David Baxter PhD
Late Founder
Post Traumatic Stress: Symptoms, diagnosis, and brain-mechanisms
by Brian Trappler, M.D., Psychology Today
August 31, 2010
In the Early versions of psychiatric classifications, the trauma literature was dominated by combat trauma reported in World War II. Many of the symptoms that we today would call "PTSD" were captured by terms such as "combat neurosis" or "war neurosis".
In fact, the DSM-II reflected the model proposed by Kardiner and Spiegel in their manuscript War, Stress, and Neurotic Illness. The manuscript was later revised and published under the title The Traumatic Neurosis of War (New York: Hoeber, 1947).
In the middle of the 1970s, "Post Traumatic Stress Disorder," otherwise referred to as "PTSD", was first proposed for inclusion in the Diagnostic and Statistical Manual of Mental Disorders, Third Edition (DSM-III).
By the time DSM-III was first publicized in 1980, sufficient data was available to justify the PTSD construct and thereby replace the "Traumatic Neurosis" construct of DSM-II.
Since then, the lay community as well as physicians tended to conform to a reductionist terminology, attempting to lump all traumatic conditions into the PTSD construct.
Despite the attempts of experts to widen the enduring effects of trauma beyond the narrow construct of "PTSD" remains as the only construct for persistent, unresolved trauma," and is categorized in the DSM IV as an "Anxiety Disorder".
Several factors will influence the outcome of a particular trauma:
There are social, legal, and political factors that can either deter or facilitate the likelihood of the occurrence of a traumatic event.
There are numerous reports of domestic and political terrorism where mandated reporters, judges, and Intelligence Agencies, leading to horrendous violence, which was entirely preventable, ignored clear warning signs.
Two clear examples of such negligence were the 9/11 attacks and the shooting at Fort Hood.
The most benign responses reported by trauma survivors would fall under the umbrella of "Trauma-Related Symptoms."
In such cases, victims may experience worry, apprehension, and sleep disturbance. However, when these victims receive or actively pursue rescue resources, even in the form of simple social bonding and "ventilation," these symptoms (despite appearing quite disruptive), tend to be benign and self-limiting.
When the trauma is of higher intensity and duration and rescue services fail, victims are much more likely to develop the more serious trauma-induced condition of "Acute Stress Disorder", viewed by experts as a harbinger of PTSD.
This explains how victims of life-altering traumatic events may show little recollection of certain details of the traumatic event. Some victims have no recollection of the entire event.
Because of the brain's inability to successfully "process" or "resolve" a serious psychological trauma, elements of the trauma are left to fester or "ferment".
According to Donald Kalsched from the Carl Jung Institute, if left unchecked this "Trauma-Complex" becomes autonomous and "self-traumatizing" (The Inner World of Trauma, Brunner-Routledge,1996)
In the world of Neurophysiology, this phenomenon is explained as "limbic kindling".
When a trauma is not "put to rest", stress-circuits in the limbic-brain, Sympathetic Nervous System, and adrenal glands, remain "primed" to be re-activated as "alert-systems" to further trauma-triggers.
Patients with PTSD are constantly vigilant to the perception of threat.( "Selective Processing of Threat Cues", McNally and colleagues, J Abnormal Psych, 1990).
Because of failed synthetic functioning in the Hippocampus, PTSD patients are prone to randomly "relive" the original trauma as if it were continuing in the present, a phenomenon known as "flashbacks".
This trauma-generated failure of synthetic brain-function also leads to the "over-memorization" of fragmented trauma-recollections, images and sensations. In contrast, victims who have coped better with trauma are more able to formulate a coherent, less emotionally- threatening memory of the trauma-narrative (Foa, 1995).
At a biological level, neurotransmitters generated from overwhelming stress exert a toxic effect on the Hippocampus, inhibiting the "processing" function that is required to organize sensory-dominated trauma-recollections into a rational coherent trauma narrative (Sapolsky, Science, 1996).
Put differently, one could say that in PTSD, the "emotional brain" assumes dominance over the "rational brain".
The reason appears to be the failure of the Hippocampus to create abstract verbal representations that inhibit the brain's access to sensory-perceptual recollections of the traumatic event (Conway & Pearce, Psychological Review, 2000).
Because of fear-sensitization, heightened threat-sensation, and failed verbal-encoding, PTSD victims continue to live their lives within a narrow "Fear Paradigm" (Brewin, 1996).
"Avoidance" refers to a victim's flight from any thoughts or feelings that could serve as trauma-reminders. The "Avoidance Defense" also shelters the victim from engaging in a world dominated by external trauma-triggers.
Activation of "negative feedback loops" and other "brake-systems" drives avoidance behaviors and serves a defensive function, but comes at a price:
Victims with dominant avoidance symptoms cannot creatively re-engage socially or into the workplace (Goleman, 1995).
"Over-arousal" is the result of persistent over-activation of central stress circuits such as the "sympathetic nervous system"." One this occurs, the individual will continuously scan the environment to identify danger-signals, which subsequently reinforce the perception of danger, hence maintaining the state of "alert."
Persistence of the three above-mentioned domains of symptoms for a month or longer constitute the core elements of PTSD.
Further downstream effects of unremitting stress include a multitude of somatic systems including chronic pain, immune function, and chronic ware and tear of the cardiovascular system (Uno and colleagues, J. Neurosci. 1989).
by Brian Trappler, M.D., Psychology Today
August 31, 2010
In the Early versions of psychiatric classifications, the trauma literature was dominated by combat trauma reported in World War II. Many of the symptoms that we today would call "PTSD" were captured by terms such as "combat neurosis" or "war neurosis".
In fact, the DSM-II reflected the model proposed by Kardiner and Spiegel in their manuscript War, Stress, and Neurotic Illness. The manuscript was later revised and published under the title The Traumatic Neurosis of War (New York: Hoeber, 1947).
In the middle of the 1970s, "Post Traumatic Stress Disorder," otherwise referred to as "PTSD", was first proposed for inclusion in the Diagnostic and Statistical Manual of Mental Disorders, Third Edition (DSM-III).
By the time DSM-III was first publicized in 1980, sufficient data was available to justify the PTSD construct and thereby replace the "Traumatic Neurosis" construct of DSM-II.
Since then, the lay community as well as physicians tended to conform to a reductionist terminology, attempting to lump all traumatic conditions into the PTSD construct.
Despite the attempts of experts to widen the enduring effects of trauma beyond the narrow construct of "PTSD" remains as the only construct for persistent, unresolved trauma," and is categorized in the DSM IV as an "Anxiety Disorder".
Several factors will influence the outcome of a particular trauma:
- The trauma itself varies in duration and intensity.
- Survivors vary in age, temperament, and coping skills.
- When someone is the victim of a serious, usually unexpected, trauma, external rescue-responses need to be rapid and robust. This is very important for psychological damage-control.
There are social, legal, and political factors that can either deter or facilitate the likelihood of the occurrence of a traumatic event.
There are numerous reports of domestic and political terrorism where mandated reporters, judges, and Intelligence Agencies, leading to horrendous violence, which was entirely preventable, ignored clear warning signs.
Two clear examples of such negligence were the 9/11 attacks and the shooting at Fort Hood.
The most benign responses reported by trauma survivors would fall under the umbrella of "Trauma-Related Symptoms."
In such cases, victims may experience worry, apprehension, and sleep disturbance. However, when these victims receive or actively pursue rescue resources, even in the form of simple social bonding and "ventilation," these symptoms (despite appearing quite disruptive), tend to be benign and self-limiting.
When the trauma is of higher intensity and duration and rescue services fail, victims are much more likely to develop the more serious trauma-induced condition of "Acute Stress Disorder", viewed by experts as a harbinger of PTSD.
This explains how victims of life-altering traumatic events may show little recollection of certain details of the traumatic event. Some victims have no recollection of the entire event.
Because of the brain's inability to successfully "process" or "resolve" a serious psychological trauma, elements of the trauma are left to fester or "ferment".
According to Donald Kalsched from the Carl Jung Institute, if left unchecked this "Trauma-Complex" becomes autonomous and "self-traumatizing" (The Inner World of Trauma, Brunner-Routledge,1996)
In the world of Neurophysiology, this phenomenon is explained as "limbic kindling".
When a trauma is not "put to rest", stress-circuits in the limbic-brain, Sympathetic Nervous System, and adrenal glands, remain "primed" to be re-activated as "alert-systems" to further trauma-triggers.
Patients with PTSD are constantly vigilant to the perception of threat.( "Selective Processing of Threat Cues", McNally and colleagues, J Abnormal Psych, 1990).
Because of failed synthetic functioning in the Hippocampus, PTSD patients are prone to randomly "relive" the original trauma as if it were continuing in the present, a phenomenon known as "flashbacks".
This trauma-generated failure of synthetic brain-function also leads to the "over-memorization" of fragmented trauma-recollections, images and sensations. In contrast, victims who have coped better with trauma are more able to formulate a coherent, less emotionally- threatening memory of the trauma-narrative (Foa, 1995).
At a biological level, neurotransmitters generated from overwhelming stress exert a toxic effect on the Hippocampus, inhibiting the "processing" function that is required to organize sensory-dominated trauma-recollections into a rational coherent trauma narrative (Sapolsky, Science, 1996).
Put differently, one could say that in PTSD, the "emotional brain" assumes dominance over the "rational brain".
The reason appears to be the failure of the Hippocampus to create abstract verbal representations that inhibit the brain's access to sensory-perceptual recollections of the traumatic event (Conway & Pearce, Psychological Review, 2000).
Because of fear-sensitization, heightened threat-sensation, and failed verbal-encoding, PTSD victims continue to live their lives within a narrow "Fear Paradigm" (Brewin, 1996).
"Avoidance" refers to a victim's flight from any thoughts or feelings that could serve as trauma-reminders. The "Avoidance Defense" also shelters the victim from engaging in a world dominated by external trauma-triggers.
Activation of "negative feedback loops" and other "brake-systems" drives avoidance behaviors and serves a defensive function, but comes at a price:
Victims with dominant avoidance symptoms cannot creatively re-engage socially or into the workplace (Goleman, 1995).
"Over-arousal" is the result of persistent over-activation of central stress circuits such as the "sympathetic nervous system"." One this occurs, the individual will continuously scan the environment to identify danger-signals, which subsequently reinforce the perception of danger, hence maintaining the state of "alert."
Persistence of the three above-mentioned domains of symptoms for a month or longer constitute the core elements of PTSD.
Further downstream effects of unremitting stress include a multitude of somatic systems including chronic pain, immune function, and chronic ware and tear of the cardiovascular system (Uno and colleagues, J. Neurosci. 1989).
