Friday, April 25, 2014

A Trauma-Based Model of Mental Illness (preliminary thoughts)

Here is another section (still in the process of being written) from the paper I have been working on for a couple of months now - or maybe it will be a monograph, since it keeps getting longer and longer.

This section (much of which is still missing citations) proposes a new model of mental illness that does away with many of the diagnoses we now find in the DSM. Rather, it proposes a trauma-based model that sees symptoms as adaptations to the traumatic experience.

As I said, this is VERY preliminary - just began writing it yesterday. Any feedback is welcome.

A Trauma-Based Model of Mental Illness

It is my belief, based on years of reading the trauma literature and working with sexual trauma clients in therapy, that nearly all the traits we label as mental illness are more accurately understood as adaptations (or clusters of adaptations) to traumatic experience, either interpersonal or "shock."
Interpersonal traumas are those occurring between people in relationship, such as neglect, abuse, bullying, and attachment failures. The younger one is when these traumas occur, the more profound their impact on brain development.

"Shock" traumas are those single frightening events that can seriously disrupt our lives and our basic understanding of the world. These may include natural disasters, accidents, stranger rape, muggings, and other unexpected, unpredictable violent disruptions of our lives.

The greater the severity of the trauma, the more extreme the adaptations a survivor makes to cope with the experience. Early interpersonal trauma tends to be more difficult to treat than shock traumas, unless the person experiencing the shock trauma has also experienced adverse child events. I propose that we can create a spectrum of how these adaptations are generated and how they function, ranging from less extreme to more extreme.

At one end we might have the adaptation cluster often labeled as an adjustment disorder, with anxiety or depression being common expressions. Addictions and other forms of self-numbing behavior would also likely be in the first half of the spectrum.

An issue with some of the adaptations, particularly addictions, is that they generally co-occur with other adaptations. For example, post-traumatic stress disorder (PTSD) often co-occurs with mood symptoms, addictions, or disordered personality structures.

PTSD would be somewhere near the middle, although its manifestation can be mild to severe. Further down the spectrum would be dissociative disorders, the most extreme form of PTSD, with the most extreme adaptation being dissociative identity disorder (DID).

At the far end would be full-blown psychosis, representing a cumulative experience so awful and unbearable that reality become intolerable, necessitating a retreat into an alternate reality often imbued with a sense of importance or specialness, which is even true in paranoid iterations of psychosis.

It's important to keep in mind that when these interpersonal traumas occur during development, they create changes in the way the brain is wired, particularly the right hemisphere, the source of affect regulation, interpersonal skills, and body-mind integration.

Likewise, many of the adaptations noted here will manifest in the brain as shrinkage of one set of circuits or enlargement of another. For example, PTSD can produce an enlarged amygdala and a smaller hippocampus. Prolonged environmental stress also generates excessive levels of cortisol and other stress hormones that can damage brain function and leave the survivor in a near constant state of hypervigilance.

How Trauma Changes the Brain

When confronted with a stressor, a series of events occurs in the body that generates what we now call the “fight or flight response.” This process evolved early in the history of life on Earth to allow organisms to act in a situation where their life was in danger. In response, the body generates the energy for either a “fight” or a “flight” through activation of the nervous system and the endocrine system in order to maximize resources for surviving the threat (the stressor).

The following is paraphrased from Neigh, Gillespie, and Nemeroff (2009).

Researchers have identified two phases to this process. When the stressor is detected, the initial phase of the stress response begins. The sympathetic nervous system (associated with action, the "fight or flight" response) releases norepinephrine from nerve terminals and epinephrine from the adrenal medulla into the general circulation. Both of these neurochemicals and stimulants in their effects on the body.

In the secondary phase, moments later, corticotropin releasing factor (CRF) is released by “parvocellular neurons of the hypothalamic paraventricular nucleus into the hypothalamo-hypophyseal portal system for transport to the anterior pituitary gland where it stimulates the release of adrenocorticotropic hormone (ACTH) into the general circulation” (Swanson, Sawchenko, Rivier, & Vale, 1983; cited in Neigh, Gillespie, and Nemeroff, 2009). The ACTH travels to the adrenal cortex where it stimulates the release of glucocorticoids (cortisol is the primary stress hormone in primates). It generally takes several minutes for these processes, which are characteristic of the hypothalamic-pituitary-adrenal (HPA) axis stress response, to become fully activated.
Following the crisis, activity in the HPA axis is dampened through negative feedback (the parasympathetic nervous system, associated with "recuperation") via stimulation of glucocorticoid receptors within the hippocampus, hypothalamus, and anterior pituitary (Jacobson & Sapolsky, 1991). When there is a crisis, this stress response allows an organism to shift biological resources away from whatever activity was the focus and engages physiological functions that promote survival.

However, if the stress response becomes chronic due to repeated exposure to stressors, or a physiological deficit in the negative feedback system (or both), the organism experiences an on-going excess in stress hormone levels, which can trigger pathological changes in a variety of physiological systems, leading to stress-related diseases (McEwen, 2008).
This near-constant state of "activation" also leads to many of the symptoms of PTSD, including anxiety, memory deficits, hypervigilance, and the exaggerated startle response. The inability or failure of the body to metabolize the stress hormones, representing in essence that the situation cannot be escaped, results in the third and fourth of the Four F's - fight, flight, freeze, and fold. The freeze response is the most common experience for those who experienced on-going trauma, and the fold represents complete surrender, a profound state of "giving up."   
Whitehouse and Heller explains it this way:
Part of the problem is that when these states occur, discharge of the intense energies mobilized to meet threat often becomes thwarted. Often we just don't have the time necessary to complete them. Nevertheless, the survival energy has mobilized for fight or flight, but literally has no place to go and ends being converted into symptoms. (Whitehouse & Heller, 2008)
The freeze response (fold is very rare, so it will not be discussed here) is characterized by a simultaneous activation of the sympathetic and parasympathetic nervous systems. According to Peter Levine, the creator of Somatic Experiencing:
We have several synonyms for freeze, including dissociation, immobility, spacing out, deer in the headlights look. In the healthy nervous system it still serves and protects us humans, but often freeze is associated with the residual crippling effects of trauma. Here's what happens that causes humans to get stuck in trauma. (Levine, 1992)
References (partial)
  • Neigh, GN, Gillespie, CF, and Nemeroff, CB. (2009, Aug 6). The Neurobiological Toll of Child Abuse and Neglect. Trauma Violence Abuse; 10: 389-410. DOI: 10.1177/1524838009339758
  • Jacobson, L., & Sapolsky, R. (1991). The role of the hippocampus in feedback regulation of the hypothalamic-pituitary-adrenocortical axis. Endocrine Reviews, 12, 118-134.
  • McEwen, BS. (2008). Central effects of stress hormones in health and disease: Understanding the protective and damaging effects of stress and stress mediators. European Journal of Pharmacology, 583, 174-185.
  • Whitehouse, B., & Heller, DP. (2008). Heart Rate in Trauma: Patterns Found in Somatic Experiencing and Trauma Resolution. Biofeedback, 36(1).
  • Levine, P. (1992). Somatic Experiencing. The Foundation for Human Enrichment. http://www. traumahealing. com/index. html.

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