Talk:Dopamine hypothesis of schizophrenia

message: Isn't there a possibility that there is a chicken and egg problem.  Is the dopamine activity the cause or the effect of the psychosis?  Has this been explored?--Jack Upland 06:14, 28 November 2005 (UTC)
replies: text: Well dopamine antagonism seems to relieve some of the 'positive' symptoms suggesting that the dopamine activity (if you believe in the dopamine hypothesis) underlies the psychosis to some degree.  Whether the dopamine dysfunction is secondary to some other disease process or neurological change is difficult to say, since it would require having studied people's brains before they were symptomatic, which is a very large undertaking if you expect only around 1% of people to develop it. --Coroebus 20:48, 26 January 2006 (UTC)
replies: text:  You would have to prove a dopamine difference before giving a "medicine" to a schizophrenic to help them, otherwise any and all brain changes in schizophrenia can be attributed to the drugs given by psychiatry. "Maintenance antipsychotic therapy: is the cure worse than the disease? "http://www.ncbi.nlm.nih.gov/pubmed/2021 --Mark v1.0 (talk) 12:48, 23 October 2015 (UTC)
thread_title:  Chicken & Egg 

message: This article has been recently edited to include a great deal of research by Philip Seeman. The major changes were here, by Seemanph, so I presume they were done by the author of the research himself.
Consequently, the article needs re-balancing, as it is currently quite one-sided.
: - Vaughan 13:47, 11 May 2006 (UTC)
replies: text: However, it is not clear that every psychotic experience is linked to increased dopamine release (ref the work on NMDA receptor antagonist induced psychosis that is not reverse by antipsychotics) - Vaughan 23:46, 10 December 2006 (UTC)
thread_title:  Article needs re-balancing after addition of Seeman et al refs 

message: The chicken-egg question is highly relevant.
I am uncomfortable with the unqualified assertion that schizophrenia is due to a dopamine defect. In order to prove that assertion, one would need to measure dopamine activity in a synapse and prove that it was measurably abnormal as defined by a statistically derived range. Every psychiatrist of course knows that such a test is impossible with current technology so there is no proof to be had. This is why the patient information booklet that comes with every psychotropic prescription drug contains the phrasing 'is believed to'... rather than 'is known to'...
: I am uncomfortable with leaving such a large block of criticism unchallenged - I will try and provide my little bit of balance point by point. This is a very simple initial hypothesis. For the electric engineer you seem to be, this is akin to 'A transistor is like a switch'. The scientific world has moved on, from dopamine to dopamine receptors, from dopamine receptors to GABA receptors to glutamate / glycine interactions and brain network hypotheses. Focusing on the dopamine hypothesis as anything more than a first-level abstraction is like teaching schoolkids conventional current. Egmason (talk) 04:11, 29 January 2014 (UTC)
replies: text: Neuronal transmission is a complex interaction between receptor-gated and voltage gated ion channels, exocytotic vesicles, excitatory and inhibitory receptors (which can be either presynaptic or post-synaptic) and remote humoral mediators. there are multiple feedback and feedforward connections. Egmason (talk) 04:11, 29 January 2014 (UTC)

text: Psychiatrists don't have the luxury of being able to retrofit better components. It is more like trying to fix your computer by alternately dipping it in water or oil. In the forties some advocated lobotomy / leucotomy to provide a Programmable read-only memory type modification, but this was ended with the development of the dopamine receptor antagonists. Egmason (talk) 04:11, 29 January 2014 (UTC)

text: Franz Mesmer and James Braid did the hand-waving thing too. Egmason (talk) 04:11, 29 January 2014 (UTC)

text: This comes from your unproven assertion that feedback instability is responsible for schizophrenia. Some seizures produce hallucinations or paranoia, which does actually add to you assertion. Antiepileptic medications are believed to work by focusing on glutamate interactions or regulating neuronal ion channels; not neurotransmitters directly. Egmason (talk) 04:11, 29 January 2014 (UTC)

text: Those must be the bad psychiatrists, because this is pretty much the hypothesis that I tell my patients that have a tertiary education or a strong interest in science. There is a strong model that says that schizophrenia is a neurodevelopmental disorder (Causes_of_schizophrenia#Prenatal), probably involving changes in growth factors leading to abnormal growth and / or synaptic pruning. Brain biopsy results show abnormal placement of neurons in layers where they do not usually end up. For links on the neuroscience modelling currently being done, look at the Blue Brain Project.Egmason (talk) 04:11, 29 January 2014 (UTC)

text: Destructor = Monoamine oxidase Egmason (talk) 04:11, 29 January 2014 (UTC)

text: (1) The dopamine hypothesis is itself dis-proven by the newer antipsychotic medications which are not primarily dopamine-blocking, but work on many different receptors. (2) Modern Psychiatrists try not to use the term 'schizophrenic' which labels people by just one aspect of their make-up. (3) Getting stuck on 'dopamine is solely responsible' is like demanding we stop the war on Vietnam - now! Egmason (talk) 04:11, 29 January 2014 (UTC)

text: How much use is 'natural' vs 'unnatural'. Cancer is natural. Schizophrenia is natural. Antibiotics are unnatural. Antiretrovirals are unnatural. Heart and lung transplants are unnatural.  Egmason (talk) 04:11, 29 January 2014 (UTC)

text: Deep brain stimulation is successfully being used to treat depression (see below), OCD and Parkinson's disease currently. Egmason (talk) 04:35, 29 January 2014 (UTC)

text: See Biological neuron model for your beloved calculus (yuck, don't get it, can't stand it). See Computational neuroscience and Default mode network for information about medium and large-scale brain networks, and Neural engineering for ideas about using these things for treatment. The interconnecting network hypotheses are really hot in the Neuro-cognitive circles, while the physical science boffins are still plugging away at receptor sub-types and complex gene-expression models. Egmason (talk) 04:11, 29 January 2014 (UTC)

text: I am happy to discuss the limitations of my knowledge, but when it accounts for up to 60% of my treatment effect, I also try to project certainty and boundless optimism. Perhaps you are confusing that for belief. Egmason (talk) 04:35, 29 January 2014 (UTC)

text: I am a Doctor. (Dammit Jim, I'm a doctor not an engineer!). I am a therapist, a researcher, a teacher, a neuroscientist. I acknowledge there are a lot of grey areas around (and within) what we know, but what we know, we know well. Egmason (talk) 04:11, 29 January 2014 (UTC)
replies: text: RE: Deep brain stimulation is successfully being used. This is a false claim.
"DBS surgery comes with a host of other potential surgical risks,  including: up to an 8% risk of bleeding in the brain that can lead to permanent deficit, or death 1.1% of the time. an 8% chance of stroke or permanent neurological deficits. a risk of infection of up to 15%. 5% risk of hemorrhage. 2% risk of seizure. the potential for air to enter the brain, and leakage of cerebrospinal fluid or brain fluid." source http://www.madinamerica.com/2015/09/adverse-effects-perils-deep-brain-stimulation-depression/ --Mark v1.0 (talk) 16:16, 24 October 2015 (UTC)
replies: text: 100%-8%-1.1%-8%-15%-2%-2%=60.9%; still room for hope. I'm not saying its a good option, nor that it isn't risky. Okay, after further reading, I will withdraw this claim about depression. It is still sitting in 'not proven', and given the effort that has gone into it, that probably means it's a dead duck. Egmason (talk) 04:56, 17 April 2016 (UTC)
thread_title:  Second the Motion - Rebalance please! 

message: This article strikes me as pretty balanced - evidence for and against is presented. Would anyone have an issue with removing the neutrality tag? Or could we get a list of issues that need to be addressed? StripeyBadger 11:04, 5 March 2007 (UTC)
thread_title:  Neutrality Tag? 

message: The sentence 
The blockade of serotonin (5-HT2) receptors does not contribute to either the antipsychotic action or to alleviating the Parkinsonism that can occur at high doses of antipsychotic medication.[7]
is very anachronistic.  Can its writer either elaborate or explain its function?
Insomnis 04:38, 20 July 2007 (UTC)
thread_title: Serotonin?

message: One of the cogent pieces of evidence against the dopamine hypothesis is that Parkinson's disease and schizophrenia may co-exist in the same person. The only reference this article currently makes to Parkinson's disease is that people treated with dopamine lowering medicine for this illness may show psychotic symptoms. More needs to be said on evidence against the dopamine hypothesis in this article. ACEOREVIVED 21:08, 9 November 2007 (UTC)
replies: text: Dopamine medication to treat Parkinson's (e.g. L-DOPA) increases not lowers dopamine function and can indeed can cause psychosis. - Vaughan 11:40, 10 November 2007 (UTC)
thread_title: Comorbidity with Parkinson's Disease

message: The theory has been discredited and proven as far too simplistic.
I am not expert on the subject, but as far as I am aware, this is an exaggeration. Is there any evidence to back up this claim? 
As far as I know (do correct me if I am mistaken), yes the original hypothesis was overly simplistic. However, in recent years a revised dopamine hypothesis is emerging, which focuses on hypofunction and relates to the negative symptoms in schizophrenia too. 
Moreover, it is not a deterministic hypothesis; so to state that it is discredited because other factors can influence the onset of schizophrenia would be incorrect.Ihatechoosingnames (talk) 02:24, 11 April 2008 (UTC)
replies: text: Sounds good to me. I worked on the chemical imbalance theory article and pretty well came to the same conclusion. Feel free to make the edits here, you have my blessings. --scuro (talk) 02:34, 11 April 2008 (UTC)
thread_title:  "Theory has been discredited"? 

message: If cocaine and amphetamines may be associated with schizophrenia, why not nicotine, which also messes with dopamine in a major way?  Maybe smoking makes you crazy, in addition to killing you.  —Preceding unsigned comment added by 75.72.202.72 (talk) 00:49, 6 July 2010 (UTC)
thread_title:  What about Nicotine? 

message: "The excitatory neurotransmitter glutamate is now also thought to be associated with schizophrenia. Phencyclidine (also known as PCP or "Angel Dust") and ketamine, both of which block glutamate (NMDA) receptors, are known to cause psychosis closely resembling schizophrenia, further suggesting that psychosis and schizophrenia cannot fully be explained in terms of dopamine function, but may also involve other neurotransmitters.[12]"
Unfortunately, 'psychosis closely resembling schizophrenia' is vague and subjective, and can be produced via a multitude of drugs, disorders, and illnesses. removed the entry because it cannot be considered to be unbiased. 64.186.120.109 (talk) 20:07, 12 December 2011 (UTC)
replies: text: I think you make a very good point about not conflating everything that superficially looks like a psychosis. At the same time, the glutamate hypothesis of schizophrenia is supported by sufficiently many sources that I'd rather not remove the material entirely. I restored it, but I also reworded it, to make it clearer that PCP/ketamine symptoms do not actually equal schizophrenia. --Tryptofish (talk) 22:35, 12 December 2011 (UTC)
thread_title:  Removal of entry in "Evidence against..." section 

message: I took a look at the cited sources of the introduction regarding its basis for early intervention, but it appears that the statement in the "Introduction" section regarding the effects/importance of early intervention isn't mentioned in its sources.
"...Patients on neuroleptic or antipsychotic medication have significantly less atrophy within these crucial areas. As such, early medical intervention is crucial in preventing the advancement of these profound deficits in bilateral communication at the root of all psychotic disorders.  Advanced, chronic schizophrenia can not respond even to clozapine, regarded as the most potent antipsychotic, as such, a cure for highly advanced schizophrenia is likely impossible, so the value of early intervention cannot be stressed enough."
From checking the source,  concludes possible hypertrophy of certain brain regions (found to be "higher caudate, putamen, and thalamus volumes" compared to nontreated and healthy subjects) due to antipsychotic medication,
while  discusses the relationship of certain brain regions (even apparently different from those in  - ie. "Corpus Callosum [abnormalities were] related to the severity of their psychotic symptoms") to symptoms. However, to say the least, neither source considered the antipsychotics to thus prevent deterioration or deficits, or consider it as a basis for early intervention; it seems to me that the studies were nowhere near saying that.
This is also conflicting with the Psychosis and Early intervention in psychosis articles, which on the other hand cite sources directly regarding early intervention, finding early intervention to only be controversial or questionable in its long-term benefit, with little gains sustained after 5 years.
This suggests to me that this is original research.
However, I'm not an expert on the subject myself, and a good amount of the introduction seemed to be too technical for me to really evaluate. I'm also not that familiar with Wikipedia procedure :\ so I'd like to check with you guys - would it be appropriate to, say, tag the section as original research? What should we do about this?
96.48.197.114 (talk) 10:45, 22 August 2013 (UTC)
replies: text: This is not 'original research'; as a search or the links you point to will show, there is a large body of published work around Early Intervention. As you also point out, the early hope of the field has not been proven with time, but the hope is still there that while biological progression of schizophrenia might not be slowed by medication, people might still do better psycho-socially with more initial input. The statement might be introduced better to show its balanced context in the history of psychiatry. Egmason (talk) 00:56, 3 February 2014 (UTC)
thread_title:  Original research in introduction? "Early medical intervention is crucial in..." 

message: "The antipsychotic aripiprazole occupies over 90% of D2 receptors, but this drug is both an agonist and an antagonist at D2 receptors."
is there a source for this statement?  it's contrary to my understanding (and anything i can find) of dopaminergic effects of aripiprazole is that it's a dopamine receptor partial agonist at D2-D4 receptors.  Indeed, aripiprazole also has partial agonism at the 5ht2a receptor.  — Preceding unsigned comment added by 198.49.6.225 (talk) 10:56, 6 September 2015 (UTC)
thread_title:  evidence against section 

message: "People with Schizophrenia appear to have a high rate of self-medication with nicotine; the therapeutic effect likely occurs through dopamine modulation by nicotinic acetylcholine receptors."
is there a source on this?  it seems to be highly speculative to say "the therapeutic effect likely occurs..."  perhaps a little more equivocation is in order, like saying "possibly" or "potentially".  — Preceding unsigned comment added by 198.49.6.225 (talk) 11:02, 6 September 2015 (UTC)
thread_title:  evidence for section 

message: This sentence near the beginning of the introduction "A relative excess of these receptors within the limbic system means Broca's area, which can produce illogical language, has an abnormal connection to Wernicke's area, which comprehends language but does not create it.[citation needed]" I believe requires clarification in addition to a citation. 
In healthy individuals these two areas are connected by the arcuate fasciculus, so the presence of a connection between these two areas is not atypical as the sentence seems to suggest. Even knowing this, the reinterpretation of the sentence is that there is something atypical about the connection, but without saying what that something is.
Anditres (talk) 00:05, 31 October 2020 (UTC)
thread_title:  Introduction: Broca's area and Wernicke's area (clarification needed) 

message: I was trying to add more references to the paragraph on criticisms but an other editor was too fast for me. "cite web" is accepted by Wikipedia on other pages and has a webpage on it https://en.wikipedia.org/wiki/Template:Cite_web. The additional web page reference I was about to place was https://www.medscape.com/viewarticle/823368_2 . I don't want to get into an edit war so I am leaving it for now. ( Who did the third WRONG edit? I don't know)--Mark v1.0 (talk) 17:23, 27 October 2021 (UTC)
thread_title:  Criticisms