Theory: Neurobiology of Psychological Trauma Etiology

Neurobiology of
Psychological Trauma Etiology

ETM Theory in the title of this chapter emphasizes that were it not for the application of ETM's clinical component, Trauma Resolution Therapy, its results, and the need to explain why it did what it did, there would be no theory about the neurobiology of psychological trauma to describe in this book. That is, we did not compile this information and postulate this theory as scientists trying to understand and then find a remedy to a problem, but rather as counselors who were trying to explain the problem from the perspective of what we have found to be its solution.

Consequently, all descriptions of neurobiological influences and other biological effects that result primarily from surviving were postulated from a combination of

our observations of TRT’s facilitation
the study of standard textbook information about and research data related to neurobiology, and
a review of the literature on neuropsychology, neurobiology, neuroendocrinology, and immunology of trauma, loss, stress, and bereavement (the review is provided in About/ Comparison - Contrast/ Biology).

In making this review, which took approximately 2 of the 9 years required to produce the ETM text, we discovered that neuroscientists use a language of their own, which to say the least is difficult to understand. We attempt to mitigate this problem, caused by the use of technical language, with italics; they are used and intended to show that clarification through word definition is probably required for some readers — an italicized word or term means that a definition will be forthcoming shortly (by the end of the paragraph or, where there are numerous words to be defined, in a catch-all and following paragraph). This method should save your having to buy a medical dictionary, assuming that you do not own one, to get through the chapter.

The number of studies, various models, paradigms, and the panoply of findings, many of them contradicting, make this subject, the biology of psychological trauma, worthy of its own book. Regrettably, such an undertaking would change the character of this work as a whole and divert attention from the main theme — showing counselors and therapists how the TRT and ETM models define and address the etiology of psychological trauma; the biology of psychological trauma provides only a segment of the definition and address. Consequently, we have consolidated the biological information related to psychological trauma; our thesis reflects the consolidation. If the reader would like the detailed picture of the biology of psychological trauma, the bibliography from which we drew our conclusions and prepared our consolidation is provided in About/ Bibliography.

Why Should Counselors and Other Managers
Study the Neurobiology of Psychological Trauma?

Why study the neurobiology of psychological trauma?

If you do, such study explains the theory of the relationship between your applications of TRT to trauma victims and the neurological changes they undergo as a direct consequence of your actions; the relationships of grief and emotional pain to learning are clearly understood. Subsequently, you are supported in your focus on the etiology of psychological trauma: molecular facts replace psycho dynamic suppositions. Clarity and understanding can strengthen, that is, give certitude and greater meaning, to your efforts. This strengthening of you will provide confidence and benefit to your clients and to those professionals who act in association with you. Understanding the neurobiology of psychological trauma's etiology will set you above the fray; you will be prepared for the next century: the study and understanding of the neurobiology of psychological trauma is the future for the understanding of the value of talking therapies; the management paradigms emerging from these studies and understandings will then become the forerunners of all future human management endeavor.

This Chapter Says

The etiology of continuous psychological trauma is not a consequence of individual maladaptation or disorder, but a function of outside interference with logical neurological processes inherent in the brain's attempts to integrate change. That is, the pathology known as post-traumatic stress disorder occurs when social/cultural norms and drug use interfere with that brain integrative effort. The stoppage of integration activities continues the etiology of psychological trauma until the accompanying stress disorder develops.

The Brain is an Integrator

The brain is primarily an integrator of body functions and processes, including psychological processes. A primary goal is to maintain these functions and processes as ongoing. This brain integrative capacity is phylogenetic: meaning the integrative capacity has apparently been developed through evolutionary means and is encoded into the genetic structure. The brain will always attempt to integrate changes that affect the organism.

When an extraordinary event that introduces contradiction to the current system of psychological management occurs, the brain's attempts to integrate the changes initiated by the contradictions involve the genetically encoded instructions to reorder the functioning of neuronal processes and the restructuring of the neurons that provide for those functionings.

A "neuron" is the primary cell in the brain that conducts its operations, including those involving the integrative functions. "Neuronal processes" are complex, but when simplified here they refer to those processes ongoing within the structure of the cell (neuron) and that make it work. "Restructuring" involves actual physical, morphological, changes in the structure of the cell. These changes include biological depreciation and growth of neurons.

Unlike ordinary requirements of every day brain functioning and integration where the neurons act instantaneously to coordinate body and mental processes, psychological trauma creates extraordinary demands; the changes that occur are not solvable instantaneously because the physical depreciation and growth of the cell (neuron) have to be completed. The changes take time and require biological emphasis, referring to the stress response produced during and following traumatic events. It accords the biological functions necessary to make the morphological cellular changes.

The additional time required for the brain to facilitate the process of integration of psychological trauma can be analogized to the use of a computer. Where ordinary calculations are conducted at the speed of light and the retrieval of outcomes are fast, a major intrusion upon the computer's electrical and physical system, for example, an unexpected and powerful electrical charge introduced by lightning's overloading of the circuitry, will disrupt the functioning and cause the machine to require repair; the machine's circuitry will likely require rewiring, the addition of new parts, and possibly even the reconfiguration of the software (logic) that runs the system. Likewise, the brain's integration of psychological trauma involves multiple processes that are different from those rapid and usual processes that manage every day activities. Unlike the computer, however, the brain has to repair itself, which requires emphasizing the response to the problem through creation of stress. This response often then involves eliciting help from other people. The next subsection explains these integrative or repair processes as they relate to the neuropsychology of the memory that comprises existential identity.

Once the event occurs, 3 concomitantly occurring brain integration processes, which we call "memory systems," are initiated. These systems have both separate and interrelated purposes and functionings. The 3 memory systems include:

The process of extinction of the knowledge comprising the pre trauma memory traces containing existential identity. The process of extinction provides the initiation of the neurobiological underpinning of the psychological concept of loss.
Establishment of a new (second) memory trace that recognizes the contradiction to pre trauma existential identity as historic; the contradiction occurred in the past. This establishment in memory of the contradiction resulting from extinction serves as the integrating system's analytical/evaluative process; it provides the measurement of the degree of extinction and its effects on the organism's ongoing status. The second trace (system) also provides for the resolution of the extinction process initiated as system one.
establishment of a new (third) memory trace that temporarily (during survival) provides the basis for a new system of psychological management; the new memory trace replaces trauma-contradicted values, beliefs, images and realities: the replacements allow life and its management to begin again.

Although all of these systems are explained in greater detail in the following subsections, general definitions of some of the terms used here would probably be helpful for some readers. "Process of extinction" refers to the process through which the neuronal mechanisms that have provided for the storage of the particular (eventually to be contradicted by the traumatic event) value, belief, image and reality are altered; the efficacy of the functioning of the neuronal process underlying the previous value, etc., is reduced. "Efficacy" refers to alterations in the electrical chemical charges that sustained the value, etc. in the neuron before the trauma occurred. "Process of extinction" also means that something new, which in the case of trauma the new is also the opposite of the previous identity, is learned at the same time the efficacy of the neuronal mechanism underpinning the old value is being reduced. "Learned" refers to the method through which the neuron stores the electrical and chemical charge that represents learning and memory retention. Importantly, this new learning has a direct bearing on the reduction in efficacy of the pre trauma neurons. "Reduced" means that the process of extinction in this use does not refer to a total loss of the efficacy of those neuronal mechanisms; some memory is retained. A "memory trace" refers to a consortium of multiple and integrated neuronal processes that are combined to represent, in this explanation, a particular value, belief, image or reality, or related thought, emotion, or experience (described later). More definition about these various terms is accorded through consideration of them in later paragraphs.

Although these 3 systems are initiated and proceeding functionally at the same time, their developments and functionings are different; the degree to which each system's development and functionings proceed is different. The 3 systems' developments are also interrelated and they are coordinated and facilitated by the phylogenetic integrative capacity of the brain. And finally, the 3 systems are supported by additional neuroendocrine activity: protection (analgesia and alarm responses), signalling (distress vocalization [crying/grieving/exclaiming] and perpetual recall of the event), and remedy (stimulation of neurohormonal activity to strengthen signalling and enhance learning). We call this protection, signalling, and remedial aspects of integration "PSR."

The next several subsections explain each memory system as it is developed in response to the event. When the individual explanations are completed, we describe the interrelationships including the additional signalling, protection and remedial (PSR) activities.

Memory System One: Extinction of Existential Identity

As explained earlier, extinction refers to the process through which the efficacy of a particular level of knowledge is reduced in storage in neurons and in their connections. This process is the opposite of learning in the same neuron. We sometimes refer to this opposite as unlearning. In this subsection, we describe extinction by explaining learning first and then follow in the next subsection with an explanation of unlearning.

We point out here that the following subsections consist of considerable elementary description of synaptic functionings; however, the descriptions were not elementary to us as counselors when we initially engaged in the neurobiological research. They are necessarily provided in detail in this beginning subsection because synaptic action will be shown to hold the key to understanding of not only the etiology of psychological trauma, but the resolution of that etiology. If you would like another view of this information, the bibliography provides an assortment of references that provide similar descriptions.

Neurology of Pre trauma Existential Identity: Neuronal Learning

Generally, learning is accomplished when one neuron passes an electrical charge to another neuron (and sometimes when a charge is prevented from occurring). This charge is stimulated by the influx of sodium ions through neuronal membrane channels and the efflux of potassium ions from similar channels in the same membrane. As the 2 ion groups ebb and flow across the neuronal membrane, which also carries a charge, another and greater charge is generated. When this charge is stimulated to the degree that it surpasses the voltage necessary to become involved in the participation of work, the electrical charge, which is called an action potential, flows down the axon of the neuron's body where it is converted temporarily into a chemical process. An "axon" is the primary extension, the elongation, of the neuron from the cell body. Axons in the central nervous system may be short in length, less than a centimeter, or long, 3 feet (where the neuron extends to lower muscular operations). There is only one axon per neuron.

The electrical charge passing from one neuron to another begins through conversion of the electrical charge to a a chemical process. This conversion starts with the charge's stimulation of the neuron to release a flow of calcium across the end of the cell. The "end of the cell" is actually multiphysical and functional, but when used here it refers to the pre synaptic membrane, the last physical protrusion of the neuron before intracellular space is encountered. This pre synaptic membrane houses vesicles which in turn house neurotransmitters. Neurotransmitters are chemical substances that act as messengers carrying the charge out of the pre synaptic membrane and across the intracellular space, an open area or gap (called the synaptic cleft) that exist between neurons, to a waiting receptor that is physically located on the post synaptic membrane (the receiving membrane) of another neuron. As the calcium ions (from now on also referred to as Ca2+) are stimulated by the action potential of the initiating neuron (carrying the original charge) across the vesicles housing the neurotransmitters, they are released by the Ca2+ to flow across the synaptic cleft (the gap comprising the intracellular space existing between neuronal membranes) to the waiting receptors on the receiving post synaptic membrane of the neuron receiving the charge. Upon docking in these receptors of the post synaptic membrane of the other neuron, the chemical process is then converted back to an electrical one as neuronal gates are opened that stimulate the influx and efflux of sodium and potassium ions across the charged membrane of the receiving neuron. As these currents are stimulated they achieve another action potential. This receiving neuron, then, can become the initiating neuron for passing the current on to another cell -- the current (charge) is passed from one neuron to another.

The principal location for the physical expression of learning, which is the process of storage of learning in memory, is in the action occurring between the pre synaptic and post synaptic membranes (the place where the distinct neurons chemically connect through neurotransmitter activity). For example, as a neuron undergoes a particularly intense series of firings, the stimulation of 500 to 1000 action potentials in a second, the Ca2+ released across the pre synaptic membrane builds up; the Ca2+ stays in the pre synaptic membrane. This "staying" in the pre synaptic membrane, then, has the effect of moving vesicles (that house neurotransmitters) to a more ready position; the neurotransmitters are more readily releasable because of the continued influence of the calcium that remains in the area where the vesicles are housed. This process through which calcium builds up in the pre synaptic membrane and through which vesicles are made ready to release their neurotransmitters is called post-tetanic potentiation and is the underpinnings of the beginnings of storage of learning in memory. That is, as the multiple firings occur, the synaptic action (the chemical action between the pre and post synaptic membranes representing, respectively, the sending and receiving neurons) is strengthened by the additional amount of Ca2+ remaining in the pre synaptic membrane. This strengthening, which is the increased readiness of vesicles to release their transmitters, is the underpinning of storage of learning in memory: the neurobiological/molecular expression of learning.

Long-term retention in memory or learning, like retention of learning in memory for weeks, months and years, is an extension or graded expansion of the post-tetanic potentiation process. In long term learning, however, the receiving neuron plays an integral part in maintaining, even increasing, the probabilities that a charge will be sent to it. This effect on the probabilities that a charge will be chemically transferred is maintained or increased when the receiving neuron grows an extension of the cell that loops back to the pre synaptic membrane on the sending neuron; the growth, called a dendrite, carries retrograde messengers, substances that are similar to neurotransmitters, but different in that they serve different functions: they initiate the additional release of more calcium into the pre synaptic membrane of the original sending neuron.

To summarize, the initial charge passes down the axon of the initiating neuron, releasing Ca2+ when the charge reaches the area of the pre synaptic membrane; the Ca2+ then releases the neurotransmitters to flow across the synaptic cleft and dock at their proscribed receptors. This docking carries the charge to the next neuron as the chemical action stimulates in the second neuron the additional efflux and influx of sodium and potassium across that membrane's neuron; there is a new twist. Instead of the charge's only proceeding along the axon of the receiving neuron, an action via another chemical messenger, in this case a retrograde messenger called a calcium calmodulin kinase, is initiated along the channel of the dendrite (in some cases other mechanisms are used) that returns to the pre synaptic membrane where the charge was chemically transferred. As the kinase (the retrograde messenger) loops back to the pre synaptic membrane, it is received in a similar place from which the original chemical transmission was initiated -- the pre synaptic membrane. This retrograde reception releases more Ca2+ in to the pre synaptic membrane which makes more vesicles ready to release their transmitters for crossing again to the receiving post synaptic membrane; a cycle is formed at this synapse (the joining of the pre and post synaptic membranes) where the physically joined, thus strengthened, synapse perpetuates the prospects of carrying the charge, the action potential, across the synapse.

This perpetuation is the neurocellular and molecular expression of the brain's retention in long term memory of a thought, and as related to our interests a value, belief, image or reality. The process for maintaining this perpetual retention in the connections of the neurons is called long-term potentiation (LTP).

There is an aspect of the maintenance of long-term potentiation that is key to the process of extinction, and subsequently to the etiology of trauma. In actuality, neurons do not always achieve action potentials that result in the chemical transference of charges across synapses. In the non long term potentiated synapse the transference may frequently fail to occur. This failure is not of great concern to the functioning of the brain, however, as there is much duplication and redundancy built into the system of wiring; many neurons are simultaneously engaging in the same activity that make up the work of the memory trace. Some synapses will carry the charge, while in some synapses the charge does not carry across. The determination of firing is a consequence of randomness or probability.

For example, a non long term potentiated synapse may only have a probability of 30% that it will transmit the charge across the synaptic cleft. When LTP is initiated in the synapse, the probability of the synapse's transferring the charge to the post synaptic membrane through the use of the feed backing dendritic loop (the cyclical process that maintains greater Ca2+ inflows across the pre synaptic membrane to facilitate additional neurotransmitter release) is increased. Thus LTP results in the strengthening of the probabilities of the firing of the synapse to say, for example purposes, 80%.

In simplified terms, the more important a value, belief, image or sense of reality, the higher the probabilities that the synapse will fire: the greater the LTP. As explained later, the relationship of LTP to extinction is that following the trauma-causing event, which contradicts existential identity by providing the experience of an opposite to that identity, the LTP representing the neurobiological encoding of the contradicted value, etc., will undergo an alteration in the probability of synaptic transmission: a reduction in the efficacy of LTP, which is a principal underpinning of the neurobiology of extinction.

Before explaining how trauma affects this neuronal process of memory storage of values, beliefs, images, and realities, a few additional bits of information might be helpful in explaining the neuronal network as the biological underpinning of existential identity and its development. The next several paragraphs provide, generally, this additional information.

Storage of memory, learning, does not happen just in a single neuron. When learning occurs, like the adoption by a person of a particular value with which to run his or her life, the idea is coded simultaneously in multiple neurons (hundreds of thousands) simultaneously. Moreover, these neurons are interconnected by the various synapses on each of the neurons. The physical locations of these synapses exist on the body of the neuron, the axon that extends outward to carry the main charge, and on the dendrites that also extend from the body of the cell like thin spidery legged tentacles. A neuron in the brain may have 30 to 40 dendrites which then branch into more thinly formed dendritic substances; some of these substances are called spines. Attached to most of these dendrites, as well as the cell body and axon, may be upwards of 5000 to 10000 synaptic endings that connect this neuron to a multitude of others.

Neurons are plastic -- meaning they mold themselves to the experience at hand (neurons are not made of a plastic substance). For example, as the brain goes about learning something new, the neuron will strengthen and even add synapses or increase the size and thus capacities of current ones; in the process these changes increase the capacity to store the knowledge being inculcated. Moreover, dendrites can also be changed to adapt to the new memory demands, including providing for LTP. This molding or adaptive process is similar to the brain developmental process that occurs in an individual before the age of 8 years.

It is important to note that this neuronal growth is facilitated through protein synthesis in the cell, which takes a long time, that is, hours in the individual cell and thus days, weeks or even years to develop supporting structures (new knowledge for the new psychological management structure), especially when compared to the instantaneous process, for example, milliseconds, required to just transfer a charge. The number of neurons do not change, however, as neurons may die but not grown anew (as a rule) after that age (7-8). Consequently, when we say that an individual is growing new brain neurochemistry as he or she develops an existential identity (values, beliefs, images and realities), we are not saying that new neurons are developed, but that those that exist undergo considerable change to their physical structures. This change is important to understanding the process of extinction as it occurs in the neuronal mechanisms (again, described later).

Understanding that process of extinction is also facilitated by having a general understanding of the basic influences that control charges: excitation, inhibition and integration of each's influence on the cell. "Excitation" means that a charge is depolarized through the neuron. As this depolarization occurs through the influx and efflux, respectively, of sodium and potassium ions across the neuron's membrane, the action potential is generated.

Importantly, no electrical inputs from any one neuron provides enough stimulation to generate a depolarizing effect that is adequate to initiate an action potential. However, multiple inputs from other neurons will create such an effect and produce the action potential.

"Inhibition" is the process through which the depolarizing effect is stopped and the action potential precluded. Inhibition in the neuron is a hyperpolarization, or reduction, of the processes (the opposite of depolarization) that lead to the cell's reaching the action potential.

When a cell receives inputs from say 5000 synaptic connectors carrying information (charges) from other neurons, some of these connectors are excitatory in that they are caring commands to depolarize this neuron and create an action potential. Some of these synapses, however, are inhibitory -- they receive commands to inhibit the charge through hyperpolarization. The determination of whether the action potential is reached is made by the "integrative" component of the cell.

There are at least two such components, one existing in the cell body and the other located in the axon extending from that body. The integrative component will assimilate the total of the excitatory and inhibitory commands and processes and make the determination as to the amount of charge that will, in the end, influence the action potential. If there are more excitatory commands than inhibitory ones coming from the multitude of receiving synapses and the sum is adequate to fire the action potential, then the charge is created and passed on to the next neuronal configuration. If the integrative component of the cell determines that more inhibitory commands are present, then the actional potential is stopped --the charge is not passed on to the next neuron.

Importantly, inhibition of a neuronal charge, preclusion of the action potential, can have as important a role in learning as the excitatory command that produces the charge. For example, some neurons fire spontaneously, and the inhibition of that firing becomes itself an indication that learning is occurring as the non firing influences the amount of charge going to other neurons.

Through this integrative computer in the cell, the brain controls the assimilation of neuronal information and cellular decision making. When we address the issue of extinction, we will refer back to this process as a primary means of altering the efficacy of the long term potentiation housing the values, beliefs, images and realities intruded upon by the traumatic event.

Here we change the focus from cellular and wiring ("wiring" = neurons and inter neurons that connect memory traces in order to complete various functionings) considerations to organizational ones. "Organizational" refers to the location in the brain of the particular neurons in question. For example, neurons that form memory traces, that are in this hypothesis the physiological manifestation of thoughts making up values, beliefs, images and realities, are believed to be retained and synthesized in long term memory in the hippo campus, the neocortex and the amygdala; the literature does not validate conclusively these organizational locations (the specific locations are not important to the biological etiology hypothesis, only the functioning of LTP is important). There are connectors, inter neurons that connect neurons, that tie the existential identity to other brain processes. For example, management and decision making which may use aspects of existential identity, or think to change such identity, is likely to occur in the frontal lobe or other areas of the brain. Emotional activity, which is considered later, is spawned out of the limbic system. We will discuss the organizational aspects of emotion later (under the heading of PSR: protection, signalling and remedy) as we explain the effects of the trauma on the brain, but now focus on the emotional activity as it supports the formation of existential identity. This discussion centers on the role of the opioid system.

The opioid system produces neurotransmitters called peptides. Some of these peptides have strong influences on brain operations. In this instance (the focus on existential identity), as an element of identity is formed, for example, a particular belief is inculcated into memory, a parallel system of wiring reaching into the limbic system complex connects to a system of opioid correlative response. The parallel system of inter neuron connectors carries the command to initiate an action potential releasing the peptide, which is probably enkephalin, into the synaptic cleft where it binds to the receiving neuron. Upon this binding, a feeling of satisfaction, positiveness, and so forth is experienced; a positive feedback system of reward is established to cement actions that conform to the particular belief being adhered to. The wiring connecting the hippo campus, temporal and limbic systems also passes through the hypothalamus, which provides for the integration of the opioid system with the existential identity. Organizationally, this activity is also thought to be locused in the amygdala (and other brain subsystems described later). Thus, existential identity is underpinned in formation in another part of the brain by an ongoing motivational process -- the stimulation of enkephalin or other peptides that provide a natural opiate high when the ongoing status of the existential identity is affirmed and reaffirmed. The more enkephalin release and binding the greater the motivation to strengthen the belief, which requires additional long term potentiation activity supported by the addition of more synapses, dendrites, and other neurons that are then incorporated into the memory trace comprising the belief. Beta endorphin, a lesser powerful peptide, modulates the opioid-based interaction as neurohormonal support for neuronal learning.

The ongoing system of organism psychological management is an integrated system of neuronal and ever changing electrochemical activity dedicated to maintaining the ongoing status of itself and the organism. As we are about to explain, psychological trauma occurs when an event changes this construction. The more rapid the change the more demands put upon the system to adapt. The greater the demands, the longer the time required and assistance needed in making the necessary neurobiological adaptations. The next subsection explains this process as beginning with the extinction of neuronal memory comprising existential identity affected by the traumatic event.

Neurobiology of Post-trauma Existential
Identity: Unlearning (Extinction)

Following the event, all memory traces related to the particular aspect of existential identity being contradicted enter a process through which each cell comprising that trace no longer carries the knowledge as it did prior to the trauma. We distinguish this change with "as it did prior to the trauma" because the cell still retains the information, but without its previous influence on CNS (central nervous system) and psychological functioning. This phenomenon of neurological change as a response to trauma, which is not fully understood and explained within the literature, is called extinction. We also refer to extinction as unlearning.

In this work, you will find that extinction of the memory traces comprising existential identity is the biological underpinning of loss and the etiology of psychological trauma. This subsection explains our theory of this process as it relates to the trauma-induced contradictions to existential identity.

There are 2 functional, interrelated (to the degree that they are inseparable), and simultaneously occurring processes comprising extinction. One process involves the recording of a newly learned experience into memory; the establishment of a trace that is located parallel to the pre trauma existential identity trace. The other process involves the inhibiting effects of the new trace on the trace that existed before the trauma occurred. The inseparability results from the fact that were it not for the old trace, it would be impossible for the new one to exist at all. Moreover, the nature of the new trace is that it only exist as a contradiction -- a perception that a value, belief, image or element of reality does not exist, when in fact it still does exists as a diminished recording.

Where the old trace is replete with well developed dendritic and synaptic interrelators (between the neurons comprising the trace), the second and newly forming trace is initiated only with enough structure (newly forming synapses and dendritic growth) to alter the LTP comprising the pre trauma trace. The functional aspects of this new structure involves the new neuronal path acting on the old one to inhibit (retard) its neuronal (electrical-chemical) actions. We speculate that this inhibition occurs through the addition of commands initiated from the new trace and passed on through inter neuron connection to the old trace; the commands change the sum of the excitatory or inhibitory actions on the pre trauma neuronal circuitry to the degree that the integrative functions in the cell body and axon make a different decision to regulate the neurons involved before the trauma occurred. For example, if the pre trauma trace is comprised of a learned experience that is manifested by an excitatory command to initiate an action potential, the commands coming from the new trace representing the opposite of the previously stored learned experience will provide enough inhibitory charges to reverse the action potential, or at least interfere with the charge carrying process enough to reduce the probabilities that the action potential will be transferred. There will be a cascading, if not direct, effect on long term potentiation. Reduction in the probabilities of the action potential stops calcium flows, pertinent neurotransmitter crossings and dockings in the proscribed receptors required to open the channel gates that allow the impetus of the charge to be cycled back to the pre synaptic membrane. In other words, the new and inhibiting memory trace reduces the efficacy of the pre trauma trace by reducing the probabilities of LTP action (firing) from, say 80%, which may have developed over years as the particular value, belief, etc. was inculcated to serve the organism's needs, to, say 30%, probability of firing; the LTP action is neutralized.

If this trace has developed over many years (the neurons and synaptic connections comprising the trace are mature), and it serves a primary management need, then it will no doubt be comprised of considerable redundancies. The greater the contradiction to the original pre trauma traces, that is, the more threatening the traumatic event, the more the redundancies are also altered; the process of neutralization of the ongoing management system is made more profound. Moreover, this neutralization is locked into a continuing state of equilibrium-sustaining maintenance. That is, as the contradicting trace is learned, the LTP underpinning it is increased (from 30% to 80%) and the older trace is being inhibited (LTP is reduced from 80% to 30%) by the increase.

This locked state, the interlocking relationship between the old pre trauma and now inhibited traces and the new one creating the inhibition, is the neurobiological configuration of unresolved loss. Specifically, the neuropsychological concept of loss is posited in this theory to be the depreciation of the efficacy of the memory functionings of the existential aspects of the psychological management system that existed before the trauma occurred -- inhibition of the memory trace representing existential identity as it existed before the event occurred.

Moreover and very importantly, the inhibiting contradicting trace does not distinguish the contradiction by changing time or tense. In other words, the contradiction is simply the recording of an opposite -- the original identity does not exist, which opposite recording is maintained in its interlocked relationship with the now depreciated trace representing the pre trauma existential identity. The loss will remain unresolved until the neuronal commands inhibiting the original pre trauma trace are reversed and the LTP supporting the pre trauma trace is restored to its maximum probability of firing. This restoration can occur through restoration of the trace as it existed before the contradiction or through restoration of it within the context of some change. For example, the tense of the information may change from the way the person "believes" to the way he or she "believed." Such reversal is the function of the interplay of memory system two on the contradicting and contradicted traces and is described in greater detail as a component of the loss/trauma resolution process.

Before explaining the establishment of the brain's adjustments that are made in memory to this neutralized state, it might be helpful to remind the reader that other parts of the brain and the endocrine system also provide responses to the altered states described in this subsection. Those responses include the providing of protection (analgesia and alarm responses), signalling (distress vocalization and perpetual recall of the event) and remedy (continued stimulation of noradrenergic, adrenergic and hormonal activity to strengthen signalling and enhance learning: reversal of the altered memory state). As indicated earlier, we call this series of biological processes post-trauma PSR (from herein only "PSR") and discuss them after completing this section that explains the 3 general memory systems that are established by the integrative component of the brain as adaptations to the changes resulting from the traumatic event's effects on existential identity.

Memory System Two Places
Contradictions into the Past

If there is a singularly most important statement that can be made about the development of the system of memory considered in this subsection, it is that the subject matter is over viewed here because this second system is only initiated simultaneously with the development of the inhibitory process described in the preceding subsection. "Only initiated' emphasizes the fact that the trace is barely functional and does not play an important role until it begins to be strengthened during the resolution phase; hence, the reason for keeping the discussion to an overview. The detail of its influence is postponed until the resolution chapter.

The integrative component of the brain establishes a second system of learning that parallels the process through which the traces representing existential identity are being inhibited (as described in the preceding sections, the LTP comprising these traces is being reduced while the inhibiting traces are being strengthened) and the psychological management system stemming out of, and thus relying upon, those traces is being incapacitated. As different from the contradicting trace in memory system one, which trace is established and maintained as an ongoing (present tense) recording, this second system of learning is grounded in the reality that the contradiction occurred in the past. Because this perspective is the opposite of the contradicting or "not" trace comprising system one, that is, the contradiction is continuing to occur and maintained as an ongoing inhibitor of the original existential identity trace, the second system acts (or will continue to act as the resolution/integrative process develops) to inhibit the contradicting trace and excite, that is, return to its former levels of firing probability, the original and now inhibited trace representing existential identity.

Moreover, this second system is capable of analyzing the degree of change resulting from the inhibitory process. Importantly, during the resolution process this analysis or appraisal itself provides for the strengthening of this second system to the extent that the contradiction is learned to be historic -- the contradictory trace is inhibited and the existential identity trace is returned to its pre trauma firing levels. The reader will remember that this subject is emphasized as one of the neurological keys to the trauma's resolution and addressed again after considering the influence of PSR on the inhibited existential identity.

To summarize the second memory system, it is established at the time of the event, but weakly because it represents the fact that the contradiction occurred and in the recent past. As this past is lengthened, the second memory system will be strengthened; it will eventually offset the process of extinction ongoing in memory system one.

Memory System Three Provides for New and
Immediate Psychological Life Management

When pre trauma existential identity memory becomes inhibited to the degree that it is neutralized, the existential aspects of psychological management are incapacitated, the integrative component of the brain develops a third system of memory (learning) that provides for survival during the incapacitated state. "Survival" means that the system takes over almost as if it were a separate person, a separate psychological management system. The operational thought and behavioral manifestations of this system are described in a later subsection and the relationship of this third system to the 2 preceding memory systems is explained in the next subsection. We hope that it will suffice to say here that the excitatory commands (integrative neuronal motivation) for this system's development come from the effects of the incapacitated state resulting from the trauma on brain functioning. Moreover, this system is greatly stimulated and strengthened by PSR and thus addressed again with descriptions (examples) in the pertinent subsection that describes PSR.

Overview of the Interrelationship
of the 3 Memory Systems

Before explaining the 3 memory systems' interrelationships, a summary of the preceding sections may be helpful. The first memory system provides for the undoing of the neurobiology underpinning the psychological system of management that existed before the traumatic event. The second memory system is initiated to reconcile that undoing. The third system is providing for a new system of management that provides ongoing direction during the trauma's disruption to pre-trauma existential identity.

The three post-trauma memory systems are interrelated through the common brain integrative process; brain integration activities effect and manage the following neuronal changes in memory. As time passes memory system two produces additional synaptic and dendritic growth commensurate with the reality of the fact that the intrusion to memory system one is increasingly becoming an experience of the past. As this system two growth is stimulated, the person learns that the intrusion is past, the LTP of system two strengthens the influence of system two on system one. Thus, system two eventually inhibits the intrusion by inhibiting the contradicting trace that has inhibited the original trace comprising existential identity. This inhibition of the contradicting trace provides for the eventual interruption of the equilibrium existing between the trace representing existential identity (where LTP has been rapidly reduced) and the contradicting trace (the contradiction is maintained in the present tense as the reduction is always ongoing). The outcome of the disequilibrium: the contradicting trace is prevented from inhibiting the pre trauma existential identity trace; LTP underlying the existential identity trace sundered by the event is restored. This restoration occurs for existential identity either exactly as the trace existed before the event occurred or in the context of a different (past) tense -- the person says that this was my value, belief, etc. Regardless, the process involving the ongoing maintenance of extinction is reversed and the psychological management system previously stymied by the changes is again operational. Simultaneously, memory system three adapts; it is inhibited as the identity initially affected by the contradiction is strengthened. In this scenario, the brain's integrative component provides a final outcome: reconciliation of the 3 memory systems into a current reality. This reconciliation is discussed again in the resolution chapter.

There is another scenario; the reconciliation does not always occur. Invariably, this failure is a function of (absent comorbity with other biologically based mental health conditions like manic-depressive illness, borderline personality, or compulsive disorder) system three, the survival system, maintaining its strengths via the intervention of exogenous variables (see the heading, "Interfering Variables"). For now, hopefully it will suffice to say that the maintenance of survival system three blocks the integrative processes by interfering with the reconciling interactions that would be ongoing between memory systems' two and one were it not for the exogenously introduced and supported system three maintenance activities. Thus, some trauma resolution processes last longer than others; some last indefinitely.

Before explaining how this interruption occurs neurobiologically, we need to leave this overview and complete the descriptions of the 3 memory systems by describing their functionings as they are supported or otherwise influenced by PSR (protection, signalling and remedy). That description is provided in the next subsection.

PSR (Protection, Signalling, Remedy)

At the onset of this discussion, we emphasize that the components of PSR, protection-signalling-remedy, are not mutually exclusive processes. For example, biological activities that provide protection might also induce signalling and remedial processes, and vice versa. Moreover, as the reader will see, a biological process described as pertinent to one of the three categories is likely to be shown again to be pertinent to another category. These interchanges are a consequence of our attempting to provide an orderly schematic of an otherwise very complex and convoluted neurological series of processes. Our method for telling this story will be to, as we over viewed the 3 memory systems described above, explain PSR in terms of the individual categories; we will then provide a description of their interrelationships at the end of the individual descriptions.

To reiterate: protection stands for analgesia and alarm responses; signalling refers to distress vocalization and perpetual recall of the event; remedy refers to continued stimulation of noradrenergic, adrenergic and hormonal activity to strengthen signalling and enhance learning, a requirement for reversing psychological trauma's biological etiology: post-trauma memory system one.

Protection

Protection is provided through 2 primary processes: alarm responses and analgesia; the analgesia blunts physical and emotional pain. Each of these processes are underpinned by specific neurobiological functionings that are initiated by memory system one's cascading effects on locus ceruleus activity. The "locus ceruleus" is located in the center of the brain stem, which itself is found in the center and lower portion of the brain. The locus ceruleus is known for providing a biological, also referenced as primal, stress response to survival. "Primal' refers to the fact that the locus ceruleus is a part of the brain that formed during its earliest development. We consider the alarm response component of protection first; the anesthetic protective component is addressed second.

Alarm Response: Fight or Flight

Simultaneous with the contradiction to existential identity in memory system one, the locus ceruleus initiates a warning by exciting norepinephrine and epinephrine producing systems. "Norepinephrine" and "epinephrine" are chemical messengers, neurotransmitters, that are identified with producing and carrying out the stress response; norepinephrine and epinephrine interact to stimulate the autonomic (the sympathetic component) nervous system. This stimulation provides for increased heart and lung activity as a response to alarm -- the organism is aided in either fighting or fleeing.

Linked to the fight or flight response is the primal emotional response of fear; it drives the production of the norepinephrine and epinephrine. Fear has its own neurological basis, which is apparently locused in the brain differently from other emotions comprising the loss response. The neurological origin of fear is the locus ceruleus. The fear response is not as important to this theory and thus its explanation is saved for the review where the prominent neuroscientist Michael Davis's work on the neurology of fear is referenced.

Analgesia

When the trauma occurs, it may be accompanied by either physical or emotional pain, or a combination of both. The locus ceruleus initiates norepinephrine producing activity that carries the message through neuronal pathways that analgesia is required. In fact, the reader will find in the bibliographical section that norepinephrine and opioid neurosystems have an organizational and mutually supporting interrelationship. The message passes through the hypothalamus where it is then disseminated through a complex system of neuronal wiring to the pituitary gland (found just below the hypothalamus) and opioid system where the opioids endorphin and enkephalin are released to cross the pertinent synapses. As the opioids (primarily enkephalin, as it is the most powerful opioid) bind on pertinent receptors, the analgesia feeling is experienced. This analgesia experience protects the individual from the physical pain by blocking pain pathways.

Moreover, if the pain is psychologically derived, the binding of enkephalin will also create a similar analgesia experience; emotional pain is shunted too. The thought, state, and behavioral manifestation of enkephalin binding on its pertinent receptors is usually shock, disbelief and denial of the event and its effects. The emotional experience is equated to the feelings of numbness that accompany shock following a traumatic event.

Signalling

Signalling involves two processes: the retention of the event in memory as an ongoing (as opposed to historic) experience and the use of distress vocalizations (a scientific term used to objectify crying and exclamations for help). Both are explained in this subsection.

Retention of the Event in Memory

The event is retained in memory and receives much individual and social attention, apparently because the retention seems abnormal; the event happened in the past and the person should stop focusing upon it. The key to the event's retention in memory is the relationship that exist between the event's being maintained as an ongoing experience and the inhibited existential identity. "Ongoing" in this use refers to the repeated movie-like replay of the recollection, which recall is accompanied by a stress and emotional response. "Ongoing" retention in memory is different from the retention of the event as a historical, non repeatedly recollected, and without incapacitating stress or emotional effect, fact -- a recollection held by trauma victims who have resolved the trauma.

This relationship between the ongoing recollection and the inhibited (contradicted) identity is cyclical and reciprocal; moreover, the repeated recollection serves as a signal that the inhibited biological state, that is the particular contradicted value, belief, image or reality, or combination of the same, has not been disinhibited or behaviorally reconciled. "Cyclical and reciprocal" means that the relationship is self supporting of both the retention of the event and the inhibited state; there is no need for exogenous (outside the organism) processes to continue either the recollection or the inhibition.

An example of an "exogenous" process that might initiate recollection and continue inhibition is a new stressor or life experience that evokes the memory of the earlier event; the recollections and contradictions can perpetuate themselves even if additional bad things do not happen. The rest of this subsection explains the neurobiological aspects of that cyclical and reciprocal relationship.

The inhibited post-trauma existential identity sends a series of excitatory commands: maintain the memory of the event in the same state that the contradiction exists -- ongoing. The purpose of this maintenance of the ongoing status of the event is that it serves as a mirror or displacement of the ongoing status of the inhibited (stopped) post-trauma existential identity.

The result is a constant, obvious, and unequivocal message to the integrative component of the brain and to other people that the contradiction to existential identity, that is, the stoppage of existential identity functioning (interruption to the logic of the neurosystem), continues unreconciled. When the commands are sent, they form a new memory trace in association with the factual recording of the event.

This new trace is strengthened, like all long term memory traces, through long term potentiation. It is important to reemphasize that this trace is different from the recording of the event itself -- the new trace described here only provides for the event to be characterized as ongoing as opposed to past; the characterization is a direct consequence of the inhibited post-trauma existential identity.

The proof of this affair is in the logic; were it not for the contradiction to existential identity, there would never have been a traumatic event to record in memory in the first place -- there is no trauma or issue for concern absent the contradiction to existential identity. Thus, without the contradiction, the event would be maintained in memory like last week's trip to the grocery store.

Once this new trace characterizing the event as ongoing is established, it in turn sends an excitatory command back toward the inhibited post-trauma existential identity trace. However, rather than the target being the inhibited state, it is instead the parallel trace that provides for the inhibition -- the trace that represents the counter or opposite to the existential identity.

This opposite is stimulated again; the existential identity that existed before the trauma occurred is not in existence following the traumatic event, which is now also repeatedly and cyclically replaying. Excitation of this contradicting trace results in the strengthening, to the degree that it is maintained, of the command that inhibits the trace representing existential identity -- LTP is interfered with and continues to reduce the probabilities of synaptic firing. This command to inhibit the existential identity trace completes the cycle, which is summarized again here for emphasis.

Step 1:: The event occurs which, because it is a contrary phenomenon to the traces comprising existential identity, initiates a trace parallel to the pretrauma trace -- the initiation of the trace represents the learning of something new: the opposite of the pretrauma trace is true. We call this opposiste the contradicting or "not" trace. It is inhibitory of existential identity.
Step 2:: The contradicting trace sends a command to inhibit that which is said to no longer be -- the pretrauma existential identity trace is inhibited. This inhibition hyperpolarizes the cell and interferes with synaptic LTP. This interference stops the ongoing system's ability to use this trace in the management of the organism's affairs. Memory system is one is fully formed.
Step 3:: A series of commands are sent from system one to establish a new learned contradiction (trace) that manages the organism's perceptions of the trace maintaining the factual recording of the traumatic event. This perception is that the event is ongoing (as opposed to past). The ongoing recollection serves as a signal that the contradiction to existential identity has not been reconciled. Proof of this trace's existence and functioning is found in the logic of the theory itself -- if there were no contradictions to existential identity, the event would not be emphasized.
Step 4:: Once established as ongoing, the new trace that manages the perception of the event as ongoing sends commands back to the contradicting or "not" trace representing the opposite of the original pretrauma existential identity trace.
Step 5:: Excitation of the contradicting trace results in the reinitiation of the cycle: inhibition of the original and now contradicted post-trauma existential identity trace results in a reduction of the efficacy of LTP, the incapacitation of the management system, excitation of the memory of the event as ongoing, restimulation of the contradicting pathway, etc.

There are several features of this cyclical process that warrant emphasis:

The traces comprising the cycle have reciprocal relationships to the degree that they perpetuate the cycle (until the integrative component of the brain reconciles the changes resulting from the occurrence of the event).
The cycle provides for continued signalling that the traces comprising post-trauma existential identity have not been disinhibited -- restored to their pretrauma levels of LTP functioning.
The five steps described above and the traces comprising them are, while in engaged in this cycle, at the same time both inseparable and separate processes: each trace serves a specific and individual function, but is simultaneously dependent for its continuation on the cycle of reciprocal relationships existing between itself and other traces.

Distress Vocalizations

As memory system one becomes incapacitated by the equilibrium existing between the contradicting trace and the existential identity trace (where LTP for the first trace has been reduced), a command is sent to the opioid system that has been supporting the establishment of the original LTP in the pretrauma existential identity (see the previous subsection entitled "Neurology of Pretrauma Existential Identity: Neuronal Learning"). The reader will remember that when a value, etc., is established and then reaffirmed, a simultaneous binding of peptide, such as endorphin, or possibly enkephalin, provides a feeling of satisfaction.

Through the combination of this continued affirmation of existential identity, including the opioid stimulation (binding on receptors), the neuronal system is experienced as ongoing. Reductions in the existential identity's LTP produces an interruption not only to the existential identity (memory system one) ongoing status, but simultaneously an interruption to the parallel neuronal actions in the opioid system. This interruption results in the inhibition of the opioid neurons and thus a failure to complete the sequence across the synapse; the particular peptide fails to bind on the pertinent receptor.

The behavioral manifestation of this opioid failure to bind, to pass the charge via transmission of neuropeptide from presynaptic to post synaptic membrane, is crying and calling for help. The emotional experience is loss, mourning, sadness, and grief. Both the crying and experience of grief provide signals that the contradicting trace is still inhibiting the existential identity (traces) that existed before the event occurred; the modulating neuropeptide's failure to bind is reflecting the depreciation or rapid depression of LTP hosted in the original existential identity synapse.

Remedy

The remedy for ending the inhibiting effects of the contradicting trace (memory system one) on existential identity lies in the ability of the integrative component to produce adequate chemical responses to simultaneously provide for protection, produce and amplify signalling for identification of the problem's locus, and learn that the contradiction is past. This process will be explained in following subsections in this chapter and also in the chapter on resolution (and the bibliographical section). For now, the explanation is limited to a general discussion of the primary remedial influences of norepinephrine on protection and signalling, and learning that the contradiction is historic.

Norepinephrine (NE) and epinephrine (as a stimulator of NE) greatly influence learning; when they are present in larger quantities, learning (retention of an experience in memory) is enhanced proportionately. For example, when a rapidly changing event occurs, epinephrine and norepinephrine production (release from presynaptic vesicles) is increased; the additional neurotransmitter enhances the length of the period that information can be retained in memory.

The specifics of how NE accomplishes this enhancement is provided in the bibliography section, but for now, NE is influencing the probabilities of synaptic transmission of a charge, obviously resulting in the increased occurrence of long term potentiation. Thus, NE is instrumental in enhancing the learning process.

For now we can say without too much diversion, that NE strengthens protein synthesis to synaptic plasticity (the structural adaptation of the synapse to handle more LTP -- neuronal learning) and through stimulation of Ca2+ flows across post- and even pre-synaptic membranes; the post - synaptic flows also influence retrograde transmissions, which additional transmissions then lead to increasing presynaptic neurotransmitter release: completion of the enhanced LTP cycle.

This relationship of NE to learning is cyclical -- it provides a positive feedbacking loop for the brain as it integrates (through learning) the changes that have occurred in existential identity. Moreover, there are several of these feedbacking processes and they are interrelated. The feedbacking processes, their effects on learning (memory), and their interrelationships are described in the next several subsections.

NE Influences Memory System One

When the initial traumatic event occurs, the contradicting trace that inhibits the old existential identity is the new process being learned (the contradiction is being learned). Thus, as the locus ceruleus produces its norepinephrine during the fight or flight response to that contradiction, the contradicting trace is strengthened (LTP for the new trace is increased).

Through this strengthening, the inhibitory action on the original existential identity is also increased, incapacitating further the particular (or group of) values, beliefs, images and realities being contradicted. The positive feedback relationship between the contradiction and the production of NE is that the greater the contradiction created by the event, the greater the stimulation of the locus ceruleus; the more NE is produced, the more enhanced the contradiction, the greater the inhibition to existential identity, the greater the incapacitation: the cycle is completed with the production of more NE. Moreover, this cycle is continued indefinitely as NE continues to be produced after the event has passed; with considerable vigor, the contradiction is encoded into memory.

This encoding (in this use to mean the establishment of additional and stronger synapses) is, in effect, the encoding of loss in memory, which concomitantly encodes the event recollection cycle used for signalling (described under "Retention of the Event in Memory"). In this cycle, NE also plays a role as an important catalyst; the encoding of the event as an ongoing experience is strengthened through the locus ceruleus's production of norepinephrine, obviously leading to the enhancement of that recollection, which supports the continued strengthening of the contradicting trace and subsequent (and cyclical) locus ceruleus activity. Signalling through event recollection can remain clear and intense for long periods.

The other signalling method, distress vocalization, is also enhanced. It too, can remain loud and intense for long periods.

NE Influences on Memory System Three

The reader will recall that memory system three is the system that has been created by the brain's integrative component to provide for a new survival reality during the period in which the pre-trauma one is incapacitated. This new reality can include the retention in memory system three of blocks against the activity ongoing in memory systems one and two. Behaviorally, the person may believe as a consequence of system three activity that the traumatic event never even occurred.

Moreover, if the contradictions never occurred, the event is not recognized as ongoing. In some instances, both the contradiction (including the depreciation of the efficacy to existential identity) and the event can be blocked from conscious recollection entirely; the entire signalling cycle where the retention of the event in memory is maintained as an ongoing experience is blocked from consciousness by memory system three's strengthening. Where part of this strengthening is underpinned by stimulation of enkephalin (produced in and linked to the opioid system), norepinephrine's simultaneous production can strengthen system three: the learning (LTP enhancement) of the behavioral equivalent of denial.

As indicated, through the production of NE two helping processes are pitted against each other: signalling through retention of the event in memory as an ongoing experience and the development of a temporary survival reality to protect the organism against the changes. This new survival system and its associated protection is needed until memory system two, which integrates the contradicting trace into memory as a historic (as opposed to ongoing) event, has had an opportunity to develop its own strengths -- which development is primarily based on time. That is, the reality of passing time provides for synaptic and dendritic growth to eventually counter the strengths of memory systems one and three.

There is another neuronal process (related to NE activity) influencing memory system two's development. That process is discussed in the next subsection.

NE Influences Memory System Two

Memory system two, which provides for evaluation of the depreciation of efficacy of existential identity and the placement of the contradicting trace and event recollection into historic tense, is stimulated in this process through use of the signalling method -- distress vocalization. Distress vocalizations, themselves, then produce NE which enhances the learning of all the memory processes, but also has the effect of removing the previous blocks provided by memory system three (the new and temporary survival system). This subsection explains these processes and their relationships to the strengthening of memory system two -- the primary reconciling integrative memory system.

As synaptic and dendritic growth accompany neuronal development comprising memory system two, learning that the contradiction and the event are past tense is enhanced. This learning produces an inhibitory effect on the learning process established as memory system three (the survival reality); system three inhibition removes blocks against the realization that the contradictions and the event are ongoing. Inhibition of these memory traces underpinning denial also interrupts the binding of enkephalins as analgesia. The combination of enkephalin receptor blockade (of the opioid neurons that previously supported the denial through receptor binding) and inhibition of the traces comprising the actual thought responses making up the denial result in the more complete use of distress vocalizations.

As the reader will recall from having read the subsection "Distress Vocalizations" under "Signalling," the reduction in the efficacy of the existential identity trace also produces a blockade of opioid receptors; opioid blockade produces the behaviors and experiences, respectively, of crying/mourning and sadness/grief. Distress vocalization (DV) resulting from opioid receptor blockade is somewhat different from other CNS functionings in that DV requires the manifestation of motor activity: expression of the vocalization is required for it to have its desired positive neuronal feedbacking effect.

In other words, opioid receptor blockade produces a physical crying (cathartic) behavior which is in turn received by the same and other organisms sensorily. Sensory neurons pick up the cry and enhance an already ongoing autonomic system (respiratory and cardiac) response -- cyclically increasing production of NE.

Moreover, when reading the bibliographical sections, the reader will find that there is an even more direct relationship between opioid receptor blockade and NE release; opioid binding (excitation of opioid peptides like enkephalin and endorphin) inhibits (prevents) the release of NE. Opioid receptor blockade then releases norepinephrine. Thus, simultaneous with the DV's, NE is being produced to effect learning.

This time, the NE, which is distributed to all memory systems, has the effect of strengthening the system that is becoming ascendent, memory system two (where the trauma is being placed into its rightful historic context). This strengthening of this system over the others occurs because an inhibitory trace has already been established that reduces the efficacy of the traces underpinning the temporary survival identity (memory system three). This repeated and repeating inhibitory action accelerates the cascade of opioid receptor blockade (reduction of the thought system supporting denial of the changes ongoing in memory systems one and two) and concomitantly accelerates a similar blockade of those opioid system receptors that underpin existential identity -- extraordinary DV is produced.

Through this cycle, the production and influence of NE (through the DV cycle) and the passing of time, to include the process of synaptic and dendritic growth, memory system two comes face to face with the contradicting trace that has inhibited the pretrauma existential identity -- the etiology of loss. Inhibitory action produced by the growing memory trace two ensues; the action eventually begins to counter the strengths of the contradicting trace and a reversal of the cycle that has maintained the inhibition of existential identity and continued the retention of the event as an ongoing experience.

Over time, and supported by the frequency of distress vocalizations and the consequent production of NE, memory system two becomes ascendant, quashing altogether the former contradictions and ongoing aspects of the event recollections. The existential identity trace is restored to its pretrauma LTP levels and the event recording is left in memory without its ongoing memory appendage initiating movie like replays.

The ending of the contradicting trace's influence and the reversal of the post-trauma incapacitated state (of existential identity) produces an end to the commands directing the blockade of opioid receptors. In other words, the loss is resolved and the neurobiology is returned to a level of functioning unimpeded by the effects of the trauma.

The battles between the growths of memory systems one, two, and three is phylogenetically directed -- they are logical processes whose purposes all serve the brain integrating command. In some cases, however, these processes do not work themselves out in the best interest of the organism. We believe this failure is not, as a rule, a function of a particular person's brain integrative processing, but primarily a function of exogenous variables that interfere with the phylogenetic capacity. We address these interfering variables in the next section.

Interfering Variables

Generally, cultural/social processes that support memory system three over the integrative processes that occur between one and two will slow the brain's ability to integrate the traumatic event: interfere with the brain's ability to reverse the etiology. More specifically, any cultural/social response that blocks the use of the protection, signalling, and remedial methods by preventing such methods from functioning fully and properly, will also stifle the integrative process. There are two such responses that we delineate as interfering variables: stoicism philosophy and the use of pharmacological agents as medication of the stress responses that produce PSR. This subsection explains how these interfering variables influence the brain's integrative effort.

Stoicism Interferes with the
Brain Integrative Process

Where stoicism may be valuable for the achievement of certain tasks over the near term, for example, being stoic helps people to survive during and immediately following an event, over the long term stoicism's support of memory system three, against the propensity and need to manifest DV's resulting from the blockade of opioid receptors (opioid activity that modulates existential identity LTP), prevents the extraordinary productions of norepinephrine, the biochemical remedy that accompanies the cathartic experience. Blocking of NE production interferes with the opportunity to learn (see the previous subsection entitled "Remedy"). "Blocking" occurs through social/cultural admonitions to strengthen the new values of being strong and so forth; the new values supporting denial of the event and its effects. The society supports the enhancement of the opioid receptor binding process underpinning the be-strong-indentity: memory system three. Both processes then underpin denial, the primary encumbrance to brain integrative activities: learning.

There are some social/cultural exceptions to this pathological use of stoicism; funerals for the loss of loved one are supported by the culture and time-outs are accorded for grief to be expressed over such losses. In this case of rapid change to LTP, which stores the memory of the relationship being lost, the society often supports the existential approach that provides for the time to develop the appropriate synapses and dendritic connectors for memory system two. Moreover, this existentially-based cultural process emphasizes the value of distress vocalizations and heeds the signalling apparent in the repeated recollections of the loved one and his or her death. Through this existential process, and emphasizing the caring by others for that trauma victim, the integrative process between memory systems one and two are facilitated; memory system three is staved off after it has served its initial purposes.

Apparently, where various cultures have come to incorporate this brain integrative method when the change to identity is obvious, for example, immediately following the death of a family member, less obvious changes, for example, as occurs through a sexual assault, a battering, or near death experience, have not always warranted the existential approach where a period of time provides for synaptic growth and the encouragement to use DV's. This failure is probably a result of the lack of continuing physical evidence of the change; such evidence is always available when a person dies, the person is no longer available to be seen. We can note that recently, the last 30 years, a trend is developing toward the application of the grief process to these less obviously experienced losses.

We believe that stoicism, from the beginnings of the use of philosophy as a coping instrument, was produced out of an unresolved individual response to trauma; stoicism philosophy rightfully did and still does protect individuals from the etiology of trauma. When the philosophy is adopted collectively, many people within a culture use it, they become vested in protecting themselves from their collective etiologies through the imposition, projection, of stoicism onto individually and newly (trauma) affected people within the culture; projection of stoicism by the polity interferes with the brain integrative process of the individual, which interference, culminating in individual unresolved trauma, is assimilated into the collective psychopathology -- intergenerationally and intercivilizationally, the trauma is protecting itself, preventing its resolution for newly affected individuals and for the society as a whole. Without this collective-to-individual-to-collective cycle (systemic protective process), the etiololgy would always be reversed: psychological trauma would not be a problem; PTSD would not exist. There is one exception; like stoicism, drug use also interferes with the brain integrative etiology reversal process. This interference is described in the next subsection.

Drug Use Interferes with the
Brain Integrative Process

Drug use's effects are similar to stocism's; drug use interferes with the operations of both the opioid and noradrenergic systems, which effects in turn interfere with memory system two's attempts to integrate the brain's functionings into the current reality. Drug use affects are both general and specific. This subsection explains the differences between the two categorizations.

"General" interference by drug use refers to the means through which the drug, almost regardless (it needs to be at least psychoactive) of its pharmacology, works generally to strengthen the development of memory system three -- the survival system -- in its long term blocking of the prospectively integrative interactions between systems two and one. This "works- generally-to- strengthen" refers to the timing of the use and the timing of the integrative battle that is being waged by the development of system two and the influence of that development on memory systems one and three. In this timing, as the integrative process attempts to develop, periodic pharmacological applications retard (described in the next paragraph) the noradrenergic and opioid systems' participation in the integrative process. This retardation experience can occur to the degree that memory system three is supported indefinitely as the ascendent memory system; the person learns that anesthesia is available as an offset against the more painful brain integration process.

"Specific" refers to the actual influence of the various drugs' pharmacologies on norepinephrine and opioid producing and binding activities. Alcohol, the most prolific drug used, and unlike other drugs, is soluble in every brain cell. With regards to its role as an interfering variable, ethanol acts on the locus ceruleus to reduce noradrenergic activity. For example, it has been shown that ethanol, used in certain amounts, is a powerful retardant of the need for alarm responses -- the behavioral manifestations of locus ceruleus action.

Moreover, alcohol has anxiolytic and anesthetic effects through its ability to strengthen GABAergic transmission and reception. The GABAergic system is principally an inhibiting neurotransmission system; its neurons reduce excitability in other neurons. When alcohol invades the GABA neuron, gates that control the reception and passage of the charge are left open; the probabilities of action potential being reached are enhanced and more inhibition of exciting neurons occurs; reduction in excitability of neurons produces the anxiolytic (positive high) effect. More profound anesthetic effects occur when the presynaptic component of general neurotransmission is influenced: Ca2+ flows in all neurotransmitter systems are increased and more transmitter is repeatedly produced. Alcohol influences every brain neurotransmitter system and these effects are described in greater detail with accompanying bibliographical information in appendix E, section 3.

Opioid interactions are fairly precisely understood. For example, morphine can be applied in doses that prevent distress vocalizations entirely. This prevention occurs because the morphine binds on the receptor that has been blockaded by the integrative command -- in this theory the command responding to the contradictions to existential identity previously underpinned by opioid receptor binding. However, as the exogenously introduced opioid degrades, the receptors are again empty -- DV's are reinitiated. Through repeated frequency of use, the exogenously introduced opioid binding and degradation-resulting-in-non binding process can result in replacement of endogenous opioid transmission; the transmission of opioid neurotransmitters stops because the system no longer needs them. This stoppage can lead again to the need for more exogenous opioids to bind on the empty receptors.

Regardless of whether this process leads to addiction, the important factor relating to this process's influence upon our description of TRT theory is that the cycle of opioid binding interrupts the brain integrative process by interjecting an exogenously controlled, as opposed to brain integratively controlled, variable. That is, the brain integrative component no longer has control over the outcome as control belongs to the availability of the externally induced opiate; the outside interfering variable is replacing endogenous opioid activity, a necessary modulator of neuronal learning: the exogenous variable interrupts the opioid system's functionings under the brain integrative system; there are no more DV's nor NE productions available for reconciliation of memory systems one, two, and three otherwise natural interactive/integrative processes. Under either exogenous ethanol or opioid use, it is impossible to also fully and properly use PSR to continue the brain's integrative functions.

Two notes are required at this time. First, many people who have not been traumatized become addicted to psychoactive substances. In the process, considerable alterations to brain physiology occur similar to the changes being described in this chapter. We discuss this issue more fully in the bibliographical section; the subject is multiple sources of trauma -- comorbity of pathological chemical use and other causes of trauma. Second, there are other pharmacological products that influence the integrative process. Some are intended to end the symptoms of post-traumatic stress, but in the process, have the effect, in our view, of interfering with overall brain integrative functionings; the trauma's resolution is prevented by such pharmacological introductions, which is why we do not allow the application of TRT simultaneous with the application of pharmacological therapies.

Interruption of Circadian Systems

There is a long term neurobiological aspect of bereavement that has been introduced by Hofer (1983) that should be explained as likely playing a role in the biological change resulting from trauma (loss). We overview it here because we believe it describes an additional part of the biological process that follows traumatic episodes, especially where the traumatic event includes a loss or near loss of life.

Hofer hypothesizes that when relationships, or even abstractions of relationships (the memory of past relationships), are severed through the loss of one of the participants, there is an interruption of the biological systems that operate rhythmic regulators. That is, relationships or abstractions of relationships past, help to regulate daily biological processes that are based on daily timing. Disruptions of this regulation occur when either the person or the abstraction providing the regulatory effect is lost. Hofer then shows that the symptoms of biological disregulation are the same as symptoms of the long term aspects of bereavement (Lindeman, 1944).

Hofer's idea (interruption of rhythmic regulators) can be extrapolated to the loss that results from the contradiction to a value, belief, image, and reality that comprises existential identity; the abstractions forming existential identity are similar in composition to those psychological components that form the abstractions of relationships past and, more emphatically, of the actual relationships. To summarize this concept's influences on psychological trauma, in addition to the changes in memory described in the previous sections, existential identity includes the experience between people and disruption of this experience has a biological effect on rhythmic regulators.

Delayed Response: Additional Neuronal Change

If the social/cultural interfering variables, inappropriate (prolonged) applications of stoicism philosophy and drug use (described in a preceding section), are administered indefinitely, memory system three (the survival system) will likely predominate the integrative process for an equally indefinite period; eventually, the battle between the 3 memory system's attempts to reconcile the trauma can and probably will culminate in the dissolution/breakdown of the entire psychological apparatus. This breakdown is usually referenced as chronic post-traumatic stress disorder (PTSD).

During this psychological dissolution, PSR activity will become more acute and be seen as a problem (by those surrounding the trauma victim) in and of itself. If the acute and non positive applications of PSR are allowed to continue, additional and even more damaging neuronal change is likely to occur. This subsection overviews these additional prospects (various author's theories of the biological basis of post-traumatic stress disorder, the nosotropic perspective of psychological trauma, are referenced in the bibliography).

Generally, long-term failure (months and years) of the culture/society to resolve the trauma for a particular trauma victim will result in the elaborate encoding of the survival memory system for that person. "Elaborate" means that the LTP of the survival system is strengthened by not only increasing the probabilities of neuronal firing, but through extensive synaptic and dendritic growth -- an entirely new neuronal support is developed for an altogether new psychology. All the while, the neuronal interactions, cycles, supporting the inhibition of the existential identity that existed pre-trauma are continuing also, making the differences between the traces representing the loss to identity and the survival system more pronounced and dramatic. The pronunciation is that the new system thinks everything is OK and the neuronal paradox underpinning system one gives ever continuing evidence that everything is not all right. The drama results from the war between additional neuronal interplays that are equally offsetting and supporting; the contradictions represented by the ongoing actions of memory system one are creating survival activities that protect the organism against system one's dislocated state and at the same time the survival system not only keeps the dislocation going, but it adds to it as the behaviors created by the dislocated condition continue to contradict additional elements of existential identity: more system one configurations are created. This neuronal paradox and dislocation is the underpinning and basis of psychological dissociation. Add interfering variables, stoicism and drug use, into this melee and the phylogenetic brain integrative process has little chance of doing its job.

This paradoxical and increasingly conflictive neurological and behavioral state is exacerbated by an also increasingly dramatic need for and use of PSR; wide emotional swings, ever continuing event recollections, hyperarousal and hysteria hallmark the behavioral manifestations of PSR's more dramatic usage. During this hyperactive period, which may be prolonged if the culture doesn't know how to respond, the over use of the PSR system is likely to create sensitization to the various neurochemicals required to operate the brain functionally; the changes invariably include over and under productions of such neurochemicals. These changes are discussed more fully in About/ Comparison - Contrast/ Biology when considering the views of those professionals (Kolb, van der Kolk, Kosten and Krystal, and Charney) who focus on the chronic aspects of PTSD. For now, we can say that the principal neurochemical under-production that causes the greatest concern to us is that of the transmitter serotonin, an invaluable neurochemical element to the learning process; serotonin acts as a second retrograde messenger that stimulates increased pre-synaptic Ca2+ flows: learning is thwarted without adequate serotonin.

Moreover, lower amounts of serotonin are statistically linked to suicide. Other neurochemicals, for example, transmitters like dopamine and norepinephrine and the neuroenzyme monoamine oxidase (MAO), are increased or decreased at different times in response to psychological trauma. These other neurochemical changes in response to psychological trauma and their influences on behavior are discussed in the appendix.

Neurological Axioms of TRT Theory

There are several axioms of the TRT theory of biology of psychological trauma that can serve to synthesize the linkages between the trauma-causing event and the subsequent neurobiological change. Those axioms are described here.

The greater the importance of a particular value, belief, image or reality to the ongoing status of the organism, the greater the pretrauma long term potentiation (LTP) of the memory trace comprising that aspect of identity.
The greater the difference between the event and the correlative element of existential identity, and the more rapidly the difference is introduced (without the benefit of time to provide for adaptive neuronal learning, including the physical development of synaptic and dendritic additions to provide for preparation for the changes long term), the greater the contradiction and subsequent rapid (and discombobulating) reduction in the efficacy of pre-trauma existential identity LTP.
The greater and more rapid the reduction of the efficacy of LTP in the original memory trace comprising the contradicted existential identity, the more distinctly initiated the three memory systems and more pronounced the need for and use of PSR.
The greater the interference (applications of stoicism and drug use) with the brain integrative process, that is, the longer the interferences require PSR activity past the point phylogenetically required of the particular brain integrative process, the more likely that additional and destructive neurochemical change, as different from the change that predominates during the constructive usage of PSR, will occur.

Summary: ETM Theory of Psychological Trauma

This section summarizes the ETM hypothesis of the biological underpinnings of psychological trauma. The summary also correlates the biological hypothesis to its thought and behavioral (psychological) correlates, the 4 psychological trauma patterns and the paradoxical system of control, described in Part One.

The etiology of psychological trauma is the establishment of a new and contradicting memory (neuronal) trace that inhibits the pre-trauma traces that comprised the pre-trauma existential identity; the new inhibiting action reduces, by reducing LTP, the efficacy of the knowledge stored in the traces' LTP. Following these reductions in LTP, the existential identity aspects of psychological management are incapacitated. The newly inhibited state is represented psychologically as loss; a depreciation of the existential identity LTP is a loss of the Self.

The brain's primary evolutionary directive is integration of all processes affecting the organism. In that regard, the brain attempts to integrate the changes brought about by the event. These integrative efforts include, in addition to the inhibitory commands of the contradicting trace on the original neuronal activity comprising pretrauma existential identity (called memory system one), the establishment of a memory system (two) that places the contradictions to existential identity into the past (and increasingly proper historical perspective), and the establishment of a temporary memory system (three); it is used for survival. The integrative functions of these 3 memory systems are supported by 3 neural activities: protection of the organism (autonomic activation for fight or flight and opioid system activation for analgesia), signalling for assistance (repeated recall of the event through reciprocal excitatory - inhibitory interneuron activity and the use of distress vocalizations) and remedy (the production of neurochemicals like norepinephrine to enhance neuronal learning -- the underpinning of the brain integrative process). We call this protection, signalling, and remedial response "PSR."

Barring exogenous interferences, the phylogenetic brain integrative process will be successful at providing the integration. Such interferences can occur when memory system three is emphasized by externally initiated processes over the other memory systems and against the phylogenetic capacities available through the brain integrative process. These interferences usually include the use of philosophies like stoicism that encourage the application of survival philosophies long past their original value (stoicism provides much needed action defense during survival) and the use of psychoactive drugs that medicate the stress response. Both variables interfere with brain integration activities by preventing the full and unfettered uses of PSR; PSR is used to end the inhibitory effects on the neurons comprising existential identity. PSR enhances neuronal learning.

If the interferences are allowed to continue, additional and destructive neurochemical changes may occur. For example, the availability of serotonin may be reduced, which reduction is linked statistically to depressive episodes that lead to suicide. Absent suicide, this condition can remain long lastingly destructive; the condition can become apparently chronic PTSD.

Thought/behavioral manifestations of this biology, include paradoxical and dichotomous activities; some survival responses have opposite goals and missions. In that regard, the responses are attempting to resolve the trauma and at the same time prevent the resolution. The result is a continuing psychological and internal tug-of-war and the likelihood that some of these activities will themselves serve to place more neurons representing existential identity into the process of extinction. Additional neuronal interactions similar to those comprising the first 3 memory systems and PSR will develop, except that these new survival initiated ones will serve to support the original survival memory system three's predominance against the integrative efforts of the original memory system two. The psychological result of this increasingly disparate and at the same time convoluted neuronal process is dissociation -- the ascendence of a paradoxical system of control that influences all psychological decisionmaking processes.

In addition to the paradoxical system of control, the neuronal composition of trauma described by the 3 memory systems is represented in TRT theory by 4 psychological trauma patterns. They, and their synthesis with the biological/neuronal elements of the theory, are described in the following (1-4) paragraphs.

Psychological trauma pattern 1:: Psychological trauma pattern one includes the initial experience of the event; it contradicts existential identity (the values, beliefs, images and realities that underpinned the psychological management of the person before the trauma occurred). The process of extinction for the neurons representing this existential identity trace is initiated and accompanied by the introduction of PSR (protection, signalling and remedial neurological activities).
Psychological trauma pattern 2:: The contradictions to existential identity result in loss. This loss is represented neurologically as a combination of an equilibrium established between the contradicting and contradicted trace (that we call memory system one), the maintenance of a cyclical and reciprocal relationship between the contradictions to existential identity and a new memory trace that carries the event in memory as an ongoing experience, and the establishment of another memory system (two) that evaluates and measures the degree of depreciation resulting from the contradiction; system two eventually strives to place the contradictions and the ongoing event recall traces into extinction.
Psychological trauma pattern 3:: Survival responses develop. These responses, that are eventually manifested psychologically as a paradoxical system of control, are initially underpinned by the formation of neuronal memory system three, the new memory system that the brain develops to provide for psychological management during the initial trauma-induced incapacitation of existential identity. Moreover, these survival responses, themselves, can become contradictions to existential identity; they then create more loss and additional neuronal change, culminating in psychological dissociation (see the next pattern 4).
Psychological trauma pattern 4: Loss resulting from the survival responses' contradictions to existential identity is underpinned by neuronal processes similar to those representing patterns 1 and 2. There is an exception. These neuronal processes will take their commands from the original memory system three and thus always serve to divert conscious focus from the brain integrative and psychological reconciliation process that is attempting to end the extinction to existential identity resulting from the original trauma-causing event. Thus, the 4 psychological trauma patterns are connected motivationally and logically in their underlying neuronal configurations.

There are several axioms to this theory that when synthesized state that the more important the pretrauma existential identity is to the ongoing status of the organism, the more dramatic the cascade of neuronal and psychological change; the greater the demands placed upon the integrative functions of the brain. Moreover, the further these integrative functions are pushed (by external forces and then the person's paradoxical system of control) past their phylogenetically determined limits, the greater the propensity for the effects of psychological trauma to become more destructive; greater neurochemical change and the occurrence of the chronic condition are more likely

Why Should Counselors and Other Managers
Study the Neurobiology of Psychological Trauma?

This Chapter Says

The Brain is an Integrator

Memory System One: Extinction of Existential Identity

Neurology of Pre trauma Existential Identity: Neuronal Learning

Neurobiology of Post-trauma Existential
Identity: Unlearning (Extinction)

Memory System Two Places
Contradictions into the Past

Memory System Three Provides for New and
Immediate Psychological Life Management

Overview of the Interrelationship
of the 3 Memory Systems

PSR (Protection, Signalling, Remedy)

Protection

Alarm Response: Fight or Flight

Analgesia

Signalling

Retention of the Event in Memory

Distress Vocalizations

Remedy

NE Influences Memory System One

NE Influences on Memory System Three

NE Influences Memory System Two

Interfering Variables

Stoicism Interferes with the
Brain Integrative Process

Drug Use Interferes with the
Brain Integrative Process

Interruption of Circadian Systems

Delayed Response: Additional Neuronal Change

Neurological Axioms of TRT Theory

Summary: ETM Theory of Psychological Trauma

Home

ETM Pro

About

Theory

Why Should Counselors and Other Managers Study the Neurobiology of Psychological Trauma?

This Chapter Says

The Brain is an Integrator

Memory System One: Extinction of Existential Identity

Neurology of Pre trauma Existential Identity: Neuronal Learning

Neurobiology of Post-trauma Existential Identity: Unlearning (Extinction)

Memory System Two Places Contradictions into the Past

Memory System Three Provides for New and Immediate Psychological Life Management

Overview of the Interrelationship of the 3 Memory Systems

PSR (Protection, Signalling, Remedy)

Protection

Alarm Response: Fight or Flight

Analgesia

Signalling

Retention of the Event in Memory

Distress Vocalizations

Remedy

NE Influences Memory System One

NE Influences on Memory System Three

NE Influences Memory System Two

Interfering Variables

Stoicism Interferes with the Brain Integrative Process

Drug Use Interferes with the Brain Integrative Process

Interruption of Circadian Systems

Delayed Response: Additional Neuronal Change

Neurological Axioms of TRT Theory

Summary: ETM Theory of Psychological Trauma

Home

ETM Pro

About

Theory

Why Should Counselors and Other Managers
Study the Neurobiology of Psychological Trauma?

Neurobiology of Post-trauma Existential
Identity: Unlearning (Extinction)

Memory System Two Places
Contradictions into the Past

Memory System Three Provides for New and
Immediate Psychological Life Management

Overview of the Interrelationship
of the 3 Memory Systems

Stoicism Interferes with the
Brain Integrative Process

Drug Use Interferes with the
Brain Integrative Process