The WordPress.com stats helper monkeys prepared a 2012 annual report for this blog.
Here’s an excerpt:
4,329 films were submitted to the 2012 Cannes Film Festival. This blog had 20,000 views in 2012. If each view were a film, this blog would power 5 Film Festivals
The WordPress.com stats helper monkeys prepared a 2011 annual report for this blog.
Here’s an excerpt:
The concert hall at the Syndey Opera House holds 2,700 people. This blog was viewed about 15,000 times in 2011. If it were a concert at Sydney Opera House, it would take about 6 sold-out performances for that many people to see it.
As they say in The Music Man, “You can talk all you want…but you gotta know the territory.” To really understand what peritraumatic dissociation is all about, you gotta know the territory — namely, peritraumatic dissociation’s historical context and its role in several important debates.
Near-Death Experiences
About a decade before peritraumatic dissociation was ‘discovered’ in California. [Where else! :-)], Russell Noyes published a series of articles about “transient depersonalization syndrome” (Noyes, Hoenk, Kuperman & Slyman, 1977). Noyes was a near-death researcher; he studied motor vehicle accident victims and those who had experienced near-drownings, near-fatal falls, heart attacks, and so on.
A significant proportion of Noyes’ subjects reported that their brush with death was characterized by a sense of detachment, unreality, time-slowing, emotional calm, and accelerated thought. Noyes, by the way, was the scholar who retrieved, translated, and republished Heim’s (1892) account of the experiences of mountain climbers who had survived potentially fatal falls. As we noted in an earlier post, Heim’s mountain climbers who fell had experienced the same phenomena that Noyes described.
Because there had been little academic interest in dissociation for decades, Noyes’ articles about near-death depersonalization experiences largely ‘took place in a void.’ There was no ‘hook’ on which to hang his findings — except the fringe area of near-death experiences. Hey! It was the seventies!
The Battle Over PTSD
During the late 1960s and the entire 1970s, the Veterans Administration treatment system was flooded with Vietnam veterans who were angry, emotionally reactive, and haunted by recurrent memories and flashbacks about their time in Vietnam. The diagnosis of PTSD did not yet exist (it would not enter the DSM until 1980).
Prior to 1980 (and afterwards, as well) an intense political battle surrounded the diagnosis and treatment of Vietnam veterans. The ‘old guard’ claimed that these veterans were largely psychotic and that they should be treated as such. The ‘new wave’ insisted that these veterans were suffering from “Post-Vietnam syndrome,” a consequence of their wartime trauma. The ‘old guard’ would have none of it. They insisted that war does not cause mental illness — unless the soldier had a preexisting psychological problem or weakness.
A lengthy political battle ensued. The new wave won the debate and Posttraumatic Stress Disorder became part of the DSM. Prior to that, however, opponents of PTSD sought to minimize the number of PTSD diagnoses by seeking a restrictive Criterion A (which defines trauma in PTSD) in DSM-III. They lost that battle, too. DSM-III’s Criterion A for PTSD was quite broad. It defined trauma as:
“a recognizable stressor that would evoke significant symptoms of distress in almost everyone.” Criterion A further stated that a trauma is a stressor that “is generally outside the range of usual human experience.” (DSM-III)
The important point about this DSM-III definition of trauma is that it suggests that traumatic events will cause PTSD “in almost everyone.” Time and research data has shown that assumption to be incorrect.
Across all kinds of trauma, only about 25% of trauma survivors succumb to PTSD. Some kinds of trauma (e.g., physical and sexual assault) produce higher levels of PTSD. Nevertheless, it is now crystal clear that trauma (even rape) does not cause PTSD “in almost everyone.”
As a consequence of such findings, the DSM-IV Criterion A is much more restrictive:
“(1) the person experienced, witnessed, or was confronted with an event or events that involved actual or threatened death or serious injury, or a threat to the physical integrity of self or others (2) the person’s response involved intense fear, helplessness, or horror.” (DSM-IV, emphasis added)
Notice that Criterion A2 requires a specific peritraumatic reaction (Aha! Peritraumatic reaction!). The person is required to experience “intense fear, helplessness, or horror” at the time of the traumatic event. In part, this peritraumatic diagnostic requirement is designed to distinguish between the 25% of trauma survivors who develop PTSD and the 75% who don’t.
The Trauma Field’s Belated Interest in Dissociation
During the struggle to define and defend PTSD, the trauma field had little interest in dissociation. In fact, it is probably accurate to say that the trauma field was actively disinterested in dissociation. After all, dissociation is weird and it’s connected to multiple personality disorder which is even weirder. Certainly, few paid much attention to Noyes’ articles about “transient depersonalization syndrome.”
Then fate took a hand. Card-carrying members of the trauma field discovered that many trauma victims dissociated during trauma: e.g., Are Holen (1993), David Spiegel (1991), Charles Marmar (1994). More importantly, Holen’s (1993) longitudinal study of the survivors of a North Sea oil rig disaster found that dissociation during the disaster predicted the subsequent development of PTSD. With that, the trauma field suddenly developed an interest in what quickly came to be called peritraumatic dissociation. This interest dove-tailed with the effort to define trauma and traumatization in terms of peritraumatic emotional reactions (Remember “intense fear, helplessness, or horror”?).
But the ambivalence of the trauma field about dissociation soon returned — for two reasons. First, as we have discussed in previous posts, research on the relationship between peritraumatic dissociation and PTSD has produced inconsistent findings. Second, Acute Stress Disorder became a lightning rod for attacks on dissociation.
Acute Stress Disorder
Amid the interest about peritraumatic reactions, a new diagnostic entity was born: Acute Stress Disorder.
According to the DSM diagnostic criteria, PTSD cannot be diagnosed unless the person has been symptomatic for 30 days. Thus, even if trauma survivors were intensely symptomatic during the 30 days after the trauma, they could receive no diagnosis or treatment until reaching the 30-day mark. This ‘gap’ in the nosology led David Spiegel and colleagues to propose a new diagnostic entity that would ‘fill the gap’ between the day of the trauma and PTSD’s 30-day diagnostic requirement.
Spiegel’s proposal was accepted (mostly) and DSM-IV ushered in a new diagnosis — Acute Stress Disorder. Unlike PTSD, a diagnosis of acute stress disorder requires that a person be very symptomatic for only 2 days (but for less than 4 weeks). Why less than 4 weeks? Because 4 weeks + 2 days = 30 days; at which point, a symptomatic person could receive a diagnosis of PTSD.
So what does acute stress disorder have to do with peritraumatic dissociation? A great deal. Spiegel was one of the fathers of peritraumatic dissociation (Spiegel, 1991). Acute stress disorder is the direct progeny of peritraumatic dissociation. In fact, Spiegel originally proposed that this disorder be called “Acute Dissociative Disorder.”
In keeping with this idea, Spiegel proposed a set of diagnostic criteria that emphasized dissociative symptoms. His proposed diagnostic criteria were mostly accepted, but his proposed name was not. Opponents said that the name made little sense because a person would have a dissociative disorder (Acute Dissociative Disorder) for a few weeks and then, suddenly, would switch to having an anxiety disorder (PTSD). Accordingly, the disorder was named acute stress disorder and, like PTSD, classified as an anxiety disorder.
The diagnostic criteria for acute stress disorder (ASD) are quite similar to those of PTSD (i.e., reexperiencing symptoms, avoidance symptoms, and hyperarousal symptoms), but with the addition of dissociative symptoms. Overall, ASD has fared reasonably well in subsequent research, but its dissociative diagnostic criteria have not. Just as peritraumatic dissociation has been an inconsistent predictor of PTSD, so too, have the dissociative symptoms of ASD proved to be an inadequate predictor of PTSD (e.g., Bryant, 2007; Marshall, Spitzer & Liebowitz, 1999).
The Territory of Peritraumatic Dissociation
Over the last 35 years, the territory of peritraumatic dissociation has ranged from (a) near-death experiences (Noyes’ transient depersonalization syndrome), to (b) the question, “Does peritraumatic dissociation predict PTSD?” (Answer: Not very well), to (c) the shift from the question, “What is a trauma?”, to the question, “What constitutes traumatization?” (According to DSM-IV: peritraumatic emotional reactions [i.e., “intense fear, helplessness, or horror”]), to (d) inspiring the creation of a new diagnostic entity (acute stress disorder).
My own contribution to this territory consists of asking two questions: (1) “What is peritraumatic dissociation, really?” and (2) “How much of it is a normal, hard-wired animal defense?” We will take a closer look at these two questions in my next post.
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.
…sigh.
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!”
Victims of rape and childhood sexual abuse frequently describe dissociation-like experiences which occurred during the assault. Typically, we assume that these are dissociative experiences. But are they? I don’t think we really know. To be blunt about it, we have little idea where our animal defenses leave off and our dissociative functioning begins.
Tonic Immobility During Rape
In my last post, I described the first empirical study of tonic immobility during rape. Galliano et al. (1993) reported that 37% of rape victims had experienced tonic immobility during the assault. Furthermore, tonic immobility during rape was not a blessing. Galliano and colleagues found that tonic immobility seemed to breed guilt and self-blame. As one member of our discussion community recently put it:
“I was an athlete; 21 yrs old, strong, feisty, self-assured. my experience of tonic immobility during rape [generated] an identity crisis that had me feeling profoundly confused about who I was and ashamed that I did not fight back. it took me a long time to fully understand this response as a defense mechanism and let go of the guilt I felt about not fighting back.”
According to Tiffany Fusé, almost half of women who experience tonic immobility during rape find it to be terrifying. As the quotation above illustrates, the autonomous intrusion of tonic immobility not only takes away what little power that a rape victim still possesses, it may challenge her very identity:
“Animals and humans do not choose TI [tonic immobility] … TI is more akin to a hardwired response, a response that can be quite frightening itself.” (Marx, Forsyth, Gallup & Fusé, 2008, p. 80)
“the TI experience itself might be so aversive and frightening that having such an experience promotes the onset of posttraumatic stress symptomatology.” (Marx et al., 2008, p. 84, emphasis added)
Uh oh — “promotes the onset of posttraumatic stress symptomatology?” That would go far beyond the old saw about ‘adding insult to injury.’ Marx and colleagues are saying that, in the case of sexual assault, tonic immobility adds injury to injury. Does it?
Does Tonic Immobility Generate Posttraumatic Complications?
In a word, “Yes.” Every study that has examined this issue reports the same finding: trauma survivors who experienced tonic immobility have more posttraumatic symptoms than do trauma survivors who did not experience tonic immobility. Let’s take a closer look at this finding.
The size of the correlations between tonic immobility and posttraumatic symptoms are consistently modest. With few exceptions, these correlations range from .21 to .37. This means that tonic immobility and posttraumatic symptoms share 4% to 14% of their variance. On the other hand, Fusé and colleagues (2007) factor analyzed their Tonic Immobility Scale and found two factors: (1) Tonic Immobility and (2) Fear. When Heidt, Marx, and Forsyth (2005) correlated the Tonic Immobility factor with a good measure of PTSD symptoms, they found a correlation of .49.
This begins to be rather impressive. Rape is known to be an especially potent generator of PTSD symptoms (e.g., Rothbaum, Foa, Riggs, Murdock & Walsh, 1992). Now, Marx and colleagues have shown that tonic immobility, all by itself, accounts for 24% of those symptoms! What is going on here?
Let’s take a look at “the internals.” What the heck are internals? Those of you who are major political junkies may know. On TV, when they present the latest poll results, they soon get around to “the internals” — the detailed numbers within the major result. For example, the poll may say that Obama’s positive rating is 48%. The most interesting stuff, however, lies in “the internals” — that is, Obama’s positive ratings among Democrats, Independents, Republicans, men, women, and so on. Similarly, the most interesting findings in these eight tonic immobility studies can be found in the internal details.
PTSD has three clusters of symptoms: (1) re-experiencing (e.g., flashbacks, intrusive memories), (2) avoidance/numbing (e.g., avoiding anything that reminds you of the trauma, loss of interest in daily life), and (3) hyperarousal (e.g., hypervigilance, jumpiness). The key internal result from the eight studies is that the relationship between tonic immobility and PTSD symptoms is mostly driven by tonic immobility’s effect on re-experiencing symptoms.
So, there is something about tonic immobility that can make a bad event (especially rape) more traumatic. There is something about tonic immobility that worsens flashbacks and intrusive memories. And by the way, some of these studies examined nonsexual traumas and found the same thing. Tonic immobility somehow makes trauma worse.
Bottom Line: Our gifts from evolution and Mother Nature are usually quite beneficial. Here, however, our phylogenetic inheritance (i.e., tonic immobility) may have some very unpleasant consequences.
And now, a Question: “Is tonic immobility an aspect of peritraumatic dissociation?” Or not? If not, why not? This may be an annoying or useless question for some of you. For me, it’s really important. Remember: I’m the guy who is trying to sort out the boundary between animal defenses and dissociation. So, what do you think?
Spontaneous tonic immobility is common during rape, but it doesn’t discourage many rapists. The problem is that tonic immobility was designed by Nature to deal with animal predators (e.g., big cats and bears), not human ones. Human predators usually don’t lose interest if their human prey suddenly passes out or ‘looks dead.’
As we saw in my previous post, experimenters don’t lose interest when the rat or dog becomes immobile. In fact, as we saw with Richter, the experimenter may become curious and repeat the experiment again and again with other animals. Tonic immobility has a long research history. It used to be called “animal hypnosis” (Ratner, 1967). Under that appelation, you can find many published accounts that date back to the 1800s. Under whatever label, this has phenomenon fascinated researchers. They have conducted study after study on different species (including psychology students!). Similarly, its close ‘cousin,’ learned helplessness, has fascinated experimenters since Richter’s mid-50s experiments.
Why Don’t We Hear More About Learned Helplessness?
Learned helplessness and tonic immobility have occasionally been invoked to explain the behavior of victims of human violence. For example, “Why don’t battered wives leave their abusers?” Or, “Why don’t women fight their rapists?” Or, “Why don’t child abuse victims tell someone?” By and large, these explanations have not ‘caught on.’
Domestic violence counselors, rape counselors, and therapists who treat abuse victims know that these questions are bad news because — whether based in ignorance of abusive dynamics or driven by misogynistic prejudice — these questions blame the victim. These counselors and therapists have an understanding of these dynamics, which can easily be described as “learned helplessness,” but this conceptualization has never become part of mainstream thinking and writing.
Why? Probably for several reasons. Perhaps most importantly, frontline workers have ‘bigger fish to fry.’ They are busy providing direct clinical care and fending off societal resistance to the realities of domestic violence, rape, and child abuse. Oddly enough, one of the big reasons that learned helplessness and tonic immobility have not ‘caught on’ has to do with style. One of psychology’s dirty little secrets is that trends in research are substantially governed by what is ‘in style.’ A blunter way to say this is that psychological research is often swept along by fads.
Learned helplessness was ‘in style’ in the late 60s and 70s, but not now. Tonic immobility has probably never been much ‘in style’ — certainly not today. As Gordon Gallup once said, ‘when discussed at all, [tonic immobility] often is referred to as a behavioral aberration of little interest’ (Woodruff, 1977, p. 161).
Finally, there is a technical reason why learned helplessness has not been applied much to human victims of repeated violence. A great deal of research indicates that learned helplessness in rats “dissipates” rapidly. Lab research shows it to be a short-term phenomenon that dissipates in 48 to 96 hours (e.g., Maier, 2001).
Anyway… Enough about that for now. We’ll return to the issue of dissipation in later posts. Meanwhile, let’s get back to tonic immobility.
What Happens During Tonic Immobility When the Predator is Human?
This question has two sides, one of which we’ve already discussed: (1) How do human predators react to their prey if they become tonically immobile? (Answer: Human predators are seldom dissuaded from their predatory intent); and (2) What goes on ‘inside’ the tonically-immobile human prey (both during tonic immobility and afterwards)?
The first important step toward understanding what happens during human tonic immobility came in 1979. Suarez and Gallup (1979) pointed out that tonic immobility was a common occurrence during rape. Tonic immobility during rape, they noted, was quite similar to the tonic immobility of animals:
“In most instances…practically all of the salient elements associated with the onset of tonic immobility in animals are also present during rape, including fear, contact, and restraint… For victims who report being paralyzed, the state has a rapid onset and abrupt termination. It is also accompanied by an inability to vocalize or call out. Loss of consciousness does not occur, as evidenced by a victim’s ability later to relate the sequence of events that occurred during the attack. Some victims even report feeling ‘freezing cold’…which may parallel the characteristic decrease in body temperature of immobile animals. Additionally,.many rape victims relate that they felt completely numb or insensitive to pain during the ordeal…” (Suarez & Gallup, 1979, p. 317, emphasis added)
This was a wonderful start. Unfortunately, this important article has largely languished in obscurity. True, it has been cited from time to time, but mostly in passing. The first effort to investigate tonic immobility during rape did not occur until 14 years later (Galliano, Noble, Travis & Puechl, 1993). This study produced some very important findings.
First, 37% of rape victims reported that they became completely paralyzed during the rape; 23% reported being partially immobilized. Second, careful analysis revealed that the occurrence of tonic immobility was unrelated to ‘the usual suspects’:
— previous exposure to violence during childhood
— whether the rapist had a weapon
— number of injuries sustained
— whether the rapist was a stranger or an acquaintance
Third, tonic immobility had significant consequences for the rape victim. Compared to those who did not experience tonic immobility, paralyzed survivors (a) had a stronger belief that they could have stopped the rape if they had resisted; (b) had a stronger belief that if they had resisted, other people would be more likely to believe that they had been raped; and (c) less often sought immediate help after the assault.
These results have a variety of serious implications. I will focus on just one of them. Tonic immobility is our phylogenetic inheritance from our animal ancestors. It is designed to aid biological survival during an encounter with a predator. Whenever a prey animal succeeds in not being eaten, its tonic immobility is a huge victory. It won! It survived!
But, as I keep emphasizing, tonic immobility in humans is often of little help (unless the predator in question is a big cat or a bear). When the predator is a rapist, the tonically-immobilized rape survivor does not feel victorious. Anything but. That is why Olivia Benson on Law and Order: Special Victims Unit is always having to tell her rape victims, “You did the right thing. You survived!” — often receiving a vaguely hopeful, but mostly dubious look in return.
So, enough for today. More about rape and tonic immobility next time. Notice that we’re still walking the trail of our animal defenses. We haven’t reached clinical dissociation yet. And think about how difficult it will be to disentangle tonic immobility from clinical dissociation when we focus on what happens during childhood sexual abuse. Perhaps some of our ‘insider’ experts can find a way to talk about some of this. They have much to teach us.
Let’s take a closer look at tonic immobility. When does it happen? How does it affect the animal? How does it affect the predator? And, perhaps most importantly for our purposes, “Does tonic immobility have after-effects?” As we will see, it does indeed.
To preview: The after-effects of tonic immobility are determined by what caused the tonic immobility in the first place, what happened during the time that the animal was immobile, the manner in which the animal emerged from its immobility, and what happened to the animal afterward.
When Psychologists Take Away All Safety
As you remember, the autonomic nervous system has two branches: (1) the sympathetic, emergency, fight-or-flight system, and (2) the parasympathetic, withdrawal/immobility system. As Porges (1995a) has emphasized, the parasympathetic nervous system has two very different functions. Mostly, this system becomes active when the environment does not need to be dealt with; at those times, the parasympathetic nervous system facilitates homeostatic functions such as digestion, growth, healing, and conservation of energy. The parasympathetic nervous system’s second function is triggered when the sympathetic nervous system’s fight-or-flight operations fail. Then, there is a sudden, massive parasympathetic innervation of the heart and the animal may collapse into immobility.
The noted fear researcher, Joseph LeDeux, conditioned rats to fear a tone that occurred whenever they were shocked. Later, something very interesting happened (Iwata & LeDeux, 1988). If the conditioned rats heard the tone while they were roving freely about their cage, their heart rate and blood pressure increased (i.e., fear and sympathetic innervation). On the other hand, if they heard the tone while they were restrained, their heart rate and blood pressure decreased (i.e., inability to flee and parasympathetic innervation): So:
Signal of pain when they could flee ==> Sympathetic Activation
Signal of pain when they could not flee ==> Parasympathetic Activation.
This same duality of response occurs naturalistically. If free-ranging woodchucks are approached in the open by a human, their heart rate accelerates and they flee (i.e., sympathetic activation). On the other hand, if woodchucks are approached when they are near or in their burrow, their heart rate slows (i.e., parasympathetic activation). The woodchucks’ bradycardia was greatest when their danger and helplessness was greatest — namely, when a dog was digging into their burrow (Smith and Woodruff, 1980).
Bottom line: An animal’s parasympathetic innervation is greatest when it is approached in its place of safety by a potential predator. Remember: Submerged alligators (submergence is their place of safety) dropped their heart rate from 30 bpm to 2-5 bpm when approached by a canoe. The alligator then remained submerged for 30 minutes (instead surfacing every 5-7 minutes as alligators normally do).
What does this have to do tonic immobility? Quite simply, parasympathetic innervation may culminate in full-blown tonic immobility if the experimenter continues to restrain the animal (thereby increasing the animal’s helplessness in the face of pain and danger).
Restraint and Inescapable Danger
One of the most dramatic examples of inescapable restraint and utter loss of safety is the series of studies that were conducted by Curt Richter. Richter (1957, 1958) dropped domestic rats into a vat of water where they were harassed by a jet of water that produced turbulence in the water. Nevertheless, these rats swam for about 60 hours — until they became exhausted and drowned. Then, Richter performed the same experiment with rats who had been shorn of their vibrissae (whiskers). This was not an inconsequential thing to do; a rats’ vibrissae are a major sensory organ. To Richter’s surprise 2 of these whiskerless domestic rats drowned within minutes; the other 10 continued to swim strongly for a long time.
Curious about this mysterious “death response,” Richter launched a new series experiments — this time with 34 brown, sewer rats (Rattus norvegicus). Norway rats are incredibly fierce and suspicious. In fact, they are so fierce that, in order to avoid being severely bitten, Richter was forced to concoct a special device to pick them up and restrain them. He then trimmed their vibrissae and dropped them into the vat of water. All 34 of these fierce rats died in 2 to 8 minutes!
Despite the influence at that time of Walter Cannon’s writings about the fight-or-flight function of the sympathetic nervous system, Richter noticed, to his surprise, that his rats’ deaths were preceded by their hearts slowing (rather than accelerating from sympathetic activation). Autopsies confirmed his observation. Their hearts were found to be in a state of diastole, engorged with blood. They had died ‘a vagus death.’ [The vagus is the major nerve in the parasympathetic nervous system that controls heart rate.]
Richter then did something very strange. He wrote that the rats had become “hopeless” — that they had just ‘given up’ and died. I cannot convey adequately how strange it was for Richter to say this. His comment about hopelessness was a very ‘un-rat-psychologist’ thing to say. Academic psychology in the late 1950s was profoundly behavioristic. Everything was behavior. And there was no room in behaviorism for things like ‘hopelessness’ or ‘giving up.’
Richter was especially taken aback by the fact that some of his fierce Norway rats ‘gave up’ even before they were dropped into the vat of water!
“a reaction of hopelessness is shown by some wild rats very soon after being grasped in the hand and prevented from moving. They seem literally to give up.” (Richter, 1958, p. 120)
This mysterious ‘giving-up’ “death response” was so striking to him that he sought to ‘cure’ it. [He may also have wanted to justify his ‘heretical’ comments about hopelessness.] 🙂
Richter intuitively sought to teach the rats that ‘all was not hopeless’:
“Support for the assumption that the sudden death phenomenon depends largely on emotional reactions to restraint or immersion comes from the observation that after elimination of the hopelessness the rats do not die. This is achieved by repeatedly holding the rats briefly and then freeing them, and by immersing them in the water for a few minutes on several occasions. In this way the rats quickly learn that the situation is not actually hopeless; thereafter they again become aggressive, try to escape, and show no signs of giving up. Wild rats so conditioned swim just as long as domestic rats or longer.” (Richter, 1957, p. 196, emphasis added)
Martin Seligman, one of the fathers of learned helplessness, was fascinated by Richter’s experiments. Not surprisingly, Seligman referred to Richter’s rats as “helpless.” Seligman described a Richter-related, unpublished study about tonic immobility in baby chicks (Seligman, 1975).
H. J. Ginsberg induced tonic immobility in baby chicks by restraining them [Note: Restraint is the classic procedure that psychologists use to induce tonic immobility.]. Ginsberg allowed half of these chicks to come out of tonic immobility at their own pace. He forced the other half to come out of their state of tonic immobility prematurely — by repeatedly prodding their breast with his finger.
Ginsberg then dropped the chicks into vats of water where they swam until they drowned. He compared their time-to-drowning with a third group of chicks that had never experienced tonic immobility. The chicks who had been forced to come out of tonic immobility prematurely died the fastest. The control group of chicks who had never experienced tonic immobility swam the next longest. Finally, the group of chicks that been allowed to come out of tonic immobility at their own pace swam the longest.
Seligman interpreted these results in terms of helplessness vs. control. The more control that a chick had experienced over its own fate, the longer it resisted drowning.
Why Did Evolution Select For This Automatic Response of Tonic Immobility?
The survival value of tonic immobility presumably lies in the fact that immobility causes the predator to lose interest in its prey. The Internet, in fact, provides a plethora of news reports and advice articles about the survival value of ‘playing dead’ when attacked by a predator.
For example, a woman described a bear attack that happened a few months ago when she was camping in Yellowstone Park (The Early Show, CBS, 7-29-10):
“Next thing I know, this bear is chewing on my arm. I screamed. He bit harder. I screamed harder.” She then realized that “screaming was not working… I don’t know if you call it instinct, but something inside me just said… ‘I want to live.’ And I just told myself, ‘Play dead.’ …As soon as I went limp, I feel his jaws get loose and then let me go and he went away.”
Notice the difference between (1) this woman who ‘played dead’ and (2) the chicks that Ginsberg forced to come out of tonic immobility prematurely (and then dropped into a vat of water). The woman was delighted and empowered. The chicks were defeated and helpless. And they died quickly.
‘Playing dead’ worked exactly the way Nature designed tonic immobility to function — when the predator was a bear. The chick’s immobility also worked the way Nature had designed it to function, but the experimenter was not a bear. Human predators behave differently. Tonic immobility usually does not cause a human predator to lose interest.
Tonic immobility is the ‘last chance’ biological reflex that is triggered when an animal is caught by a predator. Today’s post focuses on a rarely noted fact about tonic immobility — it has 4 possible outcomes, not two: (1) death (the predator eats the animal); (2) survival (the animal escapes and recovers); (3) biological survival, but physical/psychological defeat (e.g., physical assault, rape); and (4) captivity (which may include repeated incidents of #3). Note that #3 and #4 only happen when the predator is human.
Human Predators Are Different From Animal Predators
Humans have some important differences from other animals. As noted above, human predators may inflict two very different kinds of defeat: (1) biological death, and (2) instrumental or sadistic use of the person or animal (e.g., rape, captivity, torture) to serve the needs of the predator.
Yes, some animals settle their fights for dominance when one animal surrenders and bares its vulnerable throat to the other. Occasionally, some human fights are settled in this way, but this is rare. Unlike other animals, humans wield an instrumental cruelty (and, sometimes, frank sadism) that has no true counterpart in the rest of the animal kingdom.
The closest parallel that I can find to human cruelty is a cat ‘toying with’ a mouse — which, I think, is actually a very different phenomenon. When a cat ‘toys with’ a mouse, it’s actually an interaction between the mouse’s animal defense of freezing (which causes the cat to stop attacking) and the mouse’s animal defense of flight (which is a powerful ‘releaser’ of hunting/pouncing in the cat). The cat may seem to be toying with the mouse, but there is a hidden instinctual orderliness in what is happening (which involves neither cruelty nor sadism).
Uncontrollable, Inescapable Pain
What happens when a human (or any other animal) is subjected to uncontrollable, inescapable pain? Inescapable pain occurs in single-incident rape, recurrent child abuse, recurrent rape during incarceration, torture, and so on. And, of course, inescapable pain may occur in a psychology lab when experimenters inflict uncontrollable/inescapable shock on dogs or rats. These psychology experiments are our core topic for today.
Learned helplessness was discovered serendipidously in the animal learning laboratory of Richard Solomon at the University of Pennsylvania in 1964 when his graduate students exposed a dog to repeated trials of inescapable shock.
Learned helplessness is best described by comparing the behavior of dogs who have never been shocked with the behavior of dogs who had recently been subjected to repeated trials of inescapable shock:
When placed in a shuttle box [a box that is divided by a shoulder-high barrier that the dog can jump over], an experimentally naive dog, at the onset of the first electric shock, runs frantically about until it accidentally scrambles over the barrier and escapes the shock. On the next trial, the dog, running frantically, crosses the barrier more quickly than on the preceding trial; within a few trials it becomes very efficient at escaping, and soon learns to avoid shock altogether. After about 50 trials the dog becomes nonchalant and stands in front of the barrier; at the onset of the signal for shock it leaps gracefully across and never gets shocked again. (Seligman, 1975, p. 22)
A dog that had first been given inescapable shock showed a strikingly different pattern. This dog’s first reactions to shock in the shuttle box were much the same as those of the naive dog; it ran around frantically for about 30 seconds. But then it stopped moving; to our surprise it lay down and whined quietly. After one minute of this, we turned the shock off; the dog had failed to cross the barrier and had not escaped from the shock. On the next trial, the dog did it again; at first it struggled a bit, and then, after a few seconds, it seemed to give up and to accept the shock passively. On all succeeding trials, the dog failed to escape. This is the paradigmatic learned-helplessness finding. (Seligman, 1975, p. 22, emphasis added)
Eventually, the experimenters removed the barrier from the shuttle box — in vain. The dog continued to lie there, passively enduring (accepting?) the continuing electric current. It took repeated trials where the experimenter physically dragged the dog to the other side of the box before the dog began to escape the shock on its own.
When these experiments were reported in 1967, they evoked an amazing amount of interest and controversy. The controversy was not about shocking the dogs, but about the theoretical meaning of the phenomenon of learned helplessness. Learned helplessness challenged the prevailing S-R models of learning. The proponents of these S-R models were subsequently defeated in the ensuing debate and learned helplessness became part of the “cognitive revolution” in psychology [The cognitive revolution supplanted the barren S-R models of learning and functioning that had dominated academic psychology for half a century] (for a detailed historical account, see Peterson, Maier & Seligman, 1993).
Inescapable shock research continues to the present day. Although I am not a PETA person, I think it bears mentioning (again) that other species do not deliberately inflict uncontrollable, inescapable pain. Only humans do this — in the psych lab, in abusive families, in prisons, and in the extreme sadism of sexual psychopaths. Deliberate cruelty and the instrumental use of others is the sole province of homo sapiens.
Curiously, the experts (Peterson et al., 1993) have applied learned helplessness to depression, physical health, growing up Black in America, and a variety of other problems, but they have largely avoided applying it to child abuse. In fact, they prefer to study the minor forms of learned helplessness. They worry that if learned helplessness is applied to severely traumatic situations that the model could be lost to the rest of psychology:
While there are instances of general helplessness, they seem most likely to occur in highly unusual situations, like the aftermath of concentration camp internment or a natural disaster. We would not wish to reserve “learned helplessness” only for these instances of generalized passivity. (Peterson et al., 1993, p. 147)
Concluding Comment:
We have been studying the animal defenses in order to distinguish their phenomena from the phenomena of clinical dissociation. We have now arrived at the concept of learned helplessness. When tonic immobility fails to stop a predator’s attack, learned helplessness is one of the possible outcomes. Evolution ‘created’ tonic immobility to deal with animal predators. I want to emphasize today that human predators are a much later phylogenetic development than tonic immobility and the other animal defenses. This phylogenetic circumstance has a crucial consequence: tonic immobility –the ‘last chance’ animal defense — is of little or no help when the predator is human.
By the way, we are still creeping up on clinical dissociation, but we haven’t gotten there yet. Next time, we will examine in detail what happens when tonic immobility encounters the predator that it was never designed to handle — humans.
Thoughts? Reactions?
Today, we focus on the ‘last chance’ animal defenses — those that spontaneously activate when an animal (which includes us!) is threatened with imminent death. So far, we have examined two ‘last chance’ defenses: (1) the evolution-prepared switch to accelerated information-processing that increases the animal’s ability to survive during a fall, car wreck, or plane crash; and (2) tonic immobility. Let’s take a closer look at tonic immobility so that we have a better understanding of where it fits in the larger scheme of things.
Conservation/withdrawal and the parasympathetic nervous system
In tonic immobility, the animal doesn’t move. It is unresponsive to the predator and appears to be dead. Because this immobility is so striking, it tends to dominate our thinking about tonic immobility. There is, however, much more to tonic immobility than its absence of movement:
“As a profound, but reversible state of motor inhibition, TI [tonic immobility] is often accompanied by intermittent periods of eye closure, diminished vocal behavior, Parkinsonian-like tremors in the extremities, and waxy flexibility. In addition to these overt changes, other physiological concomitants include changes in respiration rate (hyperventilation), heart rate (bradycardia), core temperature (hypothermia), and altered EEG patterns… [D]espite the animal’s outward appearance, ..subjects in TI continue processing information and remain aware of events occurring in their immediate environment…” (Gallup & Rager, 1996, pp. 59-60)
Tonic immobility is part of a broader category of coping that George Engel called conservation-withdrawal:
“conservation-withdrawal”…involves disengagement, withdrawal, and inactivity and serves to conserve energy, to reduce engagement with a threatening, overloading, or unsupporting environment, and sometimes to render the organism less conspicuous to predators. Sham death, ‘animal hypnosis’ [i.e., tonic immobility], hibernation, and aestivation represent some of the more obvious manifest expressions of conservation-withdrawal. (Engel, 1978, p. 408, emphasis added)
The biological goal of conservation-withdrawal is to conserve resources and to assure the autonomy of the organism until environmental conditions are once again more compatible. We postulate that such regulatory mechanisms for protection against environmental extremes characterize all forms of life and we place them at one end of an activity-inactivity continuum of the homeostatic processes serving survival.” (Engel & Schmale, 1972, p. 58, emphasis added)
The human autonomic nervous system has two reciprocally activated branches: (1) the sympathetic nervous system, which supports strenuous engagement with the environment (by increasing heart rate, vasoconstriction, and blood pressure; by inhibiting digestion; and by increasing the transport of oxygenated blood to the skeletal muscles, lungs, heart, and brain); and (2) the parasympathetic nervous system, which promotes disengagement from the environment in order to facilitate growth, restoration, and conservation of energy (by slowing the heart, facilitating digestion, and optimizing the functioning of the internal viscera).
Engel’s conservation-withdrawal and the animal defense of tonic immobility are extreme operations of the parasympathetic nervous system (Porges, 1995a). In other words, the normal homeostatic functioning of the parasympathetic nervous system should be supplanted by extreme defensive functioning (Porges, 1998) only when the animal encounters an inescapable predator or an overwhelmingly hostile environment.
Porges (1998) notes that the mammalian parasympathetic nervous system has two vagal nerves, whereas reptiles and earlier phylogenetic creatures have but one. The mammalian myelinated vagus operates as an ongoing brake on heart rate (and other things). The phylogenetically earlier unmyelinated vagus is “a neural component of a vestigial immobilization system” (Porges, 1998, p. 843).
Immobilization, hunh? Hmmm.
Porges goes on to say that reptiles use their primitive dorsal vagal complex as “an avoidance system [that] provides a shutdown of metabolic activity to conserve resources during diving or death feigning” (p. 843). In the diving reflex, a submerged animal undergoes a variety of physiological changes, including a slowing of the heart, that enable it to remain underwater for many minutes.
Fear Bradycardia
Interestingly, however, there is a profound difference between spontaneous diving and submergence under threat (Campbell, Wood & McBride, 1997). For example, a free-ranging alligator will remain submerged for 5 to 7 minutes at a time, with a heart beat of 25 to 35 bpm. Under threat, however, (due to the approach of a canoe) the submerged alligator’s heart rate plunged from 31 bpm to 2 bpm (Smith, Allison & Crowder, 1974)! Variations of this phenomenon have now been found to occur in a wide range of vertebrates, including those that are purely terrestrial. Under severe threat, different species undergo 37% to 90% slowing of the heart (Campbell et al., 1997)
This remarkable deceleration of the heart is called fear bradycardia. It is driven by the primitive unmyelinated vagus of the parasympathetic nervous system. The important thing to know is that fear bradycardia occurs when there is no escape. When escape is possible, tachycardia occurs (due to the strong activation of the sympathetic nervous system). Thus, free-ranging woodchucks that are approached in the open will experience tachycardia and flee. On the other hand, if they are approached near their burrow, they hunker down and bradycardia occurs (Smith & Woodruff, 1980).
Bottom line: “Fear bradycardia is directly proportional to the intensity of the threatening stimulus” (Campbell et al., 1997, p. 60; see also Smith & Woodruff, 1980).
Of still bodies and slow hearts
I think the immobility of the threatened alligator is a behavioral ‘choice,’ whereas the immobility of tonic immobility is anything but a voluntary choice. During tonic immobility, the animal is paralyzed. Whether voluntary or involuntary, both kinds of immobility are driven by the ventrolateral periaqueductal gray (vlPAG) in the brainstem. Fear bradycardia is also driven by brainstem structures — the dorsal motor nucleus of the unmyelinated vagus, the nucleus of the solitary tract, and the area postrema. The dorsal vagal complex and the vlPAG seem to operate in concert when the animal is exposed to extreme threat. Whether one controls or inhibits the other is still unclear.
Final comment
My apologies for all the neurophysiology today. This groundwork is crucial because, as we will discuss next time, some authorities are convinced that dissociation is inseparable from massive parasympathetic inhibition of the heart. Also next time: learned helplessness and conditioned freezing. We are finally sneaking up on clinical dissociation!
My unvarnished opinion is that the dissociation literature’s discussions of animal defenses (1) routinely conflate different kinds of immobility (freezing) and (2) fail to appreciate crucial differences between trauma and biological survival. I have been reviewing that literature lately. The most complete accounts are provided by Ogden, Minton and Pain (2006) and Scaer (2005).
Animal Defenses in Humans
Today, I will try to lay a foundation for a deeper analysis of animal defenses and how they operate in humans. To do this, I will discuss animal defenses simultaneously from three points of view: behavior, the autonomic nervous system (i.e., sympathetic and parasympathetic nervous systems), and the three levels of the brain (i.e., neocortex, limbic system, and brainstem). Discussions of animal defenses in the dissociation literature routinely focus on freezing. Each author, however, defines and classifies freezing in different ways. In what follows, I discuss 6 important biological, hard-wired phenomena — 4 of which involve immobility.
1. Immobility I (Orienting reflex): When an unexpected or novel event (a sound, sight, etc.) occurs (but is not extreme enough to provoke the startle reflex), the organism will reflexively become immobile for a few seconds, with its sensory organs focused intently on what just occurred. This is a deeply biological, normal reflex. And, as Pavlov (1927) said, “The biological significance of this reflex is obvious” (p. 12).
In humans, the immobility often ‘freezes’ the person in mid-motion, leaving him or her with arms or whole body frozen in mid-movement. To borrow a term from the attachment literature — a term that seeks to reference a very different kind of freezing — the orienting reflex is marked by “behavioral stilling.”
The immobility of the orienting reflex is accompanied by a rapid deceleration of the heart (i.e., bradycardia), an event that is driven by the parasympathetic nervous system. To be more precise, experimental evidence (see Sokolov & Cacioppo, 1997) indicates that orienting involves both an increased activation of the sympathetic nervous system and an even greater activation of the parasympathetic nervous system (that culminates in cardiac deceleration). Even reptiles have an orienting reflex (albeit one that is not accompanied by cardiac slowing). This means that the ‘machinery’ of the orienting reflex lies in the brainstem — the reptilian brain. In humans, the orienting reflex is rapidly followed by a conscious, higher-brain decision (about whether to continue to attend, and so on).
2. Immobility II (Unconditioned, instinctive freezing): The research literature on animal defenses calls this immobility “freezing.” Such freezing is classified as a post-encounter defense because the animal freezes just after it detects the presence of a predator in its environment. Thus, “Freezing is is an unconditional reaction to an encounter with an innately recognized predator” (Fanselow & Lester, 1988, p. 194). Unlike the immobility of the orienting reflex, however, this kind of freezing is not instantaneous. It is prompt and tactical. The animal freezes in a location and body position that is optimum for concealment from the predator.
Respiration is shallow and rapid. The animal is hypervigilant and hypertensive (elevated blood pressure). Fear is present, as is fear-induced opioid analgesia. Muscle tension increases as the predator comes nearer. In short, the sympathetic nervous system is increasingly activated as it prepares for fight or flight. Research (Vianna et al., 2001) suggests that this “reactive immobility” is an integral component of the active (mostly circa-strike) defenses that are organized by the dorsolateral PAG (dlPAG). Finally, this kind of freezing is a hard-wired, ‘instinctual’ reaction to an innate threat to life. As such it is not a conditioned response; it is an unconditioned response that is not based on previous experience.
3. Immobility III (Conditioned fear response –> freezing): This freezing is a conditioned fear response to cues that are associated with past pain and trauma. In fact, I suspect that it would be even more accurate to say that this kind of freezing is associated with past experiences of helplessness in the face of inescapable pain and abuse. My current intuition is that this is where Martin Seligman’s (1975) learned helplessness fits into the scheme of things.
Conditioned freezing is clinically very important; it repeatedly occurs in some survivors of abuse when they encounter a cue that is associated with previously inescapable abuse. This freezing involves intense fear, helplessness, a sense of weakness and defeat, and a general inability to take any self-protective action. The inability to protect the self implies that the dlPAG (the organizer of active defense) is inhibited or somehow ‘knocked offline.’ This freezing is driven by a different part of the PAG — the ventrolateral PAG (vlPAG). Conditioned freezing is probably characterized by a simultaneous activation of the sympathetic and parasympathetic nervous systems, but the parasympathetic nervous system is dominant. Despite this parasympathetic dominance, conditioned freezing is not the same as tonic immobility’s frank paralysis (see below).
I suspect that when a person experiences conditioned freezing, he or she is very much aware of all that is happening, but is unable to muster any clear, problem-solving thinking that could lead to action.
Finally, in a rather technical point for this blog, Vianna & Brandão (2003) have suggested that
“it is wiser to propose a dissociation of dlPAG and vlPAG as mediating responses to immediate and cued danger, respectively, than one based on the conditioned-unconditioned dyad” (p. 563).
I disagree with this proposal because, as a trauma/dissociation clinician, I am all too familiar with complex trauma survivors who not only freeze when they encounter cues that remind them of their past abuse, but remain passive (i.e, are unable to activate their dlPAG) when a stranger leads them out behind some building and rapes them.
4. Flight: Flight is the first of the three circa-strike defenses. Prior to flight, as the predator comes nearer, the animal is in a state of growing, hyperalert tension. At this point, the animal has a hair-trigger readiness to explode into action. At the last possible moment, if escape seems possible, the animal explodes into flight. Needless to say, the parasympathetic nervous system is inactivated and the sympathetic nervous system is highly activated. Flight is organized and driven by the dlPAG in the brainstem. Forebrain or cortical input at this point is minimal. De Oca, DeCola, Maren, and Fanselow (1998) suggest that the dlPAG can inhibit forebrain structures.
5. Fight: Fight is the second of the circa-strike defenses. The dlPAG switches to fighting if physical contact with the predator is unavoidable. The views of De Oca and colleagues about the dlPAG’s contribution to fighting are even stronger than their views about its contribution to flight:
“the role of the dlPAG emerging from this work is that of a structure that can inhibit activity in the forebrain structures during times of extreme risk, such as elicited by shock and predatory attack.” De Oca et al., 1998, p. 3432, emphasis added)
“Thus, it may be necessary for the amygdala to be inhibited in order to engage in active defensive behaviors like circastrike attack. It may be that in times of physical contact between predator and prey, the defensive needs of the animal are best served by complete midbrain control and activation of circastrike behaviors.” (De Oca et al., 1998, p. 3431, emphasis added)
Recent research has shown that De Oca and colleagues are quite right about this. Mobbs and colleagues used fMRI to study brain functioning during a game that involved a realistic virtual predator. The results were clear and dramatic:
“As the virtual predator grew closer, brain activity shifted from the ventromedial prefrontal cortex to the periaqueductal gray [PAG].” (Mobbs et al., 2007, p. 1079)
6. Immobility IV (Tonic Immobility): While the animal is fighting for its life, the sympathetic nervous system is in overdrive. If the animal’s fight is successful, it breaks free from the predator and flees to a place of safety. On the other hand, if the animal is unable to escape, a dramatic shift in behavior and functioning takes place. The animal collapses into total stillness and paralysis. It becomes totally unresponsive to the predator and seems to be dead.
This remarkable change is brought about by a complete shift from dlPAG dominance to vlPAG dominance. The sympathetic nervous system remains active, but it is now strongly suppressed by a massive activation of the parasympathetic nervous system. Powerful vagal control of the heart produces bradycardia, hypotension, and hyporeactivity (Depaulis, Keay, & Bandler, 1994; Porges, 1995). Evolution and natural selection have demonstrated that tonic immobility significantly increases survival when an animal is seized by a predator.
In my next blog post, I will discuss in detail the various possible outcomes (for humans and other animals) of tonic immobility. I hope to show that remarkably different outcomes may ensue when the predator is a human.
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Understanding Dissociation 