David Berceli PhD is an international expert in the areas of trauma intervention and conflict resolution. He is also the energetic and creative founder and CEO of Trauma Recovery Assessment & Prevention Services (TRAPS 1998). The goal of TRAPS is to provide specialized trauma recovery assistance to international and local organizations whose employees are living and working in trauma inducing environments. For the past 22 years he has lived and worked in nine countries providing trauma relief workshops and designing recovery programs for international organizations around the world. Dave has lived and worked extensively in Israel/Palestine, Sudan, Uganda, Kenya, Yemen, Egypt, and Lebanon. Fluent in English and Arabic, David brings a keen understanding of the intertwining dynamics of religion and ethnic customs and has developed specific processes to enable people to manage personal trauma as well as bring healing and reconciliation between diverse groups. He is the creator of a revolutionary and unique set of Trauma Releasing Exercises (TRE) that release the deep chronic tension created in the body during a traumatic experience. (read more)
International Consultations: As a trauma consultant David has designed and implemented comprehensive and individualized programs of...
trauma recovery,
stress management and
conflict resolution .
These individualized programs are specifically for....
Multinational Corporations
International Relief Agencies, Embassies and Consulates
Government and Non-Government Organizations (NGO) Emergency Services Agencies whose staff are living and working in trauma inducing environments. (read more) For the past 15 years he has provided training and supervision of senior staff regarding individual and organizational trauma behaviors and the need for a healthy recovery process. He has updated senior staff on the most recent developments in the theory and practice of organizational trauma recovery. His work has included programs in numerous countries including:
Sudan * Israel * Palestinian West Bank * Northern & Southern Ireland * Ethiopia * New Zealand * Yemen * Egypt * Lebanon * Kenya * Brazil * Germany * Uganda
Educational Background PhD (2007) Research/Dissertation: The use of neurogenic tremors for the alleviation of post traumatic stress disorder (PTSD) symptoms. Arizona State University. M.S.W. (1993). Clinical Social Work. Fordham University. M.A. (1987). Theology. State University of New York. Maryknoll School of Theology. LIC. (1984). Post Graduate License in Arabic and Islamic Studies. Pontificio Istituto di Studi Arabi edIslamistica. Roma, Italia.
ADDITIONAL EDUCATION LICENSE. (1998). Reilly School of Massage Therapy. (Swedish Massage). CERTIFICATION. (1994). International Institute for Bioenergetic Analysis. (Body Psychotherapy). CERTIFICATION. (1981). Jesuit University of Beirut, Lebanon. (Arabic Language). CERTIFICATION. (1979). American University of Cairo, Egypt. (Arabic Language). CERTIFICATION. (2005). Human Participant Protections Education for Research.
PROFESSIONAL LICENSE Field Traumatologist Cert. # 5026 Academy of Traumatology 2005 - Certified Traumatologist Cert. # 10027 Green Cross Foundation 2005 - Certified Disaster Assistant IS-7 A Wash. D.C. 2005 - Certified Cont. Ed. Provider#412278-00 National 2004-2006 Massage Practitioner License#03100436 Phoenix, AZ. 2003-2004 Clinical Social Worker License# 00529 Providence, R.I. 2001-2003 Massage Practitioner State Approved Richmond, VA. 1998-1999 Clinical Social Worker License # 046677-1 Israel 1995-1997 Certified Social Worker License # 046677-1 New York, N.Y. 1993-1995
Conferences, Presentations & Workshops
Luke Air Force Base, 56th MDOS/SGOMH 2007 Traumatic Stress Response Team Workshop: Post deployment training in Combat Operational Stress (COS), Rucksack Palsy, and post traumatic stress symptoms for OIF and OEF soldiers. Luke AFB, Arizona
National Association of Social Workers Arizona (NASWAZ) and Arizona State University 2007 Workshop: "Mass Trauma: A New Paradigm for Recovery" Phoenix, Arizona
Department of Behavioral Health, US Army, Ft Sill 2006 Post deployment training in Combat Operational Stress (COS), Rucksack Palsy, and post traumatic stress symptoms for OIF and OEF soldiers. Rach, Oklahoma
Phoenix Vet Center 2006 Trauma Releasing Exercises (TRE) for veterans of Vietnam, Afghanistan, Gulf War, OEF & OIF. Phoenix, AZ
Sociedade de Analise Bioenergetica do Nordeste Brasileiro 2006 O tratamento neuropsicomotor dos traumatismos, desordens e stress pos-traumticos. (The use of the neuro sensory motor response for the alleviation of post-traumatic stress disorders) Recife, Brazil
Genesee County Mental Health Association 2006 Keynote speaker: Mass trauma and its psychosocial impact on health practitioners. Workshop Presenter: The Neuro-anatomy of trauma and extinction of the hypothalamus-pituitary-adrenal (HPA) axis. Batavia, New York.
Socit Franaise d'Analyse Bio-Energtique 2006 Le traitement neuropsychomoteur des traumatismes, dsordres et stress post-traumatiques. (The use of neurogenic tremors for the alleviation of post traumatic stress disorder (PTSD) symptoms) Paris, France
Internationales Institut fr Bioenergetische Analyse 2006 Posttraumatische Belastungsstrung (PTSD) Symptome und deren Behandlung (Post-traumatic Interference (PTSD) Symptoms and its Treatment) Heidelberg, Germany
The National Institute for the Clinical Application of Behavioral Medicine 2006 Neurogenic tremor release technique for the alleviation of PTSD symptoms. Hilton Head, South Carolina
International Yoga College 2006 Mass trauma: A body-based recovery method for large-scale populations with PTSD. Tucson, Arizona
164th Corps Support Group (CSG) S-1 2006 Pre-deployment training in Combat Operational Stress, Rucksack Palsy, and post traumatic stress symptoms. Mesa, Arizona
National Association of Social Workers (NASW) 2005 Trauma recovery methods for large-scale traumatized populations. Phoenix, Arizona
Walter Reed Army Medical Center: Deployment Health Clinical Center (DHCC) 2005 Neurogenic tremor release technique for the alleviation of hyperarousal PTSD symptoms among Operation Iraqi Freedom (OIF) and Operation Enduring Freedom (OEF) soldiers. Washington, D.C.
United States Association for Body Psychotherapy (USABP)2005 Trauma releasing exercises (TRE): The use of neurogenic tremors for the alleviation of PTSD symptoms. Tucson, Arizona
Foundation for Global Leadership 2005 Trauma assistance and hotline protocol for first responders to traumatic events. Manama, Bahrain
Alpha & Charlie Co. 1st Battalion 151st Field Artillery 2004/2005 Post deployment training in Combat Operational Stress (COS), Rucksack Palsy, and post traumatic stress symptoms for OIF and OEF soldiers. Morris, Minnesota
International Institute for Bioenergetic Analysis 2005 Neurogenic tremors and the alleviation of hyperarousal post traumatic symptoms. Boston, Massachusetts
National Organization for Continuing Education of Roman Catholic Clergy 2004 Bioenergetics and sexual celibacy: A bodily experience. San Diego, California
Non-Government Organizations 2002 Unicef, World Health Organization (WHO), Doctors without Boarders, Med Air, Concern for the World, Friedrich Egert Stiftung. The effects of trauma among local and foreign volunteers in Sudan. Lokichokio, Kenya
El-Ahfad University. Department of Psychology 2002 Sudan and trauma: A new paradigm for healing a nation. Khartoum, Sudan
Imute The effects of trauma on the individual, institution and society. 2001 Tel Aviv, Israel
YMCA West Jerusalem 2000 The relational effects of trauma and PTSD in a multi-cultural workplace. Jerusalem, Israel
Non-Profit Organizational Workshop; Daughters of Charity 1999 The Disruptive Effects of Post War Trauma within organizations. Addis Ababa, Ethiopia
INTERNATIONAL RESIDENTIAL EXPERIENCE Sudan Trauma Recovery Therapist 1999-2002 Developed and implemented a national trauma recovery program in conjunction with Sudanese non-government organizations and German relief agencies. Trained and supervised local Sudanese leaders in trauma recovery awareness, education and somatic psychotherapy techniques.
Israel Conflict Resolution Consultant 1995-1997 Provided stress management & trauma relief programs to embassy and consulate staff. Designed trauma intervention programs for local Israeli and Palestinian organizations. Supervised therapists, social workers, counselors and emergency medical teams on the psychological and physical interventions necessary in the trauma recovery process.
New Zealand Bioenergetic Analysis Training Supervisor 1994-1995 Provided supervision for the local Bioenergetic Training Program. Supervised thirteen 2nd and 3rd year trainees in issues pertaining to somatic psychotherapy. Facilitated individual and group psychotherapy sessions. Designed and taught workshops on the psychobiological effects of stress and trauma.
Western Samoa Substance Abuse Counselor 1985-1986 Designed culturally sensitive substance abuse programs. Provided clinical counseling and staff support to Alcoholics Anonymous programs.
Lebanon War Relief Service Provider 1980-1981 Provided social services for victims of war and political violence. Engaged in war relief social work efforts among military, civilian populations, women and abandoned children.
North Yemen English Teacher 1979-1980 English teacher for grades 1-6 in a high security adolescent, residential school for delinquent and/or orphaned boys.
Egypt Youth Coordinator 1978-1979, 1982 Assisted in supervising and facilitating individual and group therapy programs for Egyptian teenage youth with histories of family violence, severe poverty, juvenile delinquency and domestic violence.
ADDITIONAL INTERNATIONAL EXPERIENCE Bahrain, Kenya, Ethiopia, Uganda, Northern Ireland, Chile, Bolivia 1999-2004 Trauma and Conflict Resolution Consultant Developed and facilitated culturally sensitive trauma awareness and training workshops. Provided on-going training, educational and supervisory programs for local populations for the purpose of developing trained trauma professional within the host countries.
PROFESSIONAL EXPERIENCE Founder of Trauma Recovery Assessment & Prevention Services 2000-present International Trauma Therapist & Consultant Provide specialized trauma recovery assistance to international organizations whose employees are living and working in trauma inducing environments. Design, organize & implement comprehensive trauma recovery and stress management programs for International Relief Agencies, Government and Non-Government Organizations (NGO). Train and supervise senior staff on individual and organizational trauma behaviors and a healthy recovery process. Supervised programs in Ethiopia, Eritrea, Israel, Kenya, Northern Ireland and Sudan.
Formation Consultation Services 1998-2000 Staff Psychotherapist Provided clinical assessments of international clients as well as short-term counseling to in-house residents. Developed and implemented community organizational workshops in Ireland, Ethiopia, Eritrea, Kenya and Sudan.
Maryknoll International Society 1976-1998 International Cross-Cultural Consultant Promoted global relationships for the peaceful cohabitation of diverse cultures through large-scale and long-term intercultural projects and assistance programs. Designed intercultural training programs that addressed barriers to effective cross-cultural management. Implemented training programs on diversity in a multicultural workplace.
Massage Therapist 1998-2005 Private Practitioner Provided professional massage to a diverse clientele as a state certified massage therapist. Massage techniques included: Osteopathic Massage, Psychotherapeutic Massage, Neuromuscular Massage and Swedish Massage.
Bioenergetic Therapist 1994-present Private Practitioner Provide a bioenergetic analytic approach to the psychotherapeutic process by combining psychotherapeutic insight with body sensitivity. Promote an integration of body, mind and spirit approach to resolving psychosomatic patterns of distress.
Spiritual Director 1976-2001 Engaged in spiritual/religious dialogue and practices as well as provided spiritual direction within diverse cultural and religious contexts.
Publications: Books and Monographs
Berceli, D. (2007). Exerccios para Libertao do Trauma: Um revolucionrio novo mtodo Para a recuperao de stress e trauma. [Trauma releasing exercises: A revolutionary new method for stress/trauma recovery]. (Silveira, Tai, Trans.). Recife, Brazil.
Berceli. D. (2005). Trauma releasing exercises: A revolutionary new method for stress/trauma recovery. Charleston, S.C: Book Surge Publishers.
Refereed Journal Articles Berceli, D., & Napoli, M. (2007). A Proposal for a Mindfulness-Based Trauma-Prevention Program for Social Work Professionals. Complementary Health Practice Review, 11(3), 1-13, (In print).
Okamoto, S., LeCroy, C., Tann, S., Rayle, A., Kulis, S., Dustman, P., & Berceli, D. (2006). The implications of ecologically based assessment for primary prevention with indigenous youth populations. The Journal of Primary Prevention. 27, 155-170.
Additional Published Articles
Koch, L. & Berceli, D. (2005). The Iliopsoas muscle: A bio-reverent approach. Massage, 114, 74-82.
Koch, L. & Berceli, D. (2005). The Psycho-emotional aspects of the Iliopsoas muscle. Massage, 115, 106-113.
Berceli, D. (2000). Missionaries in trauma. Irish Missionary Union Report, 11, 3-4.
Berceli, D. (1999). Embodying politics: Recovering from political violence. Bioenergetic Analysis, 10, 18-20.
Berceli, D. (1999). Trauma and the startle reflex: Its creation and resolution. Bioenergetic Analysis, 10, 22-24.
Translated Journal Articles
Berceli, D. (2002). Missionarios traumatizados. (Traumatized Missionaries). Translated in Vida Espiritana: Missao Em Situacoes-Fronteiras, 13, 65-69.
Berceli, D. (2003). Trauma die unsichtbare epidemie symptome, Auswirkungen und heilungsanstze. (Symptoms of trauma). Translated in Forum Weltkirche, 4, 28-3.
Book Chapters
Trauma Releasing Exercises: TRE. (2004). Post-Conflict Healing: Trainer manual for peace building in Uganda (Module 4). Jamii Ya Kupatanisha P.O. Box 198, Kampala, Uganda. pp. 22-26.
Conference Papers Berceli, D. (2006, December). Neurogenic Tremor Release Technique (NTRT) for the alleviation of PTSD symptoms. Conference proceedings of the 18th International Conference of the National Institute for the Clinical Application of Behavioral medicine (NICABM), Hilton Head, South Carolina.
Berceli, D. (2005). Trauma releasing exercises: The use of psychogenic tremors for the alleviation of post traumatic stress disorder (PTSD) symptoms. Conference Proceedings of the 4th national conference of the United States Association for Body Psychotherapy. (USABP) Tucson, Arizona.
Publications in Progress
Napoli, M., & Berceli, D. The art of effective communication: Mindfulness and family therapy. Will be submitted to: Family Social Work Journal.
Video Publications
Rabin, M. (2005). One hour television interview. David Berceli's Trauma Releasing Exercises (TRE). A Better World Media. Manhattan, New York.
Berceli, D. (2004). Trauma Releasing Exercises (DVD): A self-help trauma recovery methodology. Trauma Recovery Assessment and Prevention Services (TRAPS). 435 W. Rio Salado Pkwy. Suite #101. Tempe, AZ 85281.
Berceli, D. (2001). Pathway to Healing. (VHS). 90 minute video of a self-help trauma recovery process. Trauma Recovery Assessment and Prevention Services (TRAPS). 435 W. Rio Salado Pkwy. Suite #101. Tempe, AZ 85281.
National Organization for Continuing Education of Roman Catholic Clergy. (2004). Bioenergetics and working with sexual celibacy in the body. (2004). Videotaped presentation at the thirty first annual convention. 1337 W. Ohio St. Chicago, IL. 60622.
Radio/TV Broadcasts
A Better World Productions July, 2006 One hour television interview. Trauma Releasing Exercises (TRE). Channel 57, Manhattan, New York.
KRUP 91.5FM. Dec. 2003, Jan. 2004 One hour public radio interview. Trauma and recovery: A somatic process. San Jose, CA.
Crescendo Dec. 2003, Jan. 2004 30 minute TV interview on the program. Trauma recovery and prevention. Comcast Channel 27. San Jose, CA.
Sudan Radio, Khartoum. 2002, May, 2002. 15 minute English to Arabic translated interview. The effects of post war trauma at the cultural and family levels.
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While there are many theories of war, there is one root cause that seems not to have been widely acknowledged. And yet it is perhaps the single most important root cause of the form modern warfare has taken. Its perpetuation, escalation, and violence, at least, can be attributed to post traumatic stress. (Levine 2000).
It is unfortunate, but trauma and Post Traumatic Stress Disorder (PTSD) have forced themselves indelibly onto the global scene as well as into the lives and psyche of this generation. Due to an increase in armed conflict, violence, terrorism and extreme poverty, trauma and PTSD are terms that have begun to dominate this era of human history. As a result of the increased awareness of trauma and its damaging effects of the psyche of individuals, institutions and entire societies, science has begun to explore this phenomenon in a more thorough and pervasive manner then ever before. The findings of these studies are both startling and disturbing.
Through advanced scientific studies and historical research, it has been recognized that there is no avoiding the traumatic aftermath of war; it reaches into every segment of society (Levine, 2002). The effects that trauma has on the general population has been thoroughly studied. It has been demonstrated that work impairment due to secondary comorbid disorders of PTSD such as anxiety, depression, irritability, disturbed sleep and elevated mood disorders all damage the cognitive and interpersonal skills of individuals. This has a staggering impact on the social structure of any country or society. Since the average duration of each trauma episode is reported to be more than seven years, Kessler alerts us to the daunting fact that the typical person with PSTD has a duration of active symptoms for more than two decades. The process of healing therefore will have to be measured in terms of generations rather than years (Kessler, 2000).
SOMATIC TRAUMATOLOGY One only has to read the most basic of the literature on the function of the brain, the nervous system and the physiology of stress to understand that the mind and the body are undeniably linked. Rothschild (1994).
Until recently most research programs on trauma and post traumatic stress symptomatology were conducted in the field of psychology. Subsequently all of the recovery programs designed to help relieve symptoms of PTSD addressed the psycho-emotional behaviors of the individual. However, the most recent research in the field of traumatology is helping to dispel this limited view of trauma and PTSD. The cross-fertilization of fields of study such as psycho-biology, neuro-physiology and physiological psychology are revealing new levels of understanding of the effects of trauma on the human organism. This dialogue among diverse fields of medical science has increased scientific awareness of the critical interaction and mutual interdependency of autonomic body responses and neurological processes.
This shift in awareness is increasing the recognition that trauma is primarily an autonomic, physiological and neurological response and this somatic reaction creates a secondary psychological response. Acknowledging that the human organism has a systematic set of autonomic responses that become engaged during the time of trauma allows us to study these unconscious responses. If these autonomic responses can be reversed, then the secondary psychological disruptions can be limited and the psyche of the individual can be restored to health much more readily.
To understand these unconscious physiological reactions, we have to look at the human person as an animal species in the process of evolution. During any traumatic experience the extensor muscles are inhibited so that the flexor muscles can contract. This allows the body to bring the extremities together, creating an enclosure that gives us a sense of safety while protecting the soft, vulnerable parts: the genitals, vital organs, and the head and its contents the eyes, ears, nose and mouth. (Koch, 1997).
A key set of muscles that assist in this complex series of contractions are the psoas muscles. This pair of muscles that connect the trunk, pelvis and legs are considered the fight/flight muscles. These muscles stand guard like sentinels protecting the center of gravity located just in front of C3 of the spine. These muscles help pull the body into a semi-fetal position as a way of protecting it from anticipated harm. Since this contraction response of the human body is autonomic, instinctual and primarily unconscious it is not necessarily under the control or awareness of the individual. Because the human organism is genetically encoded to preserve its existence, this process of contraction is the emergency survival system designed to engage itself in any real or imagined life threatening experience. Since this emergency mode is not under the control of the conscious brain, the behaviors, actions and reactions of the individual(s) are instinctual rather than calculated and conscious. So, unlike other psychological issues, traumatic experiences cannot be immediately dealt with via conscious and logical methods to achieve a resolution. It is precisely this conscious and logical resolution of a psychological crisis versus the unconscious and illogical resolution of trauma that has tremendous implications for the therapeutic session.
TRAUMA RELEASING EXERCISES Since the psoas muscles are primary muscles that contract to protect the center of gravity, it is imperative that these muscles are relaxed so that the somatic recovery process can be engaged. Liz Koch (1997) writes very clearly and at length on this subject in her book The Psoas Book. As Koch tries to point out, traditional stress reduction techniques are designed to release surface level tension and are often insufficient and ineffective in releasing the deep chronic tension created in the body during traumatic episodes, particularly if they are prolonged or repeated experiences of trauma. Likewise, Trauma Recovery Assessment and Prevention Services (TRAPS) has designed a unique set of Trauma Releasing Exercises (TRE) specifically designed to release the deep, chronic muscle contractions created by severe shock or trauma. By releasing the chronic tension created by trauma the individual feels some immediate relief from the debilitating physical effects of trauma. This relief naturally provides the individual with the psychological insight necessary to continue to integrate their psycho-somatic experience in their trauma recovery process.
Although deep relaxation is the answer to somatic recovery, a fast, effective and efficient method for this deep relaxation still eludes us. However, if we return to our study of the human species we will discover that our trauma recovery process is very similar to most other mammals. As a living species on this planet, we like all other living species are genetically encoded to experience, survive and resolve trauma. It is part of our natural instinct that guarantees we will not only survive but actually evolve as a species. Without it the human animal would already have become extinct.
This mysterious and elusive key that activates the release mechanism of the humans natural recovery process can be found discretely hidden right within the natural psycho-neuro-physiology of our bodies as well. We are already familiar with this mechanism. We use it regularly although we try desperately to control it. Children are our best examples of unguarded behaviors. When a child is frightened or highly charged by some experience, their knees will begin to shake involuntarily. As adults we say I was so angry I shook! When we are unable to control our overwhelming emotions our lips, jaw, legs or hands may shake involuntarily. This shaking is the bodys natural method of releasing tension that has become so high within the system that it requires a discharge. It is precisely this shaking mechanism that needs to be reactivated in the human species after a traumatic event. This shaking mechanism actually stimulates the parasympathetic nervous system, discharges the tension in the muscles, reduces the high biochemical levels and restores proper neurological functioning. This combination of effects helps to turn off the organisms emergency protective response and restore it to normal functioning.
By understanding why and how this physiological process occurs we are able to use it to help restore the person to normal functioning. A specific series of anatomical movements and exercises must be followed in order to evoke this shaking mechanism. These exercises create the natural shaking of the iliopsoas muscles (fight/flight muscles). When the natural shaking mechanism of the body is evoked at this powerful center of the body where the protective organismic contraction began, the shaking reverberates throughout the entire body looking for deep chronic tension in its path and naturally dissolving it.
RE-ENACTMENT AND REPETITION COMPULSION Fear is lodged in our bodies. It vibrates in the nervous system and is easily evoked. Although fear is often a subtle experience, we attempt to control this unpleasant feeling of anxiety by adding more muscular tension, resulting in layer upon layer of rigidity. (Liz Koch, 1981)
Post trauma reactions are caused by the residual undischarged excitement (biochemical energy) generated at the time of the traumatic event. If this high state of aroused energy is prevented from being discharged in the body it remains trapped in a bio-neural-physiological loop that causes a repetition compulsion behavior. Until the brain receives a signal from the central nervous system that the danger is over, the body will continue to repeat the bio-neural pattern of protection and defense. The key to a successful recovery from trauma is to activate the organisms natural releasing (shaking) mechanism that signals the body to return to a state of rest and recuperation. Because the excessive energy created in the body during a traumatic event continually seeks an organismic discharge, it will continually repeat some form of the trauma creating a cycle of compulsive reenactment an endless and unstoppable neurobiological feedback loop that keeps the individual locked into a kind of psychophysical imprisonment.
TRANSFORAMTION AND FUTURE Letting go is not for the purpose of forgetting or forgiving the past, it is about releasing the energy of the past to give us back our lives in the present which is necessary to deliver us into a new future. (Holloway, 2002).
Trauma and tragedies often find their way into our lives despite our greatest attempts at protecting ourselves from the suffering and pain that they inflict on ourselves and our families. As living organisms our bodies know we are capable of experiencing, enduring and recovering from even the most severe of tragedies. It is our egos that try to avoid, deny and refuse to forgive and let go of our past tragedies so we can move into a new future. What we are recognizing however is that it is precisely our inability to forgive and let go that adds to the pain of the tragedy of loss that is already in our hearts. This inability to forgive and let go of the past leads us into an excruciating double bind. Our refusal to forgive the past imprisons us in our own resistance to our natural, evolutionary instincts and thereby has the power to deny us a healthy movement into our future. (Arendt 2000). The question that haunts us is how do we get through this painful egotistical refusal to let go and move on? Why is this so difficult? Once again we are faced with the paradoxical experience of being part reflective human and part animal instinct. One the one hand, the ego refuses to let go of the past because it is equivalent to a second injury or death experience. The primary blow to our existence came from the initial trauma and the second threat to our existence comes from our need to re-experience the painful scars and memories left behind in order to heal. This therapeutic process of remembering, forces us to face the residual reminders of trauma that belie our fragility, vulnerability and precarious place on this planet. This experience is often a shattering of ones self-identity and a destruction of ones entire belief system.
One the other hand, as living organism we are compelled biologically to rid ourselves of anything that is obstructing our growth process. To exist and evolve we have an instinctual (nature-like) mechanism genetically encoded in us so that we can complete our process of letting go of the past and begin something new. This process is nothing more than part of our unending cycle of evolution. This ability to let go only seems to happen when we diminish the egos resistance and increase the bodys natural biological instincts. This process allows the life-force to work in us with less constraint. In this respect, forgiving and letting go are like natural control mechanisms in us that assure our unending process of evolution. There is a quote by Friedrich Nietzsche in Untimely Meditations (1997) that says; we possess the power to grow uniquely from within, to transform and incorporate the past and the unknown, to heal wounds, to replace what is lost, and to duplicate shattered structures from within.
Inevitably, whether we like it or not, whether we want to or not, our trauma recovery process will force us deeper into our bodies and further into the reflections of our minds than we would dare to go. As painful as this exploration may be, in the end we have to resign ourselves to the fact that this is the way things are and that they have been made that way by factors that are not in the persons control. (Holloway, 2002).
Refusing to let go of the past can only force us into a neural feedback loop that causes the trauma to be replayed over and over in our minds in an endless loop of madness. Eventually, the neurological process of our brains will transform this excess neural energetic activity into ideations of hate, revenge, shame, suicide or depression. Once we enter this arena we can be forever trapped into the compulsion and vengeance of victimhood rather than the freedom and forgiveness of survivorhood.
Letting go of the past is, in the end, the individual responsibility of each trauma survivor. It is our responsibility to guarantee that revenge does not steal the future of our life from us. Only this radical experience of letting go can restore our natural biological process. This restoration of our natural instincts of survival and evolution are so powerful that we even give up the need for past ideations of hatred and revenge. With the recovery from each traumatic episode of our lives, we give into and accept more easily the way the universe has treated us. Paradoxically, the more we let go into life the more we discover that we can re-take control of our lives and participate once again in the precariousness nature of being human. Only by letting go can we unlock ourselves from the past, be delivered into the future and prepare ourselves for our next evolutionary experience.
References
Babette Rothschild, M.S.W. & Erik Jarlnaes. (1994). Nervous system imbalances and post-traumatic stress: a psycho-physical approach Members: European Association of Body-Psychotherapy and European Society for Traumatic Stress Studies. Hannah Arendt, The Portable Hannah Arendt, Penguin, London, 2000, pp.180-181. Holloway, Richard (2002). On Forgiveness. Canongate Books Ltd. Edinburgh, Scotland. Kessler, L. This report is from the Department of Health Care Policy, Harvard Medical School, Boston, MA. It can be found in the Journal of Clinical Psychiatry 2000;61 [suppl. 5]:4-12. Koch, Liz (1981). The Psoas Book. Felton, CA. Guinea Pig Publications. Levine, Peter (2002). We are all neighbors. Foundation for Human Enrichment. P.O. Box 1872 Lyons, CO 80540. Nietzsche, Friedrich (1997). Daniel Breazeale, (Editor), R. J. Hollingdale (Translator), Untimely Meditations, Cambridge University Press, Cambridge, 1997, p.62.
IMPORTANT NOTICE: Information on this site is for information purposes only and not intended to constitute professional advice as circumstances will vary from person to person. Likewise, the results and the performance of Trauma Releasing Exercises and the additional trauma information is assumed by the user, and in no event shall TRAPS or David Berceli be liable for any consequential, incidental or direct injuries suffered in the course of using the exercises or information in this web site. Use of the information contained in this web site may contain restrictions on use.
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posted
The Perfect Accompaniment to the book The Revolutionary Trauma Release Process�
A man approaching sixty years of age tells a group of friends that most of his life, he was never really happy. No matter how he tried to find joy in his life, somehow it eluded him.
Then, he was introduced to Dr. David Berceli's Revolutionary Trauma Release Exercises�, and began performing the simple routine several times a week. After two or three months, he reports that his life was completely changed. The happiness he had sought broke through into his everyday reality.
Stress, anxiety, and especially trauma can block the natural flow of joyous energy with which we are born--that wonderful excitement, sparkle, and sense of wonder that arises so spontaneously in little children.
When trauma of any kind assaults us, energy that should course freely and li berally throughout our body becomes stuck. It is trapped by mu sculature that has become tense as a result of physical, mental, and emotional experiences that cause the body to clench and tighten.
Talk therapy can help free our psyche from the multiple hurts we have experienced in life. But it can require more than talk therapy to unblock the tension in the body that prevents the free-flow of the life force. The Revolutionary Trauma Release Exercises� are designed to do just this.
The muscles of the body become tight, roped, and knotted from our traumatic experiences. Just as tree rings record the harsh winters and stressful summers of a tree's life, so also does the musculature of the body, from head to toe, retain an accurate memory of all the stress, anxiety, and trauma that has bedeviled us in life.
Globally, our species is experiencing an extraordinary period of trauma. Millions in multiple nations from East to West are suffering the ravages of hurricanes, mass flooding, drought, wildfires, and earthquakes.
Simultaneously with the onslaught from nature, the financial world is being rocked on an epic scale. The mortgage crisis is throwing huge numbers of people out of their homes and into rental property. People's financial stability is being affected by the collapse of major institutions. The economic squeeze means that many are losing their jobs, with the added trauma of the divorces and other relationship breakups that often accompany such hard times.
In addition to all of this, a spate of plane crashes, train crashes, and the constant presence of automobile accidents--accounting for more than 43,000 deaths a year in the United States alone--add to the toll of misery that comes with accidents both on the job and at home, whether from a fall that results from tripping over a rug or tumbling off a ladder.
For many, simply living is a traumatizing experience, whether from spousal abuse, child abuse, being a victim of a crime, or multiple other causes.
The Revolutionary Trauma Release Exercises� are a simple and practical way to address the trauma that results from the many ways in which everyday life stresses us. They are performed in your home, in most cases without any need of professional supervision, and can restore health and vitality to the body with very little effort.
Now, to make it easier to use the exercises regularly, Namaste Publishing has released a 105-minute DVD, in which Dr. Berceli guides us through the exercises step-by-step in real time with three models who show us exactly how to perform the exercises.
First watch the introduction in which Dr. Berceli explains how and why the exercises work, then follow along as the models demonstrate the techn i que. Next, listen to the group discussion, and finally learn all about how the exercises were discovered and what they can do to enrich your life in the in-depth interview with Dr. Berceli.
After you have watched the complete DVD, you can simply select the exercises directly under ``scene selection'' each time you want to perform them.
The Revolutionary Trauma Release Exercises� DVD is the perfect accompaniment to the newly released book, The Revolutionary Trauma Release Process�.
Coming mid-October
Listen to Sample Chapters from The Revolutionary Trauma Release Process� (MP3) Chapter 1 Making Sense of Stress, Anxiety and Trauma Chapter 16 Tough Times Can Make You Stronger Chapter 18 The Body and the Present Moment
The Revolutionary Trauma Release Process� To Be Taught to One Million in Earthquake-Stricken China
This is an exciting time for Dr. Berceli and The Trauma Release Process�.
In conjunction with the release of his long-awaited new book, The Revolutionary Trauma Release Process: Transcend Your Toughest Times, David Berceli, PhD, has been invited to China for the month of September. He is training 1,000 Trauma Release Process � trainers in the Sichuan Province, where millions were traumatized by the recent earthquakes.
The goal is to provide Trauma Release Process� training to one millio n p eople by the end of this year. ``This is what the trauma release exercises were developed to do,'' says Dr. Berceli, who envisioned providing this self-healing tool so whole populations could be taught to aid their own healing.
Before the end of the year, Dr. Berceli will provide Trauma Release Process� trainings in California, Canada, Denmark, Sweden, Germany, Spain, Amsterdam, London, Geneva, and Rome.
Sherry Mills, LCSW, has joined Dr. Berceli in providing Trauma Release Process� trainings, as well as in getting the word out about his new book--and now, also, The Revolutionary Trauma Release Exercises� on DVD. Sherry has thirty-three years of experience in the treatment of trauma and addictions in Canada and the United States. For twenty-two years, she was in private psychotherapy practice in Tallahassee, Florida. She now devotes her energy to supporting Dr. Berceli's work and to getting the Trauma Release Process� out into the wider world. Sherry has studied extensively with Dr. Berceli and provided Trauma Release Process� training since 2003.
The Neurophysiology of Dissociation and Chronic Disease by Robert Scaer, M.D. Download The Neorophysiology of Dissociation and Chronic Disease .PDF CLINICAL TYPES OF DISSOCIATION MEMORY, TRAUMA AND DISSOCIATION THE ANIMAL MODEL TRAUMA AND DISSOCIATION: THE WHIPLASH MODEL THE AUTONOMIC NERVOUS SYSTEM IN DISSOCIATION SOMATIC DISSOCIATION REFLEX SYMPATHETIC DYSTROPHY THE DISEASES OF TRAUMA CONCLUSIONS BIBLIOGRAPHY AUTHOR'S NOTE ABSTRACT
Published in: Applied Psychophysiology and Biofeedback, (2001), 26(1), 73-91, based on a Keynote Address presented at the 31st annual meeting of the Association for Applied Psychophysiology and Biofeedback, March 29-April 2, 2000, Denver, CO.
During the last two decades of the 19th century, psychiatrists in Europe began to explore and define the peculiar behavior manifested by patients of theirs who fell under the diagnostic category of hysteria. Pierre Janet at the Salpetriere` described dissociation as phobias of memories, in the form of expressions of excessive or inappropriate physical responses to thoughts or memories of old traumas (Janet, 1920). After visiting Janet, Freud adopted many of these concepts of dissociation as a splitting of consciousness, often associated with bizarre physical symptoms and manifestations, and ultimately attributed such symptoms in his hysterical patients to a history of childhood sexual abuse (Freud, 1896). Evolution of the concept of dissociation led to the description of a constellation of varied clinical manifestations attributed to it, including altered perceptions of physical sensation, time, memory, and the perceptions of self and reality. Complex expressions of these states came to include conversion disorder, fugue states and multiple personalities (dissociative identity disorder) (Freud & Breur, 1953, Mayer-Gross, W., 1935, Spiegal & Cardena, 1991, Bremner, et al, 1992). Thus the concept of dissociation evolved to include not only mental and emotional aberrations, but also stereotyped and unusual somatic perceptual and motor experiences and expressions.
All of these symptoms and behaviors were felt to be the sequellae of prior life trauma. The basic mechanism of dissociation was felt to involve the splitting off of parts of memory or perception in order to escape intolerable anxiety triggered by those areas of the mind that retained elements of the traumatic conflict. Relief from that conflict through hysterical dissociation resulted in relief from anxiety, resulting at times in the seemingly blas� acceptance of disabling physical conditions (la belle indifference`).
Freud, however, soon began revising his concepts of hysteria, and by 1925 had recanted his theories of the relationship of hysteria and dissociation to prior childhood trauma (Freud, 1959). He ultimately attributed the stories of childhood sexual abuse in his hysterical patients to fabrication, based on unacceptable sexual wishes and fantasies that they could not acknowledge. As a result, the role of childhood trauma in the etiology of dissociation was basically ignored for decades The introduction of the diagnosis of Post Traumatic Stress Disorder (PTSD) into the Diagnostic and Statistical Manual of Mental Disorders, 3rd edition (DSM III) in 1980 also resulted in the reclassification of many of the conditions formerly attributed to trauma and dissociation, and in some cases, ignored their association with prior life trauma (American Psychiatric Association, 1980). Van der Kolk et al (1998) note that in the DSM IV, dissociative symptoms are included under the diagnostic categories of not only Post Traumatic Stress Disorder, but also of Acute Stress Disorder, Somatization Disorder and Dissociative Disorders themselves (van der Kolk, et al, 1998). In fact, in the DSM IV, Dissociative Disorders do not include Conversion Disorder, which has now been placed under the Somatiform Disorders. Since the DSM III, the diagnosis of hysteria is nowhere to be found. Van der Kolk et al (1998) make a strong case for the consideration of dissociation, somatization and affect dysregulation as late expressions of trauma even in the absence of continuing criteria for the diagnosis of PTSD. In doing so, they echo the concerns of Nemiah (1995), who notes that the diagnoses of PTSD, conversion disorder and dissociation are connected by the common process of dissociation itself, whereas their disparate placement in different categories of the DSM IV inhibits investigation of the psychodynamics of trauma.
This attempt to return to the concepts of a relatively broadly-based response of the organism to traumatic stress is critical to our consideration of the neurophysiology of trauma and its effects not only on systems of the brain and endocrine systems, but also on the body itself. When one accepts the tenet that the clinical expressions of a multitude of psychiatric syndromes derive not only de novo or through gene expression, but perhaps also through life experience and its lasting effects on brain physiology, one must return to the concept of a physiological continuum between many psychiatric diagnoses.
[top] CLINICAL TYPES OF DISSOCIATION
One of the dilemmas of classification of symptoms of dissociation is that these symptoms assume many and varied forms and expressions. They may be emotional, perceptual, cognitive or functional. They may involve altered perception of time, space, sense of self and reality. Emotional expressions may vary from panic to numbing and catatonia. Altered sensory perceptions may vary from anesthesia to analgesia to intolerable pain. Motor expressions frequently involve weakness, paralysis and ataxia, but may also present as tremors, dysarthria, shaking and convulsions (Please see discussion of conversion reaction later). Cognitive symptoms may involve confusion, dysphasia, dyscalculia and severe deficits in attention. Perceptual symptoms include ignoral and neglect. Memory alteration may appear as hypermnesia in the form of flashbacks, or as amnesia in the form of fugue states or more selective traumatic amnesia. The varied symptoms of dissociation therefore mimic the intrinsic bipolar nature of the defining symptoms of PTSD (arousal, reexperiencing, avoidance).
Time perception is often greatly altered, most commonly characterized by a sense of slowing of time (Terr, 1983). Altered perception of self (depersonalization) may manifest as an out-of body experience, or a sense of intense familiarity (de ja` vu) (Pynoos, et al, 1987). In its most extreme expression, depersonalization may encompass perception of several separate states of self in the form of distinct and separate personalities (dissociative identity disorder), each with distinct personality characteristics and even physical attributes (Mayer-Gross, 1935). Strange persons or events may appear familiar, whereas familiar faces and scenes may appear alien and strange.
Abnormal memories also constitute a significant dissociative phenomenon. Simple amnesia for the traumatic event is common, and may present as complete amnesia, or as distorted or inaccurate memory content (Torrie, 1944, Terr, 1983). Fugue states present an extreme state of amnesia, characterized by periods of time for which the dissociative patient has no memory, often triggered by exposure to cues reminiscent of prior trauma. During that time, the person may appear distracted and may not remember personal facts. More often, they may appear confused, histrionic, socially inappropriate or bizarre (Fisher, 1945).
Perhaps the most unique symptom of dissociation is that of flashbacks. These episodes are distinctive in that they involve intense arousal and reexperiencing, symptoms more related to acute PTSD than to dissociation (Mellman, & Davis, 1985). During these episodes, which may last briefly or for several hours or even days, the person will also usually experience more typical dissociative experiences such as depersonalization. Sensory processing and perception may be greatly distorted. During flashbacks, the person may appear confused and detached, but later may report vivid sensory and memory experiences, often associated with intense emotions and states of arousal. The accuracy of the associated memories may be variably valid or distorted.
Conversion reaction and hysteria no longer are described in the DSM IV under dissociation (American Psychiatric Association, 1994). In fact the DSM IV goes so far as to assert that if dissociative and conversion-based symptoms occur in the same patient, both diagnoses must be made. The neurophysiological and pathophysiological basis for dissociation proposed in this paper, however, demands that conversion be reintroduced as a specific form of dissociation, one that is closely linked to somatic perceptual alterations that are an acceptable and in fact intrinsic feature of the dissociative process. The model presented proposes that the atypical neurologic symptoms and signs that characterize conversion constitute perceptual alterations based on prior trauma, and represent the same splitting of consciousness that produces disorders of perception of time, space, reality and self presented above. As such, conversion may be associated with the same spectrum of positive and negative phenomena as PTSD as well as other symptoms of dissociation (analgesia/pain, paralysis/seizures).
[top] MEMORY, TRAUMA AND DISSOCIATION
Disorders of memory constitute one of the diagnostic categories for PTSD in the form of reexperiencing. As noted above, this may be in the form of hypermnesia, amnesia or distortion of memory. Trauma-based memory phenomena often involve declarative (explicit, semantic) memory in the form of variably accurate verbal and imaginal recall of the traumatic event. Declarative memory, the form of memory that relates to facts and events, initially involves hippocampal and prefrontal cortical pathways and plays an important role in conscious recall of trauma-related events. It also is notoriously inaccurate, and subject to decay. Procedural memory relates to acquisition of motor skills and habits, to the development of emotional memories and associations, and to the storage of conditioned sensorimotor responses. Procedural memory is unconscious, implicit and extremely resistant to decay, especially if it is linked to information of high emotional or threat-based content (van der Kolk, 1994). Although declarative memory may account for much of the arousal-based cognitive symptoms of PTSD, procedural memory provides the seemingly unbreakable conditioned link that perpetuates the neural cycle of trauma and dissociation.
Endogenous opiate reward systems very likely contribute to the establishment of conditioned procedural memory in trauma. Researchers have known for decades that exposure to overwhelming trauma in combat often results in a sustained period of analgesia. Soldiers wounded in battle frequently require much lower doses of morphine than in other types of incidental injury (Beecher, 1946). Stress-induced analgesia is a well-documented phenomenon in many forms of traumatic stress (van der Kolk, Greenberg, Orr & Pittman, 1989). Release of endorphins at the time of acute stress has a distinct survival benefit. An animal ministering to his wounds due to pain at the time of aggressive, life-threatening injury would suffer significant compromise of his defensive capabilities. Endorphins also persist during freeze/immobility, rendering the animal analgesic in the face of the injury from the attack. This also has potential survival value, since the persistence of immobility in the face of painful injury might serve to end the predator's attack behavior. In the event of lack of completion of the freeze/immobility response, however, persistent recurrent dissociation with associated endophinergic reward might well potentiate the kindled trauma reflex. Endorphinergic influences might also contribute to the phenomenon of compulsive trauma reenactment (van der Kolk, 1989).
[top] THE ANIMAL MODEL
The behavior and physiology of the freeze response have been studied for decades. Freezing of course is routinely seen in the wild, initially as a state of alert immobility, as in the fawn that assumes an immobile state in the presence of a predator. This state may proceed to sudden flight, or if the fawn is attacked and captured by the predator, to a deeper state of freeze, one associated with apparent unresponsiveness, and associated with marked changes in basal autonomic state. Early immobility has the advantage for the prey animal of remaining hidden, especially since movement cues often are necessary to elicit attack by the predator. All animals manifest alert immobility, a state termed "animal hypnosis" by Krystal (1988).
In the event of attack, when the creature is rendered helpless, a different state of freezing is elicited, as noted above. Laboratory studies of this phenomenon yield interesting results. Hofer (1970) exposed rodents to a variety of predator-related stimuli in an open space with no means of escape. All rodents entered a deep phase of freeze, persisting for up to 30 minutes. This state was associated with marked bradycardia associated with cardiac arrythmias, suggesting a pronounced state of vagal or parasympathetic tone.
Ginsberg (1974) immobilized chicks, and then allowed one group to recover spontaneously, and one to recover, but with prodding and stimuli to terminate the freeze. These groups, along with a third group of chicks that had not been immobilized, were then tested for resiliency to avoid death by drowning. The group that had not been allowed to complete recovery from immobility died first, the group not exposed to immobility next, and the group that had spontaneously recovered from the freeze survived the longest. Clearly the experience of and the spontaneous recovery from freezing carries survival benefits, whereas not being allowed to go through this recovery process seemed to reduce resiliency to life threat.
The key to this process appears to revolve around the state of helplessness, or lack of control. In drowning experiments, wild rats will swim for up to 60 hours before dying from exhaustion. If these rats experience immobility in the hands of the investigator, and then are placed into the water, they will drown in minutes. Some rats experience sudden death during induced immobility (Richter, 1957). The freeze response clearly is associated with high risk to the creature if it is not allowed to dissipate spontaneously.
Studies in animals with inescapable shock (IS) further illustrate this dilemma. Animals exposed to significant shock stimuli in an escape-proof environment predictably freeze with subsequent shock exposure. Subsequent introduction of routes of escape in these animals do not elicit escape behavior- the animals remain frozen, and continue to exhibit helplessness (Seligman, 1975). They appear to be unable to learn from new experiences, even from those experiences that promote escape or survival. Animals exposed to escapable shock (ES), however, soon learn to use the escape rout and do not freeze (Fanselow & Lester, 1988). The critical factor in trauma therefore appears to be controllability of the outcome of the threat vs. a state of helplessness. Van der Kolk, et al, have noted the remarkable similarities between the human response to trauma, and the animal response to inescapable shock (IS), and have suggested that IS may be a biological model for PTSD (van der Kolk, et al,1985). Nijenhuis, et al (1998) have presented the novel model of dissociation in humans as an analogy to the alteration in defensive and recuperative behaviors in animals exposed to IS (Nijenhuis, et al, 1998). Threat-associated conditioned stimuli (CS) in this model would automatically elicit a dissociative or freeze response, rather than a conditioned response more specific to the stimulus. Persistent dissociation would therefore prompt the animal, or human, to be sensitized to continue to freeze, or dissociate, to a wide range of stimuli that might be associated with threat.
Levine (1997) takes the phylogenetic model a step further, by equating the lack of recovery from the freeze, or immobility response with retention of the stored and undissipated energy of the truncated fight/flight response. This sustained state of sympathetic arousal serves as the drive for the memory and arousal-based symptoms of trauma and PTSD. He attributes the tendency for traumatization in the human species to the inhibitory influence of selected neocortical centers that block the instinctual capability that other wild animal species possess, to "discharge" this retained energy. Noting that animals emerging from immobility often manifest repetitive, almost seizure-like motor activity, he postulates that these stereotyped motor responses are able to allow completion of the motor sequences of successful escape or defense, and therefore to effect an energetic discharge.
Dissociation in the animal model, then, appears to have many similarities to behavior in animals in whom freezing has been elicited in a state of helplessness with subsequent prevention of spontaneous recovery from immobility. Furthermore, dissociation also may be associated with predominantly parasympathetic tone, impaired cognition and learning behavior and a tendency for conditioned perpetuation.
[top] TRAUMA AND DISSOCIATION: THE WHIPLASH MODEL
We have previously presented an hypothesis that the Whiplash Syndrome constitutes a model for traumatization rather than physical injury, and that many of its symptoms and clinical manifestations are in fact a universal response to a life threat in the face of helplessness (Scaer, 1997, 1999, 2001). This hypothesis is based on the occurrence of dissociation at the time of the motor vehicle accident (MVA) in the form of numbing and the altered state of awareness often attributed to concussion. Subsequent clinical symptoms are based on theories of limbic kindling in the development of the arousal-memory cycle in PTSD (Goddard, et al, 1969, Post, Weiss & Smith, 1995, Miller, 1997). Kindling is the name given to the phenomenon in rats of the progressive development of self-perpetuating neural circuits produced by repetitive time- and frequency-contingent regional electrical brain stimulation (Goddard, et al, 1969). The behavioral expression of kindling may include epileptic seizures, but kindling is also widely felt to be a model for a number of clinical syndromes, including PTSD.
The neural pathways involved in the process of acquisition of this kindled physiologic response to threat probably involve a series of events involving primarily the locus ceruleus, amygdala, thalamus, hippocampus and right orbitofrontal cortex (van der Kolk, 1994). Arousal-based input from a variety of sensory organs, especially those of the head and neck, is transmitted to the thalamus and locus ceruleus. The locus ceruleus then provides input to the thalamus and to the amygdala, which evaluates this input for its emotional content. The amygdala then transmits this information to the hippocampus, the center for declarative memory, which establishes a cognitive context to the information. This data is then transmitted to the right orbitofrontal cortex (OFC), which organizes the appropriate cortical and autonomic response based on the implications of the sensory information for survival. The OFC therefore functions as a master regulator for organization of the brain's response to threat. Inadequate development of the OFC resulting from a maladaptive childhood experience, or from prior brain injury may result in faulty modulation of this arousal response (Schore, 1994).
Further regulatory control is provided by the anterior cingulate cortex, a center that may provide a gating function inhibiting fear conditioning by inhibitory input to the amygdala ( Morgan, et al, 1995). The locus ceruleus, through intense adrenergic input triggered by an acute arousal stimulus, inhibits both the anterior cingulate and the OFC, thereby inhibiting the gating and modulation functions of these two centers. This in turn would allow exposure of the amygdala to overwhelming internal and external arousal cues, thereby promoting the kindled development of pathways producing the clinical syndrome of PTSD (Hamner, 1999).
Dissociation at the time of trauma is the primary predictor for the later development of PTSD (van der Kolk & van der Hart, 1989). Individuals who actively dissociate at the time of a traumatic event are much more likely to develop subsequent symptoms of PTSD than those who do not (Bremner, et al, 1992, Holen, 1993, Cardena & Spiegel, 1993). Children are especially prone to dissociate at the time of a traumatic experience, and therefore people with a history of past trauma, especially child abuse, are more susceptible to arousal, freezing and retraumatization after exposure to even non-specific arousal or traumatic stimuli (Kolb, 1987).
In the whiplash hypothesis, spontaneous recovery from dissociation, or freeze/immobility at the moment of traumatic impact often will not occur, based on the premise that involvement in an MVA is by its very nature a model of helplessness. The potential for dissociation to occur will predictably be greatly enhanced by a prior history of trauma and dissociation. This state of altered memory, perception and autonomic function may potentiate kindling between centers for memory and arousal (amygdala, hippocampus, locus ceruleus) that we have described above. The resulting self generated and maintained kindled loop will then serve as the substrate for development of clinical PTSD.
From a somatic standpoint, procedural or conditioned memory for sensory input and motor responses to the physical events associated with the actual accident will also be incorporated into this kindled trauma response. In an event of great arousal and threat, only one trial may be necessary for a conditioned response to be established. Thus vestibular, ocular, and sensorimotor experiences of the accident will be imprinted on procedural memory through traumatic operant conditioning. These perceptions will then subsequently be elicited in exact form by memories, flashbacks, nightmares as well as internal and external cues reminiscent of the MVA. All of the elements of the post-concussion syndrome - vertigo, blurring of vision, tinnitus, headache, myofascial pain - now constitute symptoms precipitated by cue- and memory-based stimuli, and eventually by a wider and wider range of nonspecific arousal-based events. Myofascial pain probably represents procedural memory for the specific defensive motor stretch reflex and its proprioceptive template precipitated by the movement of the body in the MVA, thereafter elicited by stress or any movement pattern reminiscent of the accident, in the form of bracing and muscle spasm. Cognitive impairment may appear and in fact worsen based on well-documented attention and memory deficits in dissociation and PTSD (Gill, et al, 1990, Alexander, 1992, Miller, 1992, Bremner, et al, 1993, Grigsby, et al, 1995). None of this diverse array of symptoms would therefore require tissue injury to produce them.
This hypothesis is dependent on the occurrence of dissociation contributing to an unresolved freeze response as a result of life threat in the face of helplessness. Resulting kindling would then incorporate not only the centers for memory and arousal noted above, but also the centers providing the sensory information of the MVA (visual, auditory, vestibular, proprioceptive sensory receptors), and the motor centers that organized the defensive response (cerebellum, brainstem, basal ganglia, motor cortex). Kindling and dissociation would explain the vexing tendency for whiplash symptoms to be resistant to most forms of physical therapy, to persist indefinitely in many cases and to worsen dramatically in situations of ambient life stress. The proposal also incorporates somatic symptoms into the basic theories of PTSD and dissociation, leading to a somatic definition of dissociation that is the core of this paper.
[top] THE AUTONOMIC NERVOUS SYSTEM IN DISSOCIATION
Patients with chronic PTSD cycle in and out of exaggerated levels of arousal and avoidance, of panic and numbing, of terror and confusion. The panorama of autonomic symptoms includes pallor and flushing, nausea, abdominal cramps and diarrhea, tachycardia and light-headedness, diaphoresis and shivering. The DSM IV criteria for PTSD (arousal, reexperiencing, avoidance) reflect dramatic cycling of mood from panic, hypervigilence and irritability, to numbing, withdrawal and flattened affect. Physiologic markers of PTSD referenced in the DSM IV include measurements of pulse rate, electromyographic and electrodermal responses, all primarily measures of sympathetic tone. The role of the cyclical increase in parasympathetic tone or function in trauma, however, has been largely neglected. PTSD is in fact a bipolar syndrome, one that reflects remarkable cyclical autonomic instability, with patterns of heightened sympathetic arousal alternating at times with clear and dramatic parasympathetic dominance.
Oscillatory phenomena in a variety of biological systems have been studied and documented in a number of settings. Many physiologic subsystems (endocrine, autonomic, neurohumoral) operate in a bimodal fashion based on a variety of rhythmic environmental and internal physiologic influences. Antelman et al (1997) propose that exposure of such systems to chemical or behavioral stressors of sufficient intensity can induce cyclical patterns of increase and decrease in response to each subsequent exposure (Antelman, et al, 1996, Antelman & Caggiula, 1996). This phenomenon seems to be applicable to such a variety of physiological systems that the authors conclude that oscillation in response to chemical or behavioral input may represent a general principle of biological functioning (Antelman, et al, 1997). This may well be an innate biological reflex designed to reestablish homeostasis, the rhythmic and balanced fluctuation of all biological systems, be they endocrinological, neurophysiological, metabolic or immunological (Antelman et al, 1997).
In PTSD, through unresolved peritraumatic dissociation, internal and external stimuli impacting the central neural circuits mediating memory and arousal will contribute to kindling, leading to internally-based stressors of associated neural subsystems, especially the autonomic nervous system. By this model, cyclical autonomic dysfunction will result, leading to many of the divergent but dramatic autonomic symptoms of the traumatized victim. Thus periods of sympathetic arousal will include symptoms of muscle bracing, bruxism, ocular divergence, tachycardia, diaphoresis, pallor, tremor, startle, hypervigilence, panic, rage and constipation. These states will alternate with parasympathetic dominance, including symptoms of palpitations, nausea, dizziness, indigestion, abdominal cramps, diarrhea and incontinence. Although many of these symptoms are often attributed to somatization disorder, they in fact represent the extremes of the cyclical autonomic dysfunction seen in trauma, are inherently self-perpetuating, and contribute to continued abnormal autonomic oscillation. The syndrome of trauma has now literally taken control of the body.
As the kindled cycle of PTSD continues and becomes chronic, avoidance and withdrawal become increasingly prominent, often with subsidence of symptoms of arousal, hypervigilence and phobia. At this point, the DSM IV-based criteria of PTSD no longer specifically justify the diagnosis, and patients are usually given diagnoses of somatization disorder, dissociative disorder, conversion or depression. With time, the role of trauma in the patient's syndrome may be ignored. Although autonomic oscillation is still apparent, it is clear that the prevailing symptom complex reflects a state of parasympathetic dominance. Endocrinological measures now tend to show a state of low serum cortisol (Mason, et al, 1986, Yehuda et al, 1990), also commensurate with evolving parasympathetic tone. This trend is associated with behavioral responses including social isolation and withdrawal, substance abuse, constricted affect, denial, cognitive impairment and dissociation, all relatively parasympathetic states.
Another compelling rationale for this process may be drawn from the phylogenetic role of the parasympathetic nervous system, specifically the vagal system, as presented in the Polyvagal Theory of Emotion by Porges (1994). Porges emphasizes the phylogenetic layering of arousal responses in mammals, based on the varied functions of the vagal nuclei. The dorsal vagal complex (DVC), composed of the dorsal motor nucleus of the vagus and nucleus tractus solitarius, is a vestigial and primitive center, primarily useful in reptiles for energy conservation. In the low oxygen-demand system of the reptile, the DVC shuts down the energy-use system by inducing marked bradycardia and apnea, as in the reptilian dive reflex. The ventral vagal complex (VVC), unique to mammals, is a recent adaptation to the high oxygen need of this class of animals, and finely tunes energy utilization by subtle and flexible influences on heart rate. The early alerting response seen in animals consists of raising the head from grazing, orienting with the head to the source of the new, potentially threatening stimulus, widening of palpebral fissures, and sniffing for scents. This energy-conserving reflex is mediated by the VVC, and employs the locus ceruleus, which has rich connections with sense organs of the head, as well as the muscles of the head and neck. If sufficient information of threat is attained through this reflex, the VVC response is inhibited and the animal will progress to the neuromuscular and cardiovascular mechanisms of the epinephrine-based fight/flight response. If deterrence of the threat through defense or flight fails, the animal enters a state of helplessness, associated by a marked increase in DVC tone, initiating the freeze/immobility response. This state of deep parasympathetic tone is associated with marked bradycardia, apnea, sphinctor relaxation and gastrointestinal activation.
A persistent state of DVC activation, however, is common to reptiles, but in fact dangerous for mammals due to its association with marked bradycardia and life-threatening arrythmias. The spontaneous death of wild animals during induced states of immobility in the laboratory setting attests to this danger, as does the remarkable mortality rate of wild mammals introduced to the zoo environment (Seligman, 1987). In humans, this state of immobility and "suspended animation" perhaps has its most extreme expression in the phenomenon of Voodoo death, as described by Cannon (1942). The study of death in the freeze/immobility response in animals reveals that death occurs by cardiac arrest during diastole, or relaxation of the heart, in a state of complete cardiac flaccidity and engorgement with blood (Richter, 1957, Hofer, 1970). The extremes of vagal parasympathetic tone as manifested in the state of DVC activation therefore contribute greatly to the generation of severe emotions, especially those of terror and helplessness. Although freeze/ immobility states in mammals may be useful for short-term survival, prolongation or repeated activation of that state clearly has serious implications for health and long-term survival. The model of disease presented here suggests that the gradual descent into dissociation and parasympathetic dominance in chronic unresolved PTSD constitutes just such a state of peril.
[top] SOMATIC DISSOCIATION
As suggested earlier, dissociation may be accompanied by split or altered perceptions not only of self and reality, but also of parts or regions of the body. The clinical impairment experienced by the dissociated individual under those circumstances will almost always present as physical deficits that defy physiologic explanation by examination, laboratory tests or imaging studies. Diagnoses entertained by physicians in these states include hysteria, conversion and psychosomatic disorders. The cause for these states is uniformly assumed to be psychological, and the common factor to be stress. Almost all of the deficits have a neurological nature, and may affect any system, including visual, auditory, vestibular, speech, balance, sensation and motor function. Seizures and fainting are common expressions of this state.
Symptoms associated with conversion may appear to be exaggerated, and findings do not conform to those objectively seen in actual disease or injury of the nervous system. Thus, sensory loss usually presents in a "stocking/glove" distribution, rather than the layered dermatomal loss seen is lesions of the spinal cord. Weakness is diffuse and inconsistent, with a "give-away" quality. Symptoms are often one-sided, and findings may fluctuate in time, with ambient stress often enhancing the symptoms. Conversion symptoms occur more commonly in lower socioeconomic and less developed countries and cultures, and in women (American Psychiatric Association, 1994). From patient to patient and culture to culture, however, the seemingly varied syndromes of conversion have a remarkably constant theme that demands consideration of a common and as yet undefined neurophysiologic mechanism.
The medical literature does not address this attempted crossover between psychological and physiological factors in conversion and related disorders. Concepts presented in this model are based on the evaluations of thousand of patients who have experienced physical trauma in motor vehicle and other types of accidents, and who, to a varying degree, have also manifested symptoms of having been traumatized as well. Many of these patients have presented with symptoms and signs of conversion, and with minute observation of their physical states and behavioral symptoms, several conclusions appear to be inescapable.
Patients with conversion in this setting seldom present with la belle indifference, but rather exhibit early symptoms of arousal and distress consistent with PTSD. Their symptoms are remarkably common from patient to patient. Difficulties with speech elocution and mechanics are common, with word blocking, stutter and unusual dysarthric patterns of speech. One-sided or one upper extremity sensory loss is almost universal, associated with severe problems with dexterity on the same side. This sensory loss is invariably "non-physiological", often stocking and glove in distribution. Balance is impaired with variable swaying and staggering patterns not consistent with impairment of intrinsic brainstem balance centers. With careful observation, many such patients experience a physical sensation of arousal if the examiner presents a visual stimulus to them from a part of the room on the same side as their predominant non-physiologic symptoms. This pattern of arousal is most commonly experienced as nausea or dizziness, and may be associated with flushing, suggesting the influence of VVC activation as part of the early response to threat.
The concept of peripheral perceptual boundaries in psychological terms relates primarily to subtle areas of our sense of self that we perceive in relationship to others, the regions of appropriate limitations in personal and social interaction. In the model of somatic dissociation presented here, this concept of boundaries relates to an actual physical perceptual whole, or continuity of self, that represents the limits of the unconscious but perceived area defining the safe extent of our physical expression. The area comprising this space is directly proportional to the experience of previously unresolved life threats, and the continuity of the perceptual boundaries surrounding this space is dependant on the perceptual experience of severe threat within a specific boundary sector. Findings in testing the boundaries of a traumatized patient reveals that the area of a person's perception where they first experienced the warning of the impending threat (eg - the approaching automobile) will thereafter be an area where accessing any stimulus is intrinsically threatening. As a result, passing a hand around the periphery of that person's visual field at the distance of 3-4 feet will often produce an arousal response in the region of perception of prior threat. Such patients have developed a conditioned arousal reflex within areas of their perceptual surround, or boundary. Predictably, persistent ambient subliminal sensory perceptual experiences within that region, whether visual, tactile or proprioceptive in nature, will result in conditioned arousal and will perpetuate the kindled trauma reflex. Just as the chronic victim of PTSD will freeze or dissociate in the face of familiar threat, the part or region of the body representing the proprioceptive and somatic procedural memory for the threat experience will be selectively dissociated, leading to the nonphysiological signs of conversion. It will come as no surprise, therefore, that many patients with localized signs of conversion will experience symptoms of discomfort and arousal with presentation of visual or other seemingly benign stimuli within those regions of their boundary perception that now possess the sensory perception of threat.
In addition, with further close observation of such patients, one may detect unusual but reproducible physical changes in the dissociated portions of their body. My awareness of these physical phenomena began when one patient with "hysterical" right sided hemianesthesia, weakness and clumsiness related that her hairdresser had noted that her hair grew much more slowly on the right side, and was of a different texture. Close observation revealed that in addition, her hair was more sparse on the right side of her head. Examination of the patient's right hand and arm then revealed that her fingernails were broken and ridged, the hand was cooler than on the left, and finger hair growth was diminished. Close observation of other similar patients subsequently documented signs of dystrophic skin, hair and nail changes in many patients in parts of the body manifesting signs of conversion. Finally, several of these patients proceeded to develop clear-cut signs of sympathetically maintained pain, or reflex sympathetic dystrophy (RSD).
[top] REFLEX SYMPATHETIC DYSTROPHY
Sympathetically maintained pain, complex regional pain syndrome, and RSD comprise fairly common, well recognized but controversial and poorly understood pain syndromes, by definition associated with vasomotor autonomic symptoms and signs in the affected body parts. The extremities, especially their distal portions, are predominantly affected. Described by S. Wier Mitchell in the Civil War, the syndrome perhaps is most common in traumatic injuries of the extremities, but also may follow seemingly trivial injuries such as minor bruises or overuse injuries (Mitchell, et al, 1864, Schwartzman & McLellan, 1987). The syndrome is characterized by severe, often burning pain in the affected area, associated with variable signs of vasomotor dysfunction, both parasympathetic and sympathetic. These signs may include abnormal hair growth or loss, erythema and warmth, or pallor and coolness.
With unsuccessful treatment and progression of the syndrome, signs of vasoconstriction and dystrophy predominate, hence to term sympathetic. Attribution of the syndrome to abnormal sympathetic autonomic tone is supported at least in part by the fact that the injection of related ganglia of the sympathetic nervous system may provide variable relief of pain. Many investigators feel that the central nervous system may be involved. Dystonic postures of the affected limbs are common. Electromyographic and nerve conduction studies of RSD reveal that the character of this dystonia is more typical of voluntary holding of the posture than of comparable dystonias in patients with brain lesions (Koelman, et al, 1999). The authors go so far as to say, "In causalgia-dystonia, central motor control may be altered by a trauma in such a way that the affected limb is dissociated from normal regulatory mechanisms" (p. 2198).
The model presented here proposes that regional somatic dissociation exposes the dissociated member or region of the body to selective vulnerability to the effects of existing cyclical and oscillatory autonomic dysfunction associated with the neurophysiological changes of unresolved trauma. In this state, that region or part may then be vulnerable to vasomotor oscillation, with vasoconstriction and functional reduction in blood flow ultimately creating the ischemic tissue pathology characteristic of RSD. This syndrome, as often is the case, comprises a continuum, or spectrum of clinical expression, from the subtle signs seen in most patients, to the full-blown pain, dystrophic changes and dystonia of RSD. Dissociation, by this model, is a neurophysiological syndrome of central nervous system origin. It is initiated by a failed attempt at defensive/escape efforts at the moment of a life threat, and is perpetuated if spontaneous recovery from the resulting freeze response is blocked or truncated. Lack of recovery from this freeze response results in conditioned association of all sensorimotor information assimilated at the time of the traumatic event into procedural memory, to be resurrected at times of subsequent perceived threat as a primitive conditioned survival reflex. This procedural memory acquisition initially is elicited by internal and external cue-specific stimuli, but because the threat itself has not been resolved, internal cues persist without inhibition from external messages of safety, and kindling is triggered in the cortical, limbic and brainstem centers previously discussed. Recurrent dissociation in response to arousal accompanies this cycle and facilitates the development of pathologic autonomic oscillation. Physiologic inhibition of perception of those parts or regions of the body for which the brain holds procedural memory of their sensory input at the time of the threat results in the syndrome of conversion and regional somatic dissociation. Divorced from the normal trophic benefits of cerebral perception, these regions are subject to the extremes of vasomotor instability of late trauma, and develop syndromes of pathologic vasoconstriction and ischemia, leading to RSD.
[top] THE DISEASES OF TRAUMA
Selye (1936) has generally been credited with the concept that prolonged or excessive exposure to stress could contribute to the development of a group of specific diseases. These diseases predominantly reflected exposure to elevated levels of adrenal cortical hormones as part of the modulating role of cortisol on the hypothalamic/pituitary/adrenal (HPA) axis in stress. Thus rats exposed to prolonged and excessive stress developed erosion of the gastric mucosa, atherosclerosis and adrenal cortical atrophy. Other specific pathologic effects of excessive cortisol exposure include immune suppression, elevated serum lipids and atherosclerosis, diabetes, osteoporosis, hypertension, peptic ulcer disease, obesity and cognitive/emotional impairment. Many of these effects are now well described in the medical and lay literature as "diseases of stress".
The relationship of the long-term effects of trauma (as opposed to stress) and disease are less well documented. Whereas ongoing stress is easily identified, the past experience of traumatization is masked by the evolution of the resulting syndrome into experiences, symptoms and behaviors that ultimately are attributed to characterological and psychological causes - i.e. - that are due to internal rather than external events. This perception is basically correct in that the internal events in trauma are self-driven and capable of changing somatic physiology in the absence of external influences. This concept is also in keeping with the physiologic effects of somatic dissociation, which are driven by internal brain-based mechanisms that are self-perpetuating. Therefore, one would not expect the diseases of trauma to reflect the generally cortisol-based syndromes of acute and even chronic exogenous stress. Rather, one would predict that diseases of trauma would reflect autonomic regulatory impairment, both sympathetic and parasympathetic, with a predominance of vagal and parasympathetic syndromes in the later stages.
This model of disease in trauma would predict that vasomotor symptoms and signs would be likely, with both trophic and dystrophic components, the latter reflecting vasoconstriction and ischemia. Cardiac, pulmonary, bowel and exocrine gland dysfunction should be predictable. Abnormalities of strength, muscle tone and endurance should be common. Lowering of serum cortisol in late stages of trauma might lead to relative lack of immune inhibition, and therefore to hyperimmune syndromes. One would also expect these syndromes in some cases to manifest remarkable periods of exacerbation and remission based on autonomic oscillation, and to be specifically sensitive to exacerbation by external stress. Fluctuating symptoms of cognitive impairment especially related to attention and memory would be common in many of these conditions. One would expect an unusual association of the emotional symptoms of late trauma, including affect dysregulation, dissociation, somatization, depression, hypervigilance and denial/avoidance. A psychosocial trauma history in many cases might reflect a history of substantial life trauma, especially in childhood.
Among other manifestations, these diseases would at least in part show evidence of abnormal parasympathetic tone, perhaps along with sympathetic vasoconstrictive dystrophic and ulcerative phenomenona. Diseases and syndromes of the gastrointestinal system that fall into this general concept of diseases of trauma include peptic ulcer and gastroesophageal reflux disease, irritable bowel syndrome, Crohn's disease (regional ileitis) and ulcerative colitis. All reflect organ hypermotility, excessive glandular secretion and in some, ulcerative features. Cardiac syndromes would likely reflect the cardiac abnormalities associated with DVC dominance, and be associated with a variety of tachy- and bradyarrythmias, including those seen in mitral valve prolapse. Bronchial asthma, a syndrome primarily manifested by stress and hyperimmune-induced abnormal organ-specific parasympathetic events (bronchospasm and hypersecretion) has many of the criteria predictable in diseases of trauma. Interstitial cystitis is a condition characterized by pain, spasm and ulceration of the bladder wall, combining the parasympathetic/dystrophic elements of many of these syndromes.
One of the most perplexing and controversial chronic syndromes that may fall into this category is that of fibromyalgia/chronic fatigue. Protean symptoms include diffuse and severe musculoskeletal pain, impaired and nonrestorative sleep with chronic fatigue, stiffness, headaches, anxiety, hypervigilance, cognitive impairment, ocular and vestibular symptoms and paresthesias. Associated syndromes include irritable bowel syndrome, interstitial cystitis, mitral valve prolapse, and esophageal dysfunction (Clauw, 1995). Low serum cortisol and HPA axis dysfunction similar to that in late PTSD have been documented (Crofford, 1996). Fibromyalgia syndrome primarily affects women, and controversial but suggestive evidence for an increased incidence of childhood sexual and physical trauma in fibromyalgia patients has been documented (Boisset, et al, 1995). Fibromyalgia arising de novo from a traumatic experience has been well-documented (Waylonis & Perkins, 1994). While recognizing that overwhelming circumstantial evidence does not constitute medical scientific proof, fibromyalgia/chronic fatigue syndrome appears to present a prototypic syndrome for the model of the diseases of autonomic dysfunction seen in late trauma.
The rationale for RSD as a dissociative/autonomic posttraumatic disease has been presented. Chronic pain in instances where documented structural pathology is not apparent very likely represents another syndrome of late trauma. Phantom limb pain appears to represent the prototype for this model. This syndrome occurs much more commonly when the amputation was associated with a traumatic injury. Persisting representation of pain in an absent organ or body part suggests procedural memory for that pain as a conditioned response. The critical element for that memory to be conditioned, of course, is the unresolved threat associated with the injury producing the pain itself. One must remember that severe pain itself may be traumatizing, and that the medical system in which that pain was managed has many potential sources of traumatic stress (Scaer, 2001, Chapter 9). Conditioned imprinting of pain in procedural memory of course implies that trauma will have occurred in a state of helplessness without opportunity for spontaneous resolution of a freeze response. Under those circumstances, the specific pain will continue to represent the threat, and be retained for late survival purposes in conditioned procedural memory.
An underlying state of vulnerability to traumatization would also be a predictable substrate for the development of chronic pain in the injured individual. Victims of child abuse or multiple prior traumatic events clearly possess this vulnerability, and would be predicted to be susceptible to the incorporation of a newly painful experience into procedural memory in the model described above. The trauma literature amply documents the high incidence of chronic pain of many types seen in victims of child abuse relative to the general population. Types of pain represented in these studies include pelvic, back, abdominal, head, orofacial pain, and chronic pain in general. Also documented is the extremely high incidence of childhood abuse in patients referred to centers for chronic pain treatment (Rapkin, et al, 1990, Wurtele, et al, 1990, Toomey, et al, 1993, Walling, et al, I, 1994,Walling, et al, II, 1994,).
A number of studies and proposed models of disease suggest that trauma may in part contribute to the autoimmune diseases. As noted, the lower serum cortisol documented in late PTSD might be related to increased immune activities in vivo (Yehuda, et al, 1993). Indeed, Watson et al (1993) have documented increased reactivity of skin to antigens in combat-related PTSD (Watson, et al, 1993). Other authors have specifically proposed that the low cortisol state of late PTSD might well present the substrate for a hyperimmune state (Friedman, & Schnurr, 1995, p. 518). More recently, the ratio of lymphocytic phenotypes documented in victims of childhood sexual abuse with PTSD showed a pattern indicative of lymphocytic activation. This finding supports the likelihood of increased immune activity in these patients, suggesting the potential for a hyperimmune state in late PTSD (Wilson, et al, 1999). Supported by an exhaustive literature review, Rothschild and Masi present a strong argument for a vascular hypothesis for rheumatoid arthritis (RA) incorporating as a cardinal feature vasoconstriction and tissue hypoxia, both of which have been well-documented in RA. Hypoxia of the arteriolar wall leads to vascular permeability with release of antigens into surrounding tissues. The resulting immune response therefore represents a relatively secondary feature of RA (Rothschild, & Masi, 1982). This theory, supported by an extensive array of studies, is in keeping with the model of autonomic and vasomotor dysfunction presented previously as a template for trauma-related disease processes. Such findings by no means provide a specific link between prior trauma and the autoimmune diseases, but suggest an avenue for further investigation of a possible relationship between trauma and autoimmune processes.
Perhaps a more compelling and immediate avenue for investigation relates to the studies of morbidity and mortality in trauma. Victims of trauma have long been known to experience increased morbidity and mortality rates (Friedman & Schnurr, 1995). Many of these studies focus on the late health problems of former prisoners of war (POW's) (Beebe, 1975, Page, 1992). Cardiovascular and gastrointestinal diseases predominate in this group of late trauma victims, although emotional sequellae related to depression and cirrhosis of the liver associated with alcoholism contributed significantly to mortality. When the diagnosis of PTSD is added to the equation, however, the health effects of trauma are noted to increase substantially, with the cardiovascular diseases predominating (Friedman & Schnurr, 1955, Wolff, et al, 1994,).
From the early morbidity intrinsic to Selye's model of stress, to the late effects of autonomic dysregulation, and pathologic vagal dominance, the potential and real health effects of trauma are clear. Unfortunately, the trauma necessary to place the individual at risk may be as subtle as adverse childhood experiences. Felitti et al, (1998) found a strong graded relationship between the breadth of exposure to abuse or family dysfunction during childhood and multiple risk factors for several of the leading causes of death in adults (Felitti, et al, 1998). Adult diseases that were endemic in those who had experienced childhood abuse or family dysfunction included ischemic heart disease, cancer, chronic lung disease, skeletal fractures, obesity and liver disease. Additional diseases attributable to risk exposure and behavior included sexually transmitted disease, alcoholism, drug abuse, depression and suicide. This study is particularly disturbing in that it shows that the "trauma" of childhood in these high-morbidity cases was often as indirect as living with family members who were mentally ill or substance abusers. The sensitivity and vulnerability of the developing child to a loss of nurturing and safe boundary structure, and the adverse effects of this loss throughout life on emotional and physical health appear to be frighteningly clear.
[top] CONCLUSION
We have presented a model of altered brain function precipitated by a traumatic event whose completion or resolution was truncated or aborted by lack of spontaneous resolution of a freeze/immobility response, a phenomenon closely allied to the clinical psychological state of dissociation. In addition to the arbitrary psychiatric diagnosis of PTSD, this state is associated with a complex set of somatic pathologic events characterized by cyclical autonomic dysregulation, and an evolving state of vagal dominance involving primarily the dorsal vagal nucleus. The sympathetic portion of this cyclical physiologic complex primarily involves vasoconstriction, with dystrophic and ischemic regional changes, especially in regions of the body that have been subject to dissociation due to their residual representation of sensory messages of threat stored in procedural memory. The experimental model of kindling is intrinsic to the self-perpetuation of this pathologic process, driven by internal cues derived from unresolved procedural memory of threat, and enhanced by endorphinergic mechanisms inherent to both the initial response to threat, and to subsequent freeze/dissociation.
In this context, a variety of chronic diseases are postulated to represent late somatic expressions of traumatic stress. These diseases are of remarkably varied expression, but with a common thread of autonomic cyclical instability, frequently subtle vasoconstrictive/ischemic features, and usually pain. They are generally distinct from those diseases frequently attributed to stress, although these "stress-related" diseases often occur simultaneously and are definitely also more frequent in the adult population of those persons who have experienced trauma.
This model rejects the concept that the terms "somatization", "conversion", "hysterical", "psychological", or "psychosomatic" have any viable meaning in the definition of a symptom complex or disease state. It places all of these terms in a pathologic somatic context associated with subtle, but definable and objective clinical findings and manifestations of disease. It moves beyond the concept of mind/body medicine to the concept of a mind/brain/body continuum.
By attempting to isolate psychosomatic disease processes into a distinct category, we are ignoring perhaps the major cause for the group of diseases that members of the healing professions probably understand the least, and treat the most ineffectively - chronic diseases of unknown cause. Many of these diseases are due to impairment of regulation, rather than due to the invasion of microbes, toxins or other extrinsic agents. As such, they present a unique opportunity for those practitioners, researchers and teachers in the area of applied psychophysiology and biofeedback who have dealt with concepts of self-regulation and healing for the past 40 years. If one accepts the concepts of myofascial pain, visceral dysfunction, chronic pain and systemic diseases such as fibromyalgia presented above, it quickly becomes apparent that biofeedback practitioners have been treating symptoms and conditions primarily driven by past trauma in most of their patients. Not surprisingly, their techniques have often been more effective than polypharmacy and many medical/surgical techniques. Application of advanced techniques such as cerebral regulation through neurofeedback and autonomic regulation through control of heart rate variability (HRV) may have profound implications for healing trauma by providing a unique means of access to the conditioned autonomic responses that drive the trauma reflex.
Finally, as clinicians, we must look beyond the dysfunctional behavior apparent in many of these patients, to the neurophysiological and autonomic dysregulation that is the source of their symptoms and eventually their disease. Medical science must shed the concept that a symptom not measurable by current technology is "psychological", and therefore invalid. And physicians must reject the pejorative implications of the term somatization, and stop further traumatization of patients by subtly implied rejection.
[top] BIBLIOGRAPHY
Alexander, M. (1992). Neuropsychiatric correlates of persistent postconcussive syndrome, Journal of Head Trauma Rehabilitation, 43:29-45 American Psychiatric Association (APA)). (1980), Diagnostic and statistical manual of mental diseases, (3rd edition), Washington, D.C. American Psychiatric Association (APA). (1994), Diagnostic and statistical manual of mental diseases, (4th edition), Washington D.C. Antelman, S., Caggiula, S., Kiss, D., Edwards, D., Kocan, D., Stiller, T. (1995). Neurochemical and physiological effects of cocaine oscillate with sequential drug treatment: possibly a major factor in drug variability, Neuropsychopharmacology, 12:297-306 Antelman, S., Caggiula, A. (1996). Oscillation follows drug implications, Critical Revue of Neurobiology, 10:101-117 Antelman, S., Caggiula, A., Gershon, S., Edwards, D., Austin, M., Kiss, S., Kocan, D. (1997). Stressor-induced oscillation: A possible model of the bidirectional symptoms of PTSD, New York Academy of Sciences, 21:296-305 Beebe, G. (1975). Followup studies of World War II and Korean War prisoners: II Morbidity, disability, and maladjustments, American Journal of Epidemiology, 101:400-422 Beecher, H. (1946). Pain in men wounded in battle, Annals of Surgery, 123:96-105 Boisset-Pioro, M., Esdaile, J., Fitzcharles, M. (1995). Sexual and physical abuse in women with fibromyalgia syndrome, Arthritis and Rheumatism, 38(2):235-241 Bremner, J., Southwick, S., Brett, E., Fontana, A., Rosinheck, R., Charney, D.: (1992). Dissociation and posttraumatic stress disorder in Vietnam combat veterans, American Journal of Psychiatry, 149:328-332 Bremner, J., Scott, T., Delaney, R., Southwick, S., Mason, J., Johnson, D., Innis, R., McCarthy, G., & Charney, D. (1993). Deficits in short-term memory in posttraumatic stress disorder, American Journal of Psychiatry, 150(7):1015-1019 Cannon, W. (1942). "Voodoo" death
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