Science topic
Psychotic Disorders - Science topic
Psychotic Disorders are disorders in which there is a loss of ego boundaries or a gross impairment in reality testing with delusions or prominent hallucinations. (From DSM-IV, 1994)
Questions related to Psychotic Disorders
By Trialogue, I mean Trialogue events like the Psychosis Seminar or the Borderline Trialogue in the field of social psychiatry.
How would you theoretically underpin the Trialogue? Which theories would you use?
And specifically, from the perspective of Clinical Social Work: with which theories would you connect the Trialogue?
Thanks a lot!
The psychosis (break from reality) known as schizophrenia involves symptoms such as paranoia, trouble thinking logically, socially unusual behaviour, and suicidal thoughts. The “hollow mask illusion” is a common visual misconception that causes most healthy people to view the concave side of a mask as though its features were convex or sticking out in their direction. This illusion occurs because we fill in the hollows with our expectations, accumulated over a lifetime of observing and committing to memory convex faces. Curiously, people with schizophrenia see the hollow mask as just a hollow mask and have an increased ability to see hidden patterns in reality (“The Faulty Weathermen of the Mind” – Nautilus magazine, Issue 52, Page 59 – reporting the neuroscience of Paul Fletcher and Christoph Teufel.)
Many researchers believe that psychosis actually exists as a continuum, that the general population exhibits varying levels of susceptibility to it, and that these manifest in ways that do not greatly disturb the healthy person’s functioning. While full-blown psychosis or schizophrenia is obviously incompatible with a breakthrough like physically uniting everything in both space and time, a trace of it – a tiny, unrecognizable hint of its symptoms – may be vital to intuiting how unification works ie what was previously referred to as “increased ability to see hidden patterns in reality”. The hormonal and biochemical changes in the brain which accompany this barest trace of the condition conceivably result in insights into the nature and connectedness of space-time.
While this speck of psychosis would possess the great benefit of allowing discernment of the so-called “secrets of the universe” and “the mind of God”, it’d also produce problems like intermittent delusions of persecution and awkward – even totally unacceptable – social interactions. Perhaps the most well-known example in science of unacceptable interactions is Isaac Newton’s hostility towards, and clashes with, other academics. I wouldn’t be surprised if he often regretted his own hostility. Despite the tendency to be harsh and inhuman, my World Book encyclopedia says he had a sensitive nature which, besides aiding his scientific pursuits, manifested as great generosity to his nephews and nieces.
Hello everyone,
I am planning to design a model that can predict individuals with high or low psychosis-proneness by looking at the brain connectivity measures in 114 regions, age, gender, IQ, SES, polygenic risk score for psychosis (PRS), and environmental risk score for psychosis (ERS). In this way, I am planning to investigate the brain regions that serve to distinguish high and low psychosis-proneness by using machine learning. However, my sample includes healthy twin and sibling data; hence, my data is not independent. I could group the sample into high and low psychosis-proneness based on weighted positive symptom severity.
Therefore, I would like to ask whether there are any codes or approaches that you can share with me.
My data looks like the image I shared (I did not add the PRS since I do not have the information yet).
Thank you for your help!

As often in medicine animals are ( SADLY) used in experiments .A new study of mice shows there are important links between human and mouse minds in how they function -- and malfunction. Researchers at Washington University School of Medicine in St. Louis devised a rigorous approach to study how hallucinations are produced in the brain, providing a promising entry point to the development of much-needed new therapies for schizophrenia.
The study that was published in the journal Science, lays out a way to probe the biological roots of a defining symptom of psychosis: hallucinations. The researchers trained people and mice to complete a computer-based task that induced them to hear imaginary sounds. By analyzing performance of the task, the researchers were able to objectively measure hallucination-like events in people and mice.
This approach allowed them to study the neural circuits underlying hallucinations, potentially fully opening up the study of mental illness to the kind of scientific studies that have been fruitful for diseases of other parts of the body. My concern is that despite the positives and even if there are similarities, can a study like this be of great value when it comes to humans who has a fundamentally different cognitive ability and brain structure? I agree that we can see tendencies and the study gives an insight, however can this ever fully be transferred to humans? also see other risks as well as grave ethical concerns that applies with all experiments on animals. What are your thoughts?
Best wishes
Henrik
There are many reports of psychosis in patients who have symptomatic COVID-19 disease. Usually there is no past psychiatric history and onset of psychosis seems sudden within first few weeks. How long should the antipsychotic used if initiated in first place?
High expressed emotions is a major determinant of psychiatry disorder prognosis. Especially when it comes to schizophrenia. Research suggests that being in a developing country has better prognosis in psychosis. Partly due to low levels of EE. Is it still a truth ? Do we have enough evidence to prove this fact ?
Although the relationship between alexithymia and primary psychotic disorders (e.g. schizophrenia) has been studiedad, I have had difficulties in finding any research on alexithymia in patients with schizophrenia that also have any substance use disorder. Someone knows any publications on this issue?
Thank you,
I sincerely request all the experts working on schizophrenia to provide their valuable explanations/views on the above topic.
My concern is that PCP, MK-801, and ketamine are anesthetics, these drugs induced unconsciousness (sleep) whereas schizophrenia patients are hyperactive and do not sleep properly.
Melancholic depression is a form of depression that should be considered separately from other forms of depression. I'm interested in why this is the case? How are the mechanisms different from other forms of depression? In addition, considering the severity of the symptoms (e.g. psychomotor, psychosis (in some cases), poor concentration, slowed speech, lack of concentration) is it worth increasing physical activity levels or altering diet? Anyone performed research in this area?
Basically I`ve done a review of the literature on disengagement from Early Intervention Psychosis services using systematic methods. There was heterogeneity across the studies, no RCTs and I`ve used `vote counting` to make sense of the results
GABA- ergic interneurons are responsible for sinchronization of different neural networks ( provide balance in excitation and inhibition) in brain cortex. If there is a disruption of this balance, via excitotoxic degeneration in interneurons, are positive symptoms in schizophrenia a result of released improper activity of neural networks ? Vulnerability for excitotoxicity depends on our congenital conditions ( gene polymorphisms, enzyme conditions, et c.), maybe so, vulnerable people, prone to interneuron disturbance during first episode lose this balance and exhibit psychosis, which leads to connectopathy and brain degeneration?
Infectictous, metabolic, endokrinological, toxic, drug abuse, ect.
As aripiprazole, brexpiprazole, and cariprazine are partial-dopamine agonists with potent binding affinities to the D2 receptor, do they prevent augmentation effects (or worsen psychosis) when two or more antipsychotics are combined?
Certainly, there is data suggesting worsening psychosis when aripiprazole has been added to other agents (Takeuchi and Remington, Psychopharmacology 2013). Additionally, the idea of competitive inhibition is supported by the reversal of hyperprolactinemia when aripiprazole is added to another antipsychotic.
I can find no data of this phenomenon occurring yet with brexpiprazole or cariprazine.
During the psychosis irrespective of particular diagnosis the dopamine synthesis capacity is increased (https://www.ncbi.nlm.nih.gov/pubmed/?term=A+Test+of+the+Transdiagnostic+Dopamine+Hypothesis+of+Psychosis+Using+Positron+Emission+Tomographic+Imaging+in+Bipolar+Affective+Disorder+and+Schizophrenia).
But, would not be better in the case of psychosis to talk about increased dopamine release instead of increased dopamine synthesis capacity, if we do not know directly, whether the hyperdopaminergic striatal state is caused by increased dopamine synthesis or only by increased dopamine release or even disruption of termination of synaptic dopamine action (https://www.ncbi.nlm.nih.gov/pubmed/?term=Putative+presynaptic+dopamine+dysregulation+in+schizophrenia+is+supported+by+molecular+evidence+from+post-mortem+human+midbrain)?
I am currently looking into developing a tool which can be used clinically with young people 14yrs-25yrs who may present with both suspected ASD and psychotic symptomology. Before i begin i though it could be helpfuul to see what is already available.
Any information or pointers would be most helpful.
Thank you in advance
It is my understanding that from a Kraeplinian perspective, and as outlined in the DSM-V and ICD-10, cognitive dysfunction is one of the fundamental diagnostic criteria for schizophrenia, schizoaffective, and affective psychosis.
I have recently been reviewing literature regarding attempts to outline dimensional or spectral criteria for schizophrenia and other psychotic disorders. What I have taken to be the majority consensus is that it may be reasonable to postulate a schizophrenia spectrum disorder which incorporates schizophrenia, schizoaffective disorder, and affective psychosis. This view seems to generally include the caveat that it would not be reasonable to go further and propose a psychotic spectrum disorder since this would lead to the inclusion of etiologically distinct disorders such as psychosis NOS, psychosis in dementia, and drug induced psychosis.
I was curious if it would be plausible to conceptualize schizophrenia as a comorbid condition, which one could describe as “persistent psychosis with cognitive impairment” (PPCI), rather than its own entity which is distinct from other psychotic disorders. This conceptualization would permit for a possible shared etiology underlying psychotic disorders (i.e. the “psychotic core”) by placing schizophrenia along the broader psychotic axiom. To avoid overinclusion, one could assess the phenomenological characteristics of psychotic experiences associated with other disorders to differentiate symptoms which result from a “psychotic core” from psychotomimetic symptoms that are secondary to another disorder and have a separate etiology. For example, if the presence of psychosis in dementia does in fact have its own unique neurological mechanism (as compared to say schizophrenia), it would make sense to assume that it also possesses unique phenomenological qualities that could be differentiated.
This small distinction would have significant clinical implications. Since it has been shown that cognitive impairment is the most significant determinant of poor prognostic outcome in schizophrenia, conceptualizing this as a separate symptom would merit a dual approach to therapeutic intervention in which the positive and cognitive symptoms should be addressed differentially. This could be accomplished by combining therapeutic approaches, given the existence of interventions which are specific to targeting either positive symptoms or cognitive impairment. I would imagine this would also have implications for how samples are defined (i.e. construct validity) in research methodology.
If anyone reading this can understand my train of logic and would be able to provide some insight or relevant literature, it would be greatly appreciated.
Hello,
I have a question about treatment protocols and standardization of services in mental health care in the US. I am aware of numerous treatment guidelines and recommendations that have been published, for example by SAMHSA, WHO, NICE, etc. However, it would seem that theses materials function more or less as suggestions rather than as actual standard procedures.
What I would like to locate is data on the services provided in either the treatment of chronic schizophrenia or in the case of first episode psychosis. Specifically, I would like to find information on the treatment plans which are actually constructed and used in routine clinical practice. My suspicion is that there is a significant gap between the quality of services actually provided and those which have been recommended.
This question stems from a perceived overreliance on psychiatric drugs in treating psychotic disorders as well as from the recognition that there seems to be a persistent lag between psychopathology research and clinical practice. This can be seen in our current models of mental illness which is still heavily rooted in the biomedical model dating back to its initial rise to power in the 1950's. And while clinical practice still holds these views as the dominant model in the field, a recent push back against medicalization has gained popularity amongst researchers, and with it, a renewed interest in psychosocial models of treatment.
This leads me to another question about treatment standards for psychotic disorders. If you consider the poor prognosis despite available medication and the generally pessimistic attitudes toward the effectiveness of psychotherapy for psychosis, one would imagine that the development of innovative psychosocial therapies would be of great service to the unmet needs of this population. Accordingly, the literature would suggest that there has indeed been growing interest in this endeavor, and a number of therapies designed specifically for psychosis have been gaining attention. Of these approaches, a few notable examples include Metacognitive Training, ACT for psychosis, AVATAR therapy, Voice Dialogue Therapy, and IMR, among others.
So the question remains, why does it seem that CBTp is still the only intervention regularly employed in mental health care services? (I would also be interested to know how the rates of providing CBTp compare to the use of psychiatric drugs proportionally) Where is it that these alternative therapies are actually being made available to patients, and if they are not, by what process and on what timeline will they become available?
Any input on these matters would be appreciated. I would be particularly interested in locating actual statistical data on these practices. These seem to be important questions to consider, especially if my suspicions are true. From my perspective, the bias resulting from the overemphasis of a biomedical model in conjunction with a lack of enforcement of standardized protocols leads to an environment which carries significant risk of resorting to ineffective, poor quality services.
Benign hallucinations are usually non-threatening hallucinations in patients with Parkinson´s disease associated psychosis, in which the patient has a well-preserved sensorium and is aware of the hallucinations.
Minor hallucinations are: 1. a sense of presence hallucinations, which are characterized as a vivid feeling that somebody or an animal is closely present when in reality it is not. 2. Passage hallucinations are described as a person or a animal quickly passing in the peripheral visual field.
These terms are more used by neurologists as by psychiatrists.
Do you use them?
Do you also use them outside the context of Parkinson's disease?
DSM-5 (2013) defines anhedonia in schizophrenia spectrum and other psychotic disorders as "the decreased ability to experience pleasure from positive stimuli or a degradation in the recollection of pleasure previously experienced."
If so, and if there is anhedonia in relation to the presence (consummatory anhedonia), and in relation to the future (anticipatory anhedonia), is there any anhedonia in relation to the individual's past? And how we can name it?
Caffeine is an antagonist of A2A adenosine receptors that are coupled to D2 receptors in striatally located heteromers. Antagonism on A2A has a similar effect as D2 agonism, so the dopaminergic effect (and also a psychostimulating one) of caffeine is mediated precisely by this mechanism. But is caffeine itself strong enough to cause psychosis?
From the Beatles to Bob Marley, David Hockney to Duke Ellington, artists and musicians alike have long credited cannabis with enhancing creativity. In psychiatry however, cannabis is known to be associated with an increased incidence of psychosis and schizophrenia. Does cannabis enhance creativity? And is this related to the drug’s ability to induce psychosis? Is there any research that provides empirical evidence that cannabis increases creativity that you would suggest? Are psychotic symptoms and creative outbursts mutually exclusive? Any papers/articles/meta-analyses on the topic would be highly appreciated!
I am seeking databases that includes variables for women that have been diagnosed with postpartum psychosis or postpartum bipolar disorder or major depressive mood disorder with psychotic features in the first year postpartum.
There is some research indicating possible mitochondrial dysfunction in Psychosis. Currently a client with psychosis has been given melatonin for sleep in combination with therapies done by myself - Cognitive restructuring, talking to voices and cognitive therapy. This was after ALL normal (medical and psychotherapeutic) treatments had been applied for a 2 year period with little success before I received the client. The only two differences in treatment was talking to voices and melatonin prescribed by the doctor. Naturally this is not enough to propose that melatonin may have an impact, however there was a distinct improvement in cognitive processing abilities. Has anyone done any trials or research on the use of melatonin. Studies suggest that melatonin may or may not partially or fully repair mitochondria, whilst no research has been found on the possible utilisation of Gh.
My program is experiencing an influx of re-referrals. Our assessments are showing that their cognitive levels have dropped to levels seen prior to beginning the first round of treatment. Has anyone else experienced this?
1. What is it include in schizophrenia spectrum? are those the same with psychotic disorder?
2.Is it ok if I say that schizoaffective is part of schizophrenia spectrum? or schizoaffective is part of psychothic disorder?
3. In DSM V, why schizotypal personality disorder include in schizophrenia spectrum and other psychotic disorder?
4. Schizotypal personality disorder is categorized as personality disorder or schizophrenia spectrum disorder?
Thank you
recently saw a 6 year old who reported hearing a voice telling her to kill her mother
For example, using the Aberrant Salience Inventory (ASI)?
Hi all
OPCRIT is a reliable diagnostic algorithm known to produce valid ICD-10 (and other) diagnoses of psychotic disorders, based on standardised case note review of 90 symptom items.
Using OPCRIT to produce ICD-10 diagnoses is useful for the major psychotic disorders including schizophrenia (F20), schizoaffective disorders (F25) and bipolar disorder (F30-31) and psychotic depression (F32-33). However, substance-induced psychotic disorders are not assigned their own category under the algorithm used to produce ICD-10 diagnoses, instead being lumped with other psychotic disorders, nos (i.e. F21-29 + F1X.5, excluding F25).
How would you go about teasing out people with a substance induced psychosis? Is this even possible? Various papers have noted this limitation, but I have not seen a workaround. Within the 90 OPCRIT items there is a section on lifetime dependence to alcohol, cannabis and other drugs (with or without affecting psychopathology), and I also have separate clinical ratings of ICD-10 diagnoses, so I could combine these with OPCRIT to code anyone who receives an OPCRIT non-affective diagnosis NOS AND a clinical diagnosis of F1X.5 to indicate a SIP. Would I be on safe ground here?
Thanks to the community,
James
In my thesis, which I am currently writing, I'm focusing on the links between (risky) sexual behaviour and Kernberg's concept of personality organization.
I have found information about sexual behaviours in patients with neurotic and borderline personality organization. However, when it comes to the psychotic personality organization I have not found any satisfactory information.
Would be grateful for any tips!
We use many agents "off label" (eg carbamazepine for bipolar) yet given history of abuse and psychotic reactions to both ketamine and phencyclidine we need to be cautious. In what situations should clinicians cross the line and administer ketamine?
In psychiatry, mindfullness has been mostly used for mood and anxiety disorders. It seems that researchers and clinicians have been more reluctant to examine the effects of mindfulness in people with psychotic disorders.
This refers to the various ways in which individuals and their families understand the "process of healing" in the process of recovery
Can we devise a quasi-quantitative solution that establishes a formula to show the threshold or statistical probability for sz or sz-like disorders to manifest? The formula might look something like this: Gene A, allele a (all components weighted, perhaps a beta-weight in a regression equation) + Gene B, allele a + Gene C, allele b + Environmental factor (Env) A + Env B + Interaction of Env A & Gene A, allele a = the statistical probability that a sz-like disorder will manifest.
Will the new diagnostic criteria improve differential diagnoses, and thus make treatment more effective?