/s0193-953x(02)00014-x. Retrieved 2 November 2017.
  3. ^ Patel, K. R.; Cherian, J.; Gohil, K.; Atkinson, D. (2005). "Schizophrenia: Overview and Treatment Options". Pharmacy and Therapeutics. 62 (3): 247. doi:10.1001/archpsyc.62.3.247. Retrieved 2 November 2017.
  4. ^ Patel, K. R.; Cherian, J.; Gohil, K.; Atkinson, D. (2005). "Schizophrenia: Overview and Treatment Options". Pharmacy and Therapeutics. 62 (3): 247. doi:10.1001/archpsyc.62.3.247. Retrieved 2 November 2017.
Please adjusted per the advance on your talk page. Best Doc James (talk · contribs · email) 07:17, 10 November 2017 (UTC)

Semi-protected edit request on 25 November 2017

Change: Schizophrenia is a mental disorder characterized by abnormal social behavior and failure to understand what is real.[2] Common symptoms include false beliefs, unclear or confused thinking, hearing voices that others do not hear, reduced social engagement and emotional expression, and a lack of motivation.[2][3] People with schizophrenia often have additional mental health problems such as anxiety, depressive, or substance-use disorders.[11] Symptoms typically come on gradually, begin in young adulthood, and last a long time.[3][5]

to Schizophrenia is a mental disorder characterized by abnormal social behavior and failure to understand what is real.[2] Schizophrenia includes positive and negative symptoms. Positive symptoms are those experienced in addition to normal experiences, these include Hallucinations (in relation to any sense), as well as Delusions. Negative symptoms include Avolition or loss of motivation, and speech poverty. People with schizophrenia often have additional mental health problems such as anxiety, depressive, or substance-use disorders.[11] Symptoms typically come on gradually, begining in young adulthood, and last a long time.[3][5] TheblueDoggo (talk) 16:04, 25 November 2017 (UTC)

Not done: Please next make you changes clear by underlining what was removed, added or altered. Now it is hard to see the difference. But this edit is not done because you did not give any new sources so such altering will only be synthesis or cosmetic –Ammarpad (talk) 12:50, 26 November 2017 (UTC)

A blurry line between science and art

Dear Wikipedia,

Your mental illness pages often seem overly concerned with what I would attribute to an entirely separate page. Take Schizophrenia for example. The main image is an artistic representation of the illness, and a quite abstract one at that. I think that the artistic side of the illness and other illnesses should be presented on a different article page titled "Schizophrenia in art" or something. Physical illnesses such e.g. cancer are not given such a treatment and are instead treated wholly scientifically on their main wiki article pages. I think a similar treatment for mental illnesses would be right in the name of good science, good information storing, and right to those who have the illnesses or have interests in the illness. It would go a long way to help the issue of stigma associated with mental illness, which is at the end of the day a physical illness of the brain. The first image on this article in questions clearly portrays a certain view of scitziophrenia, when perhaps some brain scans or medical images (like on physical illness pages) would be more accurate and of better taste.

Your sincerely, A wikli user — Preceding unsigned comment added by 82.42.185.241 (talk) 13:05, 5 January 2018 (UTC)

There are no physical tests that have an image that would go in the infobox. I understand the issue - illustrations that we could use are tricky to come up with. Cas Liber (talk · contribs) 13:17, 5 January 2018 (UTC)

John Forbes Nash

The reference in the History section) to John Forbes Nash as a Nobel Prize winning Mathematician. Perhaps edit it to "a Mathematician who won the Nobel prize for Economics". That would stop people (like me)becoming distracted due to half-remembering that there isn't a Nobel for mathematics.41.188.70.156 (talk) 21:52, 10 March 2018 (UTC)

tweaked Cas Liber (talk · contribs) 22:32, 10 March 2018 (UTC)

Objective test

In the diagnosis section, it is stated that "there is no objective test". Perhaps add the following paragraph: "However, a niacin flush test has been moderately successful in distinguishing patients with schizophrenia. The test is based on applying a topical skin cream or patch containing a formulation of niacin. Healthy individuals exhibit a flush response (inflammation and swelling). This response is usually attenuated or absent in schizophrenic patients." [1] [2] [3]

References

  1. ^ Bosveld-van Haandel, Linda; Knegtering, Rikus; Kluiter, Herman; van den Bosch, Robert J. (30 August 2006). "Niacin skin flushing in schizophrenic and depressed patients and healthy controls". Psychiatry Research. pp. 303–306. doi:10.1016/j.psychres.2005.10.010.
  2. ^ Puri, B. K.; Easton, T.; Das, I.; Kidane, L.; Richardson, A. J. (NaN). "The niacin skin flush test in schizophrenia: a replication study". International Journal of Clinical Practice. pp. 368–370. {{cite web}}: Check date values in: |date= (help)
  3. ^ Chang, Shu-Sen; Liu, Chih-Min; Lin, Sheng-Hsiang; Hwu, Hai-Gwo; Hwang, Tzung J.; Liu, Shi K.; Hsieh, Ming H.; Guo, Shi-Chin; Chen, Wei J. (2009). "Impaired Flush Response to Niacin Skin Patch Among Schizophrenia Patients and Their Nonpsychotic Relatives: The Effect of Genetic Loading". Schizophrenia Bulletin. pp. 213–221. doi:10.1093/schbul/sbm153.

--ChinaTwist (talk) 18:38, 12 March 2018 (UTC)

Please read WP:MEDRS. The test is not diagnostic. Doc James (talk · contribs · email) 21:09, 12 March 2018 (UTC)
In my second quoted reference, it says: "Our results are therefore consistent with the previous published report and suggest that this test may be useful clinically in the diagnosis of schizophrenia". Obviously the test is not used clinically, but it is good quality evidence of an objective measurement. If you're going to write "there is no objective test", you should probably include the caveat that some objective tests have been shown to be moderately successful in research. Otherwise it might give the false impression that the disease is purely psychological with no physical manifestation.--ChinaTwist (talk) 23:43, 12 March 2018 (UTC)
These sources are not OK per WP:MEDRS. It is a waste of time arguing about what they say, as we will not consider them. Please read and follow MEDRS and if you don't understand it, please ask. Jytdog (talk) 23:50, 12 March 2018 (UTC)

Semi-protected edit request on 20 April 2018

Hvanvactor (talk) 19:06, 20 April 2018 (UTC)

 Note: Removed article content from edit request.
 Not done: it's not clear what changes you want to be made. Please mention the specific changes in a "change X to Y" format and provide a reliable source if appropriate. Please do not copy article content to the talk page as we cannot tell what changes you have made. ‑‑ElHef (Meep?) 19:43, 20 April 2018 (UTC)

Benefit of medicine for the negative symptoms of schizophrenia.

I see a lot of old links, some that link to studies with not even a snippet of information, that reflect outdated judgment on the benefit of medicine for the negative symptoms of schizophrenia. They state that medicine has little to no impact on them. Haven't reviewed the quality of evidence on the positive symptoms yet. Dopaminergics and noradrenergics collectively improve motivation, desire to work, keenness, greater salience of one's life experience, and in certain cases cognition. Serotonergics, 5-HT2A, 5-HT6, and 5-HT7 antagonists collectively, among other benefits, improve happiness, cognition, learning, memory, mood stablization, increased sociability, and decreased aggressive behavior/ideation. There's a wealth of information from WP:MEDRS and user reviews on sites like www.drugs.com that support this. Does anyone here have the desire to update schizophrenia with evidence showing the benefits in this area? If not, I'll probably try tackling it myself in the coming weeks. Reixus (talk) 08:00, 26 January 2018 (UTC)

What sources are you proposing?
User reviews are not MEDRS. Doc James (talk · contribs · email) 09:53, 26 January 2018 (UTC)
I know, I know :D Just meant to steer some attention to the fact that individuals taking the medicine also in many cases report the same benefits. But yeah, right now I'm studying up on some neurology but I'll try to see if I can find the time to forage for some MEDRS on the negative symptom treatment subject in the coming weeks. Reixus (talk) 13:15, 26 January 2018 (UTC)
It's a vexed topic area. Reviewing the evidence would be worthwhile though. Cas Liber (talk · contribs) 22:34, 10 March 2018 (UTC)

Except that's not what independent studies suggest at all. Relapse Duration, Treatment Intensity, and Brain Tissue Loss in Schizophrenia: A Prospective Longitudinal MRI Study https://ajp.psychiatryonline.org/doi/abs/10.1176/appi.ajp.2013.12050674 "Relapse prevention is important, but it should be sustained using the lowest possible medication dosages that will control symptoms." 'Long-term Antipsychotic Treatment and Brain Volumes' https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3476840/ "Viewed together with data from animal studies, our study suggests that antipsychotics have a subtle but measurable influence on brain tissue loss over time, suggesting the importance of careful risk-benefit review of dosage and duration of treatment as well as their off-label use." 'Lifetime antipsychotic medication and cognitive performance in schizophrenia at age 43 years in a general population birth cohort' https://www.sciencedirect.com/science/article/pii/S0165178116305893 "Higher antipsychotic exposure related to poorer cognition in midlife schizophrenia"

Of course if you work in psychology they're going to say their drugs are beneficial they're trying to push talk therapy and drugs on people. Just look at this recent headline about depression. https://www.npr.org/sections/health-shots/2015/09/30/444789771/studies-may-overstate-the-benefits-of-talk-therapy-for-depression but hey, 'the benefits outweight the risk'? Not like we could give schizophrenics placebos or anything... https://jamanetwork.com/journals/jamapsychiatry/fullarticle/211084 "more antipsychotic treatment correlated with greater frontal gray matter (GM) volume reductions. "

 — Preceding unsigned comment added by 71.167.63.166 (talk) 23:56, 20 April 2018 (UTC) 

Environmental Factors

I think you might want to emphasize that the environmental factors are correlated with and not causative. It reads initially as if you are saying that cannabis use or being raised in a city will cause Schizophrenia. Maybe say that the environmental factors, mixed with genetic components and stressors may lead to development of Schizophrenia but that no single environmental factor can definitively cause Schizophrenia. Additionally, schizophrenics use of nicotine is often a method to self medicate [1] which you might want to consider expanding on. Joannaberg4 (talk) 16:55, 16 May 2018 (UTC)

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. [2]

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)

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)

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

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.[3][4]"

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

References

  1. ^ https://www.sciencedirect.com/science/article/pii/S0149763405000874. {{cite web}}: Missing or empty |title= (help)
  2. ^ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1140960/
  3. ^ Fosse R, Joseph J, Jones M (2015-09-14). "Schizophrenia: A critical view on genetic effects". Psychosis. 8 (1): 72–84. doi:10.1080/17522439.2015.1081269.
  4. ^ Leo J (Winter 2016). "The Search for Schizophrenia Genes". Issues in Science and Technology.
  • It is true that neither journal is indexed in PubMed. However, Psychosis has an impact factor assigned by the Journal Citation Reports, and it is indexed in the Social Sciences Citation Index (SSCI), EMCARE, PsycINFO and Scopus. [19] As for Issues in Science and Technology, it is published by the National Academy of Sciences, and given that its WP article describes it as a "policy journal" I took it to be a reputable peer-reviewed outlet, albeit one not indexed in PubMed or having an impact factor. Looking more closely at its page on the NAS website [20] it appears it may not be the peer-reviewed journal I originally thought, so I guess it should not be included here. Everymorning talk to me 05:09, 20 June 2018 (UTC)
  • IST is essentially a magazine, on the level of Scientific American or National Geographic. As such, although it may contain excellent articles, it is not a MEDRS-compatible source. Psychosis is a reliable source, I believe, but because it focuses on psychosocial approaches, it is not treated as a medical journal. More importantly, I don't think the quote at the beginning of this section reflects the mainstream of opinion. The mainstream view, I believe, is that schizophrenia has a strong genetic component, but it comes from small contributions by hundreds of individual genes, not from large contributions by a few genes. Looie496 (talk) 13:56, 21 June 2018 (UTC)
    In any case, I believe this source should be included making it clear that there are serious concerns about the validity of the classical twin design on which the "80% heritable" claim is based. It was published in Frontiers in Psychiatry, meaning the journal is clearly relevant to the subject of schizophrenia, and it has a solid impact factor (3.532). It appears that it is not indexed in Medline [21] but if you check the journal's about page [22] it appears it is indexed in PubMed. I previously added this study but it was removed for, I think, no good reason. The editor who removed it claimed it was a primary source, [23] but in fact, it is a review article, not a primary source, as is evident from reading the article (it says "review article" just above the date near the top of that page). Everymorning talk to me 01:34, 22 June 2018 (UTC)
    I still think this should be treated as a "significant minority" view -- not fringe, but still far from mainstream. Although I don't have the same negative view of Frontiers journals that some editors do, I see this as a relatively unimportant review -- it has received a rousing 15 citations since it was published in 2015, mostly from articles that are themselves not very strong. Looie496 (talk) 15:44, 22 June 2018 (UTC)
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)
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)

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)

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)
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)
"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)
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)

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)

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 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 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, putatively 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 antagonists 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 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.[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)
It could definetely do with a lot of copy editing. You’re probably right about the predictive coding, but I see it so often now I thought it would be worth mentioningPetergstrom (talk) 16:48, 25 July 2018 (UTC)

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.

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)

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

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)

Differential diagnosis

I think there are more differential diagnoses than those reported here, whose : (M) TBI, PSTBI (psychosis secondary to traumatic brain injury) - (CTE) Chronic Traumatic Encephalopathy - Dementia - Catatonia - Stroke - Delusion/Hallucination (due to dehydration, malnutrition, or others) - (Psychotic) Depression - Photophobia, Behavioral and (or) "subjective" changes in the experience of emotions following the (definitive) loss or decrease of tears post-Lasik (Post-LASIK ocular surface neuropathic disease), ect...

[1] [2] [3] [4] [5] [6]

--— Preceding unsigned comment added by Seekthetruth-weigh the benefits and risks (talkcontribs) 19:20, 2 June 2018 (UTC)

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)

Support deleting the text. Perhaps it could be replaced by this review?--Literaturegeek | T@1k? 14:01, 1 September 2018 (UTC)
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)

Please change the photo.

Hi. Please change the photo. Stop of discrimination of patients. — Preceding unsigned comment added by Artystka88 (talkcontribs) 16:32, 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? TylerDurden8823 (talk) 18:25, 30 August 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. Asterixf2 (talk) 11:12, 16 September 2018 (UTC)

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)
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)
  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)
    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)
    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)
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)
Ok. Please also take into consideration another alternative that I have proposed. Asterixf2 (talk) 06:11, 16 September 2018 (UTC)
We are writing for a general audience, especially the leads.
Agree with going with "abnormal behavior" as also used by WHO[24]
The term "fixed, false beliefs" is basically "failure to understand reality" Doc James (talk · contribs · email) 17:27, 16 September 2018 (UTC)
Strictly speaking, failure to understand reality is correct but may be misleading for general audience. It is stigmatizing because -- in a sense -- it denies people with schizophrenia the right to have legitimate views or ideas about reality and therefore the need to respect their opinions. It suggests total failure instead of partial and often very limited and specific kinds of failures. Disturbances and distortions are both used by WHO. Asterixf2 (talk) 19:28, 16 September 2018 (UTC) Not to mention the fact that schizophrenia is episodic afaik. Asterixf2 (talk) 19:34, 16 September 2018 (UTC)
How about "problems understanding reality"? To make it clear that this is not black and white. Doc James (talk · contribs · email) 17:13, 17 September 2018 (UTC)
I've never been fond of failure to understand reality as it is a huge leap from " presence of delusions/delusional system". Cas Liber (talk · contribs) 21:12, 17 September 2018 (UTC)

"Culture"

The line in the introduction "During diagnosis a person's culture must also be taken into account." seems like an odd and unhelpful statement for an introduction. Why must it be taken into account? How does this information form part of an introduction to the topic?

I'm unsure where it could be reworked in, but I think it should be? Thoughts?

Nauseous Thot (talk) 11:29, 20 September 2018 (UTC)

Yes a person's culture must be taken into account when symptoms are interpreted. Doc James (talk · contribs · email) 03:26, 22 September 2018 (UTC)
I agree that a person’s culture must be taken into account before labelling a sign or symptom as related to schizophrenia. Perhaps an example could be added (if the source gives one) such as local or tribal superstitions or unusual religious belief.--Literaturegeek | T@1k? 12:47, 22 September 2018 (UTC)

Comorbidity

I've removed a sourced edit based on two studies, which gave undue weight to comorbidity of schizophrenia and gender identity disorder, as no other condition was mentioned, and g.i.d. isn't close to the major conditions which should be mentioned when discussing the subject. It could be added back, in proper context, and with proper weight, which I suspect will be very low. Mathglot (talk) 04:41, 9 November 2018 (UTC)

Research Directions

Could we please add that Naloxone is currently being studied in its effectiveness on reducing hallucinations. (https://www.ncbi.nlm.nih.gov/pubmed/351804) — Preceding unsigned comment added by Ashwolf22101 (talkcontribs) 21:32, 2 February 2019 (UTC)

Source is too old and is a primary source to make a significant medical claim such as this. Please see WP:MEDRS.--Literaturegeek | T@1k? 21:44, 2 February 2019 (UTC)
This is actually quite interesting! The study was published in 1978, however, and I note that additional studies on the subject are all mostly dating back to the early 1980s. Spyder212 (talk) 02:57, 4 February 2019 (UTC)

Interesting newish study on evolutionary theories in relation to psychosis [9] Darwinerasmus (talk) 07:48, 22 February 2019 (UTC)

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://www.nature.com/articles/d41586-019-00198-7

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.

Proposed "Mechanism" content
The following discussion has been closed. Please do not modify it.

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, and the observation that dopamine synthesis and release, as measured by positron emission tomography, is elevated during acute psychosis.[2][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][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 associativity 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]

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 post-mortem 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. Several studies that investigated perceptual processes found impaired GBR in ScZ patients over sensory areas, such as the auditory and visual cortex. Moreover, studies examining steady-state auditory-evoked potentials showed deficits in the gen- eration of oscillations in the gamma band.
  19. ^ Reilly, Thomas J.; Nottage, Judith F.; Studerus, Erich; Rutigliano, Grazia; Micheli, Andrea I. De; Fusar-Poli, Paolo; McGuire, Philip (July 2018). "Gamma band oscillations in the early phase of psychosis: A systematic review". Neuroscience & Biobehavioral Reviews. 90: 381–399. doi:10.1016/j.neubiorev.2018.04.006. Decreased gamma power in response to a task was a relatively consistent finding, with 5 out of 6 studies reported reduced evoked or induced power.
  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 (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. 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. 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, 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.
  30. ^ 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.
  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 J, Anticevic A, Barch D (2018). "Cognitive and Motivational Neuroscience of Psychotic Disorders". In Charney D, Buxbaum J, Sklar P, Nestler E (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 (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.

Petergstrom (talk) 21:49, 1 September 2018 (UTC)

Overly complicated IMO and needs substantial simplification. Doc James (talk · contribs · email) 03:37, 2 September 2018 (UTC)
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)
I don't really think this needs very much simplification. This is pretty much as simple as it gets, and I think it actually simplifies a number of topics that are covered in the current mechanism section (in particular dopamine). As for what Treetear said, this does need a lot of copy editing. I went ahead and implemented corrections to errors found, but there are probably a few more that I am missing.Petergstrom (talk) 03:16, 19 September 2018 (UTC)
This has been here for a few months, and no objections have been raised, so I'm gonna go ahead an implement it.Petergstrom (talk) 01:10, 23 February 2019 (UTC)
Yes I have stated that this is overly complicated.
A simpler overview belongs here with the more complicated details on the subpage. Doc James (talk · contribs · email) 08:23, 23 February 2019 (UTC)

Request to remove the picture

Hi all, I am making contact on behalf of the artist and my department (Queensland Centre for Mental Health Research) that holds copyright to the main picture on the page. The artist has asked us to remove this from the public domain, as he does not wish to reveal this aspect of his past health. Clim072 (talk) 03:42, 11 June 2019 (UTC)

I am not a copyright expert, but I notice this image has been published in numerous works available across Internet... From the file information on Wikimedia Commons, it has been shared with a "no copyright" license: "The person who associated a work with this deed has dedicated the work to the public domain by waiving all of his or her rights to the work worldwide under copyright law, including all related and neighboring rights, to the extent allowed by law. You can copy, modify, distribute and perform the work, even for commercial purposes, all without asking permission." Spyder212 (talk) 21:37, 11 June 2019 (UTC)
I am writing on behalf of the Queensland Centre for Mental Health Research, which owe the painting in question. This is our website https://qcmhr.uq.edu.au/ . In the past, we have been proud to allow the paintings we own to be used the conditions of Creative Commons (Attribution-NonCommercial-NoDerivs 2.5 Generic (CC BY-NC-ND 2.5)) . And, we have been delighted that Wiki has chosen to use some of the images that we own. https://qcmhr.uq.edu.au/gallery/ . However, on this particular occasion, the artist has requested we remove his material. We respect his wishes and thus, we have decided to formally withdrawn the Creative Commons licence to this image. In summary, as owners of the work, and at the request of the painter, we seek to remove this image from this page. Clim072 (talk) 23:21, 12 June 2019 (UTC)
@Doc James: Any input on this issue? Anyone they should contact higher up in Wikimedia's food chain? Spyder212 (talk) 00:04, 13 June 2019 (UTC)
I see that commons has it's own copyright claim area here. Maybe make the application through that? Removal from the en-language article page is just one small step. Ian Furst (talk) 00:49, 13 June 2019 (UTC)

Has been published under a CC BY license in PLOS Medicine.[25] The person in question is unable to withdraw the license. If PLOS pulls the picture than the chance we will aswell will increase.

Here is the full license it is under "This is an open-access article distributed under the terms of the Creative Commons Public Domain Declaration, which stipulates that, once placed in the public domain, this work may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose."

Would also need to verify a few other things. You however have email turned off. Also do you have other images that pertain to this subject that you would be willing to release under an open license? Doc James (talk · contribs · email) 04:33, 13 June 2019 (UTC)

Peer support

Would it be appropriate to add this recent Cochrane review about peer-support here Schizophrenia#Peer_support or here Management_of_schizophrenia#Other ? There insufficient evidence to support or refute peer support for SZ or other serious mental health conditions: https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD010880.pub2 There was some comparisons between peer-support and clinical support but the data was not usable. Notgain (talk) 15:47, 14 July 2019 (UTC)

Estimates of heritability

Yes this article states "It is concluded that the genetic component of schizophrenia may have been overestimated". This however is a hypotheses. Evidence for toxo remains tentative at best. Doc James (talk · contribs · email) 18:47, 16 July 2019 (UTC)

It's always confusing when the actual text in the article, as you quote, contradicts one of its highlights, which states "The heritability of schizophrenia has been over-estimated" (my emphasis). But this paper seems to definitely conclude that twin study estimates of schizophrenia heritability are too high, e.g. "An examination of the twin studies on which heritability is based shows why such studies exaggerate the genetic component of schizophrenia" (my emphasis). IntoThinAir (talk) 23:39, 16 July 2019 (UTC)
This is but one study and lots of other studies disagree. Doc James (talk · contribs · email) 02:36, 17 July 2019 (UTC)
This review provides some explanation. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4940219/ Doc James (talk · contribs · email) 02:40, 17 July 2019 (UTC)

Different types of schizophrenia

Should this article mention that there are different types of schizophrenia earlier in the article? Vorbee (talk) 18:23, 5 August 2019 (UTC)

A Commons file used on this page has been nominated for deletion

The following Wikimedia Commons file used on this page has been nominated for deletion:

Participate in the deletion discussion at the nomination page. —Community Tech bot (talk) 02:37, 19 August 2019 (UTC)

Semi-protected edit request on 21 August 2019

“Cannabis use during adolescence” not backed up by any rebuttal source. Not fact just an opinion on the matter. 174.63.182.82 (talk) 05:20, 21 August 2019 (UTC)

Not done, the sources we cite cite this review. – Thjarkur (talk) 22:04, 21 August 2019 (UTC)


They could of taken any number of drugs, but because they're less likely to get in trouble for marijuana they'd be more likely to share that they used that drug. It doesn't mean the drug itself causes schizophrenia, and psychotic symptoms could mean anything. That doesn't exactly mean it's permanent schizophrenia as in hearing voices, since schizo affective disorder is temporary.

If a drug is illegal and rare, it's more likely they tried an illegal drug that's widely available first like marijuana, rather than something that last long enough to cause psychosis, like say amphetamines, meth, LSD, MDMA, cocaine, etc. You could say kids are more likely to get a concussion if they ride bikes in this way, it doesn't mean the act of riding a bike causes a concussion just that it's likely with the risky behavior that ensues. — Preceding unsigned comment added by 67.80.69.119 (talk) 06:47, 27 August 2019 (UTC)

s/effect/affect

Under "Mechanisms", second paragraph:

Abnormal dopamine signalling has been implicated in schizophrenia based on the usefulness of medications that *effect* the dopamine receptor...

The proper word is "affect"

Abnormal dopamine signalling has been implicated in schizophrenia based on the usefulness of medications that *affect* the dopamine receptor... — Preceding unsigned comment added by MindChild (talkcontribs) 03:17, 6 September 2019 (UTC)

Addition of new section entitled Etymology

   Information to be added or removed: The term Schizophrenia comes from the Greek "Schizo-" meaning "Split" and the Greek "-Phrenia" meaning "the mind".
   Explanation of issue: Add new section to discuss the origins of the terminology. 
   References supporting change: https://www.dictionary.com/browse/schizo  https://www.dictionary.com/browse/-phrenia

66.90.153.184 (talk) 04:44, 29 September 2019 (UTC)

Currently, this etymology is given: "The word schizophrenia—which translates roughly as "splitting of the mind" and comes from the Greek roots schizein (σχίζειν, "to split") and phrēn, phren- (φρήν, φρεν-, "mind")". Your source states: "Origin of schizo- < Greek, combining form representing schízein to part, split" and "Origin of -phrenia < New Latin < Greek phren- (stem of phrḗn) mind + -ia -ia". Why would you replace the full etymology by some incomplete etymology using schizo- and -phrenia, that are actually not words in Greek? Wimpus (talk) 08:50, 29 September 2019 (UTC)

 Not done: The content currently in the article is much better sourced and much more accurate. Sceptre (talk) 21:31, 30 September 2019 (UTC)

Treatment - experimental?

https://www.theguardian.com/society/2017/nov/03/radical-new-approach-to-schizophrenia-treatment-begins-trial suggests a treatment based on an infective agent. The scientist referred to has 2 refs in the article - so presumably is not a crank. Can someone follow this up with medical knowledge enough to evaluate if it has merit enough to be added. — Preceding unsigned comment added by 88.115.204.102 (talk) 08:29, 3 November 2019 (UTC)

A Beautiful Mind

I am changing the inset to indicate that the BOOK, not the MOVIE, was about John Nash. The book was an actual biography, while the movie completely sensationalized his issues -- well beyond reality. Arbalest Mike (talk) 16:17, 14 December 2019 (UTC)

Okay, change made but it doesn't show up. Is this because of the "semi-protected" status of the page? Again, the movie took a single sliver of his life and then embellished it. One cannot honestly say that the movie was about him. Arbalest Mike (talk) 16:28, 14 December 2019 (UTC)

Symptoms not fully blown disorders

Had changed wording to reflect that the symptoms present are not always disorders this is clear from ref used. It refers to OCS, and OCD, obsessive compulsive symptoms and obsessive compulsive disorder - same as with substance use that is very common before it may develop into a disorder. ? Maybe it needs a qualifier such as when people have had schizophrenia for a long time. --Iztwoz (talk) 13:12, 14 January 2020 (UTC)

The ref states roughly that there is 25% prevalence of OCS, and a 23% prevalence of OCD. It also states that obsessive compulsive symptoms are present throughout the course of schizophrenia.--Iztwoz (talk) 13:27, 14 January 2020 (UTC)
If a bunch of symptoms make a person qualify for a syndrome, then the person has the syndrome. FWIW. Cas Liber (talk · contribs) 20:13, 15 January 2020 (UTC)
All refs seen make a distinction between symptoms and fully blown disorder..one mentions that when symptoms reach a threshhold they become a disorder. It's not only possible but evident that symptoms of either anxiety or depresson can be present in any part of the poulation without them being problematic enough i.e. a disorder to warrant intervention. A person may be anxious about something without it being seen as a disorder.--Iztwoz (talk) 08:03, 16 January 2020 (UTC)

First sentence

There is questions around how we should descript schizophrenia in the first sentence:

1) "Schizophrenia is a mental illness characterized by episodes of psychosis with hearing voices, delusions (false beliefs), and disordered thinking.[1][2]"

2) "Schizophrenia is a mental illness marked by significant changes in a person's perceptions, thoughts, mood, and behavior."

3)"Schizophrenia is a mental illness characterized by abnormal behavior, strange speech, and a decreased ability to understand reality.[2]"

In my opinion the first one is much more specific well the second one could apply to a large number of mental illnesses. The third one is what we had a month ago. Happy with that one aswell.Doc James (talk · contribs · email) 03:57, 17 January 2020 (UTC)

The first one is okay-ish but the natural history of schizophrenia is that it is generally chronic not episodic, hence "episodes" is a problem. Agree the second sentence is overly generic to the point of meaninglessness. Cas Liber (talk · contribs) 07:49, 17 January 2020 (UTC)
The third one is problematic because (a) abnormal behaviour is so vague as to offer no useful information, (b) decreased ability to understand reality is a grossly inaccurate way of describing delusions and hallucinations - a person can have a complex and bizarre delusional ssytem but still accurately know who they are, where they live and all their relatives/jobs/etc. The classic whay schizophrenia is described is by "delusions and hallucinations" and this sentence does not mention them. Cas Liber (talk · contribs) 08:10, 17 January 2020 (UTC)
Am in preference for the first one since it makes an early mention of psychosis - but perhaps it might be better changed to reflect that it doesn't have to involve more than one episode, maybe ..."is characterised by an episode of..." whether or not there are more is covered in the body, or add "which may recur". Literature on the treatment of schizophrenia makes many references to second-episode psychosis and more, that often need admission to hospital. And relapses do occur where there is non-compliance with meds which is known to be a problem. I also would like to see the word hallucinations used - according to the lit. there are often other types of hallucinations not just hearing voices.--Iztwoz (talk) 09:38, 17 January 2020 (UTC)
Auditory is way way way the most common. Others are rare. If a person comes into ER talking about visual hallucinations, one thinks about drug intoxication, delirium or dissociation rather than schizophrenia. DSM diagnoses schizophrenia as psychosis of over 1 month duration. Cas Liber (talk · contribs) 12:55, 17 January 2020 (UTC)
Thanks - but think was shoring up use for hallucinations as is the term used extensivley in defining the disorder. DSM says that schizophrenia lasts for at least six months and includes at least one full month of active-phase symptoms. (p89) ? --Iztwoz (talk) 13:54, 17 January 2020 (UTC)
  • None of the above. First, focusing on the first sentence (when there is an extensive list of work needed on this page above) is premature. Second, relying on the simplest, least useful sources in the article to cite a definition is sub-optimal. Third, I suggest paraphrasing the "Clinical presentation, signs and symptoms" of this Lancet article to better encompass all of the commentary above. It is a freely available, Lancet article, and could helpfully be used to write a better first sentence that covers all of the points discussed above, but does a better job than either NIMH or WHO. SandyGeorgia (Talk) 16:46, 17 January 2020 (UTC)
She we can go with something else. What do you propose? Doc James (talk · contribs · email) 22:42, 17 January 2020 (UTC)

References

  1. ^ "NIMH » RAISE Questions and Answers". www.nimh.nih.gov. Retrieved 29 December 2019.
  2. ^ a b "Schizophrenia Fact sheet N°397". WHO. September 2015. Archived from the original on 18 October 2016. Retrieved 3 February 2016.

Signs and symptoms

This is partly why having diagnosis and signs and symptoms is better together but whatever..issues... Cas Liber (talk · contribs) 20:18, 15 January 2020 (UTC)

  • "Schizophrenia is characterized by episodes of psychosis. " is problematic as schizophrenia (if untreated) is most commonly a longitudinal rather than episodic illness (like most mood disorders).
I chose that over the somewhat messy characterised by a whole host of symptoms. Initially it is characterised by psychosis and its symptoms more easily related as psychotic or positive. The same holds for relapses and the many references to first episode psychosis. Also untreated schizophrenia must have presented with a first episode psychosis in order to have been diagnosed in the first place.--Iztwoz (talk) 08:22, 16 January 2020 (UTC)
Had another look and changed.--Iztwoz (talk) 11:16, 16 January 2020 (UTC)
  • Another well referenced term is duration of untreated psychosis (DUP) that optimally needs to be as short as possible. - belongs more in management. It's not really a reified term but an acronym anyway (though is worth mentioning)
Removed sentence already included in Diagnosis.--Iztwoz (talk) 11:16, 16 January 2020 (UTC)
  • I am actually thinking that to make the section less repetitive, it is worth moving up mention of symptom classification (pos/neg/cog) to near the top, so the subject matter doesn't jump back and forth (i.e. describe symptoms, then classify them, then describe them again)
yes, Yes, and YES! I agree with everything you wrote. I too have never understood why "signs and symptoms" and "diagnosis" are not covered in the same (or adjacent) sections.   - Mark D Worthen PsyD (talk) (I'm a man—traditional male pronouns are fine.) 21:28, 15 January 2020 (UTC)
@Markworthen: other editors have different ideas, so am just looking at what we can do now until bigger debate is settled elsewhere Cas Liber (talk · contribs) 23:31, 15 January 2020 (UTC)
Re the comments above nobody else seems to be doing much to the article - clearly that section on signs and symptoms needs attention and to clear a lot of repetition - I shall carry on editing, any other editor is free to make their changes. --Iztwoz (talk) 08:22, 16 January 2020 (UTC)
An aside - there seems to be a real consensus here for your proposed change of order. --Iztwoz (talk) 11:16, 16 January 2020 (UTC)
Cas, I have been hard at work for days over at Tourette syndrome, and repeatedly find that a forced order and forced sections are disrupting the narrative and making for tons of repetition. You should do what makes sense for this article. MEDMOS is a list of suggested headings, and it should not constrain your writing. SandyGeorgia (Talk) 21:44, 15 January 2020 (UTC)

Not seeing an issue with the current order. Diagnosis generally goes into more technical details than either signs and symptoms or cause. Thus makes sense lower in the article IMO. Doc James (talk · contribs · email) 22:53, 17 January 2020 (UTC)

Hallucination

Are there any thoughts as to the use of 'Hallucination' in the lead. It would make definition easier; it is not such a difficult word.? As for the interpreting question - the word is the same in French, almost the same in German, and very similar in Spanish and Italian.--Iztwoz (talk) 18:03, 17 January 2020 (UTC)

It is tricky - my preference is phrasing like "hearing voices" would be good in simple wikipedia - and prefer "(predominantly auditory) hallucinations" here. Agree that "hallucination" is in general use enough for it not to need a plainer english phrase. Cas Liber (talk · contribs) 20:11, 17 January 2020 (UTC)
We could do "hearing voices (auditory hallucinations)" But everyone understands heading voices so the second is not really needed. Doc James (talk · contribs · email) 22:47, 17 January 2020 (UTC)
I just don't think that using 'hearing voices' as a synonym for hallucinations is in order. Other types are referred to in body. It is noted that auditory hallucinations are the most common (even by far the most common) yet since other hallucinations do occur seems more accurate to be more inclusive. Somebody for instance may have been diagnosed with schizophrenia yet never 'heard voices' and if they or relative etc. read the opening here it could make them think that they had been misdiagnosed. It would be more accurate to say (after an initial statement), new sentence: 'Major symptoms include hallucinations (most usually hearing voices), delusions...etc. --Iztwoz (talk) 14:16, 18 January 2020 (UTC)
I agree with Iztwoz's wording Cas Liber (talk · contribs) 02:14, 21 January 2020 (UTC)
Good point Iztwoz. I like your new sentence too.   - Mark D Worthen PsyD (talk) (I'm a man—traditional male pronouns are fine.) 04:21, 23 January 2020 (UTC)

Delusions

While we're at it, "False beliefs" is too broad - as it can be used to describe superstitions, religions (if different to your own) and a whole bunch of things. So loses eough accuracy to be a problem. "Delusions" is in common enough parlance not to be considered as jargon. Cas Liber (talk · contribs) 20:25, 21 January 2020 (UTC)

I agree. As the Delusions article states, "As a pathology, it is distinct from a belief based on false or incomplete information ...." In addition, if we remove the parenthetical ["(false beliefs)"], more visitors will read the Delusions article (as opposed to assuming they know what a delusion is, based on the parenthetical).   - Mark D Worthen PsyD (talk) (I'm a man—traditional male pronouns are fine.) 04:27, 23 January 2020 (UTC)

References problems

Can find no relevant material on DSM pages that is given for Diagnosis in infobox. Can someone indicate the page number?

There is a ref name DSM5pg101 used several times where page 101 is often irrelevant. This is misleading and unneeded – pages are noted in ref. Another hidden note for ref DSMpgxxx says its a different page than previous one yet no page numbers are given in ref.?

A sentence in first para ending ....sometimes never resolve - gives a ref that does not support any part of the sentence (as far as I can see).

The sentence in lead - “Social problems, such as long-term unemployment, poverty, and homelessness, are common consequences.”[6][19] nothing is found in DSM and only homelessness referred to in other ref? --Iztwoz (talk) 18:19, 23 January 2020 (UTC)

That is the name of the reference NOT the page numbers. If you look at the reference in question it will tell you the page numbers. "pp. 101–05"
What is the point of that ref tag why not unambiguous addition of a - DSM5a and the next DSMb and so on.?--Iztwoz (talk) 16:21, 24 January 2020 (UTC)
There is no sentence in the first para which ends in "sometimes never resolve" There is one that ends in "many cases never resolve"
Note that he re-added ref supports but the other one does not.--Iztwoz (talk) 16:21, 24 January 2020 (UTC)
In all the shuffling the second reference went missing.Doc James (talk · contribs · email) 12:12, 24 January 2020 (UTC)

Restored sentence

Have restored - 'Following a single episode of psychosis in those people that have been diagnosed with schizophrenia, around half will either recover completely, or have a significant improvement over the long term with no further relapses.' The reversion stated that scz. was not diagnosed on one episode - the sentence does read that in those people that have been diagnosed. A ref added to the reversion makes no mention of half of people only mentions 20 per cent. The reversion misses the point entirely that it can be resolved after just one episode - it does not have to progress to a second or more episode. Also severe had been changed to some - what is the point of not using a specific like severe as is used in ref and in many other refs? --Iztwoz (talk) 18:09, 23 January 2020 (UTC)

This does not make sense "Following a single episode of psychosis, about half of those diagnosed with schizophrenia will have a significant improvement over the long term with no further relapses, and a small proportion of these will recover completely."
Ref says
"Roughly half of schizophrenia patients recovered or significantly improved over the long term, suggesting that functional remission is possible."
It does not mention "Following a single episode of psychosis"
User:Iztwoz were does that come from? Doc James (talk · contribs · email) 11:57, 24 January 2020 (UTC)
It comes from the abstract ..."to cases in which a single illness episode is followed by complete remission." I agree that the meaning (to me) concerning the rest of those who recovered was not that clear in the article. Other sources say that the more relapses the poorer the outcome; and the reading of this article gave me the impression that it was the general outlook following a first episode.

::::Since this aspect is mentioned in lead does it need adding to Prognosis or is another section on Course of illness needed.?

You mean "Schizophrenia has a heterogeneous range of end states, from severe cases requiring repeated hospitalization to cases in which a single illness episode is followed by complete remission."[26]

I am not sure you can combine those two sentences. Doc James (talk · contribs · email) 11:52, 25 January 2020 (UTC)

It was one sentence - however am in agreement - hence the modification after your edit.--Iztwoz (talk) 14:42, 25 January 2020 (UTC)

Deinstitutionalization

In the 1960s in the Western world is supported by lots of references.

https://www.ncbi.nlm.nih.gov/pubmed/25683467

https://books.google.com.ph/books?id=eCCsAgAAQBAJ&pg=PA73

Which supports "although hospital stays are shorter and less frequent than they once were." though we could clarify that this applies to the Western world. Not sure about other regions.

Doc James (talk · contribs · email) 11:51, 25 January 2020 (UTC)

That's good (about those refs) I had trouble finding much before. Cas Liber (talk · contribs) 23:23, 25 January 2020 (UTC)

U.S.-focused diagnostic criterion

The article's first paragraph includes this sentence: "To be diagnosed with schizophrenia, symptoms and functional impairment need to be present for six months." DSM-5 does require a six-month duration of illness for a schizophrenia diagnosis. However, the ICD-11 description for schizophrenia does not: "Symptoms must have persisted for at least one month in order for a diagnosis of schizophrenia to be assigned."[α]

I suggest that we balance discussion of the U.S.-focused DSM-5 with the International Classification of Disease, 11th Revision. I specifically propose that we (1) Delete the above sentence ("To be diagnosed with schizophrenia, symptoms and functional impairment need to be present for six months") from the first paragraph; and (2) Revise (update) the Diagnosis section (and the Diagnosis of schizophrenia article) to include a brief discussion of ICD-11, including the duration of symptoms difference mentioned herein.[β]

I recognize that ICD-11 was released in June 2018 and that it will be implemented gradually over the next few to several years, depending on the country. However, as the World Health Organization puts it, "ICD–10 is scientifically and technologically outdated ...."[γ]

Notes

α. I intentionally used the word, "description" (above), because that is the subheading one sees when viewing the online ICD-11. In most instances, the ICD-11 description is equivalent to "diagnostic criteria", although the terminology is slightly different, i.e., "definitional requirements", e.g., 6A20.00 Schizophrenia, first episode, currently symptomatic, or "diagnostic requirements", e.g., 6A20.0 Schizophrenia, first episode are used instead of "diagnostic criteria".

β. The full name for the online ICD-11 I mention in this section is ICD-11 for Mortality and Morbidity Statistics (ICD-11 MMS). See the ICD-11 home page; ICD Fact Sheet (pithy good!); ICD-11 Implementation or Transition Guide; ICD-11 FAQ page; and ICD-11 Reference Guide (for nitty-gritty details), for more information.

γ. ICD Fact Sheet, p. 2

  - Mark D Worthen PsyD (talk) (I'm a man—traditional male pronouns are fine.) 06:49, 23 January 2020 (UTC)

Hello Mark - : It does not seem at all clear - the 'description' seems to be for a first episode psychosis.? I came across somewhere (DSM5 p 11) that ICD 11 would actually be following suit with DSM 5, and both seem to have listings for first episode, second episode and so on with or without relapses. It would not follow for schizophrenia to be defined by just one episode with symptoms relating to just one month - where would that leave differentials. I find it hard to believe that ICD 11 would veer so far from DSM 5.? But there are other differences between the two - schizophreniform disorder is not listed in ICD 11. --Iztwoz (talk) 10:45, 24 January 2020 (UTC)
@Iztwoz: ICD-11 emphasizes clinical utility for use around the world, which is a major reason for some of the differences between it and DSM-5. I don't know where you (Iztwoz) reside, but my next sentence is (hopefully) educational for most readers of this Talk page section. In the United States, we tend to assume that DSM-5 is "the" diagnostic manual, and that ICD-11 should follow DSM-5's lead. However, that is a U.S.-centric perspective.
There's a superb article on this topic if you're interested:
Clark, Lee Anna, Bruce Cuthbert, Roberto Lewis-Fernández, William E. Narrow, and Geoffrey M. Reed. "Three Approaches to Understanding and Classifying Mental Disorder: ICD-11, DSM-5, and the National Institute of Mental Health’s Research Domain Criteria (RDoC)." Psychological Science in the Public Interest 18, no. 2 (2017): 72–145. https://doi.org/10.1177/1529100617727266 (If you search for the title of the article on Google Scholar, you'll find no-cost PDFs).
I'll think about maybe adding an endnote mentioning that ICD-11 has a different description of schizophrenia. I'll post it here first if I do that. Otherwise, I won't make any changes to the article because it's a bit more involved than I can manage at present.   - Mark D Worthen PsyD (talk) (I'm a man—traditional male pronouns are fine.) 20:50, 25 January 2020 (UTC)
Thanks for the link - it is a very good article.--Iztwoz (talk) 11:44, 26 January 2020 (UTC)

Redundant sections?

Is much of the info in Criteria and Subtypes now relevant after seven years of being implemented? --Iztwoz (talk) 10:31, 28 January 2020 (UTC)

All outdated DSM IV material could probably go now. Cas Liber (talk · contribs) 11:52, 28 January 2020 (UTC)

Thanks --Iztwoz (talk) 12:41, 28 January 2020 (UTC)

Updating sections to match modern terminology

Under the "Differential Diagnosis" section, the "AIDS dementia complex" link/term should be updated to reflect the page it links to, and the modern terminology, "HIV-associated neurocognitive disorders (HAND)". — Preceding unsigned comment added by Ethanbissbort (talkcontribs) 23:10, 6 February 2020 (UTC)

You are right but I'm not sure that its inclusion is relevant. [27] relates that a small percentage (16%) of a study were found to have an existing or preexisting psychotic disorder.--Iztwoz (talk) 08:48, 7 February 2020 (UTC)

Urban

The source says "First, the risk of schizophrenia and related categories increases linearly with the extent to which the environment in which children grow up is urbanised (odds ratio [OR] ~2).3"[28]

"There are also consistent reports of higher rates of schizophrenia in individuals born in late winter or early spring,58 in individuals born and/or raised in cities" [29] Doc James (talk · contribs · email) 00:17, 15 February 2020 (UTC)

The ref used in that ref makes constant urban referrals - many other refs use the tern urban areas over cities as urban can relate to the sprawling built up areas not readily associated with the narrower (in UK) view of a city. However, have made small change to add iving in - which is referred to in many sources - and more specific ref.--Iztwoz (talk) 11:02, 15 February 2020 (UTC)