OK, What Is Peritraumatic Dissociation — Really?

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!”

This entry was posted in animal defenses, depersonalization, derealization, dissociation, evolution-prepared dissociation, peritraumatic dissociation, PTSD, Tonic immobility, trauma and tagged , , , , , , . Bookmark the permalink.

20 Responses to OK, What Is Peritraumatic Dissociation — Really?

  1. Scrappy says:

    Ahhhhhhh… it all makes sense now! Brilliant!

    It’ll be interesting to see how you go about studying the packaged components of peritraumatic dissociation.

  2. Peregrine says:

    Rats! I just posted a response, but it’s not showing up. I suspect it’s in your spam filter–I used html code to link to a couple of places, and I think WordPress associates that with spam. Would you mind checking?

    It’s either that, or I accidentally posted it in the wrong thread. If it’s disappeared and is irretrievable, let me know. I managed to grab a copy and can repost, but don’t want to end up double-posting if it’s simply waiting in your filter.


    • Peregrine,

      I cannot find an earlier Jan. 8 post from you. It is not in my spam filter. I think the Internet ate your homework. 🙂

      • Peregrine says:

        Thanks for checking! I think the html must have done it in. If I get a chance this weekend, I’ll edit the copy I saved and repost. Maybe I can tighten it up a bit too–I tend to type fast and think faster. And who knows, perhaps my thoughts will modify after I read your current post.

  3. Peregrine says:

    “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.”

    I agree with your proposal to group and, with my limited knowledge of your field, your proposed groupings make sense to me. What continues to concern me is referring to item two as “evolution prepared.” Are you trying to imply that there is no genetic basis to the other two? Might be that I’m reading things you don’t intend, because I’m persnickety on the topic of evolution, since that’s my field of training.

    From https://understandingdissociation.com/2010/09/21/persisting-peritraumatic-dissociation-is-different-from-evolution-prepared-dissociation: “Neither the researchers of peritraumatic dissociation, nor the instruments that they use to measure it, have drawn a clear distinction between defensive peritraumatic dissociation (which seeks to avoid reality) and adaptive evolution-prepared dissociation (which shines a bright spotlight on reality)!”

    This is what makes me cringe as someone with a background in the evolution of. The word “adaptive” has a very specific connotation in the context of evolution, and it’s misused by 99% of humanity. What “adaptive” means from an evolutionary perspective is that a particular gene rises in frequency in a population, because that gene confers upon individuals that carry it an advantage in surviving and producing viable offspring that carry the gene and themselves have an advantage in surviving and reproducing. This process occurs in the backdrop of the environment—the gene confers an advantage in the context of a particular environment.

    If the environment changes over time, then another gene may be more successful and the original one would reduce in frequency. But that does not imply that the traits associated with the gene that is reducing in frequency do not have a genetic component. It simply means that those traits do not have an advantage in a particular environment (whether that environment be physical, social, cultural, etc.). In other words, what is “adaptive” from an evolutionary perspective changes over time, and you cannot discern what is adaptive (or even what has a genetic component and what doesn’t) simply by observing that people who experience item 1 on your list tend to develop PTSD and people who experience item 2 don’t.

    Where I’m headed is that I think you are using the term “adaptive” in a more subjective way—to imply a human value judgment that having PTSD is Not A Good Thing. And I’d agree with you there 100%. But that might have absolutely nothing to do with how well people with PTSD survive and reproduce compared to those who do not develop PTSD as the result of a trauma, or whether the genetics underlying those who do/don’t have PTSD are the same/different/overlapping. And that’s without even considering some more complex genetic scenarios I’ll skip for brevity’s sake.

    So I agree with your groupings, and I agree with the need to group. But I believe you’re incorrectly applying evolution to create your groupings.

    I do think that studying the problem from a genetic perspective could be enormously fertile territory. I wouldn’t get into the question of whether there is evolutionary adaptation occurring, however. I’d focus more on the immediate question of trying to figure out if there are genes underlying PTSD. That has clinical application. E.g. if I have PTSD, does that mean my children may have inherited an underlying genetic tendency—in which case, perhaps that guides treatment decisions if something traumatic happens to them.

    “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).”

    One item I do want to mention. In one of your first posts, there was some discussion in the comments about infant rocking, and whether that could indicate dissociation. One commenter didn’t see the rocking as a sign of dissociation. I believe you did, though, Paul. So here’s an interesting tidbit for you:

    Zoo animals are subject to what is called stereotypic behavior. They pace and perform repetitive motions or series of motions. Zookeepers attempt to counter/prevent this by providing enrichment activities. I would hypothesize that this stereotypic behavior is an outward expression of what we call clinical dissociation in humans–assuming you’re willing to allow that a rocking infant is dissociating. I honestly think you’re barking up the wrong tree in trying to tease out a uniquely human dissociative response—and I don’t think doing so is required to justify your proposed approach or groupings to move forward with the research in your own field. Again, I think you’re conflating a human value judgment of what is Good vs. Bad with evolution here, and I don’t think that’s necessary.

    I suspect where your groupings split is along the survivor’s perceived severity of the trauma, combined with an underlying genetic proclivity toward dissociation (regardless of whether that genetic proclivity is adaptive from an evolutionary perspective). Field after field is finding this kind of interaction between genes and environment resulting in pathology. E.g. I’ve read studies that suggest at least some cancers, heart disease, multiple sclerosis, etc. result from an underlying genetic proclivity that is expressed as a result of an environmental trigger, such as exposure to a virus. Why couldn’t psychological trauma behave similarly?

    What I’ve read about the neurobiology of PTSD seems to hone in on structures like the hypothalamus and the HPA axis. These structures are certainly present in animals as well. So if there is some kind of dysfunction in these structures underlying PTSD, I certainly don’t think you can rule out genes, or the possibility that animals also develop PTSD.

    Anyway, I’m not trying to be pedantic. There is a real risk in incorrectly bringing “adaptation” into your arguments, because it implies things that are not known and may not even be true. Additionally, to conflate evolution with human value judgments can backfire on you. For example, there is plenty of research on animals to indicate that things such as forced copulation (e.g. ducks) and infanticide (e.g. lions) can be adaptive from an evolutionary perspective. But there’s no way anybody here is going to argue that such things are Good Things from a moral perspective or that they are Good Things for the victims’ quality of life. Give Nature her due, sure—but keep in mind that Nature doesn’t care about benevolence. She’s just the force we (and our genes) recon with.

    • Hi Peregrine,

      Thank you for your detailed comments about the proper role of evolution and adaptation in our discussion of evolution. I wish I had your depth of education about evolution; I very much like most of what you are saying.

      I use the term evolution-prepared dissociation to refer to a specific, hard-wired, animal defense (linked to falling from a height), which Nature began selecting long before primates ever existed. I think that this same hard-wired response is often triggered by the out-of-control experience of car crashes and some other human ‘traumatic’ experiences.

      As for the term, adaptive, it is certainly true that it has been largely co-opted to describe subjective/psychological matters that have nothing to do with evolution or natural selection.

      I am fascinated by your description of stereotyped behavior in zoo animals. I would like to know more about it. It sounds like a very close approximation of the stereotyped rocking of abused/neglected children.

      i would be surprised, however, if there is no discontinuity between the ‘dissociation’ of infrahuman animals and some of the dissociation of humans — especially amnesia.

      • Peregrine says:

        I just found the perfect link if you’d like to explore stereotypic behavior in animals:


        It’s a website for an academic text on the subject, and there are links to pictures and videos of the behavior, which includes rocking and swaying in some examples.

        If you’ve ever been to a zoo, you’ve probably seen this, but not realized what you were looking at. I remember seeing a polar bear once in a rather small pool, and it was doing repetitive circuits by pushing off in the exact same place with the exact same paw on each of the walls and gliding to the next wall over and over and over again. It’s eyes were glazed and half closed as it did this, and watching it was certainly lulling me into dissociation. I’ve done the same thing in small pools, actually. Maybe I’m a polar bear at heart?!

        • Peregrine,

          Thanks for finding the website on repetitive animal behavior. I have two thoughts about these behaviors. First, they seem mostly to be reactions to captivity. Second, they may all be repetitive, but they do not seem to be the same. Some of these behaviors seem to be outer-directed (e.g., biting cage bars or stall bars), whereas other behaviors seem to be more inner-directed (i.e., monotonous pacing that facilitates internal withdrawal). The latter feels much closer to dissociation than the former.

          • Peregrine says:

            I don’t know if these behaviors are ever documented in wild animals. I’m thinking a wild animal wouldn’t survive very long if it spent its day rocking, however. In fact, a prey animal that behaved oddly like that would attract predators. Predators are drawn to signs of distress, since a distressed animal is easier to kill.

            The main way in which I think humans and non-human animals divide is the degree to which we alter our environment to ensure survival. So I don’t think it’s so much that animals don’t have the potential to dissociate or develop PTSD. It’s just that, at least in the wild, that probably leads to death sooner rather than later. Whereas human society provides enough of a safety net that folks can get by. Likewise, a zoo animal isn’t going to get picked off by a predator or starve to death if it has psychological problems.

            Good point about the behaviors dividing between internal vs. external in direction. I agree that the internally focused ones seem a lot more like dissociation than the externally focused ones. The external ones seem more equivalent to things like nail chewing or chewing on pens/pencils in people.

  4. Laura says:

    Hello Dr. Dell,
    I am relatively new to the field of trauma and dissociation (second-year Psy.D. student), but I am very interesting in this particular field of research and have been following your blog closely.

    I think that your proposal to divide peritraumatic dissociation research into categories of mechanisms (tonic immobility, evolution-prepared, and clinical dissociation) makes complete sense. However, a couple questions occurred to me that maybe you could shed some light on.

    1. By “evolution-prepared” dissociation, do you mean any animal-defense-like dissociation that does not involve tonic immobility (freezing, hyperfocus, etc.)? Because from following your posts, I got the impression that tonic immobility fell into the category of evolution-prepared dissociation. I could see why dividing tonic immobility and all other evolution-prepared dissociation makes senses though, given the association between tonic immobility and later developing PTSD.

    2. Although I feel much clearer on the phenomena of animal-defense dissociation and tonic immobility, am still not quite sure I have a good understanding on the nature of clinical dissociation and what it actually looks like in the context of peritraumatic dissociation. Is clinical dissociation any kind of dissociation that does not allow for some enhanced processing of the traumatic event, and actually clouds the perception of it? If so, does tonic immobility allow for enhanced processing of a traumatic event, or does it allow someone to ‘space out’ from whatever is happening?

    3. I don’t have a lot of experience with research, so I am not sure whether this following question is a no-brainer to people who have more experience in that field. Given your observation that different aspects of dissociation could be involved in any one of the three mechanisms of dissociation (for example, depersonalization could be resulting from tonic immobility, animal defenses, or clinical dissociation), how do you propose would be a good way to realistically measure peritraumatic dissociation and divide it reliably into its respective “grouping”?

  5. Hi all,
    Regarding the mechanisms of the deconstructed components of dissociation:

    I think tonic immobility is a reflex shared with many animals that probably evolved to be triggered in situations where it increased survival, including as a last-ditch response to being cornered by a more powerful attacker. So here the “mechanism” I would predict would be a neural circuit that has “freezing” as its output and is triggered instantaneously by certain threatening stimuli. Since its often a last-ditch response, it may be a marker of severity of the situation, and so may correlate with certain PTSD symptoms like re-experiencing only because re-experiencing is also a reaction to the most severe situation (guessing).

    The analgesia I think may be due to a known pathway in which the adrenal glands release endogenous opiates along with their adrenaline.

    I believe the amnesia is a known response to high stress hormone (cortisol in humans) levels and has to do with direct effects of high level glucocorticoids on hippocampal function (a brain region involved in forming new memories).

    The emotional numbing strikes me as a “psychological analgesia” that may have the same mechanism as the analgesia to physical pain mentioned above (i.e. due to endogenous opiates). In fact, opiates were used to treat psychological distress before the advent of modern psychopharmaceuticals.

    The reduced awareness may also come from the endogenous opiates. I think opiates (in their synthetic form) are sometimes used at high doses for anesthesia (knocking you out) in addition to analgesia (pain killer).

    I don’t know about the derealization and depersonalization, but I suspect their mechanisms are along the lines of those above.

    Then, regarding the converting of this acute set of responses to a chronic condition, this might have to do with learning mechanisms. For example, my husband studies tonic immobility in mice where its called “freezing” and it is triggered when the animal is traumatized and there is nowhere to run away. This freezing response can afterward be elicited by putting the animal in the same box where the trauma originally occurred, and can also be elicited anywhere by sounding a tone that was playing during the original trauma. This is actually a commonly studied learning paradigm. Maybe dissociation becomes chronic in people for whom reminders of the trauma are everywhere in their environment and connot be avoided, whereas people whose acute dissociation does not convert to chronicity live in environments very different from the one in which they were traumatized (guessing).

  6. BearlyHere says:

    Tonic immobility could easily be a survival trait in many environments. Many predators preferentially pursue fleeing prey; some bears, canines, many big cats. Prey that does not flee may be ignored. I believe that cheetahs, for example, are actually unable to kill most prey animals unless they flee, the cheetah then pursues, trips the running animal, and leaps on it to rip the throat. It’s not strong enough to overcome many of its prey if they turn and fight back. Likewise, I have seen dogs spread out and bark at prey, then when it turns, whichever dog is then behind the prey leaps on it and snaps its spine, usually at the neck. I have seen pairs of dogs do this without training and repeatedly. That’s why you’re more likely to be attacked by a dog if you turn and run; you are signaling that you are prey. Finally, I am told that for some bears laying down and “playing dead” will often halt an attack (unfortunately, it apparently does not work for some other types of bears and I don’t know which kind is which, no personal experience with bears). Anyway, point is that “freezing” could very easily be an evolutionarily selected (adaptive?) response in at least some environments.

  7. Melissa says:

    Wow, this is getting quite complicated in abnormal psychology.. I appreciate the article, it does go into depth with the explanation. I’m not a professional, I’m just someone who has survived a great deal. The more I know and understand, the more things make sense to me.

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  12. Ashli says:

    Where did you acquire the tips to write ““OK, What
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  14. Diana Blaker says:

    Thank you for answers! I’ve kept this to myself all my life when I hovered above the crime scene as a young girl.(More than a few times) I’m grateful and I still am crying. I needed this information.Thanks again.

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