A study of 40 patients with schizophrenia diagnoses and 40 patients with dissociative identity disorder (DID) found that “neither phenomenological definitions of dissociation nor the current generation of dissociation instruments (which are uniformly phenomenological in nature) can distinguish between the dissociative phenomena of DID and what we suspect are just the dissociation-like phenomena of schizophrenia.” The study further found similarity between the experiences of hearing voices in both disorders. Results were published in the Journal of Trauma and Dissociation online on June 2, 2012.
Laddis, A. Dell, P.F; “Dissociation and Psychosis in Dissociative Identity Disorder and Schizophrenia.” Journal of Trauma and Dissociation, July, 2012; 13(4): 397-413
Mad in America hosts blogs by a diverse group of writers. These posts are designed to serve as a public forum for a discussion—broadly speaking—of psychiatry and its treatments. The opinions expressed are the writers’ own.
hi, i’m having trouble parsing this. would someone please explain what this is saying the similarities and differences are and what the significance of that is?
I will say what interested me, which is any contemplation of a continuum between what is seen as dissociation and what is seen as psychosis. I think that once that contemplation begins in earnest, the diagnostic categories and concepts that separate them begin to break down. This study, like many, struggles to preserve the distinction and therefore, in my opinion, is in fact a little confusing in its conclusions. So when I put something like this up it’s not so much that I agree with the conclusion as that I anticipate it to stimulate a vigorous discussion, perhaps on the validity of the concepts on which the study is premised. But I don’t feel it is helpful or appropriate for me to add my views to the discussion, except perhaps here where it may be that the relevance of this study to the themes of this website may seem a bit obscure if not tangential.
When I look for studies, I am often looking at the ones from within conventional areas of focus that somehow highlight the inconsistencies and tensions of the operating assumptions. This is because of the sheer numbers involved; there isn’t much research that is concerned with exploding the “common wisdom” of things; the financing, and professional and academic pressures make that difficult and rare. That’s just the nature of things. “Positive,” or confirming results tend to get published and noticed far more than studies that fail to prove their hypotheses and may therefore call a prevailing paradigm into question.
When I got involved in research I was dismayed at the lack of attention to what seemed the clear connection between dissociation and psychosis on every conceivable level. It seemed that everything was set up to prevent any research or contemplation along this line. I managed to get a look at a manuscript of a book laying out a traumagenic neurodevelopmental model of schizophrenia, and it felt like reading a draft of the communist manifesto. I had conversations with top researchers, established names in both trauma and schizophrenia who at first denied the connections and then acknowledged them but added that pursuing that line of thinking was “a career ender.” To even raise the question marked you as a radical and, at the time, their areas of interest could not have been sustained by pursuing what seemed from their perspectives to be a side show.
So when I see a study that takes on the question head-on, it excites me to include it. Even if the logic is dense or perhaps convoluted, I think it adds to the evidence base of a relatively little explored connection. But there is rarely if ever one “magic bullet” study that answers everything concisely, or even a string of studies that resoundingly make the point. Especially if you’re trying to tear down what had been commonly accepted wisdom. More often it’s a slow accretion of studies that vaguely circle the inconsistencies and tensions in the constructs that are commonly accepted.
So, here, I think this study’s conclusions are hard to parse. But for me the important thing is that they are looking for connections, and clearly finding them.
Basically, what it says is that dissociation in what is called DID, i.e. split-off parts of the self that take shape as different personalities, and dissociation in what is called schizophrenia, i.e. split-off parts of the self that take shape as voices, are very similar, and difficult to distinguish from each other with the currently available tools. Interestingly — though not surprisingly — the researchers seem to think that developing newer, more precise tools will make it easier to distinguish between what they presume is “real” dissociation, caused by trauma (as in “DID”), on the one hand, and “false” dissociation, caused by some brain defect (as in “schizophrenia”), on the other. It doesn’t occur to them that what they have studied might be two slightly different, although also closely related, types of very “real” dissociation, both caused by trauma. Cf. Ron Unger’s slides for a presentation, “When Trauma and Psychosis Mix”: http://www.slideshare.net/ronunger/trauma-and-psychosis-mix-for-osh Especially slides 29 – 33/34
Thank you, too, Kermit, for further clarification.
BTW, I find it interesting that in a country like Denmark, where “DID” is not an officially accepted diagnosis, people who dissociate, no matter in which way, usually are diagnosed with “schizophrenia”.
This kind of fact – the one about Denmark – is exactly the kind of juicy tidbit that really livens up the conversation. It adds to the resources needed to reframe the debate. Wow.
i think it’s really important to reframe “schizophrenia” as real dissociation and as coming out of trauma. and i think it’s important to dissolve the barriers inbetween diagnositic categories. I’d like to hear more people talk about the similarities between the diagnoses of “d.i.d” and “schizophrenia”.
in addition, i think it’s important to note that people diagnosed with “d.i.d.” are being given pretty much the same polypharmacy drug treatment as people diagnosed with “schizophrenia” and they are told by psychiatrists that though “d.i.d.” itself is not a brain disease, they also suffer from brain diseases caused by or enabling the dissociative response to the original trauma(s) and so they must take medications for the so-called brain diseases of depression, and of a severe form of anxiety that comes of a severe enough trauma to cause “did” and so are told they must take copious amounts of benzos and neuroleptics in order to deal with the anxiety and depression that is framed as is always co-morbidity with “did” (i’ve never known someone with only the diagnosis of “d.i.d.”) and so in a sense, traditional “did” treatment is both outside and inside the brain disease paradigm.
this is not usually talked about much, but usually the first thing that happens when someone is diagnosed with “did” is that they require medications to moniter their extreme moods and behavior and “to make therapy possible”. they are told it was caused by trauma, yes, but not to focus on that, to focus on now, and for the now, what got them into treatment, is their distress (feelings or behaviors), so they are told that what they require is medication first.
like people diagnosed with “schizoprhenia” , people with “d.i.d.” are told that recovery is not possible, only maintenance, and though long-term medication. so i am trying to say that it ends up being a kind of tricky thing the way that psychiatry has “d.i.d” as not a brain disease and yet always having co-morbidity with brain diseases and treated it with polypharamacy.
also, what i’m trying to say is that though it’s really really important to get people to see that “schizophrenia” is not a brain disease and is caused by trauma-this is not going to be enough as a way to keep psychiatry’s use of ideas of brain disease and medication from remaining the models of treatment for “schizophrenia”. Because i think if it was accepted that “Schizophrenia” was not a brain disease, the same thing would happen that happens with “d.i.d.” and suddenly everyone with “schizophrenia” would be said to have co-morbid brain diseases requiring the same medications they were on in the first place. Again, i am not trying to minimize the social and personal implications of these changes, but instead to highlight the ways that “d.i.d.” being seen as caused by trauma doesn’t play out the way it might seem and the implications that might have for “schizophrenia”.
In the end it’s a mixed message treatment for people who have had too many mixed messages.
i think it’s important that we take this into account when thinking about the reframing of “schizophrenia” so we can make more progress in the way both diagnoses are viewed.
Thank you. This is very important stuff.
was something wrong with my comment, it’s gone.
thank you to both of you for your helpful answers.
“I had conversations with top researchers, established names in both trauma and schizophrenia who at first denied the connections and then acknowledged them but added that pursuing that line of thinking was “a career ender.” To even raise the question marked you as a radical and, at the time, their areas of interest could not have been sustained by pursuing what seemed from their perspectives to be a side show.” _Kermit.
Sadly what is routinely ignored in all cognitive constructs about “symptom” expression is the body & the nervous systems role in feedback to the brain. Research & knowledge which address this is ignored, presumably because it threatens our inter-subjective mode of maintaining a group dynamic equilibrium (homeostasis).
People like Allan N Schore & Stephen Porges have a hard time getting a more holistic approach recognized.
“Pathological dissociative detachment represents a bottom-line defensive state driven by fear-terror, in which the stressed individual copes by pervasively and diffusely disengaging attention “from both the outer and inner [italics added] worlds” (Allen et al., 1999, p. 164). I have suggested that the “inner world” is more so than cognitions, the realm of bodily processes, central components of emotional states (Schore, 1994).
In line with the current shift from cold cognition to the primacy of bodily based affect, clinical research on dissociation is now focusing on “somatoform dissociation.” According to Nijenhuis (2000), somatoform dissociation is an outcome of early onset traumatization, expressed as a lack of integration of sensor motor experiences, reactions, and functions of the individual and his or her self representation.
Thus, “dissociatively detached individuals are not only detached from the environment, but also from the self—their body, their own actions, and their sense of identity”.
This observation describes impaired functions of the right hemisphere, the locus of the “emotional” or “corporeal self.” According to van der Kolk and colleagues (1996), “Dissociation refers to a compartmentalization of experience: Elements of a trauma are not integrated into a unitary whole or an integrated sense of self”
In a number of works I have offered interdisciplinary evidence that indicates that the implicit self, equated with Freud’s System Ucs, is located in the right brain. The lower subcortical levels of the right brain (the deep unconscious) contain all the major motivational systems (including attachment, fear, sexuality, aggression, etc.) and generate the somatic autonomic expressions and arousal intensities of all emotional states. On the other hand, higher orbitofrontal-limbic levels of the right hemisphere generate a conscious emotional state that expresses the affective output of these motivational systems. This right lateralized hierarchical prefrontal system, the system Pcs. performs an essential adaptive motivational function—the relatively fluid switching of internal bodily based states (Bromberg’s self-states) in response to changes in the external environment that are nonconsciously appraised to be personally meaningful.
On the other hand, pathological dissociation, an enduring outcome of early relational trauma, is manifest in a maladaptive highly defensive rigid, closed system, one that responds to even low levels of intersubjective stress with parasympathetic dorsal vagal parasympathetic heart rate hypo arousal and deceleration. This fragile unconscious system is susceptible to mind–body metabolic collapse, Janetian energy failure, and thereby a loss of energy-dependent synaptic connectivity within the right brain, expressed in a sudden implosion of the implicit self and a rupture of self-continuity.
This collapse of the implicit self is signaled by the amplification of the parasympathetic affects of shame and disgust and by the cognitions of hopelessness and helplessness. Because the right hemisphere mediates the communication and regulation of emotional states, the rupture of intersubjectivity is accompanied by an instant dissipation of safety and trust.
Dissociation thus reflects the inability of the right brain cortical– subcortical implicit self-system to recognize and process external stimuli (exteroceptive information coming from the relational environment) and on a moment-to-moment basis integrate them with internal stimuli
(interoceptive information from the body, somatic markers, the “felt experience”).
This failure of integration of the higher right hemisphere with the lower right brain induces an instant collapse of both subjectivity and intersubjectivity. Stressful affects, especially those associated with emotional pain, are thus not experienced in consciousness (Bromberg’s “not-me” self-states).
The critical elements of implicit unconscious intersubjective communications embedded in affectively charged attachment transactions are more than mental contents; rather, they are interactively communicated and regulated and dysregulated psychobiological somatic processes that mediate shared conscious and unconscious emotional states. Recall Freud’s remark to Groddeck: “The unconscious is the proper mediator between the somatic and the mental, perhaps the long-sought ‘missing link’”.
The essential biological purpose of intersubjective communications in all human interactions, including those embedded in the psychobiological core of the therapeutic alliance, is the regulation of right-brain/mind/body states.
Andrade suggests that it is the affective link, conveyed through intersubjective “empathetic introjective reciprocal identification” (p. 694), that leads to both psychic and somatic change.” _Allan N Schore. “Affect Dysregulation & Disorders of the Self.”
Core affect/emotion is suppressed for the sake of subjective harmony from around 18 months of age on-wards, and perhaps we all pay a price for an adult collusion of Descartes famous error?
Is it the fear of infectious emotion that sees us prefer on “objectified” sense of self that allows this presumption of symptom expression, as separate parts like experience, and a continuum of body/brain/mind expression?