Some insist that peritraumatic dissociation causes PTSD. Others say absolutely not. In some research, peritraumatic dissociation does predict PTSD; in other research, it doesn’t. One study even reported that those who experienced peritraumatic dissociation were healthier than those who did not experience it (Shilony & Grossman, 1993) What the heck is going on here?
What Is Peritraumatic Dissociation?
Here is the simple answer: The prefix peri– comes from the Greek; it means around or near. Thus, peritraumatic dissociation is dissociation that occurs at the time of the trauma. But, you can see this coming, right? Defining peritraumatic dissociation is not simple.
At we move forward in our study of peritraumatic dissociation, the more persnickety of you [Read: rigorous thinkers :-)], may ask a question: “How close to the trauma does peritraumatic dissociation have to be in order to still be peritraumatic (instead of posttraumatic or some other kind of dissociation)?” See! I told you it was a persnickety question.
As it it turns out, however, this question is important because it makes a big difference whether dissociation occurs just during the period of trauma or whether it persists for weeks afterward. Three studies have now reported that peritraumatic dissociation is not associated with subsequent PTSD, whereas persisting dissociation is associated with subsequent development of PTSD (Briere, Scott & Weathers, 2005; Murray, Ehlers & Mayou, 2002; Panasetis & Bryant, 2003).
OK, so true peritraumatic dissociation is not pathogenic, but persisting posttraumatic dissociation is. Does that solve our problem? Does this critical distinction explain the inconsistent research findings about the relationship between “peritraumatic dissociation” and PTSD?
Only sort of. Yes, it does untangle one major confusion about peritraumatic dissociation, but if you read my last few blog posts you know that we still have a problem — tonic immobility.
Tonic immobility is a form of peritraumatic dissociation that has repeatedly been shown to be followed by an increased level of posttraumatic symptoms. So, where does that leave us?
It leaves us with still more conflicting findings. Specifically, three methodologically rigorous studies have shown that true peritraumatic dissociation is not associated with PTSD (or acute stress disorder; ASD), but five studies have now shown that tonic immobility is associated with greater posttraumatic symptoms.
OK, back to basics.
What Is Peritraumatic Dissociation?
In a recent article, Richard Bryant of Australia said something that I think is quite valuable:
“the construct of peritraumatic dissociation needs to be deconstructed into more specific factors. To date, studies have focused on the general construct of dissociation, which has not provided information about specific mechanisms. Future studies should evaluate more responses, such as time distortion, reduced awareness, emotional numbing, amnesia, and derealization.” (Bryant, 2007, p. 188, emphasis added)
The simple definition of peritraumatic dissociation that I provided above ‘looks at’ the time of trauma, scoops up anything and everything that ‘looks like dissociation,’ and calls it all peritraumatic dissociation. Bryant’s point is that ‘everything that looks like dissociation’ is uselessly overinclusive. In saying this, Bryant echoes many others who have complained that the label, “dissociation,” includes too many different things (e.g., Cardeña, 1994; Dell, 2009; Steele et al., 2009).
Bryant, however, has proposed a new solution. Previous critics of dissociation’s overinclusiveness have tried to specify what should (and what should not) be classified as dissociation. Bryant doesn’t do that. Instead, Bryant suggests that research on dissociation (and peritraumatic dissociation) should assess the independent effects of each kind of dissociation (i.e., time distortion, derealization, depersonalization, analgesia, amnesia, etc.) — rather than lumping them all together and studying ‘dissociation.’
Although I find Bryant’s outlook to be both illuminating and refreshing, my proposed solution differs from his. I fear that Bryant’s solution — to collect data on each kind of dissociation — would generate data that would still be confusingly overinclusive.
Let me explain this by reviewing how my approach is different from Bryant’s. I am seeking the mechanisms and natural groupings of peritraumatic symptoms. For example, I see at least three mechanisms/groupings of symptoms: (1) tonic immobility, (2) evolution-prepared dissociation, and (3) clinical dissociation. I focus on these mechanisms/groupings because each of them seems to ‘come as a package’ — and I think the packages of dissociation-like experiences are what really matters.
Why? Take depersonalization, for example. Depersonalization is part of several different ‘packages’ of symptoms (i.e., tonic immobility, evolution-prepared dissociation, and clinical dissociation). Each ‘package’ is probably driven by a different mechanism. If this premise is correct — and I think that it is correct — then it necessarily follows that our research data on depersonalization is a mixture of data about depersonalization that occurs in Package 1, depersonalization that occurs in Package 2, depersonalization that occurs in Package 3, and so on. Such mixed data can breed neither conceptual clarity nor consistent findings — as we have seen with the research literature on ‘peritraumatic dissociation.’
All of which takes us back to our basic question: “What is peritraumatic dissociation?” The simple answer is that peritraumatic dissociation occurs at the time of the trauma. But, this apparent answer doesn’t really answer the question we are asking: “What is peritraumatic dissociation?” The simple answers only tells us when it happens — not what it is.
Bottom line: We need to rethink peritraumatic dissociation; we need to rethink this entire area of research. This phenomenon was named “peritraumatic dissociation” when the field realized that dissociation often occurred in the middle of trauma. That was a very important insight. Unfortunately, our name for that dissociation has inadvertently obscured the (now increasingly obvious) fact that peritraumatic dissociation is many things — not just one. And, those many peritraumatic dissociative things come in different packages, each with its own mechanism.
So, as I see it, the next crucial step is to identify these packaged components of peritraumatic dissociation and study them. And my intuition is that we have little hope of accomplishing that (and making sense of the heterogeneity that is pertitraumatic dissociation) unless we begin by studying our hard-wired animal defenses (some of which may, or may not, be uniquely human).
Remember: Nature ‘designed’ us to automatically alter our mode of information processing at moments of great danger. Some of that altered information processing is dissociative in nature. So, let’s give Nature her due. She comes first.
That’s why I’m so focused on animal defenses. We need to fully appreciate these evolutionary foundations before we can really understand clinical dissociation.
As Colin Quinn used to say on Saturday Night Live, “That’s my story and I’m sticking to it!”