recent research study about schizophrenia and dissociative disorders

Dissociation in Psychiatric Disorders: A Meta-Analysis of Studies Using the Dissociative Experiences Scale

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recent research study about schizophrenia and dissociative disorders

Diagnostic Group	k	N	Mean DES Score	95% CI	I (%)
Dissociative identity disorder	29	1,313	48.7	46.4, 50.9	77.9
Dissociative disorders	70	3,073	38.9	36.1, 41.6	95.3
Posttraumatic stress disorder	33	2,106	28.6	25.6, 31.5	96.9
Borderline personality disorder	27	1,705	27.9	25.3, 30.6	89.2
Conversion disorder	20	857	25.6	21.5, 29.7	93.4
Depersonalization/derealization disorder	16	759	25.1	22.7, 27.4	80.2
Anorexia nervosa	6	253	24.1	16.3, 31.9	92.9
Bulimia nervosa	8	353	22.0	16.9, 27.0	90.5
Gambling disorder	4	187	19.9	7.9, 31.8	98.5
Alcohol use disorder	12	1,467	19.7	16.5, 23.0	97.5
Somatic symptom disorder	4	132	18.8	16.4, 21.2	16.1
Feeding and eating disorders	24	1,401	18.6	16.0, 21.2	91.6
Schizophrenia	17	594	17.8	15.6, 20.2	80.5
Other substance-related disorders	14	1,107	17.7	14.7, 20.7	91.9
Panic disorder	11	319	15.6	10.8, 20.4	94.9
Obsessive-compulsive disorder	14	858	15.3	13.2, 17.4	80.3
Depressive disorders	12	833	15.3	11.2, 19.4	98.1
Anxiety disorders	19	615	15.2	12.4, 18.0	93.1
Bipolar and related disorders	7	208	14.8	8.8, 20.8	97.3
Total	216	15,219

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Dissociative Disorders
Posttraumatic Stress Disorder
Borderline Personality Disorder
Meta-Analysis
Dissociative Experience Scale

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Schizophrenia, dissociation, and consciousness

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1 Center for Neuropsychiatric Research of Traumatic Stress, Department of Psychiatry and UHSL, 1st Faculty of Medicine, Charles University, Prague, Czech Republic. [email protected]
PMID: 21602061
DOI: 10.1016/j.concog.2011.04.013

Current thinking suggests that dissociation could be a significant comorbid diagnosis in a proportion of schizophrenic patients with a history of trauma. This potentially may explain the term "schizophrenia" in its original definition by Bleuler, as influenced by his clinical experience and personal view. Additionally, recent findings suggest a partial overlap between dissociative symptoms and the positive symptoms of schizophrenia, which could be explained by inhibitory deficits. In this context, the process of dissociation could serve as an important conceptual framework for understanding schizophrenia, which is supported by current neuroimaging studies and research of corollary discharges. These data indicate that the original conception of "split mind" may be relevant in an updated context. Finally, recent data suggest that the phenomenal aspects of dissociation and conscious disintegration could be related to underlying disruptions of connectivity patterns and neural integration.

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Dissociative Identity Disorder and Schizophrenia

First Online: 20 January 2024

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Sindhura Kompella 3 &
Shivani Kaushal 4

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Dissociative identity disorder (DID) and schizophrenia have many similarities and some key differences, which are very important to ensure proper diagnosis and plan of care for patients. This chapter focuses on risk factors, diagnosis, treatment options, and notes the key similarities and differences for clinicians to render proper treatment for this population group.

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Kompella, S., Kaushal, S. (2023). Dissociative Identity Disorder and Schizophrenia. In: Tohid, H., Rutkofsky, I.H. (eds) Dissociative Identity Disorder. Springer, Cham. https://doi.org/10.1007/978-3-031-39854-4_15

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Recent advances in understanding schizophrenia

Chiara s haller, jaya l padmanabhan, paulo lizano, john torous, matcheri keshavan.

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Schizophrenia is a highly disabling disorder whose causes remain to be better understood, and treatments have to be improved. However, several recent advances have been made in diagnosis, etiopathology, and treatment. Whereas reliability of diagnosis has improved with operational criteria, including Diagnostic and Statistical Manual of Mental Disorders , (DSM) Fifth Edition , validity of the disease boundaries remains unclear because of substantive overlaps with other psychotic disorders. Recent emphasis on dimensional approaches and translational bio-behavioral research domain criteria may eventually help move toward a neuroscience-based definition of schizophrenia. The etiology of schizophrenia is now thought to be multifactorial, with multiple small-effect and fewer large-effect susceptibility genes interacting with several environmental factors. These factors may lead to developmentally mediated alterations in neuroplasticity, manifesting in a cascade of neurotransmitter and circuit dysfunctions and impaired connectivity with an onset around early adolescence. Such etiopathological understanding has motivated a renewed search for novel pharmacological as well as psychotherapeutic targets. Addressing the core features of the illness, such as cognitive deficits and negative symptoms, and developing hypothesis-driven early interventions and preventive strategies are high-priority goals for the field. Schizophrenia is a severe, chronic mental disorder and is among the most disabling disorders in all of medicine. It is estimated by the National Institute of Mental Health (NIMH) that 2.4 million people over the age of 18 in the US suffer from schizophrenia. This illness typically begins in adolescence and derails the formative goals of school, family, and work, leading to considerable suffering and disability and reduced life expectancy by about 20 years. Treatment outcomes are variable, and some people are successfully treated and reintegrated (i.e. go back to work). Despite the effort of many experts in the field, however, schizophrenia remains a chronic relapsing and remitting disorder associated with significant impairments in social and vocational functioning and a shortened lifespan. Comprehensive treatment entails a multi-modal approach, including psychopharmacology, psychosocial interventions, and assistance with housing and financial sustenance. Research to date suggests a network of genetic, neural, behavioral, and environmental factors to be responsible for its development and course. This article aims to summarize and explain recent advancements in research on schizophrenia, to suggest how these recent discoveries may lead to a better understanding and possible further development of effective therapies, and to highlight the paradigm shifts that have taken place in our understanding of the diagnosis, etiopathology, and treatment.

Historical background and diagnosis

The concept of schizophrenia as a disease entity has undergone major changes over the past century. Kraepelin distinguished chronic psychoses from functional decline, which he termed dementia praecox, and episodic psychoses, which he called the manic-depressive insanity [ 1 ]. Subsequent literature pointed to considerable symptomatic overlap between these disorders, leading to the rather loosely defined, and therefore unreliable, diagnosis of schizoaffective disorder [ 2 ]. Over the past century, these categories have—to a large extent—remained the same, as summarized in the current classificatory systems: the DSM and the International Classification of Diseases (ICD) [ 3 ].

A noteworthy recent development in psychiatry was the release of the fifth edition of the DSM in 2013. Although no major changes were made to the definitions of schizophrenia and other psychotic disorders, efforts were made to increase simplicity of diagnoses. First, the Kraepelinian subtyping of schizophrenia into paranoid, disorganized, catatonic, and undifferentiated type was eliminated because of a lack of evidence supporting the validity of these distinctions. Second, catatonia was moved to become a specifier across diagnoses rather than a schizophrenia subtype. Third, a more longitudinal approach to this diagnosis was defined. Finally, the previous emphasis on Schneider's [ 4 ] “first rank” symptoms (i.e. delusions of thought broadcast and thought insertion) and bizarre delusions was eliminated. Although all this improved the ease of use of the criteria, the validity of these boundaries remained largely in question.

Over the past two decades, it has become increasingly clear that there are neurobiological [ 5 ], genetic [ 6 ], and treatment response [ 7 ] overlaps between these disorders, bringing into question the validity of these categories [ 8 ]. A dimensional approach to psychopathology and the view that biological impairments may cut across categories have led to the recent introduction of the research domain criteria (RDoC). RDoC [ 9 ] refers to a framework of representing accruing information across molecular, cellular, circuit, and behavioral domains agnostic to symptom-based diagnoses. Although this approach is still in its infancy, it might offer a useful framework for future research that may yield a neuroscience-informed classificatory system [ 8 ].

There has also been interest in defining schizophrenia beyond the symptoms listed in the DSM, with recent consideration of cognitive decline as a core feature with psychosis considered by some as a later development [ 10 , 11 ]. Along these lines, there have also been significant efforts to better understand and characterize schizophrenia at earlier stages of the illness with the concept of schizophrenia prodome, which became of increasing clinical interest [ 12 ]. Schizophrenia prodrome, sometimes referred to as ultra-high-risk state or psychosis risk syndrome, is thought to be a spectrum of attenuated positive and negative symptoms that individuals may display several years to months before converting to schizophrenia.

Recent research has begun to elucidate risk factors for conversion to psychosis, including early impaired cognitive (e.g. inattention, concentration difficulties) and social functioning [ 13 ]. Even though not all risk factors are currently known, approximately 35% of the individuals with prodromal symptoms convert to schizophrenia [ 14 , 15 ]. The North American Prodromal Longitudinal Study, a large multicenter study, has begun to demonstrate substantive neuroanatomical [ 16 ], neurophysiological [ 17 ], neurocognitive [ 18 ], and neurohormonal [ 19 ] changes during the prodromal phase that may contribute to the risk of schizophrenia [ 20 ].

Pathophysiology and etiology

Schizophrenia has a substantial genetic component, with a high heritability (up to 80%), indicating that about 80% of the variation in the trait of schizophrenia may be attributed to genetic factors [ 21 ]. Genome-wide association studies (GWASs), which compare the genomes of thousands of healthy and affected individuals, have found several genes associated with increased risk of developing schizophrenia, such as NRGN and ZNF804A [ 22 , 23 ]. Recent research suggests that genetic risk for schizophrenia is composed of many common genetic alterations, each with a small effect, along with a few uncommon genetic alterations with a larger impact [ 24 ]. Additionally, genes that confer risk for schizophrenia may also be associated with bipolar disorder and other psychiatric disorders [ 25 ] ( Figure 1 ).

Figure 1. Etiology of schizophrenia.

The multifactorial etiology of schizophrenia including a) rare genes that have a large effect, b) common genes that have a small effect, and c) the environmental factors and gene-environmental interactions that confer risk for schizophrenia.

Various environmental factors may interact with susceptibility genes to increase the risk of schizophrenia; these interactions are the focus of an emerging area of investigation called epigenetics. One of the few replicated findings in this relatively new field is an interaction between cannabis use and the AKT1 gene on the risk of psychosis [ 26 , 27 ]. Other findings in epigenetics that have not yet been replicated include interactions between a history of fetal hypoxia and hypoxia-related genes on volume of the hippocampus [ 28 ] and interactions between childhood trauma and variants of the serotonin transporter [ 29 ] and COMT gene [ 27 ] on cognitive functioning. Although epigenetics research has the potential to greatly impact clinical practice, few studies have attempted to replicate findings. Among those studies attempting replication, few have been able to confirm previous findings, implying possible publication bias and a need for larger sample sizes in this type of research [ 30 ].

Although early neurobiological theories of schizophrenia largely focused on excessive dopamine, more recent research reflects a more nuanced role of dopamine and has pointed to the importance of other neurotransmitters such as GABA and glutamate. Recent animal models [ 31 ] and genetic studies of humans [ 32 ] suggest that hypofunction of the N-methyl-D-aspartate (NMDA) glutamatergic receptor may underlie schizophrenia. Glutamate models of schizophrenia may provide an additional explanation to the dopaminergic models for the cognitive symptoms of this illness and may ultimately yield novel pharmacological treatment approaches [ 33 ].

Neuropathology research indicates that schizophrenia is characterized by abnormal maturation of prefrontal networks during late adolescence and early adulthood, likely due to excessive pruning of synapses and dendritic spines [ 34 , 35 ]. Pre- and post-synaptic abnormalities in inhibitory neurons such as the parvalbumin interneuron may disturb these critical neurodevelopmental processes [ 36 ]. Recent research using optogenetics indicates that parvalbumin interneurons may influence gamma oscillations, which in turn are associated with cognitive function [ 37 ]. Myelination (another critical neurodevelopmental process) is also abnormal in schizophrenia, as shown by post-mortem studies demonstrating reduced expression of myelin basic protein in cortical regions [ 38 ]. Disturbances in both myelination and the inhibitory control of synaptic pruning may contribute to cognitive deficits in schizophrenia [ 39 ]. These recent advances in neuropathology build upon previous post-mortem research demonstrating reduced neuropil, but not a reduced number of neurons, in the brains of adults with schizophrenia [ 40 ].

Recent studies have shown compelling evidence that neuropathological changes in schizophrenia might set in during the critical period of adolescence, proximal to the onset of psychosis. Gray-matter declines appear to occur in the early phase of schizophrenia and may be related to poorer outcomes. The early phase of psychosis may also be associated with elevations in presynaptic dopamine turnover [ 41 ] as well as increases in glutamatergic activity [ 42 ]. These observations highlight the importance of early recognition and intervention targeted to the pathophysiological processes close to the onset of psychosis.

In the past several years, inflammation and oxidative stress have re-emerged as potentially important aspects of pathophysiology in a subset of affected individuals. Multiple studies have demonstrated elevated levels of cytokines and other signs of immune system activation in individuals with psychosis [ 43 , 44 ], and genetic studies have reported correlations between schizophrenia and genes involved in the immune response [ 23 ]. Recent rodent work has observed that exposure to infectious or inflammatory agents in utero can lead to behavioral and neurobiological alterations resembling those seen in schizophrenia [ 45 ]. Oxidative stress, which is associated with inflammation, may also be elevated in schizophrenia. For example, a recent meta-analysis of studies on oxidative stress markers observed reduced levels of the anti-oxidant red blood cell superoxide dismutase in schizophrenia [ 46 ].

Additionally, some recent work has focused on autoimmune dysfunction as a cause of psychosis. For example, anti-NMDA-receptor encephalitis is a potentially treatable but under-diagnosed cause of psychosis that results from the production of antibodies against NMDA receptors [ 47 ]. A number of young individuals presenting with their first episode of psychosis may have detectable auto-antibodies against this receptor or other neuronal proteins, such as voltage-gated potassium channels [ 48 ]. In addition, epidemiological data suggest a bi-directional association between psychosis and some common autoimmune diseases: individuals with one type of illness are at greater risk of developing the other type [ 49 ]. The potential therapeutic applications of these findings are being actively explored.

Various forms of imaging research have been critical in advancing our understanding of the neurobiology of schizophrenia. Studies have reported subtle structural alterations, including enlargement of the third and lateral ventricles, slight reductions in whole-brain gray matter volume, and slight reductions in the volumes of temporal, frontal, and limbic regions [ 50 , 51 ]. Functional imaging studies have observed reduced activation of the dorsolateral prefrontal cortex during tasks of executive function [ 52 ] and abnormalities of limbic system activation during tasks involving emotional stimuli [ 53 ]. In addition, studies using diffusion tensor imaging, a method of visualizing white matter, have found evidence of white matter changes in frontal and temporal lobes that would imply decreased connectivity among these regions [ 54 ]. Together, these findings support the conceptualization of schizophrenia as a disorder of brain connectivity [ 55 ]. Studies in the past few years have used various forms of network analysis to uncover decreased regional connectivity in both first-episode schizophrenia [ 56 ] and the broader psychotic spectrum.

The next major challenge is to translate neuroimaging findings into the clinical setting. Consequently, recent research has started to integrate various imaging modalities with genetic, electrophysiological, and clinical data to identify biomarkers, which may eventually be relevant for clinical diagnosis and management.

Pharmacological treatments in schizophrenia

Antipsychotic drugs have been the mainstay of schizophrenia treatment since the introduction of chlorpromazine, focusing on decreasing the frequency and severity of psychotic episodes as well as improving the functional capacity of individuals with schizophrenia [ 57 ]. However, adverse effects and suboptimal outcomes associated with first-generation antipsychotics (FGAs) led to the development of second-generation antipsychotics (SGAs), which due to their 5HT-2A antagonism are generally associated with reduced extrapyramidal symptoms (EPSs) as compared with FGAs [ 58 ]. However, there is controversy concerning the categorization of FGA and SGAs; some literature differentiates them based on their ability to cause EPSs, whereas other studies base it on their antagonism of the dopamine D-2 receptors [ 59 , 60 ]. The first and most efficacious SGA for the treatment of refractory schizophrenia, clozapine, is limited by the risk of agranulocytosis, which necessitates the use of periodic monitoring of blood cell counts. EPSs are lowest with clozapine and highest with haloperidol. All drugs except haloperidol, ziprasidone, and lurasidone produce more weight gain, with olanzapine and clozapine producing the greatest weight gain. Prolactin elevation is highest with risperidone and paliperidone. All drugs, except for amisulpride, paliperidone, sertindole, and iloperidone, are significantly more sedating than placebo [ 61 ].

Several large-scale investigations suggest no clear superiority of SGAs over FGAs among first-episode patients [ 62 ] or chronic patients [ 63 ] in regard to positive, cognitive or social outcomes [ 64 ]. Furthermore, both FGAs and SGAs do not sufficiently target negative symptoms (with only olanzapine and asenapine showing moderate effects [ 65 - 67 ]) and sometimes insufficiently treat positive symptoms [ 68 , 69 ]. Clozapine seems to be the most effective medicine, whereas the effectiveness of olanzapine and risperidone over other antipsychotics remains controversial [61, 70-72]. In terms of relapse prevention, SGAs have a modest benefit compared with FGAs [ 73 ]. Newer antipsychotics such as asenapine, iloperidone, lurasidone, and paliperidone do not seem to be significantly better than haloperidol [ 61 ], and for the treatment of refractory schizophrenia, clozapine has been shown to be significantly more efficacious than other agents [ 74 - 78 ]. However, several studies suggest that olanzapine and risperidone have greater efficacy over other antipsychotics, but this remains controversial and more research is necessary in this area. Additionally, amisulpride, olanzapine, clozapine, paliperidone, and risperidone show significantly lower all-cause discontinuation than several other agents [61, 79-81]. The Schizophrenia Patient Outcome Research Team (PORT) summarized strong empirical support for both FGAs and SGAs in acute and maintenance treatment of schizophrenia and for the use of clozapine for treatment-resistant positive symptoms, hostility, and suicidal behaviors [ 82 ].

Research over the past decade further investigated agents that stimulate the NMDA glutamate receptor, including partial and full agonists at the glycine site and glutamate 2/3 receptor agonists, and found that they may ameliorate negative symptoms with some success if used in conjunction with antipsychotics [ 83 ]. The PORT concludes, however, that there is still limited information on the use of adjunctive pharmacological agents as well as the treatment of co-occurring substance abuse [ 82 ]. None of the pharmacological agents to date effectively ameliorate cognitive deficits, which are a core feature of schizophrenia; larger and more rigorous studies are needed to examine the potential pro-cognitive effects of medications that impact dopaminergic, nicotinergic, glutamatergic, GABAergic, and other novel targets [ 84 ].

Long-acting injectable antipsychotics are helpful in treating patients with poor medication adherence and have more controlled distributions in the body; for these reasons, they are superior to oral antipsychotics in preventing hospitalizations [ 85 ] and may foster a better therapeutic alliance. Both FGA (haloperidol and fluphenazine) and SGA (risperidone, paliperidone, olanzapine, and aripiprazole) medications are now available as long-acting preparations. Recent preliminary investigations suggest a therapeutically beneficial response to dose reduction and alternate day dosing [ 86 ] in the early stages of remitted first-episode psychosis. However, more research is needed to confirm these observations [ 87 ].

Recent advances in the understanding of schizophrenia have restored interest in inflammatory and oxidative stress pathways as the pathogenesis for a subset of patients. Research on human and animal models supports this new insight [ 88 - 93 ]. In a review by Sommer et al ., 26 double-blind randomized controlled trials reported on the efficacy of anti-inflammatory agents such as aspirin, celecoxib, davunetide, fatty acids (eicosapentaenoic acids and docosahexaenoic acids), estrogens, minocycline, and antioxidants such as N -acetylcysteine (NAC) as treatment augmentation for schizophrenia [ 94 ]. Aspirin, estrogens, and NAC showed significant effects; in contrast, celecoxib, minocycline, davunetide, and fatty acids showed no significant difference [ 95 ]. Whereas more research is needed to investigate the therapeutic effects of both current and novel anti-inflammatory agents, current evidence does suggest a benefit in treating inflammation.

Pharmacogenomics is a growing field in the treatment of schizophrenia and can bring the field of psychiatry closer to achieving evidence-based personalized medicine with the goals of predicting better treatment response and reducing medication-induced side effects. For example, polymorphisms in the serotonergic system are associated with the efficacy of clozapine and risperidone, dopamine D 3 receptor polymorphisms are associated with response to clozapine and olanzapine, and D 2 variants are associated with the efficacy of risperidone [ 96 ]. As for side effects, the serotonergic system (HTR2C) and hypothalamic leptin-melanocortin genes (MC4R) can predict antipsychotic-induced weight gain [ 97 , 98 ], cytochrome P450 (CYP2D6) and dopamine receptor variants are associated with tardive dyskinesia [ 96 , 99 ], and major histocompatibility complex (human leukocyte antigen [HLA]) markers have been consistently found to be associated with clozapine-induced agranulocytosis. However, despite progress made in pharmacogenomics, the field has encountered obstacles such as replication inconsistencies, small study sizes, and lack of randomized control trials.

Psychosocial treatments

Antipsychotic medications are a necessary but not sufficient treatment for schizophrenia. The broad objectives of treatment should be reducing the frequency and severity of episodes of psychotic exacerbation as well as improving the functional capacity and quality of lives of the individuals afflicted with the illness. Thus, in tandem with research over the past decades, the urgently needed multimodal care has continued to evolve. Psychoanalytic treatments beginning in the early 20th century seemed to insufficiently address the burden caused by the illness. In the early ’60s, major role therapy and family psychoeducation were introduced based on the interpersonal and family theories of psychosis. With further research in the field and increased knowledge about the nature of the specific deficits (cognitive, social, and affective), more disease-specific psychotherapies started to develop in the ’80s and ’90s. These therapies target both pathophysiology and other core manifestations of the disease.

The PORT recently provided an extensive summary of the current evidence-based psychosocial treatment [ 100 ]. Cognitive behavioral therapy (CBT) is based on the theory that the way we interpret events has cognitive, emotional, and behavioral consequences, which lead to the creation and maintenance of unhelpful responses. CBT has been a successful approach for other mental illnesses such as depression [ 101 ] and anxiety [ 102 ]. More recently, CBT has been applied to the treatment of positive as well as negative symptoms. Research shows that CBT can improve positive symptoms [ 103 , 104 ] but is less consistent with the improvement of negative symptoms [ 105 , 106 ]. A recent review shows that CBT may mostly be efficient in the short term (i.e. more than 12 months) [ 107 ].

Social skills training (SST) is based on a behavioral model that targets the improvement of a person's ability to function skillfully in social situations (i.e. interactions). SST has emerged among the possible treatments for schizophrenia [ 108 ] to address social skill deficits primary to developmental derailments but also secondary due to both positive and negative symptoms [ 109 ]. SST has been found to improve both positive and negative symptoms [ 106 ], and some of the improvements may persist at follow-up [ 110 ].

Family therapy is based on a model that suggests that problematic behaviors are maintained and created by patterns in systems (i.e. proximal or distal family) [ 111 ]. System theory underlies the multifamily treatment approach that includes coping recommendations, problem solving, crisis intervention, reduction of pathogenic interactions such as high “expressed emotions” (e.g. criticism, hostility), and (in its core) psychoeducation. Psychoeducation enables not only the patient but also the family and others to recognize early warning signs, which is particularly important in an illness that shows such high vulnerability to stress.

Assertive community treatment (ACT) offers a multidisciplinary approach that is usually combined with SST, CBT, or any personal support. Teams include peer support specialists and practitioners with expertise in psychiatry, substance abuse treatment, and employment. Although ACT reduces time in the hospital for mental illnesses in general [ 112 ], it seems specifically to improve housing stability [ 113 ] and reduce hospitalization rates, especially in patients with higher baseline hospitalization rates [ 113 ].

Personal therapy was developed by Hogarty et al . [ 114 ] on the basis of supportive psychotherapy. It is one of the few approaches that was designed specifically for people suffering from schizophrenia and combines SST with some common elements of CBT. Personal therapy is modeled to the phases of recovery; thus, it is a long-term endeavor and seems to decrease the probability of relapse [ 115 ].

Cognitive remediation therapy (CRT) is a computer-based intervention that was originally designed to improve deficient cognitive abilities (e.g. attention, memory, and executive function) in people with traumatic brain injury [ 116 ] but since has proven to help in people with depression [ 117 ], eating disorders [ 118 ], and schizophrenia [ 117 ]. Whereas CRT by itself has no effect on improving negative symptoms [ 119 ], the combination of CRT with SST, groups, and problem solving has been found to be promising [ 120 ]. Although preliminary results showed improvements in speed of processing, attention, working memory, executive function, and social cognition in a cognitive enhancement therapy (CET) compared with a personal therapy group, rigorous validation is needed, and the durability of these improvements remains to be investigated.

For many patients the ability to resume work or school is the ultimate goal. Thus, supported employment interventions are of significant importance – the most commonly studied being the Individual Placement and Support (IPS) [ 121 ] model. An important principle of the IPS model is that minimal pre-vocational training is provided, and the job itself becomes the primary training environment. There is clear evidence that supported employment strategies help return people with schizophrenia to work [ 122 ], even for young people with their first episode of psychosis [ 123 ]. A recent meta-analysis of a total of 11 studies found that competitive employment rates were 61% for patients and 23% for controls and that about 30% out of the 61% worked more than 20 hours weekly. Supported employment further increased the duration of employment (47% of the 52-week year) and the time of onset of employment (approximately 10 weeks earlier than controls). In conclusion, the effect sizes support the effectiveness of evidence-based supported employment as one of the most robust interventions.

Given the clinical heterogeneity of schizophrenia, it is important to choose the right treatment for the right patient; thus, although supportive treatment might benefit all symptom domains, CBT may be particularly beneficial for those with residual psychotic symptoms and cognitive remediation, SST for those with cognitive or social cognition deficits or both, and ACT for those at risk for frequent hospitalizations or those who have had recent homelessness. There is increasing emphasis on tailoring psychotherapeutic interventions to the phase of the illness (e.g. personal therapy), since the primary goals of intervention might vary across phases. More research is needed, however, to examine active ingredients of the therapeutic modalities that work and to identify the synergistic effects of combinations of interventions that are hypothesis-driven and cost-effective.

Conclusions and Future directions

In summary, although our understanding of the causes and treatments of schizophrenia remains limited, several important paradigm shifts have occurred. The diagnosis of schizophrenia is still symptom-based, but increasing amounts of data point to the large genetic and neurobiological overlaps between psychotic, affective, and developmental disorders, suggesting that future classifications of these illnesses need to move toward more evidence-based, valid, and biologically based categories and dimensions. Pathophysiology is now seen as developmentally mediated alterations in neuroplasticity, manifesting in a cascade of neurotransmitter and circuit dysfunctions setting in around adolescence. Etiology is now seen as an interaction between multiple genes of small-effect and some rare large-effect genes and unknown environmental factors. These observations may help therapeutic interventions move beyond the current sole focus on dopamine toward novel therapeutic targets such as glutamate, GABA, and calcium channels. The focus of intervention has expanded beyond relief of psychotic symptoms alone toward restoring functionality by targeting dimensions such as cognitive deficits and negative symptoms. Research is intensifying on the possible utility of several evidence-based psychotherapy modalities in combination with pharmacological approaches. Treatments are still based on serendipitous discoveries from decades ago, and the urgent need is to discover novel interventions based on etiopathology. Finally, recent incremental advances in understanding the etiopathology have motivated vigorous prevention approaches in early phases of the illness and early interventions with novel pharmacological targets and plasticity-based treatments such as cognitive remediation.

Acknowledgments

We would like to thank all the patients that allow us to learn from them, all the collaborators who are doing terrific clinical work, and all the researchers who help us gain better insight.

Abbreviations

assertive community treatment

cognitive behavioral therapy

cognitive remediation therapy

Diagnostic and Statistical Manual of Mental Disorders

extrapyramidal symptom

first-generation antipsychotic

Individual Placement and Support

N -acetylcysteine

N-methyl-D-aspartate

Schizophrenia Patient Outcome Research Team

research domain criteria

second-generation antipsychotic

social skills training

Disclosures

This work was supported in part by National Institutes of Health grants MH 64023, 60902, 78113, and 92440 (MSK).

The electronic version of this article is the complete one and can be found at: http://f1000.com/prime/reports/m/6/57

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Attachment in Schizophrenia—Implications for Research, Prevention, and Treatment

Susanne harder.

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*To whom correspondence should be addressed; Department of Psychology, Oester Farimagsgade 2A, 1353 Copenhagen K, Denmark; tel: +45-35-32-49-07, fax: 45-35-32-48-02, e-mail: [email protected]

Issue date 2014 Nov.

Attachment is a promising area for elucidating psychosocial mechanisms important for development, prevention, and treatment of schizophrenia. This report gives a short summary of studies of attachment in psychosis. It was found that dismissing and disorganized forms of attachment were over-represented in psychosis. Evidence pointed to associations between a dismissing attachment pattern and positive psychotic symptoms, negative symptoms, and poor engagement with services. Furthermore, insecure attachment was found to predict impaired recovery from negative symptoms. Possible major risk processes in development linking dismissing attachment to symptom development were externalizing and deactivation of affects and poor mentalization. For a disorganized form of attachment, possible risk mechanisms were heightened stress-sensitivity and dissociation. Based on this initial evidence, further research in attachment in psychosis focusing on these risk mechanisms seems warranted. In addition, the evidence supported a focus on attachment-related risk processes to enhance the prevention and treatment of psychosis.

Key words: dismissing attachment, negative symptoms, disorganized attachment, stress-sensitivity, psychological treatment

Introduction

The crucial importance of attachment for normal development has long been acknowledged as attested in a large and rapidly growing body of research. 1 The developmental psychopathology approach and the new Research Domain Criteria (RDoC) approach, proposed by the American National Institute of Mental Health, both stress the importance of studying risk development in domains important for normal development. Nonoptimal forms of attachment have been found to be involved in the development of several mental disorders, such as borderline personality disorder (BPD) and depression. 1 Taken together, this makes attachment a promising area for elucidating psychosocial mechanisms important for the development of schizophrenia. Following the RDoC approach, the association between attachment and the broader psychosis domain, not only schizophrenia proper, will be discussed.

The core contribution of the attachment approach is the understanding of the unique quality of the tie between a parent and a child established through the infants first 1–2 years of life. 2 Through attachment relationships, strong emotional bonds between infants and primary caregivers are formed, which can then lead the infant to experience distress and separation anxiety when separated. This distress can only be repaired by reunion with the attachment figures, not by any other caregiver. According to attachment theory, humans have an evolution-based need for attachment, which serve the purpose of increasing survival through securing the infant’s physical closeness to the caregiver and providing optimal conditions for the cognitive and socioemotional development. It is the specific qualities of the attachment relationship, where the caregiver can serve as a secure base for exploration and as a safe haven for the regulation of distress and negative emotions, which is crucial for optimal development. The infant’s experiences in attachment relationships lead eventually to the development of an inner working model for affect regulation, exploration, and interpersonal functioning, an attachment pattern, which tends to be relatively stable over time.

Subtypes of Attachment

Three organized patterns of attachment have been described, secure, insecure dismissing and insecure preoccupied. 3 These patterns are understood as adaptations to the type of care provided, with the purpose of maintaining the caregiver’s protection. Secure attachment is characterized by adaptive affect regulation, an ability to be emotionally close and yet autonomous in interpersonal relationships and high levels of mentalization, ie, the ability to understand mental states. This is the result of early interactions with caregivers, who are sensitive to the infant’s need for both exploration and resolution of distress and anxiety.

In dismissing attachment , adults tend to deactivate emotions and attention to mental states of self and other. They prefer to keep others at a distance, valuing achievements over close relationships. This is understood as an adaptation to early experiences of consistent rejection from caregivers of open expression of distress. The person adapts to this by over-regulation of affects and distraction strategies, eg, by focusing away from the attachment relationship and attending to exploration, in an attempt to cope with distress alone.

In contrast, preoccupied attachment is thought to develop in response to inconsistent caregiver availability. In order to secure the needed attention from attachment figures, the person exaggerates expression of emotions and keeps attention to attachment figures at the expense of exploration and development of autonomy. Emotions tend to be under-regulated, and positive feelings are often mixed with feelings of anger and anxiety.

In addition to these 3 organized patterns, some individuals develop more disorganized attachment characterized by momentary ruptures of the organized pattern (unresolved type) or more profound breakdown (cannot classify type). Here, a strategy to successfully regulate emotions no longer seems present, resulting in incoherent states of mind. Disorganized attachment has been linked to adverse experiences in childhood, such as frightening or frightened caregiver behavior or other types of disrupted caregiver behaviors.

In addition to these classical subtypes of attachment, which are measured by the Adult Attachment Interview, 3 various questionnaires have been used in studies of attachment in psychosis. 4 They use subtypes conceptually related to the classical subtypes for assessing attachment, most importantly “attachment avoidance,” which is related to the dismissing pattern and “attachment anxiety” resembling the preoccupied pattern. The classical terms will be used to cover both.

Distribution of Attachment in Psychosis

In psychosis the dismissing type of attachment is found to be dominating, ranging from 48% to 71% compared with 27% in a norm group. Preoccupied attachment ranges between 12% and 20% and secure between 27% and 32%, as compared with 19% and 58%, respectively, in a norm group. 5–7 This distribution stands in contrast to most other mental disorders, where preoccupied attachment and under-regulation of affect are dominant, as in depression and BPD. 8 Only two studies 6 , 7 have reported levels of disorganized attachment in psychosis. They found high levels (29–35%) equivalent to levels found in BPD whereas, in post-traumatic stress disorder (PTSD), disorganization is higher (57%). 9 Thus, dismissing and disorganized attachment appears to be important as potential risk factors in psychosis.

Correlates of Attachment

Two recent systematic reviews have summarized the findings of correlates of attachment in psychosis 10 and association with psychotic phenomena in clinical and nonclinical samples. 11 As would be predicted by attachment theory, insecure forms of attachment taken together are related to poorer premorbid adjustment, more interpersonal problems, and impaired mentalization. 10 Dismissing attachment is robustly associated with psychiatric symptoms, positive and negative symptoms in psychosis. These findings are echoed by findings in nonclinical populations. Here, dismissing attachment is associated with subclinical psychotic symptomatology, paranoia, and endorsement of delusional-like experience; 12 and with negative symptoms, especially social anhedonia found in 3 studies 11 suggesting a robust relationship. For attachment preoccupation , only a modest association to symptomatology is found in psychosis, 10 whereas correlates of disorganized attachment in psychosis are yet to be examined. Thus, at present, the evidence is most strongly established for an association between dismissing attachment and psychotic symptoms.

Risk Mechanisms in Dismissing Attachment

Various hypotheses have been proposed concerning which risk processes link attachment and psychosis. Three risk processes might be involved in the association between dismissing attachment and psychosis, namely deactivation of affects and impaired mentalization involved in the development of negative symptoms and externalizing affect regulations strategies involved in the development of positive symptoms.

Deactivation of affects. It has been proposed that the over-regulation/deactivation of affects seen in dismissing attachment could be a risk mechanism underlying development of negative symptoms . 7 Negative symptoms include blunted affect, anhedonia, and emotional and social withdrawal. Each of these symptoms could potentially be endpoints of severe affective deactivation processes in a dismissing attachment pattern, in response to unresolved distress.

Impaired mentalization . Impaired mentalization has been suggested as linking attachment and psychosis 6 and is more profound in dismissing attachment than in secure and preoccupied attachment in psychosis. 6 Furthermore, impaired metacognitive skills—a concept overlapping with mentalization—has been found to be associated with negative symptoms in schizophrenia. 13 Impaired ability to mentalize is likely to interact with deactivation of affects and together these two risk developmental processes could be underlying mechanisms of the lack of spontaneity and engagement in social interaction described in negative symptomatology. Low mentalization has also been proposed to be involved in impaired social functioning and positive symptoms. 11

Externalizing strategies. Externalizing behavioral and cognitive strategies might be mechanisms linking dismissing attachment to positive psychotic symptoms . A line of indirect evidence supports this hypothesis. Dismissing attachment is characterized by a turning away from attachment towards exploration in situations of distress. In accordance with this externalizing affect regulation strategy, infant avoidant attachment predicts externalizing behavior, 14 which in turn has been found to be associated with hallucinations in a youth sample. 15 Externalizing cognitions are further found to underpin hallucinatory experiences. 16

Risk Mechanisms in Disorganized Attachment

In addition to dismissing attachment, disorganized forms of attachment (unresolved and cannot classify) were found in one-third of persons with psychosis. Unresolved attachment in adults can only be assigned when experience of past trauma has been identified. Corresponding to this, a recent meta-analysis 17 found significant associations between childhood adversities and psychosis with an overall effect of odds ratio (OR) = 2.78. The findings indicated a 33% reduction in people developing psychosis if childhood trauma could be prevented. Within subtypes of childhood trauma, the highest risk of psychosis was found for emotional abuse (OR = 3.40) and high as well was emotional neglect (OR = 2.90). Infant disorganized attachment status is closely linked to trauma 18 and has in itself been proposed as the result, not only of overt trauma but also of “hidden trauma” 19 of caregiver unavailability and interactive dysregulation resulting in lack of regulation of fearful arousal in the infant. Thus, early disorganized attachment is likely to be a risk factor for psychosis, in line with the established emotional abuse and neglect type of trauma. In contrast, secure attachment is an important resilience factor for resolving traumatic experiences in childhood 20 indicating that secure attachment could moderate the association between trauma and psychosis. As mentioned earlier, correlates between disorganized attachment and psychotic symptomatology in psychosis are yet unexplored, but indirect evidence points to a possible association between disorganized attachment and positive psychotic symptoms, with heightened stress-sensitivity and dissociation as underlying risk mechanisms.

Heightened stress-sensitivity . A physiological mechanism possibly linking disorganized attachment and trauma to psychosis is heightened stress-sensitivity, a vulnerability marker for psychosis. This is supported by findings that the human brain seems especially sensitive to interpersonal stress. 21 Stress-sensitivity can be measured as altered cortisol reactivity in the hypothalamic–pituitary–adrenal axis in responses to stressful experiences. Both hyper- and hypo-cortical reactivity have been found in psychosis, indicating altered functioning as response to prolonged severe distress. 22 Furthermore, altered cortisol release patterns have been found in infants with disorganized attachment 23 and in adults with childhood emotional maltreatment. 24

Dissociation . Dissociation can be understood as a mental reaction to severe distress, which cannot be regulated or overcome. The distress can partly be a result of heightened stress-sensitivity. Dissociation is well described as a result of traumatic experiences in PTSD and is thus hypothesized to be present also in persons with psychosis and a history of trauma. “Hidden trauma” within the attachment relationship may also lead to dissociation, because disorganized attachment in itself is described as an early form of dissociation, 25 and strong associations has been found between disorganized attachment in infancy and dissociative symptoms at 19 years. 26 In addition, dissociative symptoms are common in psychosis and have been associated with hallucination in PTSD and trauma and hallucinations in psychosis. 27 This line of indirect evidence supports the hypothesis of a link between disorganized attachment and the development of positive psychotic symptoms with stress-sensitivity and dissociation as underlying mechanisms.

Psychosocial Risk Mechanisms in Psychosis—An Attachment-Based Model

Several possible mechanisms have thus been proposed which could underlie associations between dismissing and disorganized attachment and psychosis. The proposed developmental pathways and risk mechanisms described earlier are illustrated in figure 1 .

Psychosocial risk mechanisms in development of psychosis—an attachment based model.

As illustrated in figure 1, the quality of the infant caregiver attachment relationship most likely interacts with parental and infant factors, as well as with various social factors. If the attachment relationships lead to dismissing or disorganized attachment, then various risk developmental processes are present, which can be involved in symptom development in psychosis. The model only illustrates the mechanisms discussed in this report. In line with the developmental psychopathology approach and empirical findings of multiple risk factors in schizophrenia, the disease is best understood as the result of multiple developmental pathways caused by several interacting risk factors and disease mechanisms. Hence, attachment is only one of many bio-psycho-social risk processes involved. Of particular note, secure attachment was found in one-third of a psychosis sample. A secure attachment pattern will most likely function as a resilience factor, and it has been found to be associated with better engagement with services and improved recovery from negative symptoms. 7

Implications for Research

The emerging findings of associations between attachment and psychosis reported earlier support attachment as a potentially important concept in psychosis. I have pointed to a number of risk developmental processes possibly involved, namely deactivation and externalizing affect regulation strategies, low mentalization, heightened stress-sensitivity, and dissociation. They seem promising areas of research, which could potentially improve our understanding of socioemotional processes involved in the development of specific symptoms and difficulties in psychosis.

Implications for Prevention and Treatment

The emerging evidence for the role of attachment for development of psychosis has implications for prevention and treatment of psychosis. Prevention should include the promotion of resilience through facilitating secure attachment relationships during childhood. Little is known directly of the role of childhood attachment for psychosis, but indirect evidence, as outlined earlier, supports such an approach and warrant further research. Attachment-based preventive interventions should be offered where risk factors for psychosis known to be associated with insecure attachment, in general, are present, such as children having a mentally ill parent, low socioeconomic status, childhood interpersonal trauma, and growing up in managed care.

Turning to treatment, attachment as both resilience and risk factor should be part of routine assessment together with the assessment of adverse childhood experiences. An understanding of attachment status contributes important information on emotional and interpersonal aspects involved in symptom formations and recovery. Findings that attachment security predicted recovery from negative symptoms at 12 months and that increase in security was associated with improvement in negative symptoms support the importance of such an approach. 7

Importantly, attachment affects the possibility of being engaged in treatment at all. Greater attachment insecurity is associated with poorer engagement with services and greater likelihood to disengage from mental health services. 10 Specifically, attachment avoidance is associated with a reduced likelihood to seek help, poor use of treatment, and lower therapeutic alliance. 10 Affective and interpersonal aspects of psychosis might thus be important to address in attachment informed psychological therapies to promote engagement with health services and promote recovery. The attachment perspective is currently informing various new integrative models for psychotherapy of psychosis, 28 , 29 but further research in attachment informed intervention models is required.

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Introduction, acknowledgment.

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The Relationship Between Dissociation and Symptoms of Psychosis: A Meta-analysis

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Supplementary Data

Eleanor Longden, Alison Branitsky, Andrew Moskowitz, Katherine Berry, Sandra Bucci, Filippo Varese, The Relationship Between Dissociation and Symptoms of Psychosis: A Meta-analysis, Schizophrenia Bulletin , Volume 46, Issue 5, September 2020, Pages 1104–1113, https://doi.org/10.1093/schbul/sbaa037

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Evidence suggests that dissociation is associated with psychotic experiences, particularly hallucinations, but also other symptoms. However, until now, symptom-specific relationships with dissociation have not been comprehensively synthesized. This is the first prospectively registered (CRD42017058214) meta-analysis to quantify the magnitude of association between dissociative experiences and all symptoms of psychosis. MEDLINE, PsycINFO, PubMed, and Scopus databases were searched using exhaustive terms denoting dissociation and psychotic symptoms. We included both nonclinical (58 studies; 16 557 participants) and clinical (46 studies; 3879 patient participants) samples and evaluated study quality. Ninety-three eligible articles considering 20 436 participants were retained for analysis. There was a robust association between dissociation and clinical and nonclinical positive psychotic symptoms ( r = .437; 95%CI: .386 −.486), with the observed effect larger in nonclinical studies. Symptom-specific associations were also evident across clinical and nonclinical studies, and included significant summary effects for hallucinations ( r = .461; 95%CI: .386 −.531), delusions ( r = .418; 95%CI: .370 −.464), paranoia ( r = .447; 95%CI: .393 −.499), and disorganization ( r = .346; 95%CI: .249 −.436). Associations with negative symptoms were small and, in some cases, not significant. Overall, these findings confirm that dissociative phenomena are not only robustly related to hallucinations but also to multiple positive symptoms, and less robustly related to negative symptoms. Our findings are consistent with proposals that suggest certain psychotic symptoms might be better conceptualized as dissociative in nature and support the development of interventions targeting dissociation in formulating and treating psychotic experiences.

The concept of dissociation has become a focus of considerable interest for the psychosis field over the past few years, with research examining its importance for the historical concept of schizophrenia, 1 the prevalence of undiagnosed dissociative disorders in psychotic populations, 2 the possibility of hybrid dissociative/psychotic disorders, 3 and the role of dissociation in psychotic symptoms. 4 The latter domain is the focus of this meta-analysis.

Dissociation has been defined by DSM-5 as “a disruption of and/or discontinuity in the normal integration of consciousness, memory, identity, emotion, perception, body representation, motor control, and behaviour.” 5 (p291) Dissociation, and the dissociative disorders, are generally seen as resulting from traumatizing experiences; in recognition of this, dissociative symptoms are now formally recognized in other disorders typically seen as trauma-related, including borderline personality disorder and posttraumatic stress disorder. 5 As trauma is increasingly seen as a causal risk factor in the development of psychosis, the relevance of dissociative experiences to psychosis is being explored with more vigor. 6 Indeed, some have gone so far to suggest that certain psychotic symptoms, particularly auditory hallucinations and delusions of control or passive influence experiences, are better classified as dissociative than psychotic. 3 , 7 The frequency with which the so-called first rank or Schneiderian symptoms are found in dissociative disorders lends weight to this argument. 8 In turn, the concept of psychiatric disorders as discrete “disease entities” linked to distinct biological or genetic etiologies only present in those who meet criteria for specific conditions is increasingly contested. 9 Considerable evidence further suggests that psychosis, like dissociative experiences, exists on a continuum with normal functioning and that its presentation cuts across diagnostic boundaries without being necessarily pathognomonic for any specific disorder. 10

The concept of dissociation refers to a range of phenomena, including experiences encompassing various forms of “psychological detachment” (eg, depersonalization, derealization) as well as compartmentalization of mental experiences (eg, identity disturbances and dissociative amnesia). 11 Significantly, meta-analytic studies have confirmed that dissociation is elevated in people with diagnoses in the schizophrenia-spectrum, 12 , 13 suggesting that dissociation may be related to symptoms commonly observed in people who receive diagnoses of psychotic disorders. The association between auditory hallucinations and dissociation has attracted particular research attention, with a meta-analysis of 19 investigations reporting large associations between the two across both clinical and nonclinical populations. 14 However, whilst the association with auditory hallucinations appears well-replicated, this does not imply that dissociation is uniquely associated with a greater predisposition to only report this symptom. In fact, research studies have found significant positive associations between dissociative experiences and both delusions 4 and paranoia 15 as well as respective subsyndromal psychotic-like symptoms in nonclinical samples. 16 A significant relationship has also been reported, albeit less consistently, between dissociation and negative symptoms. 17

Whilst recent meta-analytic evidence suggests the presence of considerable symptom overlap between diagnoses of schizophrenia spectrum disorders and dissociative disorders, 18 no evidence synthesis to date has systematically examined the magnitude and consistency of the associations between discrete symptoms of psychosis and measures of dissociation. The value of investigating symptom-specific associations is especially pertinent due to the fact that different psychotic experiences may have distinct etiologies. Furthermore, clarifying these associations would be relevant to recent trends toward more symptom-specific and personalized targeted therapies for distressing psychotic symptoms. 19

The primary aim of this meta-analysis was, therefore, to examine and synthesize associations between dissociation and the full range of psychosis symptomatology. A secondary aim was to assess the relationship between dissociation and psychosis symptomatology in both clinical and nonclinical populations and to report on the similarities and differences between them.

Search Strategy

This review was conducted and reported according to PRISMA 20 and its protocol registered on Prospero (CRD42017058214; for PRISMA guidelines, see supplementary table S1 ). MEDLINE, PsycINFO, PubMed, and Scopus were systematically searched using strings for dissociative and psychotic symptoms: ( dissociat* OR depersonali* OR dereali* OR absorption OR multiple personalit*) AND (psychosis OR psychotic OR schizophren* OR hallucinat* OR voices OR visions OR delusion* OR paranoi* OR cognitive disorgani* OR positive symptoms OR negative symptoms OR first-rank symptoms OR Schneiderian ). A hand-search of references and citations from eligible articles was also performed in order to identify additional studies. Primary searches were completed in April 2017 and updated in January 2020. Articles were subsequently assessed for eligibility based on screening of titles, abstracts, and full texts and only retained for review with consensus agreement from at least three reviewers. Details of the search and screening procedure are presented in figure 1 .

Flow diagram of systematic search.

Inclusion and Validity

Studies meeting the following criteria were included for review: (1) published in English in a peer-reviewed journal, (2) use of self-report measures of dissociation, (3) use of self-report measures of psychotic symptoms, and (4) use of quantitative methods to report on the association between dissociative experiences and psychotic symptoms. Studies meeting these criteria were subsequently excluded if: (1) they were presented in a conference abstract or single case study format; (2) global scores of psychosis measures were provided rather than separate measures of positive and/or negative symptoms; (3) the study did not report sufficient statistical information to estimate effect sizes; and (4) there were overlapping participant samples. When multiple reports considered overlapping samples, we only included the report which provided a more precise estimate of the effects (ie, considered a larger sample size) or contained more complete statistical information to estimate relevant effects. No restrictions were placed on age or diagnostic status of participants, study design, or study start date.

Study quality was evaluated using relevant items from the Effective Public Health Practice Project tool 21 (EPHPP). This is an instrument used to evaluate health research on the basis of study design and methodology, sample selection, and analytic methods and has demonstrated validity 22 and inter-rater reliability. 23 Studies were assessed by A.B. Oversight was provided by F.V., E.L., and S.B., with any queries or disagreements over scoring decisions resolved amongst these authors.

Data Extraction

Data extraction was conducted by the first two authors and systematically checked for accuracy by F.V. Information extracted from the primary studies was recorded on a standardized form and included general characteristics (eg, county, publication year), design, sample characteristics (eg, age, gender, diagnostic status), measures used to assess psychotic symptoms and dissociative experiences, the specific symptoms and subtypes of dissociation considered in the article, and statistical information to compute relevant effect sizes.

Effect Size Computation and Statistical Analysis

Analyses were conducted using CMA v.2. Results were pooled using a random-effects meta-analysis. Pearson’s r correlation coefficient was used as the primary metric, as effect sizes of the r -family were most commonly reported in the literature. When studies reported statistical information consistent with other families of effects (eg, d-family and binary effects), these were converted to effect sizes of the r family using computations methods outlined by Borenstein et al. 24 To ensure that different study designs (ie, between-group and correlational) did not impact the findings, a subgroup analysis was conducted to contrast the magnitude of the aggregated correlational and between-group effects extracted from the primary studies. In all analyses, heterogeneity was assessed using the Q -test and the I 2 statistic. Publication bias was also assessed through visual inspection of funnel plots and Egger’s tests. When evidence of publication or other selection bias was evident, analyses were followed with the trim-and-fill method to estimate the influence of potentially missing studies on summary effects.

The following analytic approach was taken. First, we summarized effects considering the relationship between dissociation and global symptom cluster measures (ie, positive, negative, and disorganization symptoms). These analyses were first conducted by including studies which reported effects for total symptom cluster measures (eg, PANSS positive symptom scores) as well as aggregated effect estimates in the case of studies that provided statistical information pertaining to specific symptoms within that cluster (ie, aggregated effects for studies reporting multiple correlation coefficients between dissociation and positive symptom measures, eg, hallucinations and delusions). These analyses were followed-up through multiple subgroup analyses, including: (1) comparison of clinical and nonclinical studies and (2) sensitivity analyses focusing on total symptom cluster measures (when sufficient numbers of studies were available). Secondly, for each cluster of symptoms, multiple meta-analyses were conducted to examine the association between dissociative experiences and specific symptoms of psychosis. Whenever the number of studies allowed it, we also explored the association between various psychosis symptoms and symptom clusters and specific subtypes of dissociation assessed by the Dissociative Experiences Scale 25 (DES-II: ie, absorption, depersonalization/derealization, and amnesia).

The search strategy resulted in 9931 articles. Following title/abstract screening, 323 studies were retained for full-text review, resulting in 93 included articles (see figure 1 ). A description of these studies is available in supplementary table S2 and effect sizes for individual studies included in the positive symptom, negative symptom, and disorganization analyses are presented in supplementary table S3 .

Demographic Characteristics

The eligible studies comprised a total of 20 436 participants. Of these, 11 791 were women and 7627 were men, with a mean age of 27.07 years. Six studies did not specify gender and 19 did not specify age. In total, 58 presented data from nonclinical populations ( n = 16 557) and 46 from patient groups ( n = 3879).

Quality Assessment

Results of the EPHHP quality ratings are presented in supplementary table S2 . Most studies fell within the “moderate” rating ( n = 43; 46.2%), with 33.3% rated “strong” ( n = 31) and 20.4% “weak” ( n = 19). Overall ratings reflected the methodological limitations typical of cross-sectional, correlational literature, namely limited control of confounding variables and selection bias.

Relationship Between Dissociation and Positive Symptoms

Global positive symptoms..

A random-effect meta-analysis of 98 effects found a robust association between clinical and nonclinical positive psychotic symptoms and dissociation, r = .437 (95%CI: .386 −.486). Heterogeneity analyses indicated that there was considerable statistical inconsistency, Q (97) = 3135.421, P < .001, I 2 = 96.907; hence, caution should be taken when interpreting this summary effect. No influential cases were found, but the Egger’s test indicated possible bias, t (96) = 5.222, P < .001. The imputation of 12 hypothetically missing studies using the trim-and-fill method led to a marginal decrease in the summary effect, which remained of moderate magnitude: r = .402 (95%CI: .353 −.448).

A subgroup analysis comparing clinical ( k = 42) and nonclinical studies ( k = 51) indicated that the relationship between dissociation and positive symptoms was significantly larger in nonclinical ( r = .475, 95%CI: .426 −.521) than clinical studies ( r = .388, 95%CI: .311 −.459; Q (1) = 3.902, P = .048). Considerable heterogeneity was apparent in both subgroup analyses ( I 2 = 93.647% and 92.616%, respectively). There was no significant difference between correlational ( r = .457, 95%CI: .420 −.492) and between-group effects ( r = .337, 95%CI: .189 −.470) extracted from the primary studies ( Q (1) = 2.821, P = .093).

We further examined associations between total positive symptoms and dissociation subtypes assessed by the DES-II. In this analysis, it was impossible to directly contrast the summary effect sizes pertaining to different subtypes due to nonindependence of the effects extracted from the primary studies. The analysis indicated that summary effects were generally similar in magnitude: absorption ( k = 33; r = .460, 95%CI: .409 −.509), amnesia ( k = 18, r = .357, 95%CI: .297 −.415), and depersonalization/derealization ( k = 24, r = .405, 95%CI: .355 −.452).

A sensitivity analysis was conducted by restricting the above random-effect meta-analyses to studies that considered total measures of positive symptoms in clinical (eg, PANSS positive scale) and nonclinical samples (ie, total positive schizotypy measures like the SPQ). The results were largely comparable to those reported above. With 267 independent effects included for analysis, the summary effects for associations between positive symptoms and dissociation across clinical and nonclinical studies was r = .401 (95%CI: .305 −.489). There were high levels of heterogeneity, Q (26) = 384.884, P < .001, I 2 = 93.246, but no evidence of publication bias was found ( t (26) = 1.808, P = .171). The summary effect for the association between dissociative experiences and positive symptoms was substantially larger in nonclinical ( k = 9, r = .511, 95%CI: .430 −.583) than clinical studies ( k = 17, r = .331, 95%CI: .208 −.444; Q (1) = 6.530, P = .011). Subgroup analyses focusing on dissociation subtypes found moderate-to-large associations for absorption ( k = 6; r = .473, 95%CI: .381 −.556) but only small associations for amnesia ( k = 2, r = .178, 95%CI: −.043 −.382) and depersonalization/derealization ( k = 5, r = .181, 95%CI: .019 −.334). These two findings may be related, as absorption experiences typically fall on the “normal” (nonclinical) end of the dissociation continuum.

Hallucinations.

A random-effect meta-analysis considering 50 effects found evidence of a robust but statistically heterogeneous association between hallucinatory experiences and dissociation: r = .461 (95%CI: .386 −.531), Q (49) = 2864.317, P < .001, I 2 = 98.289. No influential cases were identified, and inspection of the funnel plot and the Egger’s test indicated no evidence of publication or other selection bias.

A subgroup analysis was carried out to contrast clinical ( k = 18) with nonclinical studies ( k = 30). After removing one potential outlier, 26 the analysis indicated that the relationship between dissociation and hallucinatory experiences was equivalent across the two subgroups of studies: clinical, r = .432 (95%CI: .274 −.567) and nonclinical, r = .482 (95%CI: .416 −.543); Q (1) = 0.388, P = .534. A further subgroup analysis focusing on the DES-II dissociation subtypes indicated that summary affects were robust and significant in all cases: depersonalization/derealization ( k = 20, r = .470, 95%CI: .416 −.521) followed by absorption ( k = 23, r = .465, 95%CI: .394 −.531) and amnesia ( k = 13, r = .388, 95%CI: .328 −.445).

An additional subgroup analysis was conducted to descriptively compare the effects obtained in studies considering hallucinations in different sensory modalities. These analyses could only be conducted for auditory ( k = 15) and visual experiences ( k = 4) due to a low number of studies that considered hallucinations in other domains. The findings indicated that the summary effects of auditory and visual hallucinations were r = .499 (95%CI: .413 −.575) and r = .476 (95%CI: .270 −.641), respectively.

Finally, a sensitivity analysis was conducted to clarify the results of these analyses by excluding effects extracted from 9 samples that used schizotypal measures of anomalous perception (which, although overlapping with hallucinatory experiences, considered a broader range of perceptual anomalies). After the exclusion of these studies, the random-effect meta-analysis of the remaining 41 effects found evidence of a robust but heterogeneous association between hallucinatory experiences and dissociation, with results comparable to those reported above; r = .453 (95%CI: .371 −.529), Q (40) = 1900.134, P < .001, I 2 = 97.895. The results of subgroup analyses contrasting clinical and nonclinical studies as well as studies focusing on the DES-II dissociation subtypes were likewise comparable to those reported in our main analyses.

A random-effect meta-analysis with 30 effects found a moderate-to-large, but statistically heterogeneous, association between delusions and dissociation: r = .418 (95%CI: .370 −.464), Q (29) = 164.987, P < .001, I 2 = 82.423. There was no evidence of potentially influential cases or publication bias.

A subgroup analysis comparing nonclinical ( k = 17) and clinical studies ( k = 12) found a significantly larger summary effect in nonclinical samples: r = .480 (95%CI: .428 −.529) and r = .297 (95%CI: .238 −.354); Q (1) = 21.750, P < .001, respectively. Subgroup analyses focusing on DES-II subtypes indicated that that the summary effects of absorption ( k = 8, r = .402; 95%CI: .315 −.482) were somewhat larger than those of depersonalization/derealization ( k = 6, r = .305, 95%CI: .236 −.371) and amnesia ( k = 4, r = .195, 95%CI: −.090 −.384).

Only a minority of studies assessed associations between specific delusional beliefs (eg, grandiose, somatic, bizarre) and dissociation. There was also considerable heterogeneity in the type of beliefs considered in these studies, which precluded our ability to carry out more fine-grained analyses.

After integrating 22 effects, the summary effect size for the relationship between dissociation and paranoia was r = .447 (95%CI: .393 −.499). Substantial statistical inconsistency was observed, Q (21) = 73.295, P < .001, I 2 = 71.349, but there was no evidence of publication bias or studies exerting undue influence on these findings.

A subgroup analysis carried out to compare clinical ( k = 8) and nonclinical studies ( k = 13) found that the association between dissociative experiences and paranoia was largely comparable across the two groups: r = .416 (95%CI: .260 −.551) and r = .470 (95%CI: .423 −.515) respectively; Q (1) = .507, P = .476. Further subgroup analyses indicated that the summary effects for the DES-II dissociative subtypes were broadly comparable: absorption ( k = 6; r = .426, 95%CI: .280 −.552), amnesia ( k = 5, r = .401, 95%CI: .256 −.529), and depersonalization/derealization ( k = 6, r = .427, 95%CI: .307 −.533).

Relationship Between Dissociation and Negative Symptoms

Global negative symptoms..

A meta-analysis considering 27 effects found a small and heterogeneous relationship between negative symptoms and dissociation: r = .138 (95%CI .065 −.209), Q (26) = 135.706, P < .001, I 2 = 80.841. Visual inspection of the funnel plot and Egger’s test found no evidence of publication or other selection bias.

A subgroup analysis comparing clinical ( k = 14) and nonclinical studies ( k = 11) indicated that the relationship between dissociation and negative symptoms was significant in the nonclinical ( r = .173, 95%CI: .101 −.242) but not the clinical samples ( r = −.082, 95%CI: −.031 −.192). However, the differences in these summary effects were not significant: Q (1) = 1.827, P = .176. As only 1 study provided between-group effects, no subgroup analysis with correlational effects was conducted.

A sensitivity analysis was conducted on 13 studies that considered total measures of negative symptoms. These analyses indicated that the association between dissociative experiences and negative symptoms was not statistically significant: r = .0.084 (95%CI: −.025 −.191), Q (12) = 44.815, P = .129, I 2 = 73.233.

To explore potential associations between dissociation and more specific negative symptoms, we combined effects pertaining to the following categories:

Reduced Emotional Experience and/or Expressiveness.

This analysis concerned a group of symptoms comprising anhedonia, flat/blunted/shallow/flattened affect, and emotional withdrawal. It included 11 effects and found a small and heterogeneous association between dissociative experiences and the symptoms under scrutiny: r = .128 (95%CI: .043 −.210), Q (10) = 36.529, P < .001, I 2 = 72.624.

Lack of Motivation, Asociality, and Withdrawal.

This symptom category covered a lack of close relationships, poor rapport, desocialization, asociality, apathy, avolition, and lack of spontaneity. This random-effects meta-analysis considered 7 effects; a small but significant summary effect was observed: r = .190 (95%CI: .090 −.285), and heterogeneity was modest within these analyses: Q (6) = 12.394, P = .03, I 2 = 55.793.

Cognitive Symptoms.

This cluster considered stereotyped thinking and difficulties in abstract thinking and attention. Only 3 effects were available for this analysis. A small summary effect was found: r = −.108 (95%CI: −.287 −.472) but heterogeneity statistics indicated substantial variation: Q (2) = 12.684, P < .001, I 2 = 87.248.

Relationship Between Dissociation and Disorganization

A random-effects meta-analysis including 12 effects led to a moderate summary effect pertaining to associations between disorganization symptoms and dissociation: r = .346 (95%CI: .249 −.436). Statistical heterogeneity was substantial, Q (11) = 74.051, P < .001, I 2 = 85.145, but there was no evidence of publication bias or influential effects. However, one investigation 27 had an uncharacteristically negative and significant effect size. A sensitivity analysis was conducted by removing this study. The results were broadly comparable to those of the main analysis above: r = .382 (95%CI: .296 −.461), Q (10) = 52.051, P < .001, I 2 = 81.099. As all studies provided data to compute correlational effects, no subgroup analysis of correlational and between-group effects was conducted.

A subgroup analysis comparing clinical ( k = 5) and nonclinical ( k = 6) studies indicated that the relationship between dissociation and disorganization was equivalent across the two samples: r = .348 (95%CI: .036 −.587) and r = .402 (95%CI: .337 −.463); Q -test(1) = .138, P = .710, respectively. There were no sufficient data to conduct subgroup analyses focusing on dissociation subtype, nor for total measures of disorganization.

Sensitivity Analyses for Study Quality

We conducted a final sensitivity analysis to evaluate the impact of including the 19 studies deemed methodologically weaker according to EPHHP ratings. Their exclusion had minimal impact on the overall findings of our meta-analyses focusing on positive symptoms, negative symptoms, and disorganization. In all cases, the summary effects and statistical heterogeneity statistics remained comparable to those reported in our main analyses.

This is the first meta-analysis to systematically summarize and evaluate the magnitude of the associations between dissociative experiences and all symptoms of psychosis, and the findings support the existence of a robust and well-replicated relationship. Indeed, while the majority of literature examining links between dissociation and psychosis has primarily focused on hallucinations, the current analyses suggest that dissociative phenomena are robustly related to multiple positive symptoms and appear to be related to higher disorganization. Conversely, associations with negative symptoms were of considerably smaller magnitude and, in some cases, were nonsignificant. Furthermore, the effects considered in our review were observed across both clinical and nonclinical samples (although with differences in overall magnitude), indicating that dissociation may be an important factor underlying vulnerability to psychotic experiences across the continuum of psychosis.

Firstly, our review replicates and expands previous meta-analytic findings suggesting significant links between dissociation and auditory hallucinations. 14 It also indicates that dissociation is linked to hallucinations across multiple sensory modalities and that the association with visual hallucinations is of comparable strength to that of auditory. The link between dissociation and hallucinatory experiences was additionally of similar size in both clinical and nonclinical studies. Some authors have argued that this association calls for a radical shift in the way such symptoms are conceptualized by researchers and clinicians, in that hallucinations amongst psychosis patients may be better conceived as “traumatic in origin and dissociative in kind.” 4 (p521) However, others have backed more cognitive perspectives; for example, that dissociation could make individuals more prone to hallucinations by increasing confusion between inner and outer experiences, 28 or that heightened states of dissociation may interact with preexisting cognitive vulnerabilities (such as source monitoring biases affecting the capacity to correctly identify the source of internally and externally generated events 29 ).

This review also indicates that dissociative experiences present large associations with paranoia and delusions. Similarly, it identified significant links with symptoms of disorganization, although these were of a somewhat smaller magnitude relative to positive symptoms. One possible explanation for these associations is trauma-related, in that paranoia and delusions may arise from flashbacks which are not recognized as such. 30 These experiences, which are consistent with models of traumatic memory, 31 would typically be associated with powerful feelings of depersonalization/derealization that could subsequently drive the development of delusions and other psychotic symptoms. 32 In this regard, future primary and secondary research could usefully elucidate such links by examining the relationship between psychotic and dissociative phenomena in those with a history of trauma exposure relative to those without.

Our analyses also corroborate findings from previous empirical studies that suggest the magnitude of associations between dissociative phenomena and negative symptoms is less robust than for positive symptoms. When focusing on specific groups of negative symptoms (cognitive symptoms, reduced emotional experience/expressiveness, and lack of motivation, asociality, and withdrawal), we observed small but statistically significant relationships. We note, however, that the number of studies considering negative symptoms is relatively sparse and characterized by high heterogeneity in the specific symptoms examined. Although our grouping of negative symptoms is consistent with existing proposals regarding their underlying dimensional structure (eg, in terms of diminished motivation and expression 33 ), we were limited by the small number of diverse symptoms examined in the primary studies. There is an ongoing debate around the exact underlying structure of negative symptoms, 34 and concerns remain regarding the risk of conflating their assessment with extraneous complaints such as depression or medication side effects. This has the potential of biasing the accurate estimation of the relationship between negative symptoms and dissociation (as well as other psychological and neurocognitive constructs), highlighting the need for further assessment innovation and future research to corroborate these findings. There are no clear models that posit a mechanism linking dissociation to negative symptoms, and indeed patients with dissociative identity disorder are often clinically distinguished from psychotic patients by an absence of negative symptoms.

Overall, our findings support proposals that certain psychotic symptoms might be better conceptualized as dissociative in nature. 4 They are also consistent with evidence suggesting common etiological underpinnings between dissociation and symptoms of psychosis. In this respect, dissociation is common in individuals who have endured potentially traumatizing events 35 and the risk for, and severity of, psychotic symptoms has been overwhelmingly linked to similar traumatic exposures. 36 , 37 Furthermore, meta-analytic evidence suggests that dissociation in people with mental health difficulties, including psychosis, is associated with histories of childhood trauma, 38 while multiple studies suggest dissociation is a well-replicated mediator of the link between childhood adversity and psychotic symptoms. 39 However, it should be noted that our meta-analysis did not consider the potential role played by peritraumatic dissociation in the etiology of psychotic experiences. This remains an under-researched topic that could be addressed in future investigations.

In terms of different dissociation subtypes, our analyses found no striking differences in their respective associations with symptoms of psychosis, although in some analyses absorption appeared to be more linked to psychotic-like experiences in nonclinical samples. However, an important caveat should be noted: our evidence synthesis only considered the bivariate associations between dissociative and psychotic symptoms. It is, therefore, not possible to establish with high confidence whether symptom-specific associations might exist between psychotic experiences and dissociation, or between psychotic experiences and specific dissociative subtypes. Multivariate analyses accounting for covariation between different psychotic and dissociative experiences might be better placed to answer such questions. When these analyses have been conducted in primary research studies, some have reported alleged symptom-specific effects (eg, in the case of auditory hallucinations) whilst others have found no strong support for dissociation exclusively impacting individual symptoms. 40

The difference observed in multiple analyses regarding the relatively larger association between dissociative and psychotic symptoms in nonclinical rather than clinical samples might be explained by several factors. Notably, as patients are likely to be more symptomatic than nonclinical participants, it is possible that studies conducted on clinical samples present restricted variance which might impact the magnitude of effects extracted from these studies. However, a further complication that should be considered when appraising our findings is the comparability of assessment measures typically used in clinical investigations, such as the PANSS, and the various schizotypy measures employed by nonclinical studies (many of which are highly heterogeneous in terms of the experiences they intend to capture). Whilst it is widely accepted that psychosis exists on a continuum with non-pathological experiences and traits, it could be argued that certain phenomena considered in the nonclinical literature (eg, paranoid ideation) may not be fully comparable with their clinical counterparts (eg, persecutory delusions). It, therefore, remains a possibility that the larger effects observed in our nonclinical analyses might reflect fundamental differences in the constructs assessed by different measures.

Another potential limitation of the literature considered in this review relates to the possible comorbidity between psychotic and dissociative disorders. Few studies formally assessed the presence of comorbid dissociative diagnoses when investigating the association between psychotic experiences and dissociation, yet there is some suggestion that undiagnosed dissociative disorders are not uncommon in psychotic populations. 41 Future investigations may attempt to clarify the impact of comorbidity by applying diagnostic interviews such as the Structured Clinical Interview for DSM-5 Dissociative Disorders. 42 It should also be noted that medication status may have confounded results via patients exhibiting antipsychotic side effects (eg, memory problems, detachment, affective flattening) that could be mistaken for dissociation during the assessment. 43 We were additionally unable to conduct dissociation subtype analyses within groups (clinical vs nonclinical) yet some studies have suggested, for example, that different subtypes of dissociation were related to hallucinations in clinical vs nonclinical voice hearers. 44

Several other caveats should also be considered when interpreting our findings. Although the analyses found no substantial evidence of publication or other forms of selection bias, our search strategy was limited to peer-reviewed English-language studies and it is possible that certain relevant studies might have been overlooked. As mentioned previously, the bivariate approach may also have masked more subtle differences in the relationship between dissociation and specific psychotic symptoms. Furthermore, our meta-analysis could not directly contrast the effects between dissociation and specific symptoms as the same studies often examined multiple psychotic experiences within the same sample. Additional methodological and statistical developments in meta-analysis and aggregate analysis of individual participant datasets (eg, network analysis, meta-analytic structural equation modeling, and independent patient data meta-analysis) might enable future evidence syntheses to estimate such effects with greater precision. Although subgroup analyses were conducted to account for the most important methodological and clinical variances between the studies included in this review, the summary effects reported should still be interpreted cautiously in light of the statistical heterogeneity detected in most of our analyses.

Finally, the findings bear several implications for clinical practice. Research into the development of psychological interventions for psychosis has recently moved toward devising and evaluating more targeted treatments in order to improve the effect sizes of generic cognitive-behavioral therapies (which traditionally focused on a range of different psychotic symptoms simultaneously). Future meta-analyses may help refine the issue of whether the relationship between dissociation and psychotic experience varies across different diagnostic groups. However, the current review suggests that the role played by dissociation in the maintenance of presenting difficulties should be carefully evaluated in the context of targeted therapies for voices, delusional beliefs, and other psychotic symptoms for which a strong link with dissociation was observed. As dissociation often represents a consequence of adversity exposure, trauma-focused therapies could also represent a meaningful treatment option for many people with psychotic and dissociative experiences. The adaptation of protocols used to treat dissociation likewise represents a promising area of intervention development for psychosis. For example, reconceptualizing voices as dissociated parts of the self and using dialogical approaches to improve relationships between hearer and voice is one instance of applying techniques developed in the dissociation field amongst psychosis populations. 45 Such an intervention is currently undergoing controlled evaluation amongst patients with schizophrenia spectrum diagnoses (ISRCTN45308981), and if effective could represent a treatment advance that encapsulates the considerable clinical and conceptual overlap between dissociation and psychosis. In this respect, therapeutic approaches derived from dialogical principles may also have applicability beyond auditory hallucinations; a tradition notably begun by Laing’s 46 characterization of schizophrenia as the “divided self,” and expanded by the work of theorists such as Lysaker et al 47 who posit that issues of self-diminishment in psychosis can be addressed via psychotherapy that focuses on developing a coherent internal narrative.

Ultimately, our findings raise the issue of whether different psychotic symptoms do in fact have distinct etiologies. The strong association between dissociation and different types of positive symptoms suggests that they may have similar causal factors. Evidence suggests that substantial overlaps exist in biological and socio-environmental risks across diagnostic categories and specific symptoms 48 and accordingly there has been a move toward transdiagnostic therapies. 49–51 Nonetheless, there are likely to be a myriad of risk and resilience factors for each symptom and the relative importance of each is liable to vary from person to person, highlighting the importance of developing individualized formulations to help understand the development of distressing symptoms within the context of psychological therapies.

E.L. is funded by a National Institute for Health Research (NIHR) Postdoctoral Fellowship Scheme (PDF-2017-10-050) for this research project. This article presents independent research funded by the NIHR: the views expressed are those of the author and not necessarily those of the NHS, the NIHR, or the Department of Health and Social Care.

The authors have declared that there are no conflicts of interest in relation to the subject of this study.

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Introduction. The concept of dissociation has become a focus of considerable interest for the psychosis field over the past few years, with research examining its importance for the historical concept of schizophrenia, 1 the prevalence of undiagnosed dissociative disorders in psychotic populations, 2 the possibility of hybrid dissociative/psychotic disorders, 3 and the role of dissociation in ...
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Dissociation in Psychiatric Disorders: A Meta-Analysis of Studies Using
Dissociation is a ubiquitous construct in modern psychopathology. DSM-5 defines dissociation as "disruption of and/or discontinuity in the normal integration of consciousness, memory, identity, emotion, perception, body representation, motor control, and behavior" ().The corresponding phenomena cover a range from relatively common experiences, such as being completely absorbed by a book or ...
Trauma and dissociation among inpatients diagnosed with schizophrenia
1. Introduction. Psychotic disorders and Dissociative Disorders (DDs) are two different diagnostic categories of mental disorders. Schizophrenia is generally understood as a brain disease and treated with pharmacological treatments (McCutcheon et al., Citation 2020), while DDs are conceptualized as trauma-related disorders and treated with psychological interventions (Brand & Loewenstein ...
Comparing Social Stigma of Dissociative Identity Disorder
The aim of the current study was to explore how the social stigmatization of dissociative identity disorder (DID) compared to that of schizophrenia and depressive disorders. Using a between-subjects experimental design, a total of 139 participants (126 usable data [39 men, 84 women, 3 other]) from the general population were randomly assigned ...
The Challenges in Diagnosis and Treatment of Dissociative Disorders
They are often comorbid with borderline personality, substance abuse, post-traumatic stress disorder, depression, and somatoform disorders. 2 Lifetime prevalence(s) of DDs and DID are around 10% and 1% of the worldwide population, respectively. 2 Dissociative disorders are clinically rarely identified and thus under-diagnosed; 1,2 for instance ...
Relationships between childhood trauma and dissociative, psychotic
Background Childhood trauma (CT) is an important risk factor in the emergence and clinical course of psychiatric disorders. In the latest literature, an association exists between CT and patients with schizophrenia. There is also a strong relationship between the dissociative symptoms of schizophrenia and the presence of CT.Aims The aim of this study is to examine the relationship between CT ...
Association Between Psychotic and Dissociative Symptoms: Further
Psychotic experiences such as hallucinations and delusions are traditionally believed to be indicative of severe mental disorders (e.g., schizophrenia) and therefore are regarded as considerable mental health issues that should receive medical attention, although studies showed that these experiences are not uncommon in the general population too (Johns & van Os, Citation 2001; Kelleher et al ...
Dissociative symptoms in schizophrenia spectrum disorders: Historical
This article discusses dissociative symptoms in schizophrenia spectrum disorders.More recently, the links between schizophrenia and dissociation have been tested by several different lines of schizophrenia research. This research was also focused on cognitive disorganization, metacognition, the incidence and effects of stress and trauma in schizophrenia and different forms of dissociative ...
Dissociative identity disorder and schizophrenia: differential
Abstract. Schizophrenia and dissociative identity disorder (DID) are typically thought of as unrelated syndromes--a genetically based psychotic disorder versus a trauma-based dissociative disorder--and are categorized as such by the DSM-IV. However, substantial data exist to document the elevated occurrence of psychotic symptoms in DID ...
Schizophrenia, dissociation, and consciousness
Current thinking suggests that dissociation could be a significant comorbid diagnosis in a proportion of schizophrenic patients with a history of trauma. This potentially may explain the term "schizophrenia" in its original definition by Bleuler, as influenced by his clinical experience and personal view. Additionally, recent findings suggest a ...
Recent research on the interventions for people with dissociation
In a recent systematic review of psychosocial interventions for conversion and dissociative disorders (Ganslev, Storebø, Callesen, Ruddy & Søgaard, 2020), all reviewed studies focused on conversion disorder (which may be better conceptualized as a dissociative disorder according to some scholars in the field) (e.g., Brown, Cardeña, Nijenhuis ...
Dissociative Identity Disorder and Schizophrenia
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Dissociation in schizophrenia and borderline personality disorder
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Introduction. The concept of dissociation has become a focus of considerable interest for the psychosis field over the past few years, with research examining its importance for the historical concept of schizophrenia, 1 the prevalence of undiagnosed dissociative disorders in psychotic populations, 2 the possibility of hybrid dissociative/psychotic disorders, 3 and the role of dissociation in ...
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Dissociation in Psychiatric Disorders: A Meta-Analysis of Studies Using the Dissociative Experiences Scale

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Recent advances in understanding schizophrenia

Historical background and diagnosis

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Figure 1. Etiology of schizophrenia.

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Attachment in Schizophrenia—Implications for Research, Prevention, and Treatment

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Distribution of Attachment in Psychosis

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Risk Mechanisms in Disorganized Attachment

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The Relationship Between Dissociation and Symptoms of Psychosis: A Meta-analysis

Search Strategy

Inclusion and Validity

Data Extraction

Effect Size Computation and Statistical Analysis

Demographic Characteristics

Quality Assessment

Relationship Between Dissociation and Positive Symptoms

Hallucinations.

Relationship Between Dissociation and Negative Symptoms

Reduced Emotional Experience and/or Expressiveness.

Lack of Motivation, Asociality, and Withdrawal.

Cognitive Symptoms.

Relationship Between Dissociation and Disorganization

Sensitivity Analyses for Study Quality

Supplementary data

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Affiliations

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