Erika J. Wolf - The Dissociative Subtype of PTSD: Rationale, Evidence, and Future Directions

From the PTSD Research Quarterly at the end of 2013, this is an excellent overview of the justification for creating the PSTD dissociative subtype.

Full Citation:
Wolf, EJ. (2013). The Dissociative Subtype of PTSD: Rationale, Evidence, and Future Directions. PTSD Research Quarterly; 24(4).

The Dissociative Subtype of PTSD: Rationale, Evidence, and Future Directions

Erika J. Wolf
National Center for PTSD at VA Boston Healthcare System
Boston University School of Medicine, Department of Psychiatry

The diagnosis of PTSD has undergone numerous changes in the recently released Diagnostic and Statistical Manual-5 (DSM-5; APA, 2013). One is the addition of the dissociative subtype (see Friedman, Resick, Bryant, and Brewin, 2011). This subtype applies to individuals who meet full criteria for PTSD and also exhibit marked symptoms of derealization (i.e., perceiving one’s world or environment as not real) and/or depersonalization (i.e., perceiving one’s self as not whole, connected, or real). This review examines the evidence for the dissociative subtype of PTSD, discusses issues related to its operational definition and assessment, and considers its broader relevance for clinical and research applications.

To begin, it is important to define the term “subtype” and clarify how it is used in DSM-5. In general, the term implies a subordinate variant of a more general kind such that one might expect differences in the core symptoms of a disorder as a function of subtype. However, in this case, the dissociative subtype is not a subset of the core PTSD symptoms, but instead, reflects a form of PTSD marked by additional comorbid symptoms of derealization and/or depersonalization. Most broadly, the term reflects the finding that only a distinct minority of individuals with PTSD experience symptoms of derealization and depersonalization and this is relatively unrelated to the severity of their PTSD symptoms.

Empirical support for the subtype comes from converging lines of research, including psychometric and neurobiological studies. A series of articles have used structural analytic models to examine the distribution of dissociation symptoms within trauma-exposed and PTSD samples. Structural analyses, such as taxometric procedures and latent profile analyses, are ideally suited for testing subtype hypotheses because these analyses take a multivariate approach to examine if there are unobserved, or latent, constructs that distinguish groups of individuals based on their scores on a series of items submitted to the analysis. In the case of latent profile analysis, competing models can be tested and compared against each other using multiple indicators of model fit and substantive interpretability. Waelde, Silvern, and Fairbank (2005) used taxometric procedures to examine the structure of dissociation (as defined by amnesia, depersonalization, and absorption) among trauma-exposed Vietnam Veterans and found that 32% of those with PTSD could be classified as belonging to a dissociative taxon or group. Wolf, Miller et al. (2012) subsequently used latent profile analysis of items indexing PTSD and dissociative symptom severity (as defined by depersonalization, derealization, and reduction in awareness), and demonstrated that about 12% of Veterans with PTSD scored uniquely high on symptoms of derealization and depersonalization. These individuals formed a dissociative class who were distinct from those with high PTSD severity and no dissociation and from those with low PTSD severity and no dissociation. The dissociative group was also associated with higher severity of clinician-rated flashbacks and self-reported a higher level of exposure to childhood and adult sexual assault compared to the other groups. This basic pattern of latent profile results was subsequently replicated in all male and all female veteran and military PTSD samples (Wolf, Lunney et al., 2012). Approximately 15% of the male sample and 30% of the female sample were assigned to the dissociative class, which was again defined by symptoms of depersonalization and derealization. The female dissociative class was associated with higher prevalence of borderline and avoidant personality disorder diagnoses. Steuwe, Lanius, and Frewen (2012) extended this work into a civilian sample of individuals with PTSD and a high prevalence of sexual trauma and found remarkably similar results that latent profile analyses revealed that approximately 25% of the sample could be classified as belonging to a dissociative subgroup, as defined by high scores on derealization and depersonalization. Finally, Stein et al. (2013) contributed an important study of the dissociative subtype in a sample of over 25,000 individuals from 16 different countries. The large sample size and cross-cultural representation permitted evaluation of the correlates and generalizability of the subtype. The authors examined the distribution of symptoms of derealization and depersonalization in the sample (but did not use structural models for this purpose) and found that approximately 14% of the sample could be assigned to a dissociative group and that this group also showed elevations on two core PTSD symptoms: flashbacks and psychogenic amnesia. The dissociative class was associated with male sex, childhood-onset PTSD, greater levels of trauma exposure, and higher levels of functional impairment and suicidality as well as comorbid anxiety disorders. Moreover, the study demonstrated that the basic pattern of results replicated across countries that differed in income, providing strong support for the cross-cultural relevance and generalizability of the subtype.

Lanius et al. (2010), followed by Lanius and colleagues (2012), compiled the neurobiological evidence for a dissociative subtype of PTSD. Their review of functional magnetic resonance imaging (fMRI) research suggested that while the majority of individuals with PTSD responded to hearing their personal trauma-scripts with high levels of psychological distress, physiological arousal, emotionality, and reexperiencing, and hyperarousal symptoms, a separate group of individuals responded to hearing their own trauma scripts with a notable absence of such symptoms and instead, showed symptoms of dissociation. The former group was characterized by heightened activity in limbic brain regions (e.g., the amygdala) and reduced activity in areas of the brain associated with emotional control and regulation (largely in pre-frontal regions). In contrast, across studies, Lanius et al. (2010, 2012) noted that the latter group showed evidence of emotional over-modulation, as suggested by heightened activation in pre-frontal brain regions and relatively less activity in the emotional/limbic areas of the brain in response to trauma cues. This provides initial evidence of potential differences in neurobiological functioning in individuals with versus without the subtype, though more research in this area is needed to evaluate the replicability of these patterns of brain activation and their specificity to the dissociative subtype.

Dissociation is a broad term and it is important to highlight that the dissociative subtype of PTSD is formulated based on symptoms of derealization and depersonalization specifically. The focus on these symptoms is consistent with evidence that these types of dissociation reflect more pathological forms of dissociative phenomena that are distinct from other types of dissociation, such as the tendency to “zone out” or have reduced awareness of one’s surroundings. For example, Waller, Putnam, and Carlson (1996) performed taxometric analyses on the Dissociative Experiences Scale (DES; Bernstein and Putnam, 1986), the most widely used measure of dissociative phenomena. Waller et al. showed that some DES items, such as those related to absorption (a trait associated with hypnotizability and cognitive control), reflected dimensional constructs or traits that were relatively nonpathological and normative. In contrast, other items, including those assessing depersonalization and derealization, fit the model for a pathological class or taxon. Others have suggested that symptoms of derealization and depersonalization are facets of a broader form of dissociation termed detachment that is distinct from a form of dissociation termed compartmentalization (which captures phenomena such as dissociative amnesia and symptoms of conversion disorder; see Holmes et al., 2005). The definition of dissociation, its relationship to other constructs, and the key assumptions about the construct are artfully discussed in a critical review by Giesbrech and colleagues (2008) that is required reading for those interested in studying dissociation.

The operational definition of dissociation is important to consider when selecting a measure to assess the dissociative subtype of PTSD. There are many self-report and interview-based measures of dissociation and they vary widely in their approach to the assessment of the construct and in their psychometric properties. The use of dimensional or nonpathological measures of dissociation will be sensitive to normative traits such as absorption, fantasy proneness, and suggestibility that are likely to correlate with PTSD simply as a function of overall severity; their use would be expected to artificially inflate the prevalence of the subtype and fail to identify a unique subgroup. Our group has focused on the use of the associated features items in the Clinician Administered PTSD Scale (CAPS; Blake et al., 1995), the gold standard structured PTSD diagnostic interview, to assess the dissociative subtype. To date, there is no stand-alone instrument that is specific to the dissociative subtype.

The inclusion of the dissociative subtype of PTSD in the DSM-5 has both clinical and research applications. Symptoms of dissociation are important clinical phenomena that may become a target of treatment or may interfere with PTSD treatment. Individuals who are highly dissociative may have difficulty benefitting from trauma-focused therapies if dissociation interferes with the processing of trauma memories and related emotions and cognitions. To date, no study had specifically evaluated if the subtype, as defined in the DSM-5, affects PTSD treatment response or the course of the disorder; most studies evaluating dissociation as a moderator of PTSD treatment response have been under-powered to fully examine this question (as they were not originally designed to address this issue). Two recent studies have provided evidence for subtle differences in PTSD treatment response among individuals with dissociation, though both failed to support an overall dissociation by time interaction on PTSD treatment response. Specifically, Cloitre and colleagues (2012) found that baseline dissociation (broadly defined) did not moderate overall PTSD treatment response, however, dissociation assessed at post-treatment time points did interact with treatment type to yield differential effects on PTSD severity at follow-up. Those with higher levels of post-treatment dissociation fared better with respect to PTSD symptoms if they had been assigned to one of the two treatment arms that involved skills training. Resick et al. (2012) also found no overall dissociation by time effect in predicting response to PTSD treatment but observed that individuals with high levels of dissociation, including symptoms of depersonalization specifically, evidenced a faster decline in PTSD symptoms if they had been assigned to the Cognitive Processing Therapy (CPT) arm of the treatment trial as opposed to the straight cognitive therapy arm (without the written trauma accounts; CPT-C). In other words, although the overall degree of change in PTSD symptoms did not differ as a function of dissociation, the pace, or rate of change in PTSD symptoms, was dependent on dissociative symptoms in combination with treatment type. More work is needed to determine the influence of the dissociative subtype on PTSD treatment response and the best practices for delivering effective PTSD treatment for individuals with salient dissociative symptoms.

The dissociative subtype holds many potential benefits for research purposes. PTSD is a heterogeneous disorder such that any two individuals with the diagnosis may present with different (even nonoverlapping) combinations of PTSD symptoms and patterns of comorbidity. It is important to measure and account for these differences. Otherwise variability in the presentation of PTSD may make it difficult, if not impossible, to identify correlates of the disorder. The dissociative subtype of PTSD may be associated with a distinct etiology, biology, course, and treatment response. For example, individuals with the dissociative subtype may have different genetic vulnerabilities than individuals with PTSD who do not dissociate and failure to account for this phenotypic difference may contribute to statistical “noise” and problems in replicating results across samples. Providing a clear definition of the subtype should allow for research examining the specific genetic, neurobiological, cognitive, and psychosocial mechanisms of dissociation in PTSD.

The association between dissociation and trauma and PTSD has long been a topic of curiosity, speculation, and controversy, and those interested in a historical view may want to read the writings of Pierre Janet dating back to 1889 (and republished in 1973). Controversy about the nature of dissociation in PTSD persists and additional refinement of the definition of the subtype as well as research on its biological and psychosocial correlates and function is still needed. The addition of the subtype in DSM-5 formalizes the PTSD-dissociation relationship and provides a reliable definition of the subtype. This should help to advance the science and understanding of PTSD.

References

• American Psychiatric Association (2013). Diagnostic and statistical manual of mental disorders. (Fifth ed.) Arlington, VA: American Psychiatric Association.
• Blake, D.D., Weathers, F.W., Nagy, L.M., Kaloupek, D.G., Gusman, F.D., Charney, D.S., and Keane, T.M. (1995). The development of a Clinician-Administered PTSD Scale. Journal of Traumatic Stress, 8, 75-90.

Your At-a-Glance Guide to Psychology in 2013 - BPS Research Digest

From the British Psychological Society's Research Digest, this is their 2013 year in review for psychology - you can also check out their most popular Research Digest posts for the year, as well.

Your at-a-glance guide to psychology in 2013 - Part 1

JAN The year began with fall-out from the final report into the fraud of social psychologist Diederik Stapel. The scale was shocking - 55 journal papers published over 15 years are tainted. The Levelt investigating committee pointed the finger at the research culture in social psychology, but the British Psychological Society's own Social Psychology Section rejected this. So too did the European Association of Social Psychology, who argued that the discipline has actually suffered fewer frauds than other branches of science. In other news, a team of researchers in Canada attracted criticism when they spun their research to suggest that the concept of IQ is a myth. "There are many mysteries about intelligence and the general factor," Professor Richard Haier told The Psychologist. "Now there is a new one – how did this paper get published?"

FEB The first rumours of Obama's richly funded BRAIN initiative began to emerge. A new spin on a modern psychology classic: researchers showed that inattentional blindness can lead experienced radiographers to fail to notice a "gorilla on the lung". A less welcome classic also made an appearance - the left/brain right/brain myth in a report from the RSA that claimed the woes of the Western world are due to our over-dependence on the left-brain hemisphere (some astute criticism here). It was also announced this month that MPs would have access to mental health treatment in Westminster for the first time. Jonah Lehrer apologised for plagiarising the Research Digest. Contradicting all established neuranatomical fact, the Daily Mail described how evil lurks in the brain's "central lobe"!

MARCH Neuroscientists and psychologists began to react to the news of Obama's BRAIN initiative and the similarly ambitious EU Human Brain Project. Psychologists started a campaign against the publication of US psychiatry's re-worked diagnostic code DSM-5. Debate about and reaction to the crisis in social psychology continued - The Center for Open Science was launched by US psychologist Brian Nosek, and The Association for Psychological Science announced a new article format Registered Replication Reports for one its key journals. An important new study found that many mental disorders share the same genetic risk factors.
APRIL After all the questions raised about social psychology, it was the turn of neuroscience as an important analysis suggested that the majority of neuroscience studies are statistically underpowered, likely leading to unreliable findings. Meanwhile a provocative paper claimed that brain scans could predict those offenders likely to return to prison. The Neurocritic took a sceptical look at the results. After all the speculation, the BRAIN Initiative finally launched. Perfectly capturing the zeitgeist, Ferris Jabr for Scientific American wrote a wonderful article about the psychology of reading paper books vs. e-books.
MAY Days before the publication of the new DSM-5 psychiatric diagnostic code, the document received a barrage of criticism from opposite directions. The BPS Division of Clinical Psychology published their concerns, including that the code is too biologically based, while Thomas Insel of the NIMH argued that the code is already out of date because it's not grounded in biological findings. In other news, the UK government's Behavioural Insight Team went part-private; a study about the effects of fist-clenching on memory attracted severe criticism; more controversy bubbled up after the failure to replicate another social priming result; Diederik Stapel was interviewed; two psychologists were voted among the world's top 10 thinker; and Paul Bloom explained how too much empathy can actually lead us to do the wrong thing.
JUNE Many psychologists were among more than 70 signatories to an open letter to the Guardian calling for a new approach to publishing across the life sciences - pre-registered reports in which a study is accepted for publication based on the proposed methodology, prior to the collection of any actual results. The Psychologist reported on the neuroscientist Russell Poldrack who is scanning his own brain three times a week for a year. This is what happened when students and neuroscientists were asked to draw a neuron. A study used fall out from atomic bomb testing to settle the debate over whether adult humans can grow new neurons. Scientists from Germany and Canada created the most detailed map of the brain ever. The Big Brain Atlas is part of the EU's €1-billion Human Brain Project.  Mark Stokes argued there's a lot more to neuroscience than media "neuromania".

Your at-a-glance guide to psychology in 2013 - Part 2

Part 1 Jan to June is here. 

JULY UCL cognitive neuroscientist Sophie Scott was among the scholars unhappy about the call for the introduction of pre-registered reports in psychology (see June). Walter Boot and colleagues published an important paper highlighting how many control conditions in psychology are inadequate. Another paper claimed that the real-world impact of psychological and social interventions is being squandered by poor practices in the reporting of randomised trials. Doubts were raised about Milgram's classic studies into obedience. Matt Wall debunked neuromarketing. Bethany Brookshire worried that neuroskepticism was becoming excessive and called for neuronuance. Oliver Sacks turned 80 and felt happy about it. "Psychology's most original thinker" Dan Wegner passed away.

AUG A study found that people's sleep is disturbed at full moon, and not because of the light. Harvard psychologist Steve Pinker wrote a magisterial essay on why science, including psychology and neuroscience, is not the enemy of the humanities. The Guardian launched a new psychology blog "Head Quarters" featuring the dream team of Pete Etchells, Molly Crockett, Nathalia Gjersoe and Chris Chambers. UCL cognitive neuroscientist Sarah-Jayne Blakemore was this year's recipient of the prestigious Rosalind Franklin Award from the Royal Society. The RSA's Social Brain Centre launched a new project into spirituality and the brain. New data showed that dementia rates had fallen in the UK. Prisoners' performance on the classic prisoners' dilemma game was measured for the first time. "Super-recognisers" were recruited to spot known criminals at the Notting Hill carnival.

SEPT Scientists created mini brains from stem cells. Hype surrounded a study that purported to show a driving game reversed age-related mental decline. New data showed that England's Improving Access to Psychotherapies programme had failed to stall the county's rising anti-depressant prescription rates. Obama's administration announced plans to create its own "Nudge Unit" modelled on the British government's Behavioural Insight Team. The British Psychological Society's Research Digest marked its tenth anniversary with a series of research-backed self-help posts. Barbara Fredrickson, one of the world’s leading positive psychologists, admitted that a highly influential paper she co-authored in 2005 is fundamentally flawed. David Dobbs wrote a wonderfully inspiring article on the social life of your genes.

OCT Reading fiction boosts your empathy skills, but only if it's literary fiction, a study claimed. Not everyone was impressed. The purpose of Obama's BRAIN initiative became clearer thanks to publication of an interim report. Meanwhile the Guardian interviewed Henry Markram - head of the EU's Human Brain Project. The Society for Personality and Social Psychology published an important remedial report (pdf) for the discipline: "Improving the Dependability of Research in Personality and Social Psychology ..." The Research Digest hosted a Super Week in which we met individuals with psychological super powers. A charity in Wales was criticised for using NLP to treat traumatised soldiers. The science of using brain imaging to decode people's thoughts, minus the hype - a welcome overview from Kerri Smith was published this month.

NOV The World Medical Association announced important changes to its Declaration of Helsinki - an influential ethics code for conducting research with human participants that is followed by many psychology departments and journals. New data suggested that after years of increase, the diagnosis rates for autism in the UK had plateaued. Concerns were raised again about the lack of educational psychologists in Scotland and there were cuts to funding for ed psych services in England, even as demand was on the increase. A new study found that eye contact does not in fact increase persuasion. BBC Radio 4's All in the Mind celebrated its 25th anniversary (the same year that The Psychologist magazine reached the same milestone). A neuroscience journal for kids was launched. A team of over 50 international researchers published an ambitious attempt to replicate 13 existing findings in psychology. Psychology mourned the loss of two stars: cognitive neuroscientist Andy Calder and social psychologist Nalini Ambady.

DEC A twin study attracted controversy after it appeared to show that genes trump schooling and parenting when it comes to children's exam success. The Science Museum opened a new psychology-themed exhibition supported by the British Psychological Society. Mind Maps: Stories from Psychology "explores how mental health conditions have been diagnosed and treated over the past 250 years." A brain imaging study purported to show that men's and women's brains are wired up differently and that this supports gender stereotypes. Not everyone was impressed. Another new study found that stimulating part of the anterior cingulate cortex triggers a kind of "Eye of the Tiger" effect. Finally, this month a US court may have been the first to see brain imaging evidence save a killer from the death penalty. Intriguingly, one of the neuroscientist witnesses for the defence - Ruben Gur - was a co-author on that sex-differences brain wiring study … it's a small world, as they say.

Jerome Wakefield - Psychiatric Diagnoses: Science or Pseudoscience?

 

This is an interesting podcast from the good folks at the Institute for Ethics and Evolving Technologies (IEET) on the validity of psychiatric diagnoses - a very relevant topic here at the Evolution of Psychotherapy Conference. Many of the speakers we have heard so far do not use the DSM diagnostic protocols because they have little to do with the clients we see in our offices.



Jerome Wakefield is the author of The Loss of Sadness: How Psychiatry Transformed Normal Sorrow into Depressive Disorder (2007), All We Have to Fear: Psychiatry's Transformation of Natural Anxieties into Mental Disorders (2012), and several other books.

Psychiatric Diagnoses: Science or Pseudoscience?

Rationally Speaking
Posted: Dec 10, 2013 


Jerome Wakefield, DSW, PhD

The standard for diagnosis is the Diagnostic and Statistical Manual of Mental Disorders (DSM), which just released a 5th edition in 2013—but just how objective is it? This episode of Rationally Speaking features Dr. Jerome Wakefield, psychiatrist, PhD in philosophy, and author of "The Loss of Sadness: How Psychiatry Transformed Normal Sorrow into Depressive Disorder." Julia, Massimo and Jerome talk about the arbitrariness of the DSM and the controversies around the boundaries of various mental disorders, including depression and sexual fetishes.



Jerome's pick: Bertran Russells's Autobiography

Listen/View

Here is the definition of Developmental Trauma Disorder as outlined by Bessel van der Kolk - Developmental trauma disorder: Towards a rational diagnosis for children with complex trauma histories.

Developmental Trauma Disorder

A. Exposure

1. Multiple or chronic exposure to one or more forms of developmentally adverse interpersonal trauma (abandonment, betrayal, physical assaults, sexual assaults, threats to bodily integrity, coercive practices, emotional abuse, witnessing violence and death).
 
2. Subjective Experience (rage, betrayal, fear, resignation, defeat, shame).
 
B. Triggered pattern of repeated dysregulation in response to trauma cues
Dysregulation (high or low) in presence of cues. Changes persist and do not return to baseline; not reduced in intensity by conscious awareness.

•Affective
•Somatic (physiological, motoric, medical)
•Behavioral (e.g. re-enactment, cutting)
•Cognitive (thinking that it is happening again, confusion, dissociation,
depersonalization).
•Relational (clinging, oppositional, distrustful, compliant).
• Self-attribution (self-hate and blame).

C. Persistently Altered Attributions and Expectancies

•Negative self-attribution
•Distrust protective caretaker
•Loss of expectancy of protection by others
•Loss of trust in social agencies to protect
•Lack of recourse to social justice/retribution
•Inevitability of future victimization

D. Functional Impairment 

•Educational
•Familial
•Peer
•Legal
•Vocational

The research in the ACE study demonstrates how adverse childhood experiences impact later health outcomes on the physical plane, it seems pretty obvious that these experiences also impact mental health.

Responses to a questionnaire about adverse childhood experiences, including childhood abuse, neglect, and family dysfunction, included the following: "11.0% reported having been emotionally abused as a child, 30.1% reported physical abuse, 19.9% sexual abuse; 23.5% reported being exposed to family alcohol abuse, 18.8% to mental illness, 12.5% witnessed their mothers being battered and 4.9% reported family drug abuse." [Felitti VJ, Anda RF, Nordernberg D, et al. (1998). Relationship of childhood abuse to many of the leading causes of death in adults: the adverse childhood experiences (ACE) study. Am J Prev Med.; 14(4): 245-258.]

From the same van der Kolk article cited above, here is the working definition of complex trauma, a similar if not identical condition as developmental trauma disorder (DTD):

The traumatic stress field has adopted the term “Complex Trauma” to describe the experience of multiple and/or chronic and prolonged, developmentally adverse traumatic events, most often of an interpersonal nature (e.g., sexual or physical abuse, war, community violence) and early-life onset. These exposures often occur within the child’s caregiving system and include physical, emotional, and educational neglect and child maltreatment beginning in early childhood (see Cook et al, this issue, Spinazzola et al this issue).

With that background, here is a report on why the DSM-5 committee chose not to include DTD, from Psychotherapy Networker Magazine.

Developmental Trauma Disorder: Distinguishing, Diagnosing, and the DSM

How One Tenacious Task Force Worked to Separate Developmental Trauma Disorder from PTSD in DSM-5

Mary Sykes Wylie • November 21, 2013

In 2001, the Cummings Foundation convened a group of child psychiatrists, public policy experts, and representatives from the Department of Justice, Department of Health and Human Services, and Congressional staff to consider the deplorable state of services to traumatized children. This initiative led to the establishment of the Congressionally mandated National Child Traumatic Stress Network (NCTSN).

In order to study the symptomatology of the children seen within the NCTSN, Boston psychiatrist and trauma expert Bessel van der Kolk and his colleague Joseph Spinazzola organized a complex trauma task force. Between 2002 and 2003 they conducted a survey (via clinician reports) of 1,700 children receiving trauma-focused treatment and experiencing the effects of child abuse at 38 different centers across the country.

They found more evidence of what two decades of research had already revealed: Nearly 80% of the surveyed kids had been exposed to multiple and/or prolonged interpersonal trauma, and of those, fewer than 25% met the diagnostic criteria for Post-Traumatic Stress Disorder (PTSD).

Instead, these children showed pervasive, complex, often extreme, and sometimes contradictory patterns of emotional and physiological dysregulation. Their moods and feelings could be all over the place—rage, aggressiveness, deep sadness, fear, withdrawal, detachment and flatness, and dissociation—and when upset, they could neither calm themselves down nor describe what they were feeling.

In 2005, the complex trauma task force—chaired by van der Kolk—began working in earnest on constructing a new diagnosis, called Developmental Trauma Disorder, which, they hoped, would capture the multifaceted reality experienced by chronically abused children and adolescents.

In January 2009, they submitted to the Diagnostic and Statistical Manual (DSM) Trauma, PTSD, and Dissociative Disorders Subwork Group an elaborate criteria set (DSM-speak for symptom list) for Developmental Trauma Disorder: Exposure to prolonged trauma, causing pervasive impairments of psychobiological dysregulation (of emotions and bodily functions, of awareness and sensations, of attention and behavior, of their sense of self and their relationships), as well as at least two symptoms of standard PTSD, and multiple functional impairments (with school, family, peer group, the law, health, and jobs or job training).

According to van der Kolk, the DSM committee responded that the complex trauma task force had “inundated” them with too much data about Developmental Trauma Disorder, but not the right kind: They needed to submit other kinds of data concerning 17 issues, including possible genetic transmission, environmental risk factors, temperamental antecedents, bio-markers, familial patterns, treatment response, and so on.

The DSM subcommittee, chaired by Matthew Friedman, executive director of the National Center for PTSD, wrote that “the consensus is that is it unlikely that Developmental Trauma Disorder can be included in the main part of DSM-5 in its present form because of the current lack of evidence in support of the diagnosis and the lack of prospective testing of your proposed diagnostic criteria.”

The complex trauma task force argued that this was a proposed diagnosis, which didn’t officially exist yet, and so—in that great Catch-22 tradition of DSM—couldn’t qualify for the funding for the kind of research the DSM subcommittee wanted to see. But their argument was still unconvincing.

Though temporarily stymied, the NCTSN task force is by no means defeated. They’ve been able to raise the money for a Developmental Trauma Disorder field trial and enlisted the sites that are able to carry out the required research.

“We’re still going ahead full throttle,” says van der Kolk. “I feel very optimistic.”

~ Discover what it takes to get a new diagnosis recognized by the Diagnostic and Statistical Manual. Download The Puzzle of Trauma: Redefining PTSD in the DSM for FREE!

Susan C. Hawthorne - ADHD: Time to Change Course

Susan C. Hawthorne is the author of Accidental Intolerance: How We Stigmatize ADHD and How We Can Stop, and is Assistant Professor, Department of Philosophy, St. Catherine University.

In this article from the Oxford University Press blog, Hawthorne questions the current status quo around ADHD and the overuse of pharmaceutical interventions.

Recently, over lunch with a fellow therapist (and like me, a person who in his youth did a fair amount of "reality adjustment"), we were discussing the ADHD issue. We both conclude that if you give ANYONE amphetamines that person will be more focused and get more done. Just because we give the drugs to kids who we think are doing poorly in school and they begin to do better does not even begin to mean they have/had ADHD - it means the amphetamines are working.

And I now return you to the article at hand.

ADHD: time to change course

Posted on Sunday, November 10th, 2013 
By Susan C. Hawthorne

In March 2013, we learned that 11% of US children and teens have received an ADHD diagnosis, an increase of 41% in 10 years. Diagnoses among adults have sharply increased as well. Some ADHD experts welcome this change. They interpret these high rates as signs that much-needed attention is finally being given to people whose biology has been a disadvantage in work, school, and relationships. Other professionals have been taken aback by the current diagnostic rate and its purported repercussions, citing risks such as overprescription of drugs, medicalization of normal behaviors, and drug diversion to street use.

No general uproar has materialized, however. On the contrary, it’s looking like the upward trend will continue. Recent publications explain how to increase screening rates via computerized assessments, and how to hone diagnosis with a new EEG test. Most important, the new diagnostic guidelines in the American Psychiatric Association’s DSM-5 relax the diagnostic criteria, pulling more people, especially adolescents and adults, under the “ADHD” umbrella. The ADHD therapeutics market has responded enthusiastically, predicting high profits from increased diagnostic rates.

Children and their teacher in a classroom

One reason for the lack of outcry might be that people see this as the continuation of a steady trend: same old, same old. Diagnostic rates have been increasing for decades. Another might be the continued sway of the pharmaceutical business. It has effectively hyped the diagnosis for 40 years through targeted medical education; advertising to physicians, patients, and parents; and a smorgasbord of perks for “opinion leaders” and clinicians.

I think, though, that the reason for accepting this status quo involves much more than the drug industry. Basically, a lot of people—and a lot of the social systems in which they participate—like the diagnosis.

• Teachers and education administrators like it: Within the strained education system, it addresses needs of overworked teachers and overcrowded classrooms.
• Physicians and medical insurers like it: It’s a win-win in the medical system because the diagnosis (in the predominant interpretation as a biological dysfunction in individuals) falls in physicians’ purview; current care is quick and easy, often consisting only of a prescription.
• Clinical scientists like it: Research dollars flow toward it because the diagnosis—hence the fruits of research—promises to solve problems.
• And of course parents and adult diagnosees, who typically self-refer, like it: The short-term effects of medication help with behavior issues they deal with, and the promise of long-term effectiveness gives them hope. (Never mind that long-term effectiveness has not yet been demonstrated.)

If so many people like the diagnosis, what’s the problem? The much-discussed worry that we are overusing psychotropics, especially in children, is worth reconsidering. But two other issues also need to be aired

The first is that the continued reliance on ADHD as a research category puts clinical science in a rut—repeatedly studying ADHD and non-ADHD groups assumes that ADHD is a relevant and important category. More research should question that assumption. Investigating other hypotheses opens avenues of research that might better address clinical needs, as well as leading to more knowledge about mental health and illness.

The second issue is the stigmatization of those who are diagnosed as having ADHD. Years of research has shown that ADHD diagnosis correlates with multiple life choices and outcomes generally considered negative, such as increased rates of accidents, substance abuse, poor relationships, low educational and work achievement, and higher medical and education expenses. Drawing attention to “ADHD” as a contributor to these life tracks puts the blame on supposed biological facts about the individuals. Then, despite efforts to spin attitudes toward compassion for these (putatively) inborn circumstances, the opposite often occurs. The correlation between ADHD diagnosis and negatively perceived life tracks instead provides a medically and scientifically justified target for social disapproval—that is, ADHD-diagnosed people are stereotyped and stigmatized. Alternatives suggest that the biological claims are at best incomplete, and that social circumstances require investigation and intervention as well.

For these reasons, I think that it is time for new directions. More specifically, it is time to reassess clinical and research needs, and to find new ways to address both without relying on the “ADHD” catch-all. However, arguments pointing to evidence of progress via the current direction and arguments favoring the vested interests in the status quo—economic, educational, medical, scientific, and personal—weigh in the opposite direction.

Should we change course? I welcome your ideas.

Susan C. Hawthorne, author of Accidental Intolerance: How We Stigmatize ADHD and How We Can Stop, is Assistant Professor, Department of Philosophy, St. Catherine University.

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Image credit: Children in a classroom by Michael Anderson, National Cancer Institute. Public domain via Wikimedia Commons.

The p Factor: One General Psychopathology Factor in the Structure of Psychiatric Disorders

Using the Dunedin Multidisciplinary Health and Development Study as a data source, researchers Terrie Moffitt, Avshalom Caspi, and their team examined "the structure of psychopathology, taking into account dimensionality, persistence, co-occurrence, and sequential comorbidity of mental disorders across 20 years, from adolescence to midlife."

The researchers initially explained psychopathology using three higher-order factors (Internalizing, Externalizing, and Thought Disorder). However, they found that one General Psychopathology dimension explained psychopathology even better. They called this dimension the p factor. Higher p scores are "associated with more life impairment, greater familiality, worse developmental histories, and more compromised early-life brain function."

This is an interesting approach to understanding psychopathology. However, until researchers discover what many therapists already know (i.e., that most mental illness is due some form of relational trauma), they will still be wandering off into the tall grass and missing the obvious.

General Psychopathology Factor May Describe Structure of Psychiatric Disorders

Mental disorders have traditionally been viewed as distinct categorical entities, but the high incidence of comorbid, or co-occurring, disorders challenges this view.

As researchers Terrie Moffitt, Avshalom Caspi, and colleagues observe in their new article in Clinical Psychological Science, about half of the people who meet diagnostic criteria for one disorder also meet the diagnostic criteria for another disorder at the same time.

“The high rates of comorbidity observed among mental disorders suggest that there may be a more parsimonious structure to psychopathology than implied by current nosologies that identify many separate and distinct disorders,” Moffitt, Caspi, and co-authors write.

To test this hypothesis, the researchers looked at longitudinal data collected from participants in the Dunedin Multidisciplinary Health and Development Study who were between the ages of 18 and 38. The researchers examined the participants’ mental health data, testing several possible statistical models to see which model best accounted for the data.

Confirmatory factor analysis revealed that the structure of mental disorders could be summarized by three core dimensions: an “internalizing” liability to depression and anxiety, an “externalizing” liability to antisocial and substance-use disorders, and a “thought disorder” liability to symptoms of psychosis.

Furthermore, analyses suggested that the propensity to develop any and all forms of common psychopathologies could be summarized by one general underlying dimension. Higher scores on this dimension, which the researchers call the “p factor,” were associated with greater life impairment, greater familiality, worse developmental histories, and more compromised brain function in early life.

“We propose that p influences present/absent performance on hundreds of psychiatric symptoms, which are typically aggregated into dozens of distinct diagnoses, which further aggregate into two overarching Externalizing versus Internalizing domains, which finally aggregate into one normally distributed dimension of psychopathology from low to high: p,” the researchers conclude.

One way to think about the p factor is in relation to the structure of cognitive abilities:

“These abilities are dissociable into separate abilities, such as verbal skills, visuospatial skills, working memory, or processing speed,” say the researchers. “Nonetheless, the general factor in intelligence (called the g factor) summarizes the observation that individuals who do well on one type of cognitive test tend to do well on all other types of cognitive tests.”

While there are specific factors that account for variation in each test, the g factor accounts for the positive correlation among all test scores, suggesting that there may be a common etiology that influences or contributes in some way to all cognitive functions.

The new findings suggest that, just as there is a general factor of cognitive ability, there may also be a general factor of psychopathology. This general factor may, in turn, help to explain why researchers have had difficulty finding distinct causes, biomarkers, and treatments for individual mental disorders.

Moffitt, Caspi, and colleagues hope that these initial findings generate “further tests, extensions, and discussions about the structure of common mental disorders.”


Caspi, A., Houts, R.M., Belsky, D.W., Goldman-Mellor, S.J., Harrington, HL, Israel, S., Meier, M.H., Ramrakha, S., Shalev, I., Poulton, R., & Moffitt, T.E. (2013, Aug 14). The p Factor: One General Psychopathology Factor in the Structure of Psychiatric Disorders? Clinical Psychological Science. DOI: 10.1177/2167702613497473

Here is the abstract and some of the introduction to the original article (available here):

Abstract

Mental disorders traditionally have been viewed as distinct, episodic, and categorical conditions. This view has been challenged by evidence that many disorders are sequentially comorbid, recurrent/chronic, and exist on a continuum. Using the Dunedin Multidisciplinary Health and Development Study, we examined the structure of psychopathology, taking into account dimensionality, persistence, co-occurrence, and sequential comorbidity of mental disorders across 20 years, from adolescence to midlife. Psychiatric disorders were initially explained by three higher-order factors (Internalizing, Externalizing, and Thought Disorder) but explained even better with one General Psychopathology dimension. We have called this dimension the p factor because it conceptually parallels a familiar dimension in psychological science: the g factor of general intelligence. Higher p scores are associated with more life impairment, greater familiality, worse developmental histories, and more compromised early-life brain function. The p factor explains why it is challenging to find causes, consequences; biomarkers, and treatments with specificity to individual mental disorders. Transdiagnostic approaches may improve research.
 

Introduction

A psychiatric nosology—the classification of mental disorders—is a practical tool. A nosology is useful for research because it is used to integrate and guide empirical studies. A nosology is useful for health-care delivery because it is used to make prognoses and to decide on treatment need and choice of treatment. The Diagnostic and Statistical Manual of Mental Disorders (5th ed.; DSM-5; American Psychiatric Association, 2013) is the current ascendant nosology in clinical psychology and psychiatry. It may not be perfect (Sanislow et al., 2010), but it is what many of us work with in both research and clinical practice (Kupfcr, Kuhl, & Regier, 2013).

A persistent challenge to the DSM and related nosologies is comorbidity, the coexistence of two or more conditions or disorders (Hasin & Kilc-oyne, 2012; Kessler, Chiu, Demler, Merikangas, Sr Walters, 2005). Comorbidity rates are very high in psychiatry and conform roughly to the rule of 50910: Half of individuals who meet diagnostic criteria for one disorder meet diagnostic criteria for a second disorder at the same time half of individuals with two disorders meet criteria for a third disorder, and so forth (Newman, Moffitt, Caspi, & Silva, 1998). The high rates of comorbidity observed among mental disorders suggest that there may be a more parsimonious structure to psychopathology than implied by current nosologies that identify many separate and distinct disorders. This article begins by providing a brief historical review of empirical research on the structure of psychiatric disorders. It then offers an empirical update, suggesting that most common psychiatric disorders are unified by a single psychopathology dimension representing lesser-to-greater severity of psychopathology that is associated with compromised brain integrity.

Soon after the publication of the DSM-5 (American Psychiatric Association, 1994), psychological scientists noted the need for research that would examine patterns of comorbidity to "elucidate the broad, higher-order structure of phenotypic psychopathology" (Clark, Watson, & Reynolds, 1995, p. 131). We responded to this call by using confirmatory factor analysis (CFA) to evaluate alternative hypotheses about the latent structure underlying 10 common mental disorders among young adults, ages 18 to 21 years (Krueger, Caspi, Moffitt, & Silva, 1998) in contrast to the prominence of categorical models in the classification of adult psychopathologies, dimensional models had long enjoyed success in research on the classification of childhood psychopathologies, and empirical studies had converged on two primary dimensions as a way to characterize childhood disorders: Internalizing (including anxious and depression symptoms) and Externalizing (including aggressive, delinquent, and hyperactive-impulsive symptoms; Achenbach & Edelbrock, 1981). We could see no reason why this highly replicable two-dimensional structure of psychopathologies should suddenly vanish when research participants and patients suddenly turned age 18 years. Our data confirmed that a two-factor model accounted for the comorbidity of different young-adult disorders, and it bore a striking similarity to the model of childhood psychopathologies.

On the basis of this initial finding, we put forth the hypothesis that common DSM psychiatric disorders in adulthood may be characterized by two underlying core psychopathological processes: an Internalizing dimension indicating liability to experience mood and anxiety disorders, such as major depression (MDE), generalized anxiety disorder (GAD), panic disorder, and social phobia; and an Externalizing dimension indicating liability to experience substance disorders and antisocial disorders. During the past 15 years, multiple studies in different parts of the world, in different age-groups, in general community samples, and in clinical populations (e g , Forbush & Watson, 2013; Kendler, Prescott, Myers, & Neale, 2003; Krueger, 1999; Slade & Watson, 2006; Vollebergh et al., 2001) have replicated this basic finding (Krueger & Markon, 2006, 2011).
 
With the publication of the DSM-5 and debate fomenting over the need for a dimensional nosology (Insel, 2013), now is a good time to take stock of what is known about the structure of psychopathology. We have drawn on insights stemming from six recent findings about the epidemiology of mental disorders.
 
First, life-course epidemiology points to the need for longitudinal research designs to study the course of psychopathology. Previous research on the structure of psychopathology has been carried out using cross-sectional designs, focusing on individuals who report symptoms within a specified period (most often using the past 12 months as the reporting period). However, research has shown that cross-sectional snapshots mix single-episode, one-off cases with recurrent and chronic cases, which are known to differ in the extent of their comorbid conditions, the severity of their conditions, and possibly the etiology of their conditions. This is true for a variety of common disorders, including, for example, depression and alcohol-use disorders (Jackson & Sartor, in press; Monroe & Harkness, 2011), but also for psychotic experiences (van Os, Linscott, Myin-Germeys, Delespaul, & Krabbendam, 2009). That is whether manifested as recurrence or chronicity, some people are more prone than others to have persistent (as well as comorbid and severe) psychopathology. These results underscore the need to take the longitudinal course of mental disorders into account when modeling the higher-order structure of psychopathology.
 
Second, sequential comorbidity points to the need to model multiple disorders over time. Previous research has focused on comorbidity as defined by the co-occurrence of two or more disorders at the same time, but both retrospective (Kessler et al., 2011) and prospective-longitudinal (Copeland, Shanahan, Costello, & Angold, 2011) research has shown that comorbidity is also sequential. For example, longitudinal research has shown that GAD and MDE are linked to each other sequentially such that each disorder increases the likelihood of developing the other disorder in the future among individuals who presented with only one condition at one point in time (Moffitt et al.. 2007). These results underscore the need to take into account both concurrent and sequential comorbidity when evaluating the structure of psychopathology.

Third, psychotic disorders can be included in models of the structure of psychopathology. In most previous studies, researchers have omitted psychotic disorders from their evaluation of the structure of psychopathology. There are practical explanations for this omission (e g , most surveys of psychiatric disorders do not assess psychotic symptoms), but their absence from studies of the structure of psychopathology is conspicuous for three reasons: (a) New research on the dimensional model of psychosis has directed attention to the fact that psychotic symptoms are more commonly experienced in the general population than previously assumed, (b) psychotic disorders are striking in their especially high rates of comorbidity, and (c) psychotic disorders have extraordinary high economic burden. as expressed in the number of years lost due to ill health. disability, or early death (Murray et al., 2012; van Os et al., 2009). A few researchers recently have incorporated psychotic symptoms and symptoms of schizotypal personality disorders into their assessment of the structure of psychopathology, pointing to the existence of a third, distinct Thought Disorder spectrum (Kotov, Chang, et al., 2011; Kotov, Ruggero, et al., 2011). These results underscore the concern that efforts to model the structure of psychopathology without consideration of psychotic symptoms may not capture the true structure in the population.

Fourth, twin studies and risk-factor studies have suggested not only that there are substantial phenotypic correlations among pairs of psychiatric disorders but also that the liability to many disorder pairs (e g , schizophrenia and bipolar disorder; MDE and GAD; and alcohol and cannabis dependence) is influenced by the same genetic factors (Kendler, 1996; Lichtenstein et al., 2009; Sartor et al., 2010) and that many disorder pairs are characterized by shared intermediate phenotypes (Nolen-Hoeksema & Watkins, 2011). These findings imply that the causes of different disorders may be similar, highlighting the potential value of a transdiagnostic approach to psychiatric disorders. The value of a transdiagnostic approach has been further underscored by evidence that different disorders often respond to the same treatments (Barlow et al., 2011).
 
Fifth, symptom variation above and below diagnostic cut points implies modeling disorder data at the level of symptom scales. Researchers in most previous studies of the structure of psychopathology have modeled DSM disorders as dichotomous variables, although the few that have used symptom scales have generated comparable results (e g., Markon, 2010). Diagnostic thresholds increasingly have been acknowledged to be somewhat arbitrary, and it has been recognized that there is meaningful and useful clinical information both above and below diagnostic thresholds (Kessler et al., 2003; Lewinsohn, Shankman. Gau, & Klein, 2004). The DSM-5 also opted to emphasize dimensional conceptualizations of psychiatric disorders.
 
Sixth, the possibility of one General Psychopathology factor should be tested. This issue has arisen from the observation that disorders are positively correlated not just at the disorder level but substantially so at the spectrum level as well; for example, the correlation between the Externalizing and Internalizing spectra is -.5, and the correlation between the Internalizing and Thought Disorder spectra has been estimated at -.6 (Wright et al., 2013). Given high correlations at the spectrum level, Lahey et al. (2012) suggested the intriguing possibility that in addition to propensities to specific forms of psychopathology (e.g., Internalizing vs. Externalizing), there may be one underlying factor that summarizes individuals' propensity to develop any and all forms of common psychopathologies. They used confirmatory factor models to test a hierarchical bifactor model that derives a general factor from the correlation matrix between different mental disorders and found that depression, anxiety, substance use, and conduct/antisocial disorders all loaded strongly on a single factor, in addition to specific Internalizing and Externalizing spectra (Lahey et al. did not include symptoms of psychosis in their work).
 
A useful way to think about the meaning of such a general factor in psychopathology is by analogy in relation to cognitive abilities. These abilities are dissociable into separate abilities, such as verbal skills, visuospatial skills, working memory, or processing speed. Nonetheless, the general factor in intelligence (called the g factor) summarizes the observation that individuals who do well on one type of cognitive test tend to do well on all other types of cognitive tests (Decry, 2001; Jensen, 1998; Spearman, 1904). Although specific factors account for variation in each test, the g factor accounts for the positive correlation among all test scores, suggesting that all cognitive functions, to some extent, are influenced by common etiology. Just as there is a general factor of cognitive ability, it is possible that there also is a general factor of psychopathology.

Given the aforementioned new findings and insights, we used data from a comprehensive prospective longitudinal study of mental disorders; during the past 20 years, we repeatedly assessed symptoms of 11 kinds of common adult mental disorders in a representative birth cohort, from ages 18 to 38 years. The research reported here had four aims. First, we tested alternative models of the structure of psychopathology using data that take into account information about the dimensionality, persistence, co-occurrence, and sequential comorbidity of mental disorders, including psychosis. Second, we evaluated the validity of the structure of psychopathology by testing associations between the factors obtained and independent information about the study members' personality functioning and life impairment. Third, we tested the family histories and developmental histories associated with each of the factors representing the structure of psychopathology. Fourth, we tested the hypothesis that individual differences in severe and impairing psychopathology are associated with compromised brain integrity from early life.

Read the whole article.

Julian Ford, Ph.D. - PTSD Becomes (More) Complex in the DSM-5

Julian Ford is one of the experts in the field of complex PTSD (an as yet un-approved diagnosis in the DSM, and not for a lack of effort). Over at his Psychology Today blog, Hijacked by Your Brain, he has posted a two-part examination of the changes to the PTSD diagnosis in the DSM-5.

I like the addition of the dissociative subtype for PTSD. The research suggests that 15-30% of those who have PTSD have persistent dissociation as a key feature. This sub-type is very strongly coorelated with childhood abuse and neglect, which is where the notion of complex PTSD comes from - research has shown that of those who develop PTSD following an adult experience of trauma (war, rape, other violent crime, natural disasters, and so on), there is also a strong correlation to childhood abuse and neglect.

When we are abused, neglected, belittled, and shamed as children, we do not develop the resilience necessary to get through traumatic events without serious complications. This is not a perfect cause and effect, but the link is clear and there are piles of research in support of this thesis.

Dr. Ford, along with Jon Wortmann, is the author of Hijacked by Your Brain: How to Free Yourself When Stress Takes Over (2013), after which the blog is named.

About the Author:

Julian Ford is a Professor of Psychiatry at the University of Connecticut School of Medicine and Director of the University of Connecticut Health Center Child Trauma Clinic and Center for Trauma Response Recovery and Preparedness (www.ctrp.org), the creator of the TARGET© treatment model for adult, adolescent, and child traumatic stress disorders, and CEO of Advanced Trauma Solutions, Inc., the exclusive licensed provider of the TARGET© treatment model.

Ford is also co-author of Treatment of Complex Trauma: A Sequenced, Relationship-Based Approach (2012, with Christine A. Courtois) and co-editor (along with Courtois) of Treating Complex Traumatic Stress Disorders (Adults): An Evidence-Based Guide (2009).

PTSD Becomes (More) Complex in the DSM-5: Part 1

Heading in the right direction, but still not as complex as the brain

Published on June 11, 2013 by Julian Ford, Ph.D. in Hijacked by Your Brain

The diagnosis of posttraumatic stress disorder (PTSD) has undergone much more than a minor tweaking or superficial facelift in the American Psychiatric Association's DSM-5. This guidebook to psychiatric diagnoses, released in May, now defines PTSD as a trauma and stressor-related disorder, not a disorder primarily of anxiety alone. Like our understanding of the brain and behavior, PTSD has become much more complex—and for millions of trauma survivors who have experienced difficulties that go well beyond the symptoms included in PTSD up to now, and the tens of thousands of clinicians who provide treatment to affected trauma survivors, the change is long overdue, but extremely welcome.

Bottom line, PTSD is now described as a disorder of persistent reactivity in all of the domains of self-regulation, and not just troubling memories and chronic anxiety[1]. Distressing memories of past traumatic events and intense stress reactions to reminders that occur in current life continue to serve as the cornerstone of PTSD.

Now, however, these forms of "intrusive re-experiencing" of traumatization are understood as playing out across the full range of ways in which we regulate ourselves: emotions, body functions and health, thinking, motivation, behavior, relationships, and ultimately our sense of self or identity.

Trauma doesn't just terrify or horrify us—it also forces us to make profound biological adaptations in how our brain operates. Basically, the brain is a control system that keeps our body functioning properly. In other words, the brain regulates how our body functions to keep us alive, and when our body is safe and working well, the brain extends its efforts to the "higher" functions that enable us to not only survive but also to become a conscious individual—a self or an identity that makes each of us and our lives unique and not only pleasurable (or tolerably painful) but meaningful.

When the brain detects serious threats to our bodily survival, traumatic stressors such as severe accidents, disasters, violence, abuse, or betrayals, the alarm system in the brain is activated and literally hijacks the rest of the brain's operations in order to put all systems in emergency mode until the threat is escaped or overcome.

This might seem like a simple shift in brain functions that leads to a temporary fight-flight reaction or adrenaline rush that is intense but quickly passes. And in many cases, both with ordinary stressors that are not traumatic threats to our lives as well as with traumatic survival threats, the alarm reaction in the brain does rapidly subside. We’re left somewhat shaken or jangly, but no worse for the wear with a brain that re-sets automatically to its normal modes.

However, as we've described in Hijacked by Your Brain, PTSD is what happens when the brain's alarm system doesn't automatically or rapidly re-set itself. When the brain's alarm continues to signal danger even though safety has been restored, the brain's overall functioning remains in an altered state that is the chronic stress response. Survival trumps self-regulation in this case: staying alert and ready to react in fight-flight mode to the next assault or betrayal takes precedence over sorting out our emotions and thoughts, taking care of our body's health, considering our core values and who we aspire to be.

In service of a commendable goal, survival, the brain's alarm system has hijacked the "higher" operations of the brain itself, keeping us alert and ready for action, and therefore alive. In this state, however, life becomes a constant struggle that involves unbearable tension and ultimately emotional as well as physical exhaustion (hence the depression and physical health problems that so often occur with PTSD).

People living with PTSD, therefore, are not just troubled by terrible memories, worries, and anxieties. More fundamentally they have high functioning brains that have become trapped in survival mode. That's why PTSD is complex, because it's about a fundamental change in how the brain (and body, and mind) are operating. It is not a disease, and not an injury to the brain (although when this has happened as well, such as when the survival threat is a blast explosion or another severe physical injury to the head, the combination of PTSD and traumatic brain injury creates additional major challenges).

How can someone re-set a brain's alarm that's stuck in PTSD (survival mode), so that self-regulation can be restored? That is the $64,000 question, which I'll tackle in Part II of this series on the implications of PTSD becoming defined in a way that is appropriately more complex in the DSM-5.

Hijacked by Your Brain blogs are co-authored with Jon Wortmann. Visit our website at www.hijackedbyyourbrain.com. You can follow us onfacebook or join us on twitter @hijackedbook.

[1] http://www.tandfonline.com/doi/abs/10.1080/15299732.2013.769398#.UaZbsuCb8Rk

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PTSD Becomes (More) Complex in the DSM-5: Part II

Recovering from (Complex) PTSD by Regaining Self-Regulation

Published on June 16, 2013 by Julian Ford, Ph.D. in Hijacked by Your Brain

In the DSM-5 released in May, PTSD just got more complex. It added a new symptom domain of "negative alterations in cognitions or mood," and expanded the hyperarousal domain to include aggressive, reckless, or self-destructive behavior. It also added a sub-type characterized by dissociation (drastic reductions in physical arousal and conscious emotion and thought). These changes reflect advances in science and clinical practice, which echo what trauma survivors have been saying for decades (if not centuries): PTSD is a radical shift from normal self-regulation to being trapped in a constant state of alarm.

To understand, and recover from, PTSD, it's essential to understand what the brain and body do to "self-regulate" under ordinary circumstances—because this is what's lost in PTSD and must be regained in recovery. Self-regulation is a delicate and complicated balancing act in which the brain and body constantly adjust to maintain a balance between mobilizing (being highly activated) and re-grouping (down shifting into less activated states).

Mobilization is essential to experiencing pleasurable excitement, enthusiasm, and achievement. But too much mobilization for too long leads to tension, frustration, recklessness, and even self-harm. Similarly, when the body and brain re-group, this can produce pleasurable and healthy states of relaxation, calm, and mindful acceptance. However, when re-grouping becomes extreme and persistent, the result can be emotional shut-down and exhaustion, depression, despair, or dissociation. Self-regulation is the constant balancing act between mobilization and re-grouping that enables us to be optimally effective and to feel true satisfaction.

Trauma is a threat or injury that requires self-protective stress reactions—essentially fight or flight—which hijack the brain and body in order to achieve the one goal that is a higher priority than being effective and satisfied: survival. Post-traumatic stress disorder derives its name from this key fact: PTSD is a disorder because the the brain and body have become trapped on a roller coaster of dysregulation. PTSD involves rocketing into extreme states of stress reactivity (mobilization in the form of terror, rage, and uncontrollable impulses) and plunging into equally extreme states of being shut-down (exhaustion, emotional numbing, despair, and dissociation). From this vantage point, PTSD clearly is about much more than fear and anxiety, involving the full range of emotions and undermining our body's health, our ability to think clearly, to set and achieve goals, and to fully participate in and benefit from relationships.

A particularly important new symptom of PTSD highlights an important aspect of the loss of self-regulation: "Persistent and exaggerated negative expectations about one’s self, others, or the world (e.g., “I am bad,” “no one can be trusted,” “I’ve lost my soul forever,” “my whole nervous system is permanently ruined,” "the world is completely dangerous")." PTSD thus is inherently complex, and all about the loss of self-regulation that occurs when survival dominates how a person thinks, feels, and behaves in every area of his or her life. PTSD replaces the "me" who was growing, learning, and becoming a unique person before the trauma(s), leaving only a desperate survivor who may have no clear sense of identity and who may even hate or loathe herself or himself.

Although the dilemma of post-traumatic self-dysregulation is indeed complex, as is the array of therapies that have shown promise in treating (complex) PTSD , the key to recovery is not rocket science. Survival threats can cause the brain to be hijacked by its own alarm system, so the key is to re-set that alarm system so it's no longer in survival mode.

Re-setting the brain's alarm requires seven steps, which are at the heart of every effective treatment for (complex) PTSD despite their many differences:

Focus mentally on a single thought that you choose because it is what's most important and positive in your life at this moment—not what's most urgent or problematic, nor what's a lifetime away, but what you value most and what represents the very best part of your life right now.

Recognize the triggers that signal problems or danger: don't ignore them, but don't obsess or ruminate about them, just make a mental note to be alert.

Experience the emotions that are signals from your brain's alarm, but also the sustaining emotions that seem to get lost in the midst of stress reactions but actually are always present if you just look carefully for them; emotions like joy, hope, love, pride, security, enthusiasm, determination.

Evaluate your thoughts not to judge or alter or eliminate them, but to distinguish between the defensive (or offensive) thoughts that are generated by your brain's alarm from the sustaining beliefs that also can get lost in alarm reactions (but actually are always available when you focus on your core values).

Define your goals so that you can tell the difference between defensive (or offensive) goals that are potentially useful warnings from your brain's alarm and the sustaining goals that are based on your core values.

[Choose] Options that enable you to achieve your sustaining goals and to live according to your core values, while being aware of and open to using other options that are more defensive (or offensive) if you are faced with a genuine threat to your, or others', survival.

Make a contribution by doing the one thing that each of us can do to make everyone safer, healthier, and more effective: continue to practice these simple steps in your own individual ways, and in so doing become a role model for responsible self-regulation.

These seven steps spell FREEDOM. They are not a pre-packaged set of techniques for self-improvement. They have to be done by each person in their own individual way. They enable you to use your mind to shift out of survival mode and your body to resume the natural state of self-regulation that is lost whenever anyone becomes trapped in the alarm state that the DSM-5 calls PTSD.

Hijacked by Your Brain blogs are co-authored with Jon Wortmann. Visit our website at www.hijackedbyyourbrain.com. You can follow us onfacebook or join us on twitter @hijackedbook.