D Nash notes on
Trauma and Emotional Dysregulation—description and analysis, prognosis, and treatment
DESCRIPTION AND ANALYSIS:
Trauma happens when someone with a psychobiological vulnerability experiences stress
which leads to beliefs that events are unpredictable and uncontrollable and lacks coping abilities
or social supports which then leads to chronic overarousal and anxious apprehension.
S Freud: Trauma is the convergence of external and internal, real and instinctual dangers.
Dimensions of trauma…
1. actual impingement if event (e.g. physical injury)
2. what person sensed (saw, touched, smelled, etc...)
3. the person’s mental state (in particular, the assessment of risk and the capacity to act
adaptively)
4. the duration of the event
Features of traumatic events that are associated with more severe posttraumatic reactions:
1. exposure to direct life threat,
2. injury to self, including extent of physical pain,
3. witnessing of mutilating injury or grotesque death (especially to loved one),
4. perpetrating violent acts against others,
5. hearing unanswered screams for help or cries of distress; smelling noxious odors,
6. being trapped or without assistance,
7. proximity to violent threat,
8. unexpectedness and duration of the experience,
9. extent of violent force and the use of a weapon or injurious object,
10. number and nature of threats during a violent episode,
11. witnessing of atrocities,
12. the relationship to the assailant and other victims,
13. the use of physical coercion,
14. the violation of the physical integrity of the child, and
15. the degree of brutality and malevolence.
Trauma is like anxiety or panic in presentation and experience
Anticipation of future stress=> hypervigilance, attention narrowing, startle response, processing
distortions, intrusive thoughts, disturbed memory and sleep,
increased irritability, anhedonia, numbing
*** self-perpetuating feedback loop
 “if an individual becomes anxious about the recurrence of panic, a cycle of anxious
apprehension and of secondary conditioning of cues associated with the panic creates the
self-perpetuating feedback loop necessary for the development and maintenance of the
panic disorder “ (6: 121)
Trauma is like dissociative disorders in causes and effect on memory and information
processing
1. distinct, time-limited event
2. sequential stressors
3. long-term exposure to danger and insecurity
Comorbidity of trauma…
Highly associated with ADHD, panic, dissociative identity disorder (a/k/a multiple
personality disorder), bipolar and major depression
Different forms or stages of PTSD
No connection between fear and PTSD; the connection is
between a sense of horror or threat and PTSD.
Intrusive thoughts and avoidance are NOT predictors of PTSD;
rather, the destabilization of the normal arousal pattern
(a/k/a/ emotional dysregulation)
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acute
delayed
chronic
intermittent
residual
reactivated
PSYCHOBIOLOGICAL PROCESS
3 subsystems in the brain
1. brainstem/hypothalamus, which is concerned with internal homeostasis, constituted by
genetic factors (thereby relatively stable and innate)
2. limbic system, which balances internal and external reality, constituted by mixture of
genetic and environmental factors
3. neocortex, which analyzes and interacts with the external world
emotions represent the alarm system
—loss of emotional regulation leads to missed emotional cues
Auditory
Olfactory
how the brain
processes
information
Visual
Kinesthetic
Gustatory
1
Thalamus (sensory reception)
2
3
Pre-frontal Cortex
(integration and planning)
Amygdala
(significance)
4
5
Hippocampus (cognitive mapping)
Sensory information is collected and gathered in the thalamus [1], which then
simultaneously sends it [2] to the pre-frontal cortex for cognitive processing and to the amygdala
for assessment of emotional significance. The pre-frontal cortex then sends [3] cognitively
processed information to the amygdala, which colors the information emotionally and sends it
[4] to the hippocampus for a fuller integration (and to other areas of the brain as shown by the
extra arrows) and mapping. The hippocampus then sends information [5] to the pre-frontal
cortex and to other parts of the brain.
How does the traumatized brain process information? First, it is important to notice that
the sensory input reaches the center of emotional evaluation at the same time it reaches the
cognitive processor. This emotional evaluation operates at a preconscious level. People may
become autonomically or hormonally activated (activation processes which I can discuss later)
before they have a conscious appraisal of what they are reacting to. This activation is based on
fragments of information rather than full-blown perceptions.
This amygdala activation is passed onto the hippocampus, and in fact affects
hippocampal functioning. The greater the emotional significance assigned by the amygdale, the
more closely the input is attended to, and the stronger the retention of the memory is. However,
with intense emotional coloring, the integrative role of hippocampal functioning is prevented.
Memories are stored as fragments, disunified and dissociated. Memories of trauma are thus
stored as disconnected from a self with a story, as living in time and space. In this way traumatic
memories are timeless and ego-alien. PTSD is considered “non-associative” in this way, because
it is not connected to immediate circumstances.
Once the brain is traumatized, lesions are left on the cortex. It is not clear what causes
some people to develop PTSD, or its comorbid diseases, and others to heal without sinking
further into illness. Some combination of genetic and environmental risk factors is hypothesized,
and repeated trauma, such as domestic violence, exponentially invites these sad outcomes. I will
discuss later the process whereby babies are supposed to learn emotional regulation from their
caregivers. Because trauma changes brain tissue itself, clearly therapy and medications cannot
recover the original “self” connected to the pretraumatized brain. This is a permanent loss.
After the brain is traumatized in the future, fragments of sensory input, seemingly
unrelated to the original trauma, may trigger an intense emotional reaction (remember the
amygdale receives input at the same time as does the pre-frontal cortex) which overloads the
hippocampus and short-circuits the cognitive processing.
It’s also important to understand that emotions acts as physical states, not verbally coded
experiences. They are preverbal. Brain scans of chronic PTSD sufferers show that the
hippocampus shows decreased oxygen use. The hippocampus translates internal states into
language (“expresses feelings”) and exercises behavioral inhibitions. In experiments with
animals, permanent changes in limbic physiology caused lasting changes in defensiveness and
predatory aggression; in other words, whatever personality tendencies already present are
magnified—fearless animals become more so, shy animals become more withdrawn. This
altered biology responds to any arousing stimuli this way, enhancing fight or flight responses
based on premorbid conditions.
Subject to intense emotions, bodies aroused, with fragments of memories activated,
unable to form a clear mental construct of what they are experiencing, trauma sufferers need to
reestablish an internal homeostasis. They use their muscles. Discharge through smooth muscles
(stomach, intestines) leads to psychosomatic reactions and discharge through striated muscles
(arms, legs) leads to action. Either solution has adverse consequences and offers little chance to
learn from experience.
Remember, the epicenter of damage caused by trauma is emotional dysregulation.
RESPONSE TO TRAUMA
Self-mutilation is common; the younger the victim, the more self-directed the injury. The
lack of secure attachments maintains the self-mutilating behavior. The earlier the onset of
trauma, and the more repeated, then the greater the emotional dysregulation. A lack of resolution
leads to a “compulsion to repeat”, literally “re-presenting” the trauma but risking re-victimizing
the self or others. Adult trauma may lead to PTSD but childhood trauma leads to more complex
symptoms.
Victims develop intervention fantasies. These may occur during the trauma itself and
become part of the memory. These fantasies may alter the precipitating events, interrupt the
traumatic event, reverse the consequences, express safe retaliation, or present future trauma and
loss.
Klein et al. (2003) have shown victims of traumatic brain injuries to develop memory
loss to distance themselves from the pain associated with the memory. Somer (2002) claims that
the dissociation of trauma, by compartmentalizing the chaos, allows the psyche to create and
nurture areas of competence but the divided self has increased difficulty with intimacy and
aggression. In this paradoxical way, dissociation is a form of self-organization for a victim of
trauma. Victims can handle cognition but not affect.
Dissociative responses to trauma predict self-mutilation and suicide.
DISSOCIATION AS RESPONSE TO TRAUMA
Dissociation
 creates a co-consciousness between different ego states
 allows the preservation of existing schemata while a separate state of mind
processes the traumatic event
 varies the person’s cognitive schemata depending on the state s/he is in
 allows areas of competence to be created in the psyche and protected from
emotional distress or chaos
STAGES OF DISSOCIATION
1. Primary Dissociation
2. Peritraumatic Dissociation (development of symptoms)
3. Tertiary Dissociation (development of disorder)
PREDICTORS OF DEVELOPMENT OF DISSOCIATIVE SYMPTOMOLOGY
1.
2.
3.
4.
5.
6.
7.
8.
9.
younger age,
higher levels of exposure,
greater subjective perceived threat,
poorer general psychological adjustment,
poorer identity formation,
lower levels of ambition or prudence,
greater external locus of control,
greater use of escape or avoidance, and
emotion-focused coping.
Emotion-focused coping is a strategy of easing the tension aroused by the threat through
intrapsychic activity, such as denying or changing one’s attitude toward the threat. The coping
strategy with better outcomes is called problem-focused coping, which channels resources to
solve the stress-creating problem. However, there are times when resisting and fighting will not
change the outcome of events and will provoke the retaliation of an assailant.
EFFECTS OF TRAUMATIC DISSOCIATION
Straker et al. (2002) discuss the significance of dissociation from several perspectives.
When the link is broken, as it is in trauma, between primary process (regulation, development,
and maintenance of the self) and secondary process (reality orientation and mapping), the
subjective experiences of depersonalization and derealization result. The former sees the internal
world as uncanny and mysterious, and the latter sees the external world in this way.
In relation to the world, the sense of its controllability, predictability, fairness and safety
are disrupted; in relation to the self, competence and self-esteem are damaged; in relation to
others, trustworthiness, benignness, and reliability are brought into disbelief. The change from
previous to post selves is pervasive.
In this way trauma creates at least two selves. One “retains an intense need for
nurturance and dependence while another part becomes prematurely adapted. The overadapted
self then caretakes the needy self and protects it from impingements, [but also] keeps the needy
self sequestered and deeply hidden.” Paradoxically, “in the service of protection, the needy
aspect may be persecuted and humiliated by the overadapted part.” The needy aspect can never
be healed in disconnection, however, and the protector mistakes life opportunities as threats and
dangers. In flight from them, the protector perpetuates maladaption.
TREATMENT OF DISSOCIATION (several lists summarized)
1] control and master psychobiological stress reactions; stabilization and symptom-oriented
treatment
2] process horrifying, overwhelming experience; identification, exploration and modification of
traumatic memories
3] re-establish secure social connections and personal/interpersonal efficacy; relapse prevention,
relief of residual symptomology, personality re-integration and rehabilitation
Stage 1 requires knowledge that the trauma won’t return. Facilitate the person’s gaining control
over transitions in dissociative states. Define problems, set goals and “ground” the person—
identify sensations, stay in the present, mirroring back nonverbal cues and naming emotions. To
treat loss of continuous sense of time, keep schedules and routine. To avoid fatigue or stress
triggers, attend to food and rest.
Stage 2 focuses on traumatic memories. The person needs to
 overcome fear of dissociated sense of self
 overcome fear and shame of thinking about trauma
 overcome fear of memories by integrating fragments into a trauma narrative within a
personal stream of consciousness
 overcome fear of life itself—fear of re-victimization, fear of not controlling own destiny
Stage 3 involves psychic re-unification, social re-integration and support and acceptance of
personal responsibility.
It is important to remember that the quicker treatment is brought to the person, the less time the
person has had to consolidate the maladaptive beliefs constructed out of trauma. Conversely, the
longer a person develops lines of thought and growth based on trauma-based values, then the
harder it will be for them to re-integrate psychologically and socially.
TREATMENT IN PRACTICAL TERMS
Many research-based perspectives current in education and counseling emphasize the
autonomy and reliability of the self, with support, to develop into maturation. Self-advocacy,
learner-centeredness, and self-determination try to center around the person. Techniques such as
the presentation of choices, self-monitoring, negotiated rules and consequences consistently
applied, identifying and expressing feelings, and teaching metacognitive strategies all focus
interventive effort at the very mechanisms damaged in the traumatizing process, so that these
perspectives and techniques should be effective and therapeutic ways to support trauma
survivors.
THE PATHOGENESIS OF DYSREGULATION IN THE RIGHT BRAIN
Schore (2002) has described the process whereby an infant child develops trauma from
its caregiver. The primary task of the first year of a child’s life is to establish emotional
communication with a caregiver. This caregiver must be psychobiologically attuned to the rising
and falling of the child’s internal states of autonomic arousal. In activities the caregiver mirrors
the changes in the child’s postnatally developing autonomic nervous system (hereafter known as
the ANS), so that it can said to be a dyadic regulation, or co-regulation, of emotion. In times of
heightened affect, each partner learns the rhythms of the other and modifies his or her behavior
accordingly. In play, these rhythms are attuned; in “misattunement” the “good enough”
caregiver establishes a timely reattunement, repairing the infant’s negative state.
If attachment is defined as the regulation of interactive synchrony, then stress can be set
as the asynchrony and stress recovery and coping becomes the result of the re-establishment of
synchronous emotional rhythms between caregiver and child. In other words,
attachment  the regulatory processes of affect synchrony
\ ==> which creates states of positive arousal
and interactive repair to modulate states of negative arousal
resilience in face of stress  ultimate indicator of attachment security
The area of the brain involved in instinctive attachment behavior is the right orbitofrontal
cortex. Because of its proximity and connections to other areas of the brain, this area regulates
arousal and acts as a “senior executive” of the right brain, where the emotional self is centered.
The orbitofrontal cortex also is directly connected into the hypothalamus, the head ganglion of
the ANS, and so sits in control of the autonomic functions.
The ANS has two branches—1] the sympathetic, activated by a stimulus above the
organism’s threshold, which increases arousal, triggers an immediate anticipatory state, and
rapidly mobilizes resources to respond to stressors and 2] the parasympathetic, set to activate at a
higher threshold (thus following sympathetic activation) to restore normal, homeostatic function
to the body. Ideally, stressors set off the ANS, are handled, and the ANS restores normalcy.
The working model of attachment, shaped by interaction with a caregiver and stored in
the right frontal system, is a recovery mechanism that monitors and regulates the frequency,
duration, and intensity of both positive and negative affective states. Further, this mechanism
responds to uncertainty or unpredictability as sources of stress whenever novel or ambiguous
situations arise.
Enter a bad caregiver who shows emotional dysregulation. This person reacts to the
child’s signs of stress inappropriately or rejectingly and doesn’t participate in any arousal
regulating processes. This caregiver induces states of stimulation and arousal high (abuse) or
low (neglect) and provides no interactive repair so that the intense negative states last for a long
time. As long as infants are in distress, they are devoting their resources to righting homeostatic
balance instead of growing. These states in the infant will later become traits. In fact, even more
disturbing, the chemicals released in the brain during this psychobiological disequilibrium
mediate programmed cell death during periods when synaptic branches are being “pruned”. At
an age when an infant’s brain is supposed to be developing, this outcome is deadly. Males are
more vulnerable to damage because their brains mature more slowly; they tend to become
hyperaroused while females more often dissociate.
Dissociative withdrawal may develop, through a parasympathetic process to conserve
energy to foster survival in the face of internal states of sympathetic hyperarousal. When a
parent’s actions are stress-producing to a child, the resulting paradox (seeking comfort from the
source of distress) causes the simultaneous activation of both the sympathetic and
parasympathetic components of the ANS.
It is this way that trauma is transmitted intergenerationally. An infant synchronises its
own emotional rhythms with a caregiver with emotional dysregulation, typically the mother, and
imprints these chaotic patterns into the neuropsychological composition of its brain. In this way
a parent’s unresolved trauma can be copied into the mind of the infant. Some perspectives on
brain functioning emphasize critical periods wherein certain tissues or organs develop. This
description of trauma is experience-dependent.
Citations are from (citations from book are in chapter: page format)
Klein, E., Caspi, Y., and Gil, S. (2003). The relation between memory of the traumatic event
and PTSD: evidence from studies of traumatic brain injury. Canadian Journal of Psychiatry, 48,
28-33.
Luthar, S., Cicchetti, D., and Becker, B. (2000). The construct of resilience: A critical
evaluation and guidelines for future work. Child Development, 71, 543-562.
Schore, A. (2002). Dysregulation of the right brain: A fundamental mechanism of traumatic
attachment and the psychopathogenesis of PTSD. Australian and New Zealand Journal of
Psychiatry, 36, 9-30.
Somer, E. (2002). Posttraumatic dissociation as a mediator of the effects of trauma on
distressful introspectiveness. Social Behavior and Personality, 30, 671-682.
Straker, G., Watson, D. and Robinson, T. (2002). Trauma and disconnection: A transtheoretical approach. International Journal of Psychotherapy, 7, 145-158.
Van der Kolk, B., McFarlane, A., and Weisaeth, L. eds. (1996). Traumatic Stress: The effects of
overwhelming experience on mind, body and society. The Guilford Press: New York, NY. 596
pp.