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.
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.
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!
What I love about the way this discussion is going is that it is preparing the ground to be able to differentiate between various forms of survival mechanisms and experiences. I think a lot of the apparent disagreements in this field arise out of people basing their comments on fundamentally different experiences. When all things are sorted out, there may be far less for people to argue about – what a relief that would be. Then we could all focus on how to help the people who are struggling with these phenomena.
Yes! That is exactly what I am trying to do. Piece by piece, bit by bit, to sort these things out, and then interrelate them in a dynamic picture of the whole (of human’s various responses to abuse).
thank you again for your clarifying exposition.
one small comment: porges adds that along with the neurophysiological phenomena you describe that are associated with what he calls, “immobilization with fear” (or “feigned death”), is the anaesthetic effect whereby the immobilized animal, if bitten or eaten, will feel little or no pain. i think this is worthy of our attention as humans, because it may have correlates with the emotional and somatic “numbing” observed in severe forms of clinical dissociation, not to mention depression.
The anesthetic or analgesic effects are, indeed, important — but complicated. The analgesia begins early in the sequence of predatory imminence — as soon as the animal notices a predator in the vicinity. Then there is the issue of not feeling the pain of being bitten if subsequently attacked by the predator (an excellent survival-enhancing phenomenon). Then, there is the analgesia that comes with the inescapable shock of learned helplessness training. We haven’t even gotten to the analgesia/numbing of clinical dissociation yet, and already I know from the literature that the various kinds of analgesia that I just mentioned each have a different mechanism!
So, yes. I agree. And, oh boy, like the movie with Meryl Streep, Steve Martin, and Alec Baldwin, It’s Complicated!
I’m fascinated by the neurophysiology information, thank you. It feels like certain reactions I’ve had in certain circumstances are actually starting to make sense now.
“some authorities are convinced that dissociation is inseparable from massive parasympathetic inhibition of the heart.”
I’ve been puzzling over this part for awhile. Does that mean they think there is ” massive parasympathetic inhibition of the heart” only during an event that leads to dissociation at a later time, or also during dissociation at a later time? Sometimes it’s confusing trying to keep track of how “dissociation” is being used in various discussions, at least to me. Sorry.
Some authorities seem to argue that any dissociative event, whenever it occurs, is marked by parasympathetic dominance. And, yes, it is very confusing to keep track of “how ‘dissociation’ is used in various discussions.” That is why John O’Neil and I edited a book on the topic, and that is why I am writing this blog.
We may be stalking the wild dissociation, but we are searching for clarity. When I give a presentation on dissociation, I usually open with a slide that says: “The concept of dissociation has never suffered from an excess of clarity.”
I’ve recently been reading your finishing chapter ‘Understanding Dissociation’, and while discussing it with a fellow student we came upon a slightly silly question, that I hope you’ll humour me in answering anyways. What’s your position the mind-body problem?
At first, I just assumed your position was double aspectism, but while discussing it, it has become apparent that you seem to draw a sharp distinction between the psychological and the physiological. Now I’m curious. Help?
Great book, by the way.
I’m proud to have it on my shelf.
Congrats on a job well done!