The amygdala has first crack at threat-detection. If it pattern-matches for a threat, it initiates physiology we can’t ignore. Half a second later, the frontal cortex learns about it. We react first, then we get a chance to think about it. It’s already too late.
“Front-running” is an illegal activity in stockbroking whereby brokers profit at the expense of their clients by acting first on information their clients don’t have.
Trauma is a “stuck” pattern-match in the amygdala.
Using foreknowledge of the trauma trigger, we can front-run the usual reaction, NOT allow the existing protein synthesis pathway to occur (ie. not reconsolidated the same way) and then the amygdala learns “Honestly, I’m safe now. No, really. Calm down already”. The unwanted conditioned emotional response is extinguished. Emotional memories become cognitive ones.
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havening.org - A Better Life Through Neuroscience
new treatment for people who suffer from life-limiting phobias, anger, grief or pain, or who are unable to overcome post-traumatic stress issues.
remove memories with touch, erase the trauma associated with bad memories without surgery, talk therapy or drugs.
Series Editor’s Foreword
For more than 40 years, starting with Stress Disorders Among Vietnam Veterans (1978), the Routledge (originally Brunner/Mazel) Psychosocial Stress Series has published important breakthroughs in the study and treatment of the traumatized.
The book When the Past Is Always Present: Emotional Traumatization, Causes, and Cures by Ronald Ruden, MD, PhD, an internist and clinical research scientist in New York City, is a welcomed and appropriate addition to the series. Ruden’s work was familiar to me because of his theoretical treatises published in Traumatology between 2005 and 2009. Each were widely read and considered by the editorial board and ad hoc reviewer specialists to be significant contributions to an emerging field in the treatment of traumatization.
For the series, I suggested that Dr. Ruden formulate a book for the busy professional, so that practitioners would be able to pick up the book and quickly get the feel for what he had to say, and then be able use the therapeutic procedures he describes to help their clients. The publisher and I agree that Dr. Ruden has succeeded in this task.
Some who read this book will be incredulous, as were most of the reviewers for Traumatology, in the beginning. Eventually, the journal reviewers and those who reviewed the proposal for the book and this final version grasped the importance of this new paradigm and began to appreciate the positive implications of this orientation.
Dr. Ruden presents a neurobiological theory for the effectiveness of a type of exposure therapy that involves emotionally reexperiencing a trauma coupled with sensory stimulation. This theory synthesizes evolutionary biology with current neuroscience research and provides an explanation for the mysterious success of some odd and still controversial alternative therapies. Importantly, he offers suggestions for recognizing symptoms that could arise from a traumatization, and concludes that once recognized, a therapist should actively seek their traumatic origin so the event can be recalled and treated. Dr. Ruden then takes his findings one step further and suggests a new biologically consonant therapy he calls havening. This curious word, derived from the word haven, means to put into a safe place. Dr. Ruden and others believe that the ability to find a haven, while experiencing an intense emotional event, is at the core for both preventing and de-encoding a traumatic memory.
How is this accomplished? Why should this work? This book introduces the concept of psychosensory therapy, the use of sensory input to alter an emotionally traumatized brain. Before operationally defining traumatization, Dr. Ruden describes the conditions necessary and sufficient for a traumatic encoding moment. The consequences of this encoding are then illuminated. Dr. Ruden outlines in a general fashion the biology for curing a traumatization. He then specifically illustrates how applying havening fools the brain into believing a haven has been found, leading to a cure of the direct consequences of traumatization. For Dr. Ruden, a cure means that stimuli that had previously released stress chemicals and caused the reexperiencing of some or all of the encoded traumatic event are no longer able to do so. He does this without drugs or talk therapy.
The Psychosocial Stress Series, the oldest of its kind in the area of traumatic and systemic stress, welcomes this book with enthusiasm. While not the final word, it offers a different approach that will ultimately allow us to make traumatic memories a thing of the past.
Charles Figley, PhD Series Editor New Orleans, Louisiana
Treating the Phobic and Anxious Dental Patient: Introduction to Havening Therapy Steven J. Ruden, DDS, and Ronald A. Ruden, MD, PhD Dentistry Today, April 2010 This paper introduces a new therapeutic modality and suggests a neurobiological mechanism for its effectiveness. We call this Havening Therapy, as in “find a safe haven.” This approach utilizes the extrasensory aspect of touch to alter pathways that create distress.
Of all the emotional states we experience, none is more primitive or powerful than fear. If we understand how a fear response is disrupted, we may be able to understand how tapping works.
We believe that ‘affect activation’ is the critical aspect for success of this method. One needs to elicit the actual target emotions, in vivo, in order to interrupt the pathway. During affect activation, we propose that glutamate is locally released in areas corresponding to the neural circuit that initially encoded the conditioned fear. Without local release of glutamate, no amount of tapping or sensory stimulation will be effective. We hypothesize that multi-sensory stimulation (tapping, massage, eye movement, etc.) causes a generalized release of serotonin via ascending pathways. This release is non-specific and global, that is, it is not related to the content or context of the feared object. (Fig 7). This release is different than that seen by desensitization or extinction training that alters serotonin levels in the prefrontal cortex. (Santini, E, Ge H, Ren K, Pena De Ortiz S, Quirk, GJ 2004) Multi-sensory stimulation affects the entire brain including the amygdala and prefrontal cortex.
when activation of an emotional response to a thought is followed by a simple procedure, the emotional response to the event appears to have vanished, often for good.
Posttraumatic stress disorder (PTSD) is a chronic and sometimes progressive illness. It has been hypothesized that PTSD is encoded in such a way that retrieval of a traumatic memory not only causes the individual to experience fear but also reconsolidates the linkage between the memory and the fear response, thus preventing desensitization. Recent work on conditioned fear, however, has shown that reactivation of these consolidated memories returns them to a protein synthetic—dependent state that makes the linkage subject to disruption. This article describes a theoretical model for the surprising effectiveness of a therapy for PTSD. It is proposed that, after activation of the fear response, tapping on certain areas of the body increases serotonin release. This increase in serotonin appears to disrupt the linkage between the thought and the emotional response. Using this approach, other disorders such as phobias, certain types of chronic pain, and other pathologically encoded negative emotive states may also be curable.
Tapping, which would never occur under natural conditions of survival, takes advantage of the moment when this connection is susceptible to disruption. The key is to activate the pathway that produces the fear response in the amygdala making it labile and subject to disruption. The end result is emotional amnesia for the event
Pain that is ‘un-anatomical’ in distribution, for which there is no peripheral lesion and that resists traditional treatment should be considered to be of psychogenic origin. The term Complex Psychogenic Pain (CPP) can be used when autonomic changes, such as temperature abnormalities, and physical findings such as tenderness, accompany the pain. It is proposed that CPP is co-encoded centrally during a traumatizing event where the individual experiences rage or fear with concomitant pain but is constrained from responding to the circumstances. CPP is encoded as dissociated from the event. However subsequent subconscious stimuli that recreate similar emotional, somatosensory or cognitive states can activate a re-perception of the traumatic pain and engage various vasomotor processes. We speculate that CPP is generated from amygdala efferents and is encoded in such a manner that precludes simple forgetting. Therapy consists of either disrupting re-consolidation of the amygdala based linkage between the memory and the emotional/somatosensory response or directly inhibiting amygdala outflow. Successful therapy extinguishes the pain.
Traumatic memories will auto-reconsolidate unless an inhibitory process is initiated. Thus, subsequent subconscious stimuli associated with the event have the potential to reactivate the pain. They can be physical, emotional or somatosensory, and since the pain is dissociated, will have no cognitive relationship to the encoding event. To clarify this, an example is instructive. In this case a young women presented with severe hand pain of three months duration. There were no obvious peripheral lesions nor was any recent history of trauma present. A detailed history revealed however that 15 years prior she had been involved in a taxi accident in London where her hand, in the exact location where she currently experienced pain, swung around and hit her face, breaking her nose. The encoding of the traumatizing event occurred during a life-threatening accident where she could not escape. Three months ago, when she had made the decision to return to that city, the pain appeared. She was completely unaware of any connection between the accident and the current hand pain.
The process of reconsolidation is fundamentally different from consolidation of the original traumatizing event. That is, re-consolidation does not recapitulate consolidation (Bahar & Dorfman & Dudai 2004). If reconsolidation involves a final common pathway, then disrupting this pathway could potentially prevent all associative stimuli, including dissociated stimuli, from activating the BLA efferents and subsequent activation of the central nucleus that produce biological effects. We speculate that inhibition of the re-consolidation can be accomplished by various maneuvers that release serotonin. Such maneuvers have an analogy to massage (Field 2005). That is, we need to induce a rise of serotonin after activation of the memory when the linkage between the LA and BLA is in a protein synthetic dependent state. We speculate that serotonin disrupts this pathway by activating GABA inhibitory receptors that cause release of GABA (Ruden 2007) (Stutzman & LeDoux 1999) in the BLA and locus coeruleus. These GABA receptors inhibit glutamate directed protein synthesis as well as glutamate activated release of norepinephrine from the locus coeruleus.
Levine has shown that if one can physically and/or imaginatively replicate the fleeing part and be guided to an imagined safe place, protein synthesis may be inhibited and the encoding disrupted. This is the concept that Peter Levine uses in a method called Somatic Experiencing (SE). SE explores the ‘body memory’, what Levine calls a ‘felt sense’. This ‘felt sense’ represents the somatosensory memory of a traumatizing event and may activate the release of glutamate in the LC and BLA. Patients will try to bring this felt sense to consciousness and then be guided to an imaginary safe place. Dr. Levine’s approach uses the physical aspects of the event and helps the patient complete the behavioral response to the traumatizing event, finding safety, thus removing the encoded trauma. It is speculated that imaginatively running and finding a safe place raises serotonin and disrupts protein synthesis. It is extremely helpful in situations where the cognitive and emotional components are dissociated.
The consequences of inhibiting the reconsolidation are to de-link the relationship between the memory of the event and the somatosensory component. Thus, there is a loss of the ability for stimuli to activate pain.
The young woman whose hand was injured, was able to recall in vivid detail the accident where she was clearly traumatized. We applied the tapping procedure to this memory and the hand pain instantly disappeared when memory of the trauma was delinked from the emotional response.
When the Past Is Always Present: Emotional Traumatization, Causes, and Cures introduces several new ideas about trauma and trauma treatment. The first of these is that another way to treat disorders arising from the mind/brain may be to use the senses. This idea, which is at the core of psychosensory therapy, forms what the author considers the “third pillar” of trauma treatment (the first and second pillars being psychotherapy and psychopharmacology). Psychosensory therapy postulates that sensory input-for example, touch-creates extrasensory activity that alters brain function and the way we respond to stimuli.
“There are haunted souls.” a model for the formation and extinguishing of traumatic memories
I know and recommend Lizzie Bryher, Havening Practitioner, London UK
Want to front-run your amygdala? Say hello