Applied History of Psychology/Specific Disorders

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Historical Perspectives on Psychological Trauma[edit | edit source]

Introduction to Perspectives on Psychological Trauma[edit | edit source]

It has been said that whatever doesn’t kill us makes us stronger. A few people live through horrible events without experiencing much fear, but most of us react with feelings of horror and helplessness. Psychological trauma occurs in the wake of an unexpected event that is so unpleasant and shocking that the human mind and body react in an autonomic defensive manner (Thornet, 2000). For some people, surviving severe traumatic events leaves them depressed, anxious, and with other emotional scars such as Post Traumatic Stress Disorder (PTSD).

By definition, PTSD includes episodic re-experiencing of traumatic events, usually in the form of dysphoric memories. Because these memories are vivid, frightening and unexpected, they have secondary effects, causing sufferers to doubt their sanity, their progress in recovery and their fundamental sense of security (Ochberg, 1998). The original traumatic experience had elements of terror, horror, and/or helplessness, and persistent episodes of traumatic memory continue and compound such elements (Ochberg, 1998). Recent findings have indicated PTSD prevalence rates of 5% and 10% respectively among American men and women (Kessler, Sonnega, Bromet, Hugues, & Nelson, 1996).

The key to understanding the scientific basis and clinical expression of PTSD is the concept of “trauma” (Friedman, 1997). PTSD is unique among other psychiatric diagnoses because of the great importance placed upon the etiological agent, the “traumatic stressor” (Herman, 1992). Thus, traumatization is seen as being caused by the event, not because of some failing or weakness in the person. In fact, one cannot make a clinical diagnosis of PTSD unless the client has actually met the “stressor criterion”. Along with the diagnostic criteria of exposure to a “traumatic event” are symptoms from each of the three symptom clusters: intrusive recollections, avoidant/numbing symptoms and hyperarousal symptoms (APA, 1994). A fifth criterion concerns the duration of the symptoms (APA, 1994). The duration criteria for diagnosis of PTSD when the above criteria have been met is one month (APA, 1994).

Not only is PTSD typified by the automatic, involuntary symptoms such as flashbacks, intrusive thoughts and autonomic hyperarousal, but also consciously mediated attempts to make meaning of the trauma experience(s) (Clark & Ehlers, 2000). The automatic and involuntary symptoms are said to represent conditioned responding to environmental triggers associated with the trauma (Clark & Ehlers, 2000). Much less is known about the origins and consequences of victims’ efforts to understand their trauma(s) or about how best to treat the symptoms associated with personal beliefs about the trauma (Meichenbaum, 1994).

In children, an important issue in the experience of trauma is its effect on the attachment system and developing brain function.

Earliest writings on trauma cases[edit | edit source]

Humankind has never been without traumatic events. The earliest writings of history contain evidence of the manifestation of psychological symptoms related to distressing experiences. Over time theories regarding the symptoms, causes, and treatment resulting from trauma have greatly varied.

Initially, only women were believed to be inflicted by symptoms that had no physical explanation, such as sudden loss of sight, loss of ability to walk, or uncontrollable shaking. The earliest indication of these symptoms was recorded on an Egyptian papyrus from 1900 BC, which attributed the disorder to a wandering uterus. The use of the term, hysteria, to describe this constellation of symptoms dates back to Hippocrates (430-367 B.C.) who labeled the condition for its Greek meaning of uterus. Since this condition was only documented in women, his prescribed cure for the afflictions caused by a wandering uterus was marriage. Of note, trauma is a term widely used in psychology and its meaning is derived from the Greek word for wound. The term emerged into the neurological and psychiatric vocabulary in the 1860’s and 1870’s. Previously, the term trauma had been reserved for the description of physical wounds and had been documented in the surgical medicine literature.

Anton Mesmer (1734–1815) was the first to explain hysteria in a physiological way. He believed that hysteria was a direct result of a disturbed distribution of the magnetic fluid present in all humans. He appears to have been the first to document the possibility that hysterical symptoms could be present in men and women. Mesmer’s treatment for hysteria involved touching his patients with rods, which he said transmitted a magnetic force called animal magnetism from his body to the patient. He believed that this force of animal magnetism was capable of rearranging the patient’s fluids to result in healthy functioning, and thereby curing the condition of hysteria. With our knowledge today, it is widely believed that Mesmer’s approach was a predecessor of hypnotism due to his convincing manner of describing his techniques to his patients and his strong suggestions of recovery. Although Mesmer’s techniques resulted in improvement and documented cures of many of his patients, his theories and techniques were not respected by other health professionals at the time.

With the development of the railroad in the mid 1800’s, there was also an increase in accidents and death with this initially dangerous mode of transportation. Lerner (2003) found statistics of injuries related to the railway in the United States in 1889: one out of every 117 train workers was killed and one out of every 12 workers was injured. In addition, passengers and bystanders were involved in train collisions and derailings, which in that time were common. Some accident victims seemed to complain of common symptoms such as headaches, dizziness, paralysis, and general disinterest and listlessness with no apparent physical cause. In 1866, an English physician, John Eric Erichsen (1818–1896) published several cases of this condition and coined the term “railway spine”. In addition to the above mentioned symptoms, he wrote about memory loss, confusion, diminished business aptitude, ill temper, sleep disorders, sensory impairment, attitude changes, loss of motor power, numbness and sexual impotence. Although these symptoms paralleled those of hysteria, Erichsen chose the new label of railway spine since it was previously believed that only women were inflicted with hysteria and most of his patients related to the railroad were men.

With increasing numbers of mental health diagnoses related to trauma, treatment for these symptoms was in high demand. Jean-Martin Charcot (1825–1893) was a neurologist who believed that hypnotism was of value in treating hysterics. Originally, his theories on hysteria were somatic in nature. Over time, he adjusted his original theories to include psychological factors. Additionally, in 1882, he began treating cases of hysteria in male patients, which he reported were growing in large numbers. He described symptoms in these males as motor and sensory disturbances due to railroad accidents, workplace accidents, and service in war. He believed that these symptoms were directly related to a traumatic stimulus in those individuals who had an inherited, constitutional disposition.

As stated earlier, symptoms of hysteria were not initially believed to be inflictions of men. However, with men fighting in the frontlines of World War I where they took the lives of the opposition, witnessed violent deaths of their fellow soldiers, and often narrowly escaped death themselves, it is not surprising that many soldiers began demonstrating symptoms of what was then know as hysteria. Soldiers were documented as suffering from symptoms such as debilitating shakes, stutters, tics and tremors, disorders of sight, hearing, and gait (Lerner, 2003). Although there is evidence of other problems during other wars, the sheer number of soldiers with these inflictions caught medical authorities unprepared and therefore drew much attention. Since it was thought unfitting to diagnose these men with a woman’s illness, new labels were created to describe these combinations of symptoms as listed earlier. Many features of what is now called post-traumatic stress disorder were well-described in literary form during this time, such The Red Badge of Courage. However, it wasn’t until World War II that there was a creation of a formal diagnostic category. World War II had brought together soldiers, psychiatrists and other medical personnel, and they discovered that they did not always have a common vocabulary to discuss syndromes and diagnoses.

After World War II ended, the Veterans Administration (VA) developed a diagnostic manual. This provided incentive for the American Psychological Association (APA) to create its own first manual. Thirteen years after his Freud’s death, the American Psychological Association (APA) published its first diagnostic and statistical manual (DSM-1) in 1952 and re-wrote his conceptualization of traumatic neurosis for Gross Stress Reaction. During the post-war era and after there was a rise in systematic investigations of things such as the consequences of exposure to death camps and experiences of prisoners of war, as well as nonmilitary stressors such as mass catastrophes, such as fires, earthquakes and plane crashes (Adler, 1943; Andreasen, Hartford & Norris, 1971).

For reasons unknown, but perhaps because of the early links between military combat and stress disorders, Gross Stress Reaction was somehow dropped from DSM-II (Andreasen, 2004). That manual was written when the United States was not engaged in any major war. However, the scientific study of the consequences of stress continued, particularly in the area of consequences of severe burn injuries (Andreasen, 2004).

After the Vietnam War, the U.S. contained another wave of young men who had been traumatized in combat. There was no official diagnosis to give them, and therefore, no coverage for treatment. American veterans lobbied the APA to construct a diagnosis of “Post-Vietnam Syndrome” to recognize the long-term psychological damage incurred by soldiers in combat, in order to pave the way for therapeutic services. Recognizing the long history of the syndrome proposed, as well as the fact that it frequently occurred in traumatized civilians as well, and being rooted in the extensive literature on stress disorders already available at the time, the APA came up with Post-Traumatic Stress Disorder as an operational diagnosis in DSM-III. Criteria specified for the new diagnosis included an initial stressor that would evoke distress in almost anyone (Criterion A), a time frame, and a list of “symptoms”.

The diagnosis began to be used widely and its application broadened steadily. For example, it began to be used for victims of childhood sexual abuse who developed traumatic stress symptoms much later in life. The requirement that the stressor be outside the range of normal human experience was sometimes reinterpreted to include less severe stressors (Andreasen, 2004). In 1987, the criteria for PTSD was reworked in the DSM-III-R. he veteran issues again faded in importance, while feminist practitioners took a special interest in PTSD.

Feminist therapists began lobbying the APA to alter the definition of PTSD so that more of their clients would fall under its auspices (Burstow, 2005). In 1994, PTSD was revised in DSM-IV such that Criterion A now stated that the person had to either experience, witness or be confronted with an event or events that involved actual or threatened death or serious injury or a threat to the physical integrity of self or others. The person’s response must have involved intense fear, helplessness or horror and caused clinically significant distress and impairment in social, occupational or other important areas of functioning. This incorporated the concept of “vicarious traumatization” (i.e. emergency services, rescue workers, etc.). The DSM-IV also added back what was formerly called Acute PTSD, which had been dropped from DSM-III-R, under a new name of Acute Stress Disorder (ASD). In 2000, the DSM-IV-TR PTSD reformulated such that it is not required that the traumatizing event be outside the range of normal experience and explicitly makes room for common events such as childhood sexual abuse. Currently, trauma is of particular interest, at a time when the entire world is aware of the potential for terrorism to strike – a stressor of great magnitude that could strike at any time and anywhere. This is also a time when the U.S. is seeing the return of many traumatized young soldiers returning from the wars in Iraq and Afghanistan. Unfortunately, the present state of our world is likely going to provide many more opportunities to study stress reactions, and the diagnoses of ASD and PTSD are likely here to stay.

Timeline of Documented Cases of Trauma (Parry-Jones and Parry-Jones, 1994)

  • 1860: Spinal concussion, railway spins, irritable heart
  • 1870: Soldier’s heart, cardiac weakness
  • 1880: Traumatic shock, traumatic neurosis, hysterical hemianaesthesia, spinal irritation, railway brain, and nervous shock
  • 1890: Anxiety neurosis, psychical trauma
  • 1910: Traumatic neurosis, shell fever, irritable heart of soldiers, mental shock, war shock, shell shock, neuro-circulatory asthenia, disordered action of the heart, and war psychoneurosis
  • 1930: Cardiac/war neurosis
  • 1940: Battle fatigue/combat exhaustion, effort syndrome
  • 1980: PTSD

Historic Diagnostic Timeline of Post Traumatic Stress Disorder

  • 1895 - 1975: Freud’s conceptualization of traumatic neurosis dominated thinking in the medical-psychiatric profession to the end of the Vietnam War era in the U.S. In 1952, Freud’s conceptualization of traumatic neurosis was basically re-written into the DSM-I (Diagnostic and Statistical Manual of the American Psychiatric Association) diagnostic criteria for Gross Stress Reaction
  • 1975: After the Vietnam War, American veterans lobbied the American Psychiatric Association (APA) to construct a diagnosis that would recognize long-term psychological damage incurred by soldiers in combat to pave the way for therapeutic services.
  • 1980: PTSD first appeared as an operational diagnosis in DSM-III. Criteria specified for the new diagnosis included an initial stressor that would evoke distress in almost anyone (Criterion A), a time frame, and a list of “symptoms”.
  • 1987: PTSD reworked in the DSM-III-R to revise Criterion A to state, “the person has experienced an event that is outside the range of usual human experience and would be markedly distressing to almost everyone” (p. 250). The veteran issues faded in importance and feminist practitioners took a special interest in PTSD. Around this time, feminist therapists began lobbying the APA to alter the definition of PTSD so that more of their clients would fall under its auspices.
  • 1992: PTSD first appears in the International Classification of Diseases (ICD-10, 1992, World Health Organization).
  • 1994: PTSD was revised in DSM-IV such that Criterion A now stated that the person had to either experience, witness or be confronted with an event or events that involved actual or threatened death or serious injury or a threat to the physical integrity of self or others. The person’s response must have involved intense fear, helplessness or horror and caused clinically significant distress and impairment in social, occupational or other important areas of functioning. This incorporated the concept of “vicarious traumatization” (i.e. emergency services, rescue workers, etc.).
  • 2000: DSM-IV-TR PTSD reformulated such that it is not required that the traumatizing event be outside the range of normal experience and explicitly makes room for common events such as childhood sexual abuse.

Recent expansion on the conceptualization of trauma[edit | edit source]

Currently, there is increasing recognition of the complex impact of discrete traumatic experiences coupled with the impact of insidious trauma, intergenerational trauma and early trauma (Vasquez, 2006).

Insidious trauma is a term that has been coined by Dr. Maria Roots. Some of the life experiences that have informed her work include her experience of racism while growing up as mixed Filipino/Caucasian woman. She studied sociology and clinical psychology, graduating with a Ph.D. in clinical psychology from the University of Washington in 1983. Root articulated her definition of insidious trauma in 1992. Insidious trauma takes into account the impact of multiple forms of oppression anchored in race, gender, class, sexual orientation, immigration, and culture. Dr. Roots highlights that this consequences of these type of trauma are sometimes very difficult to identify and that the symptoms of insidious trauma are often attributed to people’s personalities or mental disorder. This is turns can further consolidate a distorted self-image and adoption of a view of self as sick.

Some example of insidious trauma include the lasting effects of European colonization upon indigenous people on the North American continent. The internalized oppression of many queer people, the residuals of slavery of African Americans, or the impact of violence against women.

There is increased recognition that insidious trauma as well as more direct forms of trauma often have intergenerational effects. The emerging literature appear first to focus on children of survivors and now stories of great-children of survivors of the holocaust demonstrating that they can trauma adaptation / symptoms can be passed down. Two popular Canadian case example include the experience of many children of indigenous residential school survivors (Manzes, 2003), or the children of the children of Duplessi who have higher levels of substance use and other forms of emotional problems.

Assessment of Trauma and PTSD[edit | edit source]

Assessment Instruments[edit | edit source]

Frueh, Elhai, & Kaloupek (2004) provided a list of measures of trauma and suggest that these measures can be classified within the following four categories:

  • Trauma exposure measures
Traumatic Life Events Questionnaire
Traumatic Stress Schedule
  • Symptom-referenced PTSD measures
PTSD Symptom Scale
PTSD Checklist
  • PTSD diagnostic measures based on standard interview formats
Structured Clinical Interview for DSM-IV (SCID) PTSD Module
Clinician-Administered PTSD Scale (CAPS)
  • Psychometrically derived PTSD measures
Mississippi Combat PTSD Scale
Minnesota Multiphasic Personality Inventory-2 (MMPI-2)

Treatment Throughout History[edit | edit source]

Eye Movement Desensitization Reprocessing (EMDR)[edit | edit source]

EMDR is a recently developed psychotherapy that is best known as a treatment for psychological problems relating to traumatic life experiences. In 1987, Francine Shapiro noticed that her own upsetting throughs faded when her eyes spontaneously moved rapidly from side to side. She developed a complex method, combining behavioral and client centered approaches, in which the client concentrates intensely on the most distressing segment of their traumatic memory while following with their eyes the therapist's fingers moving across the visual field. Shapiro (1995) had presented this method in detail. The literature strongly suggests that EMDR is superior to traditional forms of trauma therapy (Greenwald, 1998).

Exposure Therapy[edit | edit source]

Keane and his colleagues first applied Exposure Therapy (ET) to the treatment of PTSD in the form of single-subject designed studies to document the effects of exposure to memories of traumatic events (Black & Keane, 1982; Fairbank & Keane, 1982; Kaloupek & Keane, 1982). Significant reductions in trauma symptoms, anxiety, and other related symptoms were found as a function of ET interventions. This preliminary work led to the development of randomized clinical trials that compared Imaginal Based ET to the less intensive treatment of Anxiety Management Therapy (AMT) and wait-list controls. The results of this study were clear. Compared to the wait-list condition and AMT, those clients receiving ET showed significant reductions on standard psychometric instruments and on clinician ratings of symptoms, and changes were maintained at a 6-month follow-up (Caddell, Fairbank, Keane & Zimmering, 1989).

More recently, many studies have appeared in the literature comparing the effectiveness of ET to Cognitive Therapy (CT). For example, Barrowclough, Faragher, Graham, Pilgrim, Reynolds, Sommerfield & Tarrier (1999) examined the effectiveness of ET and CT in the treatment of outpatients with PTSD stemming from many different traumatic events. Both groups manifested significant improvements that were maintained at a 6-month follow-up. No significant differences were found between the two treatments and outcomes were favorable for both groups. Similar results have also been found by other authors, such as Astin, Nishith, and Resick (2000) who reported on the comparison of ET and CT in the treatment of rape-related PTSD. In general, the two treatments have been found to be equally effective and more effective than wait-list control groups.

Cognitive-Behavioral Therapy[edit | edit source]

Cognitive Therapy (CT) involves addressing key cognitive distortions found among people who have been traumatized. In particular, the interventions are designed to address difficulties in safety, trust, power, self-esteem, and intimacy in the lives of survivors. Combination treatments that include an array of cognitive-behavioral strategies have had intuitive clinical appeal because they address multiple problems that people with PTSD may exhibit, as well as incorporating techniques that have empirical support in the literature. For example, Fecteau and Nicki (1999) examined a treatment package of 8-10 sessions including trauma education, ET, cognitive restructuring and guided behavioral practice and compared outcomes to wait-list controls. The results of the intervention were successful as measured by clinical ratings, self-report questionnaires, and a laboratory-based psychophysiological assessment procedure. The results were clinically, as well as statistically, significant and the treatment effects were maintained at 6-month follow-up.

Emotion-Focussed Therapy[edit | edit source]

Emotion-Focused Therapy (EFT) has also shown itself to be effective in helping clients deal with the sequelae of trauma. For example, Greenberg and Paivio (1995) reported clinically meaningful, stable gains for most clients treated with process-experiential therapy (a type of EFT), and that these gains were significantly greater improvements as compared to a psychoeducational group. In addition, Nieuwenhuis and Paivio (2001) investigated a 20-session EFT applied to adults with PTSD symptoms as a result of unresolved childhood abuse issues. Clients in the treatment group were compared to a wait-list control group. EFT clients showed significantly greater improvements than wait-list controls on measures of general anxiety and PTSD symptoms, global interpersonal problems, self-affiliation, and resolution of issues with abusive others. Several other studies have also shown EFT to be effective in treating PTSD symptoms (Soulier, 1995; Clarke, 1993; Davis, Elliott & Slatick, 1998). These studies are more than adequate to support the conclusion that EFT is an efficacious and specific treatment for people suffering the effects of trauma (Elliott et al., 2003). I would argue that EFT works well with clients dealing with PTSD symptoms because often such clients have not been able to develop the skills necessary to process their emotions due to past trauma and/or early attachment experiences. EFT can help increase clients’ emotional intelligence and improve their emotional processing skills so they can better regulate their emotions (Watson, 2006). Clients move towards healing and wholeness in their lives as they learn to become aware of, label, express and reflect upon their emotions so that they may move more productively towards fulfillment of their needs, values and goals (Watson, 2006).

Expressive Writing[edit | edit source]

Emotional expression has long been viewed as a vital component of good mental and physical health, and it is an important ingredient of many forms of psychotherapy. In fact, the use of writing about stressful life events and negative emotions has been used extensively by artists and poets throughout history, who have advocated for its use in promoting healing for themselves and others (DeSalvo, 1999). Expressive writing techniques are also not new to therapeutic settings as clinicians and counsellors have used “journaling” to facilitate healing (Progoff, 1977), and have increasingly encouraged writing assignments as “homework” throughout the psychotherapy endeavor (Lepore & Smyth, 2002). Despite its frequent use however, the difference today is that many researchers are beginning to empirically study the therapeutic benefits of writing.

A number of reasons exist for this increased attention. First, a plethora of studies have demonstrated the effectiveness and success of the writing paradigm developed by James Pennebaker and colleagues (Pennebaker & Beall, 1986). This procedure, known as expressive writing (EW), involves asking participants to write emotionally about their most traumatic/stressful life event on several occasions for about 20–30 minutes. Research has continuously linked EW with improvements in reported physical health, psychological well-being, as well as medical physiological and general functioning (Smyth, 1998).

Second, this widely studied EW procedure may provide a low-cost treatment that many clinicians may find useful as a result of the demands to keep costs down and services available (Lepore & Smyth, 2002). As a result, the continued development and investigation of inexpensive treatment methods such as the EW intervention have been deemed critical in the face of these demands (Friedman, Sobel, Myers, Caudill & Benson, 1995).

Third, despite a desire to discuss personally traumatic and stressful experiences with other individuals, a number of constraints limit or prevent people from being able to do this. For instance, social constraints, personal inhibitions, a lack of availability/suitability of services offered, or limited mobility may all contribute to this problem (Lepore, Silver, Wortman, & Wayment, 1996; Pennebaker & Harber, 1993). The use of the EW intervention allows for one to overcome these obstacles by offering individuals the opportunity to express their thoughts, needs, and emotions in whatever environment they choose, without concern that they will be looked down upon or incur social/interpersonal consequences for doing so.

The initial EW study conducted by Pennebaker and Beall (1986) was grounded in the idea that a failure to disclose personally traumatic events leads to an increased incidence of distress and stress related diseases. In this seminal study, Pennebaker and Beall (1986) set out to investigate whether writing about traumatic events would impact long-term indices of health, as well as short-term measures of mood and physiological arousal. A total of 46 undergraduate participants were randomly assigned to one of four writing conditions: 1) a control condition where they were instructed to write about different trivial topics (e.g., the shoes they were wearing, or a description of their living room; 2) a trauma-fact condition where they were instructed to write about an upsetting experience in a narrative form without any reference to emotions; 3) a trauma-emotion condition where they were instructed to write about the feelings they had in response to an upsetting experience, with specific direction not to describe what the experience entailed; and 4) a trauma-combination condition where they were instructed to write about both the upsetting event, and their thoughts and emotions they had in response to the event. Participants in each group were requested to write their essays for 15 min each night on four consecutive evenings. Participants in the control condition were assigned a different trivial topic each night, and participants in the trauma conditions were given the option of writing about the same traumatic experience, or to choose a different upsetting event each night. A number of pre-writing and post-writing outcome measures were collected, as well as follow up measures four months later.

The results of this influential study indicated that overall, writing emotionally about a traumatic experience (trauma-emotion condition and trauma-combination condition) resulted in greater physiological reactivity and more negative mood immediately after writing in comparison to the control condition and the trauma-fact condition. However, at four month follow up, those participants in these two emotionally expressive writing conditions also reported fewer physical health problems. Additionally, those participants in the trauma-combination condition only reported visiting the campus health center less frequently than the other groups in the six months following the writing. Finally, it is important to highlight that writing simply about the facts of the traumatic experience was not associated with reports of feeling upset, heightened physiological arousal, or any long-term improvements in health.

Since the publication of this study, a number of investigators have examined the therapeutic effects and health improvements of the EW intervention by attempting to replicate and extend the findings. Using this writing paradigm, researchers have found differences between experimental and control groups on a variety of outcome indices including: psychological well-being, physical health, health centre visits, immune response measures, re-employment status, adjustment to college, and grade point average (Smyth, 1998). Additionally, the EW intervention has been used on a number of non-clinical and clinical populations including: undergraduate students, community samples, terminally ill and non-terminally ill patients (e.g., cancer, asthma, and arthritis), psychiatric patients (e.g., depressed, suicidal, and those with PTSD), prison inmates, and people suffering from relationship difficulties or bereavement (see reviews by Frisina, Borod & Lepore, 2004; Lepore & Smyth, 2002; Smyth, 1998). Although the literature does show some inconsistent findings (e.g., Gidron, Peri, Connolly & Shalev, 1996; Walker, Nail & Croyle, 1999), two meta-analyses have been conducted and have supported the effectiveness of the EW intervention with both non-clinical (Smyth, 1998), and clinical samples (Frisina et al., 2004).

After a review of the EW literature it is reasonable to suggest that this form of therapeutic writing results in improvements in emotional and physical health in a number of individuals. However, a continuing puzzle remains as to how and why it works. Up to this point, a myriad of theories have been posited, and a number of reviews are helpful in understanding the specifics of each theory, and the empirical support (or lack thereof) that exists for each (see Kennedy-Moore & Watson, 1999; Lepore & Smyth, 2002; Sloan & Marx, 2004a). To date, a few of the more common hypotheses proposed include: decreasing the physiological work of emotional inhibition (Pennebaker, 1989; Sloan, Marx, & Epstein, 2005), forming a narrative which strengthens cognitive-emotional integration (Park & Blumberg, 2002; Smyth, True, & Souto, 2001), being exposed to a feared memory or thoughts and habituating the fear/anxiety response, (Bootzin, 1997; Pennebaker, 1997; Sloan & Marx, 2004b), increasing self-understanding or insight into a problem or past trauma (Kennedy-Moore & Watson, 1999; Pennebaker, 1993a; Pennebaker, 1993b), enhancing positive emotional reflection (Kennedy-Moore & Watson, 1999), and impacting interpersonal interactions and/or social support (Kennedy-Moore & Watson, 1999; Pennebaker & Graybeal, 2001).

After evaluating the theories underlying the expressive writing paradigm, along with the inconsistent and overlapping empirical support for each theory, Sloan and Marx (2004a) have recently concluded that no single theory appears to account for the effectiveness of the EW intervention. To support this claim, even James Pennebaker (2004), in a commentary of the Sloan and Marx (2004a) article admits, “most likely, there was never any reasonable hope of uncovering a single theory or mediating process to explain the power of writing” (p. 138). He goes on to offer a number of reasons for this dilemma including: 1) major differences in the populations studied (e.g., age, gender, ethnicity, diagnoses, sick versus healthy, distressed versus not distressed), 2) differences in the writing topics varying from traumatic childhood experiences to ongoing current stressors, and 3) a myriad of different outcome measures that measure vastly different emotions, symptoms or behaviours. Additionally, Pennebaker (2004) suggests that the lack of one single theoretical explanation is also due to the fact that EW affects people on a variety of levels. Specifically, he argues that a number of short and long-term emotional and cognitive changes likely impact and interact with social and biological processes, making a single explanatory theory improbable.

Diagnostic Issues[edit | edit source]

By definition, PTSD includes episodic re-experiencing of traumatic events, usually in the form of dysphoric memories. Because these memories are vivid, frightening and unexpected, they have secondary effects, causing sufferers to doubt their sanity, their progress in recovery and their fundamental sense of security (Ochberg, 1998). The original traumatic experience had elements of terror, horror, and/or helplessness, and persistent episodes of traumatic memory continue and compound such elements (Ochberg, 1998). Recent findings have indicated PTSD prevalence rates of 5% and 10% respectively among American men and women (Kessler, Sonnega, Bromet, Hugues, & Nelson, 1996).

The key to understanding the scientific basis and clinical expression of PTSD is the concept of “trauma” (Friedman, 1997). PTSD is unique among other psychiatric diagnoses because of the great importance placed upon the etiological agent, the “traumatic stressor” (Herman, 1992). Thus, traumatization is seen as being caused by the event, not because of some failing or weakness in the person. In fact, one cannot make a clinical diagnosis of PTSD unless the client has actually met the “stressor criterion”. Along with the diagnostic criteria of exposure to a “traumatic event” are symptoms from each of the three symptom clusters: intrusive recollections, avoidant/numbing symptoms and hyperarousal symptoms (APA, 1994). A fifth criterion concerns the duration of the symptoms (APA, 1994). The duration criteria for diagnosis of PTSD when the above criteria have been met is one month (APA, 1994).

Not only is PTSD typified by the automatic, involuntary symptoms such as flashbacks, intrusive thoughts and autonomic hyperarousal, but also consciously mediated attempts to make meaning of the trauma experience(s) (Clark & Ehlers, 2000). The automatic and involuntary symptoms are said to represent conditioned responding to environmental triggers associated with the trauma (Clark & Ehlers, 2000). Much less is known about the origins and consequences of victims’ efforts to understand their trauma(s) or about how best to treat the symptoms associated with personal beliefs about the trauma (Meichenbaum, 1994).

Research has shown that clients with PTSD are twice as likely to suffer from a co-morbid psychiatric disorder as those without PTSD, which means there can be complicating factors in proper diagnosis (Kulka, Fairbank, Hough, Jordan, Marmar, Mavissakalian & Schlenger, 1990). Thus, PTSD is frequently a diagnostic oversight that can lead to improper treatment strategies (Kulka et al., 1990). This is, in part, because of the reticence of patients to talk about traumatic experiences, which makes the therapeutic relationship an important first step in proper identification.

Key Figures[edit | edit source]

  • Pierre Janet published L'Automatisme Psychologique, which was his first work to deal with how the mind processes traumatic experiences. "Janet claimed that vehement emotions interfere with proper appraisal and appropriate action. Failure to confront the experience fully leads to dissociation of the traumatic memories and their return as fragmentary reliving experiences, feeling states, somatic sensations, visual images, and behavioral reenactments. A century later, Janet still provides an unsurpassed framework for integrating current knowledge about the psychodynamic, cognitive, and biological effects of human traumatization" (Brown, van der Hart & van der Kolk, 1989).
  • Edna B. Foa has been described as one of the leading experts in post-traumatic stress disorder research. Among her many publications, are the popular books Posttraumatic stress disorder: DSM-IV and beyond (American Psychiatric Press, Inc: 1992) and Treating the Trauma of Rape (Guilford Publications, Inc.: 1997)
  • Judith Herman is a well-known psychiatrist in the field of trauma research. Her areas of research include the psychology of women, child abuse, domestic violence, and post-traumatic disorders. She is the author of the award-winning book, Trauma and Recovery (Basic Books:1991; second edition, 1997).

Relevant Websites[edit | edit source]

The Trauma Centre: http://www.traumacenter.org/

Sensorimotor Psychotherapy Institute: http://www.sensorimotorpsychotherapy.org/faculty.html

Other Sites Discussion Trauma[edit | edit source]

http://en.wikipedia.org/wiki/Post-traumatic_stress_disorder

Historical Perspectives on Attention Deficit/Hyperactivity Disorder (ADHD)[edit | edit source]

A Brief History of Attention Deficit/Hyperactivity Disorder (ADHD)[edit | edit source]

Children, adolescents, and adults experiencing problems with attention, hyperactivity, and impulse control have appeared throughout history. For instance, a literary reference to the malady of attention was made by Shakespeare in King Henry VIII (Barkley, 2003). A hyperactive child was the focus of a German poem, “Fidgety Phil”, by physician Heinrich Hoffman. William James, in his Principles of Psychology, described a normal variant of character that he called the “explosive will”, which resembles the difficulties experienced by those who today are described as having ADHD. However, more serious clinical interest in children with ADHD first occurred in three lectures of the English physician George Still (1902) before the Royal Academy of Physicians (Barkley, 2003).

Still reported a group of 20 children in his clinical practice whom he defined as having a deficit in “volitional inhibition”. He described these children as aggressive, passionate, lawless, inattentive, impulsive, and overactive. Still’s observations were quite astute, describing many of the features that would come to be corroborated in research over the next century such as overrepresentation of male subjects, high comorbidity with Oppositional Defiant Disorder (ODD), and a familial predisposition, among others (Barkley, 2003).

After the encephalitis epidemics of 1917-1918, interest in these children arouse in North America. Children surviving these brain infections had many behavioural problems similar to those seen in contemporary ADHD (Barkley, 2003). These cases and others known to have arisen from birth trauma, head injury, toxin exposure, and infections, gave rise to the concept of a “brain-injured child syndrome”. This concept evolved into that of “minimal brain damage” and eventually “minimal brain dysfunction” (MBD) as challenges were raised to the label in view of the dearth of evidence of obvious brain injury in most cases (Barkley, 2003).

During the 1950s and 1960s, others became interested in the more specific behaviors of hyperactivity and poor impulse control characterizing these children. The disorder was labeled “hyperkinetic impulse disorder” and was attributed to cortical overstimulation due to poor thalamic filtering of stimuli entering the brain (Barkley, 2005). This definition marked a shift in diagnostic terminology away from the obvious conclusion that such symptoms indicated brain damage or dysfunction and toward a more descriptive view of the disorder. These changes in perspective gave rise to the diagnostic term “hyperactive child syndrome”. Nevertheless, a belief continued among clinicians and researchers of this era that the condition had some sort of neurological origin.

Yet the larger influence of psychoanalytic thought held sway over child psychiatry and along with it the belief that children’s mental disorders necessarily arouse as a reaction to various environmental factors, particularly early events in the family life of the child (Barkley, 2005). Therefore, in the second edition of the DSM, hyperactive child syndrome became “hyperkinetic reaction of childhood”. Problems with attention and distractibility were included under the definition of the disorder. Also, the recognition that the disorder was not caused by brain damage created the beginnings of the major conceptual rift between professionals in North America and those in Europe that continues to some extent in the present. In North America, ADHD is viewed as a developmental disorder having substantial biological origins. In contrast, in Europe, these same children are viewed as having a conduct problem because of their often hostile, defiant and belligerent nature and it is viewed as a behavioural disturbance believed to originate largely due to poor parental management, family dysfunction and/or social disadvantage (Barkley, 2005).

By the 1970s, research was appearing that emphasized the importance of problems with sustained attention and impulse control in addition to hyperactivity in understanding the nature of the disorder (Barkley, 2005). Douglas (1983) would eventually come to theorize that the disorder was comprised of four major deficits, these being in the investment, organization, and maintenance of attention and effort, the ability to inhibit impulse behaviour, the ability to modulate levels of arousal to meet situational demands, and an unusual strong inclination to seek immediate reinforcement (in Barkley, 2005). Douglas’s seminal paper, along with the numerous studies of attention, impulsiveness and other cognitive sequel of this disorder that followed, eventually led to retitling the disorder as “attention-deficit disorder” (ADD) in 1980 (Barkley, 2003).

During the 1980s, reports began to appear that challenged the notion that ADHD was primarily a disturbance in attention, instead focusing upon problems with motivation generally, and insensitivity to response consequences specifically (Barkley, 2005). Research was demonstrating that children with ADHD did not respond in the same way to alterations in contingencies of reinforcement or punishment as did normal children. In addition, in the late 1980s, researchers employed information-processing paradigms to study ADHD and found that problems in perception and information processing were not as evident as were problems with motivation and response inhibition (Barkley, 2003). The problems with hyperactivity and impulsivity also were found to form a single dimension of behavior.

Debate continues to the present over the core deficits of ADHD, with increasing weight being given to problems with behavioral inhibition, self-regulation, and the related domain of executive function. Moreover, controversy still continues around the place of a subtype composed primarily of inattention within the larger condition of ADHD, with some arguing that it is a distinct disorder.

Presently, ADHD is defined as a complex, highly heritable, heterogeneous, and prevalent disorder, which occurs in 3% to 5% of children. It is characterized by developmentally inappropriate and impairing levels of inattentive and/or hyperactive/impulsive behavior, which initially appears in childhood and manifests itself with symptoms of hyperactivity, forgetfulness, poor impulse control, and distractibility. The disorder is also associated with a wide range of cognitive difficulties and high rates of comorbidity with learning disorders and other psychiatric disorders. ADHD tends to persist into adulthood and contributes to increased risk for problems in educational, occupational, and psychiatric domains.

Historical Perspectives on the Diagnosis of ADHD[edit | edit source]

Early Discovery and Diagnosis[edit | edit source]

Much of the early clinical work on ADHD was completed in England. A British pediatrician, Dr. G. F. Still, described hyperactive and impulsive behaviour of children in 1902, indicating that it was an unknown medical diagnosis (McNeil Pediatrics, 2007). By 1922, symptoms that are currently associated with ADHD were documented and given a diagnosis of "Post-Encephalitic Behaviour Disorder". In the 1970s, symptoms of inattention, such as lack of focus and daydreaming, were first associated with the impulsive and hyperactive symptoms described over 50 years earlier by Dr. Still.

It was not until the 1980s, however, that the American Psychological Association identified a cluster of behavioural symptoms as Attention Deficit Disorder with or without hyperactivity (ADD +/-) in the DSM-III. Shortly after, in 1987, ADD was renamed Attention-Deficit/Hyperactivity Disorder (ADHD; McNeil Pediatrics, 2007).

Current Diagnosis[edit | edit source]

Currently, the Diagnosis and Statistical Manual of Mental Disorders (see the section on the DSM-IV) provides criteria for the diagnosis of ADHD, with the following three types specified: primarily inattentive (ADHD-IA), primarily hyperactive and impulsive (ADHD-HI), and a combination of ADHD-IA and ADHD-HI.

For each type, diagnosis of ADHD is made only if the individual displays at least six of the nine symptoms for inattention, hyperactivity/impulsivity, or both, shown below:

Symptoms of inattention:

  • Fails to give close attention to details, makes careless mistakes
  • Has difficulty sustaining attention
  • Does not seem to listen
  • Has difficulty organizing tasks and activities
  • Avoids or dislikes tasks requiring sustained effort
  • Loses things needed for tasks
  • Is easily distracted by extraneous stimuli
  • Is often forgetful in daily activities

Symptoms of Hyperactivity and Impulsivity:

  • Fidgets with hands or feet, squirms in seat
  • Leaves seat in classroom or in other situations
  • Runs about or climbs excessively
  • Has difficulty playing or engaging in leisure activities quietly
  • Talks excessively
  • Acts as if “driven by motor” and cannot sit still
  • Blurts out answers before questions are completed
  • Has difficulty waiting in line or awaiting turn in games or activities
  • Interrupts or intrudes on others

In addition to the criteria listed in the DSM-IV, behavioural assessment methods are increasingly being used to identify ADHD (Lerner, 2003). These include teacher rating scales and parent rating scales, such as the Conners’ Rating Scales, and direct observation. Whether using the DSM-IV or behavioural assessment methods for diagnosis, ADHD is typically associated with activity and attentional difficulties that are present for at least six months and to a degree that is developmentally deviant by the age of seven (Santrock, Woloshyn, Gallagher, Di Petta, & Marini, 2004). It is recommended that clinicians use more than one diagnostic method when assessing a child for ADHD to prevent a misdiagnosis.

There is controversy due to the recent increase in the diagnosis of ADHD (Santrock et al., 2004) Some experts attribute the increase to improved awareness of the disorder, however, others are concerned that many children are being misdiagnosed with the disorder without extensive professional assessment using multiple sources.

Historical Perspectives on Treatment for ADHD[edit | edit source]

Although the symptoms characterizing ADHD were first described in the early 1900s (see above), effective pharmacological treatments were not available until more than a half-century later. In 1937, physicians discovered that amphetamines could effectively reduce the cluster of hyperactive and impulsive behaviours associated with what was then called “Minimal Brain Dysfunction” (MBD). However, it was not until over a decade later, in the 1950s, that stimulant medications were regularly used as therapy to treat MBD.

In 1954, methylphenidate, a mild central nervous system stimulant was patented by the Ciba pharmaceutical company. Initially prescribed as a treatment for depression, chronic fatigue, and narcolepsy, methylphenidate has effects similar to, caffeine (though more potent) and amphetamines (though less potent). In 1956, the well-known methylphenidate brand-name Ritalin was introduced as a treatment for hyperactivity and impulsivity. It has a notably calming and “focusing” effect on individuals exhibiting such symptoms and facilitates concentration on work and other tasks. It is generally well tolerated by patients when prescribed in correct dosages (Steele et al., 2006). Based on brain imaging studies, researchers believe that methylphenidate’s therapeutic effects are due to increases in dopamine (a neurotransmitter) levels (Volkow et al., 2002). Today, methylphenidate is the most widely prescribed pharmacological treatment for ADHD around the world.

In the early 1960s Dr. Stella Chess coined the term “Hyperactive Child Syndrome”, referring to the cluster of behavioural symptoms of hyperactivity and impulsivity (anon, 2007). Following the disorder’s name-change, stimulant prescription increased dramatically and quickly became a widespread treatment for the "syndrome". Despite much speculation at the time regarding the etiology of the hyperactive child syndrome (e.g., poor parenting, environmental toxins, food allergies, etc.), Dr. Chess believed that it had a biological basis (anon, 2007). Research examining the effects of diet on hyperactive behaviour began in the 1970s and while the belief that hyperactive symptoms can be traced back to the child’s diet (e.g., sugar, junk food, etc.) has been a robust one, several empirically based studies have discounted many of these claims (e.g., Wolraich et al., 1995). Further, there is little scientific evidence to indicate that dietary treatments alleviate symptoms of ADHD (Bateman et al., 2004).

In the 1970s, behaviour modification was first applied systematically to manage the behavioural problems associated with ADHD. Considering that 8-25% of children with the disorder do not respond positively to pharmacological treatment, effective behavioural interventions play an important role in symptom management (Barkley, 2004). Traditionally, behavioural treatments have been divided into three classes: direct contingency management, clinical behaviour therapy, and cognitive-behavioural procedures. Of these behavioural therapy techniques, contingency management procedures in particular (e.g., token reinforcement) have provided clear benefits, both at home and in the classroom, for children with ADHD (Barkley, 2004). Cognitive behavioural therapy on the other hand, may be more effective in laboratory compared to real-world settings (Barkley, 2004).

In 1999, the MTA cooperative group conducted an extensive study examining the effects of various treatments and their combinations on core ADHD symptoms. For the management of hyperactivity and impulsivity, the authors found that a combined treatment (where child receives both medication and behavioural treatment) yielded similar benefits as those seen medication-only management (MTA, 1999). It is important to note, however, that positive outcomes of the combined treatment group were achieved at significantly lower drug doses than those used in medication-only group.

Although research on ADHD treatment continued throughout the 1980s and 1990s, it was only in 1996 that a second stimulant medication, named Adderall, was approved by the U.S. Food and Drug Administration (FDA). Shortly thereafter, Matadate (1999), Concerta (2000), and Focalin (2001) gained FDA approval for ADHD management. Concerta was the first once-daily, 12-hour release medication available for treatment of the disorder. Research has shown that long-acting methylphenidate formulas such as Concerta are equally effective as instant release preparations (Pelham et al., 2001; Hoare et al., 2005).

In 2001, the American Academy of Paediatrics published recommendations for the treatment of children diagnosed with ADHD in the Journal Pediatrics. These guidelines, intended to be used by paediatricians working in primary care settings, outline steps to develop a treatment program in collaboration with the child’s family and school, as well as follow-up procedures.

In 2002, the American Academy of Child and Adolescent Psychiatry published parameters to guide physicians in the prescription of stimulant medication. The guidelines, which were devised following extensive, independent literature reviews, provide physicians with empirically-based recommendations for the treatment of children, adolescents, and adults with ADHD.

Also in 2002, the U.S. FDA approved Strattera, the first non-stimulant medication for the treatment of ADHD. Strattera, is a norepinephrine reuptake inhibitor (NRI), which means that it increases the level of the norepinephrine (also known as noradrenaline) neurotransmitter in the brain by partially blocking the transporters that remove it from the synapses.

In 2006, Daytrana, a once-daily transdermal patch for the treatment of ADHD was approved by the U.S. FDA. The patch delivers methylphenidate in doses of 10, 15, 20, or 30 mg, but must be applied several hours before the effect is desired (Peck, 2006). Furthermore, because Daytrana’s effect lingers for several hours after patch removal, the patch should be removed in the mid-to-late afternoon in order to avoid insomnia.

In recent years, reports of methylphenidate abuse by individuals for whom it is not prescribed have surfaced. The drug is abused for its stimulant effects of appetite suppression, wakefulness, increased focus/attentiveness, and euphoria. Addiction to methylphenidate is most likely to occur when it is taken in sudden large doses, resulting in rapid increases of dopamine (a CNS neurotransmitter) (Volkow and Swanson, 2003). Conversely, the therapeutic effect of the drug as used in the treatment of ADHD is achieved by slow and steady increases in dopamine, resembling the natural production of this neurotransmitter by the brain (Volkow and Swanson, 2003). The risk of addiction of prescribed methylphenidate, therefore, is small, as doses of prescribed by physicians start low and increase slowly until a therapeutic effect is achieved.

Historical Perspectives on Autism Spectrum Disorders[edit | edit source]

The disorder known today as autism has a tumultuous and controversial history. It was originally viewed as childhood schizophrenia, followed by the belief that the disorder was the result of a “refrigerator mother”, in Bruno Bettelheim’s words. The disorder was finally identified in the terms we know today by two doctors working half a world away from each other –in the United States and Austria. This section briefly outlines the history of how Leo Kanner and Hans Asperger identified the similar symptoms in children, arriving at very similar conclusions of what the symptoms comprised. In the 1940s, both Leon Kanner in the United States and Hans Asperger in Austria noted characteristics of children referred today as having autism spectrum disorders. Kanner and Asperger were not aware of each other's work, and it wasn't until Lorna Wing published Asperger's writings that the similarity between the two clinicians' descriptions emerged. Both described children with odd social skills. Yet, Kanner recorded more severe cases in which language and communication did not develop at all, while Asperger recorded the characteristics of children with typical or even high intelligence and language development, but odd social behaviours.

The disorder known today as autism has a tumultuous and controversial history. It was originally viewed as childhood schizophrenia, followed by the belief that the disorder was the result of a “refrigerator mother”, in Bruno Bettelheim’s words. This section briefly outlines how the disorder we know today was identified and explained by two doctors working half a world away from each other – in the United States and Austria.

In the 1980s, diagnostic measures were developed that significantly improved diagnostic validity and specificity. Michael Rutter and Catherine Lord devised the Autism Diagnostic Interview, which is a semi-structured interview that details the child’s development and probes for autistic symptoms. To complement this parent interview, the Autism Diagnostic Observation Schedule was devised. This tool puts the child or adult in a social situation with a variety of activities, and provides an estimate of the child’s social abilities.

Today, autism is considered to be a spectrum of disorders, spanning from severely autistic symptoms (e.g., no language development) to relatively mild symptoms (e.g., high intelligence with very few social skills). The disorders are therefore termed autism spectrum disorders, and include the diagnostic labels of autism, Asperger syndrome, or pervasive developmental disorder not otherwise specified (PDD-NOS). This conceptualization has broadened our knowledge of symptoms, and has enabled a large number of people to seek support and guidance which adequately suits their particular needs.