When Animal Defenses Encounter A Human Predator: Part I

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?

Posted in animal defenses, dissociation, evolution, first-person accounts, human predators, research, Tonic immobility, trauma | Tagged , , , , , , , | 7 Comments

Disentangling Animal Defenses From Dissociation: Part IV

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!


Posted in animal defenses, dissociation, evolution, neurobiology, parasympathetic nervous system, Tonic immobility, trauma | Tagged , , , , , , | 8 Comments

Disentangling Animal Defenses From Dissociation: Part III

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.

A reminder: Some of the most interesting and insightful information is not contained in my blog posts, but in the Comments and conversation that you collectively contribute to each post. So, don’t forget to click on Comments below to read these contributions (and consider clicking on RSS – Comments on the right side of the a blog post if you want to automatically receive the Comments that are submitted by others). This reminder especially applies to reading the Comments that follow the last blog post (from a few days ago).


Posted in animal defenses, dissociation, evolution, evolution-prepared dissociation, first-person accounts, intentional/voluntary dissociation, parasympathetic nervous system, peritraumatic dissociation, Tonic immobility, trance, trauma | Tagged , , , , , , , , , , , | 23 Comments

Disentangling Animal Defenses From Dissociation: Part II

We have no idea where our animal defenses end and our dissociative symptoms begin. The more that I immerse myself in this area, the more I am surprised that the dissociation literature hasn’t thought more deeply about animal defenses. Animal defenses are mentioned here and there in the literature, but they are seldom subjected to a rigorous analysis vis-à-vis clinical dissociation. Probably the best existing discussions are those of Ogden, Minton, and Pain (2006) and Van der Hart, Nijenhuis and Steele (2006).

Let’s begin with a central distinction: Animal defenses are survival-oriented; clinical dissociation is not. Animal defenses protect our survival, our biological existence. Clinical dissociation protects our mind and our self. True, there are times when protecting mind or self may result in saving our lives, but biological survival is not what clinical dissociation is all about. Now let’s examine a second crucial distinction.

Dr. Livingstone, I Presume

In 1871, British explorer and national hero, David Livingstone, had been in Africa and out of touch for seven years. The New York Herald sent a reporter, Henry Stanley, to find him. After an 8-month search, Stanley found him. He greeted Livingstone with the famous words, “Dr. Livingstone, I presume.”

David Livingstone wrote an articulate account of his own tonic immobility during a near-lethal encounter with a predator:

I heard a shout. Starting and looking half round, I saw the lion just in the act of springing upon me. I was on a little height; he caught my shoulder as he sprang and we both came to the ground below together. Growling horribly close to my ear he shook me as a terrier does a rat. The shock produced a stupor similar to that which seems to be felt by a mouse after the first shake of the cat. It caused a sort of dreaminess, in which there was no sense of pain nor feeling of terror, though quite conscious of all that was happening.It was like what patients partially under the influence of chloroform describe, who see all the operation, but feel not the knife. This singular condition was not the result of any mental process. The shake annihilated fear, and allowed no sense of horror in looking round at the beast. This peculiar state is probably produced in all animals killed by the carnivora; and if so, is a merciful provision by our benevolent Creator for lessening the pain of death. (Livingstone, 1957, p. 12, emphasis added)

The crucial point in Livingstone’s account is that this state of mind took away all pain and fear, but it did not take away his awareness of what was happening. Livingstone remained “quite conscious of all that was happening.”

We saw this same mental awareness a few weeks ago when we examined evolution-prepared dissociation (e.g., what happens during a sudden fall from a great height). During the fall, time slows down and mental and sensory acuity become quite pronounced. Some of you described this sudden change of consciousness as a “hyperfocus” and as “the opposite of dissociation.”

The literature on tonic immobility in animals emphasizes a similar point:

it is now well established that…subjects in TI [tonic immobility] continue processing information and remain aware of events occurring in their immediate vicinity.” (Gallup & Rager, pp. 59-60)

It takes but a moment’s thought for us to realize that an evolution-prepared, animal defense must PRESERVE awareness and the ability to process what is happening. Your survival is not helped by being unaware of what is happening when you are being attacked by a predator.

Clinical dissociation, on the other hand, does not have the same ‘regard’ for our ability to think while we are dissociating. In Depersonalization Disorder, the disconnect from our normal emotional contact with self, body, and world is so profound that it impairs concentration and thinking. Similarly, many other forms of clinical dissociation impair the person’s ability to reason and problem-solve while he or she is dissociating.

If we were to speak of clinical dissociation as having a “mission,” it would certainly be the opposite of the mission of the starship Enterprise (“to boldly go where no man has gone before”). The mission of clinical dissociation is to avoid, block, or escape from pain and distress. And, because its priority is to escape from pain, both awareness and the ability to think are readily sacrificed when doing so provides an escape from pain.

Freud once said something similar about repression:

The psychical apparatus is intolerant of unpleasure; it has to fend it off at all costs, and if the perception of reality entails unpleasure, that perception — that is, the truth — must be sacrificed. (Freud, 1937, p. 237)

A Plea For First-Hand Accounts

There is much more to consider about the relationship(s) between animal defenses and clinical dissociation, but  I think that this is a good stopping place for today.

Our earlier discussion of evolution-prepared dissociation was greatly facilitated by your first-hand accounts. Your personal stories highlighted the clear state of mind that accompanied your falls and car accidents.

Today, I leave you with another request for personal accounts — of dissociation during maltreatment. Specifically, would you be willing to describe (1) the nature of your awareness of what was happening (i.e., clear, fuzzy, unaware, gone away, out of body, etc.), and (2) the extent of your ability to think clearly during the dissociative event(s).

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Disentangling Animal Defenses From Dissociation: Part I

We need to disentangle the phenomena of animal defenses (e.g., freezing, hyperfocus, tonic immobility, etc.) from the phenomena of clinical dissociation (depersonalization, derealization, amnesia, etc.). Animal defenses have been built into us by natural selection; as such, their phenomena are normal. On the other hand, natural selection did not build clinical dissociation into us (see Dell, 2009); clinical dissociative experiences are abnormal.

I am convinced that our empirical data on both peritraumatic dissociation and chronic dissociation are an undifferentiated mixture of (1) genuine dissociative symptoms and (2) the operation of normal animal defenses.

A Personal Comment About UnderstandingDissociation.com

I spent the last 6 days in Atlanta, attending the Board Meeting and the annual conference of the International Society for the Study of Trauma and Dissociation (ISSTD). During that time, I was too busy to make any new posts as I was completing my term as President of ISSTD. Now, I’m done. Free at last, free at last, thank God Almighty, I’m free at last!  🙂 Well, not exactly. Now I’m the Immediate Past President (an actual position, with a one-year term of office, on the ISSTD Executive Committee ).

Anyway, today I’m back home in Norfolk and we can renew our blog-ular (bloggish? blogite? bloggy?) discussions. The last 4 posts have addressed flashbacks. We are definitely not done with that topic, but my sense is that we need a break from it for a while.

Let’s talk about animal defenses and dissociation. During a delightful conversation with Steve Frankel in Atlanta (Steve is a PhD/JD –clinical psychologist/lawyer — from the San Francisco area), I learned that Steve is very interested in tonic immobility. Tonic immobility is an animal defense whose primary manifestation is total paralysis (such that the animal may appear to be dead — but is anything but). I, too, have a longstanding interest in tonic immobility (my computer contains 250 pages of notes on the topic). Steve and I plan to work together on this topic so that we can give a presentation about it next year at ISSTD in Montreal and, hopefully, commit our thoughts to paper for publication.

I am a great believer in ‘killing two birds with one stone’ (My cats just alerted: “Burd?Burd? Where burd? I can haz burd?”). Today, I will accomplish two things. I will begin to work on my project with Steve by describing these fascinating phenomena to you –the community of UnderstandingDissociation.com.

Animal Defenses

In 1988, Fanselow and Lester published a seminal paper on animal defenses. This article built on the prior work of Ratner (1967). Fanselow and Lester proposed that there is a continuum of predatory imminence. Put simply, they (and many others since then) proposed that many species of animal automatically exhibit a series of different animal defenses as a predator comes closer and closer.

1. Pre-encounter Defensive Behavior. During periods when an animal has not recently encountered a predator, it is not defensive and is free to forage for food, and so on. At most, the animal may constrict its roaming to areas that it ‘believes’ to be safe from predators.

2. Post-encounter Defensive Behavior. When an animal detects a predator in its vicinity, it undergoes a dramatic change in behavior — freezing — in a location that reduces its visibility to the predator. While frozen, the animal is in a state of very high alert. All of its senses are heightened, but its sensitivity to pain immediately decreases. Its breathing is rapid and shallow. The animal is highly attentive to its environment.

3. Circa-strike Behavior. As a predator is about to strike, the animal’s behavior undergoes another dramatic shift. In fact, the animal may successively exhibit three quite different responses, each designed to survive this encounter with the predator. First, the animal will probably shift into explosive escape behavior. If unable to escape the predator, the animal is likely to struggle, fight, and bite. Finally, if fighting is of no avail, the animal may suddenly enter a state of tonic immobility. This immobility (as if dead) will sometimes inhibit the predator’s attack, allowing the animal to escape, perhaps injured but still alive.

4. Recuperation. The animal retreats to a safe place where its spontaneous analgesia subsides.  The animal then rests and tends to its injuries.

Do Humans Have ‘Animal’ Defenses?

Yes, we do. In previous posts, we discussed what I have called evolution-prepared dissociation — an ‘animal’ defense which is specific to us humans. Similarly, there have been a few publications that have addressed tonic immobility in humans, especially in some rape victims (e.g., Suarez & Gallup, 1977; Marx, Forsyth, Gallup, Fusé, & Lexington, 2008).

On the other hand, there is a problem. Although we have some data which shows us what these phenomena look like in human beings, the truth is that we really know very little about this topic. There are far too few studies of animal defenses in humans. We simply do not know how similar (or different) our human ‘animal defenses’ are to those of other animals.

Please understand that this caveat is neither trivial nor pro forma. There are important reasons to shine a bright light on these potential differences. Forty years ago, Robert Bolles (1980) proposed that there are species-specific defense reactions. Species-specific means that there may be important differences in the fine details of an animal defense from one species to another. In short, there is every reason to carefully study human ‘animal defenses’ to learn how they may differ from those of other species.

What Do Our Own Experiences Tell Us?

In previous posts, we discussed a form of evolution-prepared dissociation that humans frequently experience at a time of extreme danger to survival: calmness, absence of fear, hyperfocused attention, time slows down, thought speeds up, enormous mental clarity, superb problem-solving, anesthesia. Several of you described such experiences.

Today, I am asking about a very different kind of evolution-prepared dissociation: tonic immobility. Have you had an experience of suddenly being unable to move when you could not escape an assault or likely death? If so, please describe your subjective experience in detail (if you can), but describe the trauma itself with as little detail as possible.

Your experiences of tonic immobility may be uncomfortable to ‘go near,’ so please (1) be careful in your remembering, and (2) choose your words judiciously if you describe such an experience in a Comment.

Posted in animal defenses, dissociation, evolution, evolution-prepared dissociation, first-person accounts, peritraumatic dissociation, Tonic immobility | Tagged , , , , , , , | 26 Comments

Are Flashbacks Just Memories?

Today’s post is really Trying To Forge a Deeper Understanding of Flashbacks: Part III. My choice of the above title, however, nicely encapsulates today’s topic and avoids the mind-dulling repetitiveness (“O, the wretched monotony!”) of continuing to use the same title.

A few days ago, I said that flashbacks have at least four striking features:

1. Flashbacks are experiential, marked by a sense of reliving, accompanied by sensations and affects).

2. Flashbacks are distinctly fragmentary.

3. Flashbacks are autonomous and involuntary.

4. Flashbacks are frequently associated with dissociative amnesia.

I addressed only reliving last time. Today, (unfortunately?) more of the same — but from a very different perspective.

Memory Researchers Say, ‘There Is Nothing Special About Flashbacks’

To oversimplify, there are two kinds of academic challenges to the clinical concept of flashbacks. First, there are those who appear to hold an ideological grudge against the concept of flashbacks. These grudge-bearing ideologues often selectively ‘cherry pick’ scientific findings, cheerfully omit or distort scientific findings, and may use thinly veiled ad hominem arguments. I refer to this contingent as skeptics. Their views are not the topic of today’s post.

Second, there are researchers who believe that well-accepted findings about memory are quite capable of explaining flashbacks. Their logic and empirical studies are eminently reasonable, straightforward, and are usually well done. I refer to them as memory researchers. Today, I will begin to discuss a program of research by Dorthe Berntsen at Aarhus University in Denmark.

Most memory research is about voluntary memory — memories that we search for and deliberately retrieve. Berntsen’s research is about involuntary memoriesmemories that just “happen.” These memories come from ‘out of the blue.’ They are spontaneous and unbidden.

I have just finished reading Berntsen’s book Involuntary Autobiographic Memories (2009):

Often memories of past events come to mind in a manner that is completely unexpected and involuntary. They come with no preceding decision to remember, with no plans and no commitment. They may suddenly pop up in response to stimuli in our environment or aspects of our current thought.” (Berntsen, 2009, p. 1)

Sound familiar?  Hmmm. You can readily see why this scholar and researcher of involuntary memory would ask, ‘Are the flashbacks that clinicians talk about any different from this?’

Momentary aside: Many of you will immediately recognize that Berntsen’s question reflects the eternal tension between clinicians and nonclinical academics. Clinicians describe dramatic clinical phenomena and propose theories and mechanisms to explain them. Nonclinical academics then say, “Yes, but… [a] ‘How is this different from what we already understand very well to be a natural phenomenon of X,’ or, somewhat more harshly, [b] ‘You are really talking about X and you clearly have not kept up with the excellent, well-replicated research about X,.’ or contemptuously, [c] ‘You guys have no idea what you are talking about (but we true academics do) and we pity the havoc that you are wreaking upon your clients!” Thus it has always been. And, one assumes, always will be.

I find Berntsen to be enlightening and enriching because she belongs to the first of these three groups of academics.

Berntsen cites Hermann Ebbinghaus (1885), the revered psychologist who pioneered and inspired all subsequent research on human memory. Ebbinghaus stated that there are three kinds of memory, one of which is involuntary. Thus, like Ebbinghaus, Berntsen claims that “involuntary memory is a basic mode of remembering of the personal past” (p. 3, emphasis added).

This mode of remembering is associative and, Berntsen suggests, the evolutionary forerunner of voluntary memory. In keeping with her evolutionary perspective, she concludes that involuntary memory is “unlikely to be specific to humans’ (p. 18). So — other species, too. A very basic mode of remembering.

Special Mechanisms

Nonclinical academics regularly disagree with clinicians about the nature of clinical phenomena. On the one hand, clinicians tend to posit the existence of a special (pathological) mechanism which generates the clinical phenomenon in question. On the other hand, nonclinical academics typically claim that no special mechanism is needed because well-studied universal mechanisms (in this case, the mechanisms of involuntary memory) are quite capable of producing that particular clinical phenomenon (in this case, flashbacks).

A few days ago, we examined Chris Brewin’s explanation of flashbacks. Yup. Brewin uses a special mechanism to explain flashbacks — namely, a pathologically weak connection between (1) overly strong imagistic-sensation memory (S-reps) and (2) weak or nonexistent verbal-contextual memory (C-reps). Thus, according to Brewin, there are (1) fragmented imagistic-sensation memories of the trauma and (2) an impaired narrative of the trauma. As a clinician, Brewin’s model makes a lot of sense to me.

But now, along comes Berntsen (and other memory researchers) who insist that flashbacks are nothing special. Flashbacks, they say, are involuntary, autobiographical memories that predictably follow a trauma. Oh, in case you’re wondering, Brewin is well aware of Berntsen’s research. She and other memory researchers are extensively cited by him in the article that we discussed a few days ago (Brewin, Gregory, Lipton & Burgess,   2010).

Let’s examine Berntsen’s work. Is her account of involuntary autobiographical memories a better (i.e., simpler) explanation of flashbacks than our typical clinical formulations?

Involuntary vs. Voluntary Autobiographical Memories

Berntsen discusses memory in terms of encoding, maintenance, and retrieval. She firmly asserts (and adduces research data which seems to support her claim), that voluntary memory and involuntary do not differ in their encoding or their maintenance. She argues that the only difference is the way they are retrieved.

Memories are voluntarily retrieved via an intentional, top-down, frontal lobe-driven search procedure. In contrast, memories are involuntarily retrieved via a bottom-up, automatic, associative process to a cue that is (usually) encountered quite by accident.

Associative retrieval endows involuntary memory with several notable features. In contrast to voluntary memories, involuntary autobiographical memories are more often specific (i.e., they refer to a particular episode), more often distinctive, tend to have greater relevance to the person’s life story, and more often produce an identifiable emotional impact and/or a noticeable physiological reaction (Think: reliving). In addition, these memories are quicker; they have a shorter latency in response to the cue that triggers them. These features of involuntary autobiographical memory are not just theoretical speculations; they have been demonstrated empirically in study after study.

What Triggers Involuntary Autobiographical Memories?

Berntsen divides her answer to this question into three parts: (1) factors that influence retrieval in both voluntary and involuntary memory, and (2) factors that are substantially unique to involuntary autobiographical memory, and (3) factors that research has shown to be highly associated with the occurrence of involuntary memories.

1.Factors common to both kinds of recall. Berntsen is at pains to enumerate the retrieval factors that are common to both kinds of autobiographical memory. I think she emphasizes these factors because she wants to counter clinicians’ claim that flashbacks are special and different — for example, that the mechanisms of flashbacks are different from those of other forms of memory. She discusses Brewin, Dalgleish & Joseph’s (1996) Situationally Accessible Memory (SAM) system which supposedly stores only memory that “was not fully consciously processed at the time of the event” (Berntsen, 2009, p. 151) — that is emotions, bodily sensations, or fragments of perception (Think: flashbacks). Berntsen says, perhaps with a certain degree of asperity:

This is a radical idea that contradicts what is generally known about attention during encoding and subsequent memory…” (p. 151).

In any case, Berntsen lists several factors that influence the accessibility of both voluntary and involuntary memories: the recency of the event, its emotional intensity, whether it was emotionally positive, its frequency of rehearsal (i.e., how often the person talked or thought about it), its degree of life impact, its novelty, and its distinctiveness. She reviews the experimental evidence which demonstrated these factors to be associated with increased retrieval of such memories, both voluntarily and involuntarily.

2. Factors that are disproportionately conducive to involuntary recall. Based on her research, Berntsen identifies three factors that are especially conducive to triggering an involuntary autobiographical memory: (1) a very infrequent cue that matches only one past event; (2) a cluster of simultaneous cues, several of which simultaneously match aspects of a particular past event; and (3) a commonly occurring cue that evokes a memory that involved that cue as part of a novel or quite distinctive context.

3. Factors that are highly associated with involuntary recall. Finally, Berntsen summarized the results of her research on the correlates of involuntary autobiographical memories. Cues were especially likely to trigger an involuntary memory if they matched a particular part of the memory content. The most frequent triggers of these memories were specific objects, activities, people, and themes.

Berntsen also found that certain states of mind were more likely to evoke involuntary recall. Most generally, involuntary recall is more frequent when a person is relaxed or in an unfocused state of awareness. Also, certain states of mind seem to sensitize the person to cues that might relate to one’s life situation (e.g., current concerns, important unfinished personal business, or a recent especially powerful event). Berntsen concluded that, if a person has a current concern that is highly pressing, then even very vague cues may activate memories that relate to that concern.

Final thoughts

Those of us who know a bit about flashbacks must recognize that many of the above points are associated with flashbacks. Now, we also know that these points are associated with all manner of involuntary autobiographical memories. Berntsen and other memory researchers contend that they have explained flashbacks (without needing to invoke any special mechanisms).

Have they? What do you think? Is there anything about flashbacks that the above account does not adequately explain?

More to come.

Posted in evolution, flashbacks, PTSD, skepticism, trauma | Tagged , , , , | 11 Comments

Forging a Deeper Understanding of Flashbacks: Part II

Flashbacks have at least four striking features:

1. Flashbacks are experiential, marked by a sense of reliving, accompanied by sensations and affects).

2. Flashbacks are distinctly fragmentary.

3. Flashbacks are autonomous and involuntary.

4. Flashbacks are frequently associated with dissociative amnesia.

In this post, I will focus solely on the first of these — the experiential/reliving quality of flashbacks.

Why Are Flashbacks Experiential Rather Than Cognitive?

Perhaps the best current answer to this question comes from Chris Brewin in England (Brewin, Gregory, Lipton & Burgess, 2010). Brewin is one of the leading cognitive psychologists in the world. He has been studying PTSD and its intrusive symptoms for the last 15 years or so (see also Brewin, Dalgleich & Joseph, 1996). Brewin proposes that humans have two memory systems for episodic and autobiographical memory: (1) a contextual memory system that represents an event via abstract, contextually-bound representations of the event (“C-reps”), and (2) a low-level sensation-based memory system that represents events via their sensations (“S-reps”).

Although Brewin prefers to characterize these two memory system in terms of whether the context of the event IS associated with the memory representation (C-reps) or IS NOT associated with it (S-reps), he is basically talking about the difference between verbal memory and imagistic sensation memory. In a nutshell, Brewin says that both of these memory systems are part of our normal functioning. They work together.

An extreme event (i.e., trauma), however, may produce very strong imagistic sensation memory (S-reps) and weak/disconnected or even absent verbal contextualized memory (C-reps) of the event. Brewin refers to this situation as “pathological encoding.”

Brewin’s explanation of flashbacks. If a person has:

(1) a weak/disconnected or absent verbal contextual memory of an event (C-rep), AND

(2) a strong imagistic sensation memory of the event (S-rep), THEN

(3) whenever the the imagistic sensation memory is activated, “it is vividly re-experienced in the present” (Brewin et al., 2010, p. 224). AND,

(4) if the verbal contextual memory is completely absent, it will produce “extreme reexperiencing, in which all contact with the current environment is temporarily suspended” (p. 225) [i.e., a dissociative flashback]

Brewin also considers flashbacks to be adaptive:

Flashbacks are an adaptive process in which stored information can be re-presented and processed in greater depth once the danger is past” (p. 221)

From this point of view, PTSD develops when a person fails to process the information contained in the S-reps. Brewin is quite clear in stating that such a failure is AN ACTIVE PROCESS which prevents integration of the information and perpetuates the flashbacks:

“If flashbacks are to persist. there must be mechanisms to perpetuate this lack of integration. PTSD sufferers show marked behavioral and cognitive avoidance and find their intrusions (or certain parts of them) too unpleasant to attend to, which could plausibly account for the fact that the corresponding C-rep [verbal contextualized memory] remains incomplete.” (p. 225)

I think that Brewin’s model has a clean and simple elegance. In terms of the parsimony that is highly valued in science, Brewin’s model is quite nice. Nevertheless, I have a few reservations.

1. Brewin considers flashbacks to be adaptive. This position has always bothered me and, perhaps, I now understand better why I feel that way. Certainly, part of this idea –that flashbacks are adaptive — must be correct. Certainly, we have an innate tendency to find consistency in our minds and to resolve things that don’t fit. The part of this that bothers me is that flashbacks are NOT the same as normal intrusive thoughts (which Horowitz talked about in terms of “the completion principle” and coming to terms with major life events). Flashbacks are not cognitive; they are experiential. Flashbacks are not thoughts; they are (often) a bit like sticking your finger in an empty light bulb socket. I find it hard to consider electric mental shocks to be ADAPTIVE.

2. Brewin states that flashbacks are caused by pathological encoding of an event. By this, he means that an event can be so extreme that it produces very strong imagistic sensation memory (S-reps) and weak/disconnected verbal contextual memory (C-reps). So far, I like this description of flashbacks a lot. My apprehension is about the next step in Brewin’s reasoning. In his view, all that is needed for a flashback to occur is for the imagistic sensory memory to be activated. Boom! Flashback!

I feel a bit like Peggy Lee — “Is that all there is?” Is there no other factor involved? I feel like something is missing. I feel this even more strongly when Brewin uses this same formula to explain dissociative flashbacks. According to Brewin, if the verbal contextual memory is completely absent, then any activation of the S-rep will cause a flashback that produces a complete loss of contact with the here-and-now.

What is the something else that might be missing? In nondissociative flashbacks, I think the missing piece is affect — usually fear. Have you noticed that both flashbacks and their treatment (i.e., some form of prolonged exposure) operate according to the model of a simple phobia. I think that flashbacks are a perverse positive feedback loop among the amygdala and the decontextualized S-reps (and perhaps the insula as well). This is basically a phobic reaction to the images and sensations associated with the traumatic event. In short, I think flashbacks are driven by a ‘pulsing’ amygdala.

I also think that there is something missing in Brewin’s explanation of dissociative flashbacks — namely, a hypnotic brain. I would be willing to bet that dissociative flashbacks only occur in PTSD patients with high hypnotizability. High hypnotizability is a normal trait, but I think a flashback operates as something of an implicit ‘suggestion’ to remember/reexperience the event. If this is correct, then  dissociative flashbacks are a binary phenomenon (flashback + hypnotic response). Elsewhere, I have described this binary phenomenon in terms of the flashback ‘hijacking’ a normal ability (i.e., high hypnotizability) or a normal mechanism (i.e., a hypnotic brain).

Time to end this post. It has gotten too long.

But, for the research mavens in our midst, there is a bonus round.

RESEARCH IDEAS: There are surprisingly few empirical publications on flashbacks. There are even fewer articles on the phenomenology of flashbacks.

1. If PTSD patients who report having dissociative flashbacks are compared to PTSD patients with no history of dissociative flashbacks, will these two groups differ in their hypnotizability?

2. What is the difference, if any, between the flashbacks (that are experienced in the first month after trauma) of those who go on to develop PTSD and those who do not develop PTSD?

3. What is the difference, if any, between the flashbacks of trauma survivors who develop Acute Stress Disorder (ASD) and those who do not?

4. What is the difference in the flashbacks that are experienced by PTSD patients with low dissociation scores vs. those that are experienced by PTSD patients with high dissociation scores?

5. What is the difference in the flashbacks that are experienced by PTSD patients with high hypnotizability and those that are experienced by PTSD patients with low hypnotizability?

6. What is the difference in the flashbacks of ASD patients with high hypnotizability and those of ASD patients with low hypnotizability?

7. What is the difference between the flashbacks of persons with DID and the flashbacks of persons with PTSD only (and are there two identifiable subgroups among the PTSD patients — dissociative and nondissociative)?

Note: The key issue in each of the above research questions is the phenomenology of the flashbacks. Not all flashbacks are the same. There is a great need for all kinds of phenomenological research on flashbacks.

Skepticism About Trauma and PTSD

Graduate students who are interested in such research topics are counseled to beware of skeptics in academia. Graduate students should know that there are some academics with highly jaundiced views about the reality of trauma, the reality of flashbacks, and the very existence of PTSD. These skeptics can be found in some clinical psychology programs in the US and especially in academic settings in the UK. Even Chris Brewin, a very well-respected British researcher of PTSD, found it necessary to title his recent book: Posttraumatic Stress Disorder: Malady or Myth. ‘Nuf said for now.

Posted in Acute Stress Disorder, dissociation, dissociative identity disorder, dissociative subtype, flashbacks, PTSD, research ideas, skepticism, trauma | Tagged , , , , , , , | 10 Comments