Excessive sympathetic branch activity can lead to increased energy-consuming processes, manifested as increases in heart rate and respiration and as a pounding sensation in the head.1 Other symptoms include muscle tensing, clenching or grinding of teeth, tachycardia (irregular heartbeat), excessive sweating, pallor, tremor, startle, hypervigilance, panic, rage and constipation. Over the long term, such hyperarousal may disrupt cognitive and affective processing as the individual becomes overwhelmed and disorganized by the accelerated pace and amplitude of thoughts and emotions, which can be accompanied by intrusive memories as well.
FREEZE RESPONSE
Opposite to fight/flight, the parasympathetic action (freeze) is described as coming “down.” Human emotions include disappointment, grief, shame, guilt and despair; or in a positive sense, contentment, peacefulness and satisfaction. These feelings involve a decrease in tension, a drawing of energy inward with a tendency toward introspection. Laughter and tears are both usually a sign of parasympathetic activity, because both reduce tension. Other physical symptoms may include heart palpitations, nausea, dizziness, indigestion, abdominal cramps, diarrhea, incontinence, social isolation and withdrawal, substance abuse, constricted affect (a lack of apparent emotion), denial, cognitive impairment and dissociation.
In the case of the zebra we’ve described, if the fight or flight is not successful, at the point of recognizing defeat and impending death he goes into a state of helplessness and hopelessness. Physiologically, this is the freeze response. It appears as “feigning death” because of the sudden and extreme immobility, which is a last-ditch effort for survival because a lion will not eat an animal unless she kills it first. If the zebra convinces the lion that he has just dropped dead, the lion walks away and the zebra lives. The stress hormones are not discharged, as they would be after a successful fight or flight. Instead, they are counteracted by a new cocktail of hormones activated by the parasympathetic nervous system. The pulse and blood pressure, previously elevated by stress hormones, are now forced to drop precipitously. In fact, the overall vital signs drop so sharply that there is a danger that the animal will fail to recover even if allowed to do so. About one-third of animals who feign death like this die before they can recover. The endorphins released in response to a threat persist during freeze/immobility, rendering the zebra analgesic in the face of the injury from the attack. At this point the zebra is in a state of passive dissociation—not unconscious, but in an altered state of “suspended animation.”
If it so happens that the zebra survives the encounter after entering a freeze state, it enters a discharge sequence similar to the discharge of the stress hormones. The experience of escape is stored in procedural (unconscious) memory, increasing confidence and resilience for future threatening experiences.
If hormone discharge is blocked without causing death, however, the zebra suffers chronic physical symptoms of immune deficiency and a shortened lifespan, and behaviorally suffers depression and neurosis. You can see in people that excessive parasympathetic branch activity leads to an increase of energy-conserving processes, such as decreases in heart rate and respiration and a sense of ‘numbness’ and ‘shutting down’ within the mind. Such hypoarousal can manifest as numbing, a dulling of inner body sensation, a slowing of muscular/skeletal response and diminished muscular tone, especially in the face. Cognitive and emotional processing are also disrupted.
One example of this is animals in cages whose freedom of movement is severely restricted. Their resignation to “inescapable” trauma is called the defeat response, or learned helplessness, and represents a state of adaptation to living indefinitely with life-threatening trauma without further attempts to escape (fight or flight). Learned helplessness is the persistence of the non-discharged parasympathetic freeze response. We know this because blocking the parasympathetic nervous system (with a drug) also blocks the development of learned helplessness.2 Here, unable to discharge and complete the process of recovery from the freeze response, the experience of inescapable threat is consolidated in procedural memory, reinforcing the tendency to freeze in the future.
Such prolonged exposure to elevated levels of stress hormones within the context of the non-discharged freeze response creates damage to the brain’s hippocampus. And indeed, you can then imagine the impact on people who suffer regular abuse. Smaller hippocampal volumes, for instance, are reported in female adult survivors of childhood sexual abuse. This kind of damage leads to a loss of neurons and synapses (up to 18 percent), and results in corruption of thought processes and learning, particularly deficits of encoding short-term into long-term memory, and of envisioning future events that are different from the past.3
The traumatic experiences, then, etched in procedural memory but not converted into long-term memory, interfere with current working memory. In this case, past threats are perceived to be present threats, suggested by intrusive thoughts, flashbacks and hypervigilance. Not only does this obscure the ability to distinguish between past and present, but the repertoire of survival skills remains confined to those skills that were acquired up to the time of the trauma and people in this circumstance lack the resilience to learn new strategies. You could say that an aspect of these individuals is frozen in the past, because they lost part of (or much of) the connection to their essence at the time of the traumatic, shock-inducing event. In circumstances related to that trauma, at least part of their true selves is only connected to them in the past, while part of the present ego-self is a replacement from the archetypal members of the circus.
The Polyvagal Theory of Stephen Porges proposes two branches to the vagus nerve: one associated more with the older, reptilian brain and one associated with the more recent mammalian brain. He suggests that this dual nerve system gives us the freeze response on one hand and a calming effect on the other. While the polyvagal system directly operates only with the parasympathetic side of things, this control also operates indirectly as a “brake” on the sympathetic system, thus controlling both through its veto power, so to speak. Porges’s work documents how the body, through the vagal nerve system, determines whether parasympathetic activation triggers disappointment and shame on the one hand or contentment on the other.4
The good news is that, in cases where either the fight/flight or freeze response hasn’t been discharged correctly, the discharge can be facilitated therapeutically and damage to the brain and memory can be repaired. The hippocampus is part of the limbic system and is especially susceptible to hypoxic and ischemic damage (obstruction of the blood supply). Yet it is the only known region of the human brain that can replicate new neurons. Long-term potentiation (LTP) is defined as an increase in strength of synaptic transmission with repetitive use that lasts for more than a few minutes. In the hippocampus, LTP can be triggered by less than 1 second of intense synaptic activity and lasts for hours or more. This may account for the memory re-acquisition and re-contextualization that is possible when healing trauma. Through techniques such as catharsis, titration of threat cues, unwinding of bound undischarged energy and reprogramming of the perpetual fight/flight or freeze response, effective facilitation can indeed reverse the damage done and return the individual to a state of resilience and homeostasis.
Nature has given us this necessary and useful ability to enter fight/flight or freeze for self-preservation. It also gives us a way to shake off these states when they are no longer useful for us. In our zebra example, that survival after stress, which includes successful discharge of the excess stress hormones, results in