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!