Trauma does not explain schizophrenia on its own, and schizophrenia is not complex PTSD under another name. But childhood adversity is one of the best-documented environmental risk factors for psychosis: a 2012 meta-analysis found that it nearly triples the odds. Some people diagnosed with schizophrenia are living with trauma-related dissociation or PTSD with psychotic features, and telling these apart changes treatment.¹

My argument here is narrower than the one this post used to make. Schizophrenia is a largely heritable vulnerability, not a disguised trauma disorder. Inside that diagnosis, though, are people whose voices, flatness and fear are organized around what happened to them. The content of their experiences is a clue worth following, not a diagnostic test, and for those people trauma-focused therapy belongs alongside antipsychotic medication, not in place of it.

What I saw at UAB REACT

When I started my career as a social worker at UAB REACT in Birmingham, Alabama, I noticed something that nobody seemed to be talking about. The patients diagnosed with schizophrenia fell into two very different groups, and once I saw the pattern, I couldn’t unsee it.

The first group had devastating trauma histories. Sexual abuse. Confinement. Violence in the home. When these patients described their psychotic experiences, they told me about spirits that had entered their bodies, about their souls being swapped with someone else’s, about demons that whispered commands in voices that sounded like their abusers. Their eyes were flat, their affect numbed, but underneath that stillness you could sense a storm.

The second group was different. Their families had histories of mental illness. Their decline had been gradual: a slow withdrawal from friends, a quiet slipping in school performance, an increasing difficulty following conversations. When they described their experiences, they talked about machines, surveillance systems, algorithms tracking them. Their affect wasn’t numbed; it was genuinely diminished, as if someone had turned down the volume on their emotional life.

I kept asking: Are these really the same illness?

I still think that was the right question. What has changed is my answer. The first version of this article put percentages on a three-way split of schizophrenia diagnoses and called the trauma link “causation-level.” Those percentages came from no study, and the research does not support two clean groups. It does show that trauma, dissociation and psychosis overlap far more than the textbook picture suggests, in ways a clinician can learn to hear.

What the research says about trauma and schizophrenia

The standard reference is a 2012 meta-analysis by Filippo Varese, Richard Bentall and colleagues, which pooled 18 case-control studies, 10 prospective cohorts and 8 population surveys. Childhood adversity, counted as sexual, physical or emotional abuse, neglect, parental death or bullying, was associated with psychosis in every design, with an overall odds ratio of 2.78. The prospective studies, which are least affected by people reinterpreting their past after they become ill, gave almost the same figure, 2.75. If the relationship is causal, the authors estimated that about a third of psychosis cases would not occur without childhood adversity, with a wide uncertainty range of 16% to 47%.¹

The amount of trauma matters. In two large community surveys, people who had experienced two or more types of trauma were more likely to have a psychosis diagnosis, in what looked like a dose-response pattern,² and in a British birth cohort of 4,433 young people, exposure to more trauma types and at more ages carried higher odds of psychotic experiences by age 18.³ That dose-response pattern is one reason researchers take the association seriously.

Two claims from the earlier version need correcting. The first is that “up to 80%” of people with schizophrenia have severe childhood trauma. A meta-analysis of 23 studies and 2,017 patients put self-reported childhood sexual abuse at 26%, physical abuse at 39% and emotional abuse at 34%.⁴ Those are high rates, and the authors concluded that clinicians should be trained to ask about abuse in psychosis, but they are not 80%.

The second is the comparison to smoking and lung cancer. An odds ratio near 3 is a substantial association. It is not proof of causation, and it is nowhere near the size of the smoking link. Genetic factors still account for most of the variation in risk: a nationwide Danish twin study estimated the heritability of schizophrenia at 79%, yet when one identical twin had schizophrenia, the other had it only 33% of the time, which leaves real room for environment.⁵ The two are also entangled. In two birth cohorts, children with a higher polygenic score for schizophrenia were more likely to be exposed to trauma, and in the British cohort their mothers’ scores showed the same association.⁶ Part of the trauma link may run through family genetics and family environment at once.

I cover the epidemiology, the genetics and the old family theories in more depth in a companion piece on schizophrenia, trauma and the double bind. This one is about the clinical question in the title.

Is schizophrenia really complex PTSD?

Complex PTSD is a diagnosis in the World Health Organization’s ICD-11, not in the American Psychiatric Association’s DSM. It requires the core PTSD symptoms plus lasting problems with emotion regulation, self-worth and relationships, and it identifies people who have more often lived through multiple, sustained traumas and who are more impaired than people with PTSD alone.⁷ Nothing in the definition includes hallucinations or delusions. Read literally, the answer to the title is no.

Read clinically, the two overlap in at least three ways.

Trauma can produce psychotic symptoms. Psychotic symptoms have been reported in up to 40% of veterans with combat-related PTSD. In one study of 45 Vietnam veterans with PTSD and no primary psychotic disorder, 22 had psychotic features, and in them more severe psychosis went with more severe PTSD.⁸ A 2019 review argues that PTSD with secondary psychotic features may be a distinct condition with its own biology, and that people with it can benefit from evidence-based psychotherapy.⁹

Dissociative disorders can look like schizophrenia. Kurt Schneider’s “first-rank symptoms,” such as voices commenting on what a person does, thoughts inserted or withdrawn, and feelings of being controlled from outside, were long taught as hallmarks of schizophrenia. In 1987 R. P. Kluft found at least one of them in every one of 30 patients with what was then called multiple personality disorder, now dissociative identity disorder.¹⁰ Colin Ross and colleagues later counted an average of 4.9 Schneiderian symptoms across 368 such patients, against an average of 1.3 among 1,739 patients with schizophrenia in ten earlier published series.¹¹ A 2017 systematic review concluded that dissociative symptoms are common in schizophrenia spectrum disorders, that they are linked to trauma history there just as they are in dissociative disorders, and that positive and negative symptoms can appear in dissociative disorders too.¹²

Schizophrenia often comes with a trauma disorder. Across studies of anxiety disorders in schizophrenia, the pooled prevalence of PTSD was 12.4%, about one person in eight, with wide variation between samples.¹³

So some people with a schizophrenia diagnosis would be better described as having PTSD with psychotic features or a dissociative disorder, and others have both conditions at once. None of them is served by a clinician who stops listening once the word schizophrenia is in the chart.

Voices as dissociated parts of the self

The most developed version of the trauma argument is about voices. In a 2012 review in Psychological Bulletin, Eleanor Longden and colleagues noted that 1% to 16% of adults in nonclinical samples report hearing voices, that a voice’s location, content and frequency do a poor job of separating psychotic from other voice-hearing, and that voices are associated with dissociation and trauma, particularly childhood sexual abuse. They argued that voices, including those in psychotic disorders, are best understood as dissociated or disowned parts of the self.¹⁴ A 2015 meta-analysis of 19 studies found a large correlation between dissociation and voice-hearing (r = .52), while warning that most studies were cross-sectional and could not show which came first.¹⁵

That is the scientific version of what I was hearing at REACT. It also has limits. When Amy Hardy and colleagues compared trauma histories with hallucination content in 40 trauma-exposed people with psychosis, 12.5% had hallucinations that matched the themes and content of their trauma, 45% had hallucinations with the same themes but different content, and 42.5% showed no identifiable link. Sexual abuse and bullying were the traumas most often echoed.¹⁶ A 2023 network analysis of 248 people with schizophrenia spectrum disorders found that dissociative experiences formed a fairly separate cluster from the core psychotic symptoms, connected to them mainly through emotional distress.¹⁷ Some voices are dissociated parts. Not all of them are.

Two other lines of research suggest how trauma could shape a voice. Predictive-processing models, which I discuss in a profile of the neuroscientist Anil Seth, treat perception as the brain’s best guess about the causes of its input. In a 2017 Pavlovian experiment, people who hear voices were more susceptible to conditioned hallucinations, which the authors traced to perception leaning too heavily on prior expectation.¹⁸ Shitij Kapur’s aberrant salience model adds dopamine: when the dopamine system tags ordinary events and inner thoughts as urgently significant, delusions are the mind’s attempt to explain that feeling.¹⁹ In this model dopamine signals importance more than pleasure, which is also why the “dopamine detox” trend misreads the chemical. A childhood spent in danger builds strong expectations of threat, one plausible route from abuse to a voice that sounds like the abuser. It is a model, not a demonstrated mechanism.

The Hearing Voices Movement, which grew out of work by Marius Romme and Sandra Escher in the Netherlands in the late 1980s, starts from the same premise from the other direction: voices are meaningful human experiences to be understood, not only symptoms to be suppressed.^{20, 21} None of this is new to psychotherapy. Harry Stack Sullivan was publishing on a modified psychoanalytic treatment of schizophrenia by 1931,²² and his interpersonal theory of psychiatry treated mental illness as something lived out between people, not only inside one skull.

Spirits and machines: what delusion content can tell you

The second half of my REACT observation was about content. The patients with heavy trauma described spirits, possession and swapped souls; the others described chips, surveillance and algorithms. I still listen for that difference, but I no longer think it sorts people into trauma and genetic groups. The content of delusions follows the culture a person lives in, whatever caused the illness.

A study of 120 first-admission records at the psychiatric hospital in Ljubljana, Slovenia, from 1881 to 2000 found that delusions of outside influence and control, and delusions with technical themes, rose after radio spread in the 1920s and television in the 1950s. Persecution and self-reference rose after the change of political regime.²³ Joel Gold and Ian Gold described patients who believed their lives were being filmed and broadcast for other people’s entertainment, a “Truman Show” delusion, and argued that the broad categories of delusion stay stable across time and culture while the particular ideas follow the culture.²⁴ Vaughan Bell and colleagues were reporting “internet delusions” by 2005.²⁵ The internet has changed the vocabulary people use to make meaning, a shift I write about in The Search Bar and the Couch, and delusions draw on the same vocabulary.

The earlier version cited a real technology-delusion study through a broken link and garbled its numbers. Alaina Burns and colleagues reviewed the records of 228 adults with psychosis treated at one U.S. academic medical center between 2016 and 2024. Of the 201 whose records described delusions, 104 (51.7%) involved the internet or new technology, and each additional year was associated with about 15% higher odds of a technology delusion.²⁶ That is a rising trend among one center’s patients, not a 15% annual increase across psychiatry, and the study looked at age, gender and education, not at trauma or family history.

Psychiatry has seen this before. In 1810 Haslam’s Illustrations of Madness described James Tilly Matthews, who believed he was being controlled by an “air loom” worked by magnetically charged gases. In 1919 Victor Tausk gave the pattern a name in his paper on the “influencing machine,” which reached English readers in 1933 in Dorian Feigenbaum’s translation. Tausk described patients who attributed their thoughts, movements and bodily sensations to a remote apparatus, and he read the machine as a projection of the patient’s own body.^{27, 28} The machines change with each generation. The experience of being controlled from outside does not.

So content is a lead, not a test. If a person’s voices use an abuser’s words or talk about what happened, or if the sense of possession began around the time of a violation, that is a reason to ask carefully about trauma and dissociation, and in Hardy’s small study some thematic link turned up in more than half of the trauma-exposed patients. Technological content says little about cause; mostly it tells you what decade the person lives in. Spirits and demons are cultural too. In a devout family, possession may be the most available language for any frightening loss of control, whatever its source.

Shutdown or deficit: two kinds of flatness

Flatness is where getting this right matters most. In 1988 Carpenter and colleagues separated primary, enduring “deficit” symptoms from transient negative symptoms secondary to other factors, and argued that the secondary kind was more likely to respond to available treatment.²⁹ Kirkpatrick and colleagues later proposed that deficit schizophrenia may be a separate disease within the syndrome, differing in symptoms, course, biology, treatment response and risk factors, while noting that the findings needed independent replication.³⁰ Secondary negative symptoms can come from positive symptoms, depression, medication side effects, social deprivation or substance use.³¹

Trauma adds another candidate. In the defense cascade described by Kasia Kozlowska and colleagues, arousal comes first and then fight or flight; freezing is fight or flight put on hold, and tonic or collapsed immobility are last resorts when active defenses have failed.³² A related state, shutdown dissociation, in which sensory, motor and speech systems shut down under threat, can be measured in psychosis. Among 75 inpatients with schizophrenia spectrum disorders, Inga Schalinski and Martin Teicher found that the severity of shutdown dissociation was related to childhood but not adult trauma. The type and timing of childhood maltreatment accounted for 31% of its variance, vulnerability peaked at ages 13 to 14, and emotional neglect and emotional abuse were the strongest predictors.³³

Many therapists explain shutdown through polyvagal theory and its “dorsal vagal” brake. That language can be useful in a session, but its physiology is disputed, and Paul Grossman has argued that each of the theory’s five basic premises is untenable or highly implausible.³⁴ I read polyvagal theory through myth, as a story about shutdown and return, in Your Nervous System Is a Storyteller.

In practice, I watch for a few differences. Shutdown tends to fluctuate. It deepens around reminders and lifts, sometimes quickly, when the person feels safe, and it often hides an internal flood the person cannot show. Primary deficit symptoms are by definition enduring and move less with circumstance. These are observations to test over months, not a diagnostic rule, and one person can have both.

The same caution applies to the earlier post’s idea of “stormy” trauma onsets and “quiet” genetic ones. In a meta-analysis of young people at ultra high risk of psychosis, childhood trauma was very common, with a pooled prevalence of 86.8% across six studies, but in the four studies that measured them, recent life events were less common than in healthy controls, not more.³⁵ That does not fit a simple picture in which trauma-driven psychosis is set off by a fresh blow while genetic psychosis arrives quietly.

Medication, trauma therapy and what the evidence supports

The earlier version said antipsychotics “often make things worse” for trauma survivors. I know of no trial showing that. For PTSD with secondary psychotic features, a 2019 review found that only two second-generation antipsychotics, risperidone and quetiapine, had been tested in randomized trials, and that the evidence was not strong enough to recommend second-generation antipsychotics specifically for that condition.⁹ For schizophrenia itself, the relapse-prevention evidence is strong: across 65 trials, about 27% of people who stayed on medication relapsed within a year, against 64% on placebo.³⁶ Medication side effects are one recognized cause of secondary negative symptoms,³¹ which is a reason to review them with the prescriber, not a reason to stop.

Antipsychotics are also not simply dopamine blockers for a broken dopamine system. Until 2024 every approved treatment for schizophrenia blocked D2 dopamine receptors. Xanomeline-trospium, a muscarinic drug that does not, reduced symptoms more than placebo in a phase 3 trial and was approved in the United States on 26 September 2024.^{37, 38} The 2009 “version III” of the dopamine hypothesis treats stress and trauma, drug use, obstetric complications and genes as converging on increased dopamine function in the striatum,³⁹ and a small PET study found exaggerated dopamine release under psychosocial stress in people with schizophrenia and in people at clinical high risk.⁴⁰ So the earlier post’s idea that trauma can sensitize the same system antipsychotics act on is plausible. Its conclusion, that medication is beside the point for trauma survivors, is not.

Most PTSD trials have excluded people with psychosis. A Dutch randomized trial tested whether that caution is needed: 155 people with a psychotic disorder and PTSD received eight weekly sessions of prolonged exposure or EMDR, or waited. Both therapies reduced PTSD more than waiting, with no preliminary stabilization phase and no more serious adverse events than the waiting list.⁴¹ A secondary analysis found that both therapies also reduced paranoid thinking and that more patients reached remission from their psychotic disorder, while voices did not change.⁴² For persistent voices, AVATAR therapy, in which a person talks with a digital representation of their presumed persecutor voiced by the therapist, reduced voice severity more than supportive counselling at 12 weeks in a 2018 single-site London trial of 150 people. The authors called for larger multi-centre trials before treating it as established.⁴³

Brainspotting, Emotional Transformation Therapy and Internal Family Systems, which the earlier version recommended for trauma-driven psychosis, have no controlled trials in psychosis that I know of. Parts-based work fits the dissociative model of voices, and we use it carefully, but it is an extension of the evidence, not a tested treatment for psychosis. The earlier post also claimed a qEEG brain map can show whether a psychosis is trauma-driven or genetic. There is no good evidence that it can. A 1997 assessment by the American Academy of Neurology and the American Clinical Neurophysiology Society, since retired, classed quantitative EEG as investigational for schizophrenia,⁴⁴ and I know of no validated qEEG marker that separates trauma-related psychosis from other psychosis.

How the illness is explained matters too. A meta-analysis of 28 experiments found that biogenetic explanations of mental disorder reduce blame but increase pessimism about recovery.⁴⁵ That supports the earlier post’s worry that “your brain disease” can be a discouraging message. It does not make psychoeducation the problem: in a network meta-analysis of 90 trials, almost every family intervention reduced relapse, and family psychoeducation alone did better than more complex models.⁴⁶

The first version also said the patients with the heaviest trauma often had “the most dramatic recoveries.” The research points the other way: a meta-analysis found that childhood adversity was associated with psychotic symptoms persisting, though the evidence was limited and the studies varied widely.⁴⁷ The real ground for hope is broader. Across 79 studies of first-episode psychosis, 58% of people reached remission and 38% met criteria for recovery, and recovery rates held steady after the first two years, which suggests that steady deterioration is not the typical course.⁴⁸ Treating trauma matters even when it does not end the psychosis. It can make a hard illness less frightening to live with.

What this looks like in therapy

Therapy for psychosis with a trauma history starts with coordination. We work alongside the person’s psychiatrist or prescriber, not around them, and medication decisions stay with that prescriber.

The assessment takes longer than a symptom checklist. I ask about trauma directly, as the abuse meta-analysis above recommends. I ask about voices the way you would ask about people: how many there are, when each one started, how old they sound, whether any sounds like someone the person knows, what they say and when they get louder. In one small comparison study of 63 people, voices that began before age 18, more than two voices, child and adult voices together, and touch or visual experiences alongside them were more typical of dissociative identity disorder than of schizophrenia,⁴⁹ though no single feature settles the question. I also screen for dissociation, including lost time and depersonalization, and for PTSD.

Then comes pacing. For someone who is acutely psychotic, the first work is safety, sleep and stabilization with the treatment team. Once the person is stable enough, the Dutch trial suggests that PTSD treatment does not have to be postponed indefinitely. Between those points the work is often relational: getting curious about a voice instead of arguing with it, noticing which situations bring on shutdown, and building enough safety in the body that the person can stay present while talking about what happened. Grounding and somatic exercises are often part of this stage, and so is involving family when the person wants that.

What I try not to do is decide early that the voices are “just trauma” or “just illness.” The useful question is rarely which box a person belongs in. It is what their experiences are organized around, and what would make them less afraid.

If you or someone you love is in crisis, call or text 988, or see our crisis resources for Birmingham.

If you live with psychosis and a trauma history and want therapy that works alongside your psychiatric care, our page on dissociation therapy in Hoover describes how we approach dissociation and trauma, and you can contact us to ask whether we are a good fit.

References

1. Varese, F., Smeets, F., Drukker, M., Lieverse, R., Lataster, T., Viechtbauer, W., Read, J., van Os, J., & Bentall, R. P. (2012). Childhood adversities increase the risk of psychosis: A meta-analysis of patient-control, prospective- and cross-sectional cohort studies. Schizophrenia Bulletin, 38(4), 661–671. https://doi.org/10.1093/schbul/sbs050
2. Shevlin, M., Houston, J. E., Dorahy, M. J., & Adamson, G. (2008). Cumulative traumas and psychosis: An analysis of the National Comorbidity Survey and the British Psychiatric Morbidity Survey. Schizophrenia Bulletin, 34(1), 193–199. https://doi.org/10.1093/schbul/sbm069
3. Croft, J., Heron, J., Teufel, C., Cannon, M., Wolke, D., Thompson, A., Houtepen, L., & Zammit, S. (2019). Association of trauma type, age of exposure, and frequency in childhood and adolescence with psychotic experiences in early adulthood. JAMA Psychiatry, 76(1), 79–86. https://doi.org/10.1001/jamapsychiatry.2018.3155
4. Bonoldi, I., Simeone, E., Rocchetti, M., Codjoe, L., Rossi, G., Gambi, F., Balottin, U., Caverzasi, E., Politi, P., & Fusar-Poli, P. (2013). Prevalence of self-reported childhood abuse in psychosis: A meta-analysis of retrospective studies. Psychiatry Research, 210(1), 8–15. https://doi.org/10.1016/j.psychres.2013.05.003
5. Hilker, R., Helenius, D., Fagerlund, B., Skytthe, A., Christensen, K., Werge, T. M., Nordentoft, M., & Glenthøj, B. (2018). Heritability of schizophrenia and schizophrenia spectrum based on the nationwide Danish twin register. Biological Psychiatry, 83(6), 492–498. https://doi.org/10.1016/j.biopsych.2017.08.017
6. Sallis, H. M., Croft, J., Havdahl, A., Jones, H. J., Dunn, E. C., Davey Smith, G., Zammit, S., & Munafò, M. R. (2021). Genetic liability to schizophrenia is associated with exposure to traumatic events in childhood. Psychological Medicine, 51(11), 1814–1821. https://doi.org/10.1017/S0033291720000537
7. Brewin, C. R., Cloitre, M., Hyland, P., Shevlin, M., Maercker, A., Bryant, R. A., Humayun, A., Jones, L. M., Kagee, A., Rousseau, C., Somasundaram, D., Suzuki, Y., Wessely, S., van Ommeren, M., & Reed, G. M. (2017). A review of current evidence regarding the ICD-11 proposals for diagnosing PTSD and complex PTSD. Clinical Psychology Review, 58, 1–15. https://doi.org/10.1016/j.cpr.2017.09.001
8. Hamner, M. B., Frueh, B. C., Ulmer, H. G., & Arana, G. W. (1999). Psychotic features and illness severity in combat veterans with chronic posttraumatic stress disorder. Biological Psychiatry, 45(7), 846–852. https://doi.org/10.1016/s0006-3223(98)00301-1
9. Compean, E., & Hamner, M. (2019). Posttraumatic stress disorder with secondary psychotic features (PTSD-SP): Diagnostic and treatment challenges. Progress in Neuro-Psychopharmacology and Biological Psychiatry, 88, 265–275. https://doi.org/10.1016/j.pnpbp.2018.08.001
10. Kluft, R. P. (1987). First-rank symptoms as a diagnostic clue to multiple personality disorder. American Journal of Psychiatry, 144(3), 293–298. https://doi.org/10.1176/ajp.144.3.293
11. Ross, C. A., Miller, S. D., Reagor, P., Bjornson, L., Fraser, G. A., & Anderson, G. (1990). Schneiderian symptoms in multiple personality disorder and schizophrenia. Comprehensive Psychiatry, 31(2), 111–118. https://doi.org/10.1016/0010-440x(90)90014-j
12. Renard, S. B., Huntjens, R. J. C., Lysaker, P. H., Moskowitz, A., Aleman, A., & Pijnenborg, G. H. M. (2017). Unique and overlapping symptoms in schizophrenia spectrum and dissociative disorders in relation to models of psychopathology: A systematic review. Schizophrenia Bulletin, 43(1), 108–121. https://doi.org/10.1093/schbul/sbw063
13. Achim, A. M., Maziade, M., Raymond, E., Olivier, D., Mérette, C., & Roy, M.-A. (2011). How prevalent are anxiety disorders in schizophrenia? A meta-analysis and critical review on a significant association. Schizophrenia Bulletin, 37(4), 811–821. https://doi.org/10.1093/schbul/sbp148
14. Longden, E., Madill, A., & Waterman, M. G. (2012). Dissociation, trauma, and the role of lived experience: Toward a new conceptualization of voice hearing. Psychological Bulletin, 138(1), 28–76. https://doi.org/10.1037/a0025995
15. Pilton, M., Varese, F., Berry, K., & Bucci, S. (2015). The relationship between dissociation and voices: A systematic literature review and meta-analysis. Clinical Psychology Review, 40, 138–155. https://doi.org/10.1016/j.cpr.2015.06.004
16. Hardy, A., Fowler, D., Freeman, D., Smith, B., Steel, C., Evans, J., Garety, P., Kuipers, E., Bebbington, P., & Dunn, G. (2005). Trauma and hallucinatory experience in psychosis. Journal of Nervous and Mental Disease, 193(8), 501–507. https://doi.org/10.1097/01.nmd.0000172480.56308.21
17. Schlesselmann, A. J., Huntjens, R. J. C., Renard, S. B., McNally, R. J., Albers, C. J., De Vries, V. E., & Pijnenborg, G. H. M. (2023). A network approach to trauma, dissociative symptoms, and psychosis symptoms in schizophrenia spectrum disorders. Schizophrenia Bulletin, 49(3), 559–568. https://doi.org/10.1093/schbul/sbac122
18. Powers, A. R., Mathys, C., & Corlett, P. R. (2017). Pavlovian conditioning-induced hallucinations result from overweighting of perceptual priors. Science, 357(6351), 596–600. https://doi.org/10.1126/science.aan3458
19. Kapur, S. (2003). Psychosis as a state of aberrant salience: A framework linking biology, phenomenology, and pharmacology in schizophrenia. American Journal of Psychiatry, 160(1), 13–23. https://doi.org/10.1176/appi.ajp.160.1.13
20. Romme, M. A. J., & Escher, A. D. M. A. C. (1989). Hearing voices. Schizophrenia Bulletin, 15(2), 209–216. https://doi.org/10.1093/schbul/15.2.209
21. Corstens, D., Longden, E., McCarthy-Jones, S., Waddingham, R., & Thomas, N. (2014). Emerging perspectives from the Hearing Voices Movement: Implications for research and practice. Schizophrenia Bulletin, 40(Suppl. 4), S285–S294. https://doi.org/10.1093/schbul/sbu007
22. Sullivan, H. S. (1931). The modified psychoanalytic treatment of schizophrenia. American Journal of Psychiatry, 88(3), 519–540. https://doi.org/10.1176/ajp.88.3.519
23. Škodlar, B., Dernovšek, M. Z., & Kocmur, M. (2008). Psychopathology of schizophrenia in Ljubljana (Slovenia) from 1881 to 2000: Changes in the content of delusions in schizophrenia patients related to various sociopolitical, technical and scientific changes. International Journal of Social Psychiatry, 54(2), 101–111. https://doi.org/10.1177/0020764007083875
24. Gold, J., & Gold, I. (2012). The “Truman Show” delusion: Psychosis in the global village. Cognitive Neuropsychiatry, 17(6), 455–472. https://doi.org/10.1080/13546805.2012.666113
25. Bell, V., Grech, E., Maiden, C., Halligan, P. W., & Ellis, H. D. (2005). ‘Internet delusions’: A case series and theoretical integration. Psychopathology, 38(3), 144–150. https://doi.org/10.1159/000085845
26. Burns, A. V., Nelson, K., Wang, H., Hegarty, E. M., & Cohn, A. B. (2025). ‘The algorithm is hacked’: Analysis of technology delusions in a modern-day cohort. The British Journal of Psychiatry. Advance online publication. https://doi.org/10.1192/bjp.2025.10452
27. Tausk, V. (1933). On the origin of the “influencing machine” in schizophrenia (D. Feigenbaum, Trans.). The Psychoanalytic Quarterly, 2(3–4), 519–556. https://doi.org/10.1080/21674086.1933.11925189
28. Bokhari, S. A., Osman, A. A., Elnoor, M., Alnor, M. A., & Javaid, S. F. (2026). Technology-themed persecutory and related presentations of delusions in the digital age: Narrative review. JMIR Mental Health, 13, Article e102927. https://doi.org/10.2196/102927
29. Carpenter, W. T., Jr., Heinrichs, D. W., & Wagman, A. M. (1988). Deficit and nondeficit forms of schizophrenia: The concept. American Journal of Psychiatry, 145(5), 578–583. https://doi.org/10.1176/ajp.145.5.578
30. Kirkpatrick, B., Buchanan, R. W., Ross, D. E., & Carpenter, W. T., Jr. (2001). A separate disease within the syndrome of schizophrenia. Archives of General Psychiatry, 58(2), 165–171. https://doi.org/10.1001/archpsyc.58.2.165
31. Kirschner, M., Aleman, A., & Kaiser, S. (2017). Secondary negative symptoms: A review of mechanisms, assessment and treatment. Schizophrenia Research, 186, 29–38. https://doi.org/10.1016/j.schres.2016.05.003
32. Kozlowska, K., Walker, P., McLean, L., & Carrive, P. (2015). Fear and the defense cascade: Clinical implications and management. Harvard Review of Psychiatry, 23(4), 263–287. https://doi.org/10.1097/hrp.0000000000000065
33. Schalinski, I., & Teicher, M. H. (2015). Type and timing of childhood maltreatment and severity of shutdown dissociation in patients with schizophrenia spectrum disorder. PLOS ONE, 10(5), Article e0127151. https://doi.org/10.1371/journal.pone.0127151
34. Grossman, P. (2023). Fundamental challenges and likely refutations of the five basic premises of the polyvagal theory. Biological Psychology, 180, Article 108589. https://doi.org/10.1016/j.biopsycho.2023.108589
35. Kraan, T., Velthorst, E., Smit, F., de Haan, L., & van der Gaag, M. (2015). Trauma and recent life events in individuals at ultra high risk for psychosis: Review and meta-analysis. Schizophrenia Research, 161(2–3), 143–149. https://doi.org/10.1016/j.schres.2014.11.026
36. Leucht, S., Tardy, M., Komossa, K., Heres, S., Kissling, W., Salanti, G., & Davis, J. M. (2012). Antipsychotic drugs versus placebo for relapse prevention in schizophrenia: A systematic review and meta-analysis. The Lancet, 379(9831), 2063–2071. https://doi.org/10.1016/S0140-6736(12)60239-6
37. Kaul, I., Sawchak, S., Correll, C. U., Kakar, R., Breier, A., Zhu, H., Miller, A. C., Paul, S. M., & Brannan, S. K. (2024). Efficacy and safety of the muscarinic receptor agonist KarXT (xanomeline–trospium) in schizophrenia (EMERGENT-2) in the USA: Results from a randomised, double-blind, placebo-controlled, flexible-dose phase 3 trial. The Lancet, 403(10422), 160–170. https://doi.org/10.1016/S0140-6736(23)02190-6
38. Syed, Y. Y. (2025). Xanomeline/trospium chloride: First approval. Drugs, 85(1), 103–109. https://doi.org/10.1007/s40265-024-02126-0
39. Howes, O. D., & Kapur, S. (2009). The dopamine hypothesis of schizophrenia: Version III—The final common pathway. Schizophrenia Bulletin, 35(3), 549–562. https://doi.org/10.1093/schbul/sbp006
40. Mizrahi, R., Addington, J., Rusjan, P. M., Suridjan, I., Ng, A., Boileau, I., Pruessner, J. C., Remington, G., Houle, S., & Wilson, A. A. (2012). Increased stress-induced dopamine release in psychosis. Biological Psychiatry, 71(6), 561–567. https://doi.org/10.1016/j.biopsych.2011.10.009
41. van den Berg, D. P., de Bont, P. A., van der Vleugel, B. M., de Roos, C., de Jongh, A., Van Minnen, A., & van der Gaag, M. (2015). Prolonged exposure vs eye movement desensitization and reprocessing vs waiting list for posttraumatic stress disorder in patients with a psychotic disorder: A randomized clinical trial. JAMA Psychiatry, 72(3), 259–267. https://doi.org/10.1001/jamapsychiatry.2014.2637
42. de Bont, P. A., van den Berg, D. P., van der Vleugel, B. M., de Roos, C., de Jongh, A., van der Gaag, M., & van Minnen, A. M. (2016). Prolonged exposure and EMDR for PTSD v. a PTSD waiting-list condition: Effects on symptoms of psychosis, depression and social functioning in patients with chronic psychotic disorders. Psychological Medicine, 46(11), 2411–2421. https://doi.org/10.1017/s0033291716001094
43. Craig, T. K., Rus-Calafell, M., Ward, T., Leff, J. P., Huckvale, M., Howarth, E., Emsley, R., & Garety, P. A. (2018). AVATAR therapy for auditory verbal hallucinations in people with psychosis: A single-blind, randomised controlled trial. The Lancet Psychiatry, 5(1), 31–40. https://doi.org/10.1016/s2215-0366(17)30427-3
44. Nuwer, M. (1997). Assessment of digital EEG, quantitative EEG, and EEG brain mapping: Report of the American Academy of Neurology and the American Clinical Neurophysiology Society. Neurology, 49(1), 277–292. https://doi.org/10.1212/wnl.49.1.277
45. Kvaale, E. P., Haslam, N., & Gottdiener, W. H. (2013). The ‘side effects’ of medicalization: A meta-analytic review of how biogenetic explanations affect stigma. Clinical Psychology Review, 33(6), 782–794. https://doi.org/10.1016/j.cpr.2013.06.002
46. Rodolico, A., Bighelli, I., Avanzato, C., Concerto, C., Cutrufelli, P., Mineo, L., Schneider-Thoma, J., Siafis, S., Signorelli, M. S., Wu, H., Wang, D., Furukawa, T. A., Pitschel-Walz, G., Aguglia, E., & Leucht, S. (2022). Family interventions for relapse prevention in schizophrenia: A systematic review and network meta-analysis. The Lancet Psychiatry, 9(3), 211–221. https://doi.org/10.1016/S2215-0366(21)00437-5
47. Trotta, A., Murray, R. M., & Fisher, H. L. (2015). The impact of childhood adversity on the persistence of psychotic symptoms: A systematic review and meta-analysis. Psychological Medicine, 45(12), 2481–2498. https://doi.org/10.1017/s0033291715000574
48. Lally, J., Ajnakina, O., Stubbs, B., Cullinane, M., Murphy, K. C., Gaughran, F., & Murray, R. M. (2017). Remission and recovery from first-episode psychosis in adults: Systematic review and meta-analysis of long-term outcome studies. The British Journal of Psychiatry, 211(6), 350–358. https://doi.org/10.1192/bjp.bp.117.201475
49. Dorahy, M. J., Shannon, C., Seagar, L., Corr, M., Stewart, K., Hanna, D., Mulholland, C., & Middleton, W. (2009). Auditory hallucinations in dissociative identity disorder and schizophrenia with and without a childhood trauma history: Similarities and differences. Journal of Nervous and Mental Disease, 197(12), 892–898. https://doi.org/10.1097/nmd.0b013e3181c299ea