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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