Contents of this Page

Symptom Clusters of Complex PTSD

Where C-PTSD and PTSD diverge and/or overlap

Behavioural Symptoms from a ‘Schema Therapy’ perspective

Co-morbidity – Borderline Personality Disorder or Complex PTSD/Developmental Trauma Disorder?

Symptom clusters from Childhood Trauma and Abuse

This website reflects the specialist area of trauma therapy of my psychotherapeutic practise. For this reason, in outlining the long-term consequences of childhood trauma and/or abuse, I focus on the symptomatology of Complex PTSD (C-PTSD) presented by adults, rather than children or adolescents.

The following two lists of symptom clusters have been taken from the Wikipedia website (Complex Post-Traumatic Stress Disorder). The first list is given as the diagnostically indicative symptoms found in children and adolescents with histories of long-term trauma and abuse. The second list is given as the symptomatology of adults who were traumatised and abused as children. There is so much overlap that I regard both lists as relevant to any discussion of adult therapy to heal from C-PTSD. I have included (in brackets and capital letters) further descriptions to emphasise the similarities between the two lists.

For Children/Adolescents

Attachment – “problems with relationship boundaries, lack of trust, social isolation, difficulty perceiving and responding to other’s emotional states, and lack of empathy”
Biology – “sensory-motor developmental dysfunction, sensory-integration difficulties, somatization, and increased medical problems”
Affect or emotional regulation – “poor affect regulation, difficulty identifying and expressing emotions and internal states, and difficulties communicating needs, wants, and wishes”
Dissociation – “amnesia, depersonalization, discrete states of consciousness with discrete memories, affect, and functioning, and impaired memory for state-based events”
Behavioural control – “problems with impulse control, aggression, pathological self-soothing, and sleep problems”
Cognition – “difficulty regulating attention, problems with a variety of “executive functions” such as planning, judgement, initiation, use of materials, and self-monitoring, difficulty processing new information, difficulty focusing and completing tasks, poor object constancy, problems with “cause-effect” thinking, and language developmental problems such as a gap between receptive and expressive communication abilities.”
Self-concept -“fragmented and disconnected autobiographical narrative, disturbed body image, low self-esteem, excessive shame, and negative internal working models of self”.

A sandtray representation by a survivor of childhood attachment trauma. The diorama gives visual form to her felt sense of how her brain has adapted itself to an environment of neglect, unsuccessful attachment and fear of interpersonal relationships. [description by permission of client]

For Adults

Six clusters of symptoms have been suggested for diagnosis of C-PTSD. These are

(1) alterations in regulation of affect and impulses [EMOTIONAL REGULATION, LACK OF IMPULSE CONTROL etc.]

(2) alterations in attention or consciousness [DISSOCIATIVE SYMPTOMS, COGNITIVE PROBLEMS]

(3) alterations in self-perception [SELF IMAGE, SELF ESTEEM, SELF BLAME, SHAME]

(4) alterations in relations with others [ATTACHMENT DISORDERS, RELATIONSHIP DIFFICULTIES]

(5) somatization [PHYSICAL & MEDICAL PROBLEMS, SENSORY ABERRATIONS]

(6) alterations in systems of meaning [PERCEPTIONS ABOUT REALITY THAT SEEM DIVORCED FROM THE APPARENT REALITY OF THE SURVIVOR’S PRESENT CIRCUMSTANCES]

Experiences in these areas may include:

Difficulties regulating emotions, including symptoms such as persistent dysphoria, chronic suicidal preoccupation, self injury, explosive or extremely inhibited anger (may alternate), or compulsive or extremely inhibited sexuality (may alternate).

Variations in consciousness, including forgetting traumatic events (i.e., psychogenic amnesia), reliving experiences (either in the form of intrusive PTSD symptoms or in ruminative preoccupation), or having episodes of dissociation.

Changes in self-perception, such as a chronic and pervasive sense of helplessness, paralysis of initiative, shame, guilt, self-blame, a sense of defilement or stigma, and a sense of being completely different from other human beings

Varied changes in the perception of the perpetrator, such as attributing total power to the perpetrator (caution: victim’s assessment of power realities may be more realistic than clinician’s), becoming preoccupied with the relationship to the perpetrator, including a preoccupation with revenge, idealization or paradoxical gratitude, a sense of a special relationship with the perpetrator or acceptance of the perpetrator’s belief system or rationalizations.

Alterations in relations with others, including isolation and withdrawal, persistent distrust, a repeated search for a rescuer, disruption in intimate relationships and repeated failures of self-protection.

Loss of, or changes in, one’s system of meanings, which may include a loss of sustaining faith or a sense of hopelessness and despair.

Where C-PTSD and PTSD diverge and/or overlap

This is discussed under the tab “ComplexPTSD or PTSD?”

Maladaptive ‘Schemas’ – Pervasive personality or behavioural traits

The Cognitive Therapy Centre of New York offers a comprehensive list of typical symptoms in their website on Schema Therapy –

http://www.schematherapy.com/id63.htm

This site defines the theory behind Schema Therapy … as “broad, pervasive themes regarding oneself and one’s relationship with others, developed during childhood and elaborated throughout one’s lifetime, and dysfunctional to a significant degree.”

These maladaptive schemas resulting from early trauma are grouped as follows:

DISCONNECTION & REJECTION

Abandonment / Instability
Mistrust / Abuse
Emotional Deprivation
Defectiveness / Shame
Social isolation / Alienation

IMPAIRED AUTONOMY & PERFORMANCE

Dependence / Incompetence
Vulnerability to harm or illness
Enmeshment / Undeveloped self
Failure

IMPAIRED LIMITS

Entitlement / Grandiosity
Insufficient self-control / self-discipline

OTHER-DIRECTEDNESS

Subjection
Self-sacrifice
Approval-seeking / recognition-seeking

OVERVIGILANCE & INHIBITION

Negativity / Pessimism
Emotional inhibition
Unrelenting standards / Hypercriticalness
Punitiveness

The website of the Cognitive Therapy Centre of New York elaborate on these dysfunctional categories with short paragraphs of description/explanation.

http://www.schematherapy.com/id73.htm

Borderline Personality Disorder/Comorbidity – or Complex Posttraumatic Stress Disorder?

I quote from two researchers in the field of Complex PTSD and/or Trauma. This is only an introduction to the issue of BPD as a misdiagnosis of C-PTSD. It is worth noting however that on the Wikipedia website on C-PTSD, where there is a discussion about BPD, the author states that around 25% of patients interviewed did not report a history of earlier/childhood trauma. The author suggests that there may be a genetic predisposition to developing BPD, which takes us into the realm of epigenetics.(1) If so, what that would suggest is that the epigene was switched on by environmental factors, which still indicates a probable childhood trigger for the disorder.

In 2002 Martin H. Teicher published an article in Scientific American (N.Y. March 2002, Vol 286, Issue 3, pp 68-75), titled ‘Scars that won’t heal: The neurobiology of child abuse‘. This article is also referenced in the neurobiology section of this website, along with his earlier article, ‘Wounds that Time won’t Heal’ . Teicher begins the article with a mention of BPD in the context of trauma :

“It is hardly surprising to us that research reveals a strong link between physical sexual and emotional mistreatment of children and the development of psychiatric problems. But in the early 1990s mental health professionals believed that emotional and social difficulties occurred mainly through psychological means. Childhood maltreatment was understood either to foster the development of intrapsychic defence mechanisms that proved to be self defeating in adulthood or to arrest psychosocial development, leaving a “wounded child” within. Researchers thought of the damage as basically a software problem amenable to reprogramming via therapy or simply erasable through the exhortation “get over it”.

New investigations into the consequences of early maltreatment, including work my colleagues and I have done at McLean Hospital in Belmont, Mass, and at Harvard Medical School, appear to tell a different story. Because childhood abuse occurs during the critical formative time when the brain is being physically sculpted by experience, the impact of severe stress can leave an indelible imprint on its structure and function. Such abuse, it seems, induces a cascade of molecular and neurobiological effects that irreversibly altar neural development.

Extreme personalities: the aftermath of childhood abuse can manifest itself at any age in a variety of ways. Internally it can appear as depression, anxiety, suicidal thoughts or post traumatic stress; it can also be expressed outwardly as aggression, impulsiveness, delinquency, hyperactivity or substance abuse. One of the more perplexing psychiatric conditions that is strongly associated with early ill-treatment is borderline personality disorder. Someone with this dysfunction characteristically sees others in black and white terms, often first putting a person on a pedestal, then vilifying the same person after some perceived slight or betrayal. Those afflicted are also prone to volcanic outbursts of anger and transient episodes of paranoia or psychosis. They typically have a history of intense, unstable relationships, feel empty or unsure of their identity, commonly try to escape through substance-abuse, and experience self-destructive or suicidal impulses.

While treating three patients with borderline personality disorder in 1984, I began to suspect that their early exposure to various forms of maltreatment had altered the development of their limbic systems. The limbic system is a collection of interconnected brain nuclei (neural centres) that play a pivotal role in the regulation of emotion and memory. Two critically important limbic regions are the hippocampus and the amygdala, which lie below the cortex in the temporal lobe. The hippocampus is thought to be important in the formation and retrieval of both verbal and emotional memories, whereas the amygdala is concerned with creating the emotional content of memory – for example, feelings relating to fear conditioning and aggressive responses.

My McLean colleagues Yutaka Ito and Carol A. Glod and I wondered whether childhood abuse might disrupt the healthy maturation of these brain regions. Could early maltreatment stimulate the amygdala into a state of heightened electrical irritability or damage the developing hippocampus through excessive exposure to stress hormones?” . . . [Here is the link to this article, which offers some exhaustive information about the possible neurobiological mechanisms involved in the behavioural consequences of childhood abuse. ]

In 2007 psychiatrist Colin A. Ross, M.D. published The Trauma Model: A solution to the problem of comorbidity in psychiatry (Manitou Communications Inc, Richardson. 2007). Like Teicher, Ross’s personal experience had led him to question the status quo:

“21 years ago, in 1979, I did my clinical rotation in psychiatry as a medical student at the University of Alberta in Canada. I noticed then that psychiatric inpatients tended to have many different diagnoses. They would be admitted and treated for depression on one occasion, and for a psychotic disorder another time, and often would have numerous admissions. The current diagnosis was always the correct one, but at some point in the future it would become a past incorrect diagnosis. I was most troubled when I saw the diagnosis change several times in a single admission. Not uncommonly, the diagnosis was changed in order to provide a rationale for prescribing a new medication.

The problem was that the patients did not fit the conceptual system of late 20th century psychiatry. Even when the conceptual system was applied consistently, it did not work. The patients were too polymorphous, variable, complicated and, often, uncooperative. I was taught that sometimes this was because the patient was “borderline”. Borderlines, I was taught, display pan-anxiety, pan-sexuality, and polymorphous perversity. Those terms conveyed to me the frustration generated by the conceptual system.

Even if the “borderline” patients were set aside, the problem persisted. On the inpatient wards, the normal was extensive comorbidity. I have been thinking about this problem for 21 years, and have devised a solution for it, which I call the trauma model. The trauma model is a comprehensive, testable scientific theory of mental illness.

[Data provided by Bessel van der Kolk, Melbourne, 2015]

The polydiagnostic patient with extensive comorbidity is the major recipient of inpatient psychiatric treatment. In managed care terms this is the high-cost, high-utilisation, high-recidivism patient. There is no scientific modelling in psychiatry which accounts for this patient, even though he or she is the major consumer of psychiatric services. The dominant model in contemporary psychiatry is the single gene-single disease model. Insurance policies which have expanded their coverage for serious mental illness include disorders assumed to be distinct genetic biomedical brain diseases within contemporary psychiatry: schizophrenia, unipolar or bipolar depression, obsessive-compulsive disorder, and substance abuse.

Yet the patients requiring expensive psychiatric care, for the most part, do not fit the single gene-single disease model. They meet DSM-IV (American Psychiatric Association, 2000) criteria for many different disorders and are often given many different clinical diagnoses over time. The separate diseases model simply cannot account for the clinical data. The problem of comorbidity, from a financial perspective, is the core clinical problem in psychiatry. The solution for the problem of comorbidity adopted by psychiatry over the next 10 years will set the tone for research, theory, clinical practice and health care coverage in the 21st-century. In this book, I propose the trauma model as a scientifically testable solution to the problem of comorbidity.” (Introduction, pp xi-xii)

In his chapter on Borderline Personality Disorder (pp.179-183), Ross goes into more detail, but in the context here of the misunderstandings and misdiagnoses, I just quote his general conclusion:

“I view borderline personality disorder as a trauma disorder. It could be called reactive attachment disorder of adulthood. The trauma which gives rise to borderline personality is a complex and variable mix of parental rejection and neglect, difficult infant temperaments, inconsistent child rearing practices with harsh discipline, physical or sexual abuse, lack of supervision, early institutional living, frequent changes of caregivers, large family size, association with a delinquent group, and certain kinds of familial psychopathology.

I view borderline personality disorder as a normal human response to chronic childhood trauma.The trauma giving rise to borderline personality is multidimensional, and causes profound harm to the individual’s attachment systems. I have never met a borderline who had a childhood that was anywhere near normal or happy. I have given dozens of workshops in which I have asked whether anyone has ever seen a borderline with a normal childhood, and not one out of thousands of professionals have ever raised a hand.

The biology of borderline personality disorder is the biology of trauma. . . Trauma therapy will have a profound positive impact on the natural history of borderline personality disorder. However a subgroup will be unmotivated and untreatable. These trauma therapy treatment failures await the development of an alternative model and treatment method. . . . Borderline personality disorder is not a discrete entity which one either has or does not have. It is a trauma behavioural checklist. (my emphasis)”

(1) The definition of epigenetics has changed over time, and the term now refers to the potentially heritable, but environmentally modifiable, regulation of genetic function and expression that is mediated through non-DNA-encoded mechanisms (Russo et al, 1996; Wu and Morris, 2001). Epigenetics has surfaced to the forefront as a mechanism by which environmental cues can be translated into precise and highly stable alterations in chromatin structure that ultimately lead to the persistent expression of altered gene programs.