Self-Regulation Therapy (SRT) is a body based treatment that exploits the innate ability of sub-cortical brain structures to regulate arousal (Josephs & Zettl, 2001)*. Useful in the treatment of post trauma symptoms such as anxiety, panic, rage, hypervigilance, and dissociation, it is best described for its effectiveness in working with autonomic nervous system dysregulation.
Both cognitive and affect regulation are essential components of SRT. However, it is the addition of the somatosensory elements whereby SRT provides relief from the somatic symptoms of dysregulation. Its formulation builds from a growing body of evidence that directly links neurobiology to psychological processes.
Trauma changes the brain in very specific ways. These changes profoundly compromise the capacity to regulate autonomic arousal and in turn, handle everyday stress. Moreover, we believe individuals who suffer from heightened arousal are more vulnerable to developing psychological disorders. These substantive changes involve cognitive, affective, somatic and physiological neurons. We witness them through dentritic`shrinkage’, hippocampal damage, memory problems and over-activation of the amygdala, characterized by `kindled’ affect dysregulation.
Self-regulation of the autonomic nervous system has increasingly been recognized as an important factor in the etiology of several psychological and physiological problems. Clinical problems such as PTSD, anxiety based disorders including simple phobias, mood disorders, Reflex Sympathetic Dystrophy, eating disorders and some learning disorders such as ADHD are all characterized by ANS dysregulation (Josephs, & Zettl, TTB II, 2001; Perry, 1999; Scaer, R., 2001; Van der Kolk, et al., 1996).
Persistent dysregulation compells many individuals to seek various means for controlling or numbing the activation. Their inevitable failure to effectively regulate their system is believed to be the driving force behind addictive behaviours such as alcoholism and drug use or forms of distraction such as hyperactivity, aggression self-mutilation and/or avoidance behaviours (Josephs, & Zettl, TTB III, 2001; Van der Kolk, B., 1989).
Self-Regulation Therapy is a body-centered psychotherapy that uses the natural healing abilities of sub-cortical structures to regulate arousal. SRT attempts to return the ANS to a homeostatic balance and to interrupt unconscious processes that dysregulate healthy functioning. The benefits of SRT include the restoration of healthy boundaries, defensive orienting and a sense of safety. In time, clients develop the ability to modulate emotional and behavioural responses and the capacity to self-soothe. SRT addresses both physical and psychological aspects of trauma related symptoms, and in doing so, improve the resiliency of the autonomic nervous system (Joseph & Zettl, TTB I – IV, 2000-2001).
Each session using SRT is carefully orchestrated in its attempt to keep the client in a range of tolerable activation. The client is encouraged to track their attention on those aspects as they arise, often but not always, in the context of the traumatic material. Through careful observation of the clinical presentation (characterized by sympathetic arousal or parasympathetic downregulation) and in combination with client reportage, repeated exposures of trauma material are renegotiated via the ANS. The client is largely able to do so through resources established in the context of a safe therapeutic environment.
Resources entail anything that somatically resonates in a positive way. Working via imagination, clients evoke resources such as nature, supportive family and friends, memories, strengths, passions, and humour, among others. For many, finding resources within their own bodies serves as an immediate stabilization.
One of the difficulties in working with shock trauma is the danger of exposing the client to the full impact of this energy, re-traumatizing them with the initial trauma experience. Flashbacks in the session might represent a clear sign of activation that’s been triggered too fast. Calibrating with minute quantities of activation however, enables a reintegration—not a reliving—of the trauma material. Attending to minute exposures of trauma material the client is able to gently titrate between the two, reducing the activation and associated somatic symptoms with the original trauma. As clients learn to self regulate they a gain a sense of greater control, over what was previously felt as unpredictable and intractable symptoms.
Important implications for clinical practice are evident in our understanding of the triune brain. The phylogenetic development of the brain dictates that the lower, earlier formed, ‘reptilian’ brain‘ potentiates the human response to threat. Even though higher level structures are more complex in their operation they depend, in part on the optimal functioning of the lower level centres. The lower cortical structures, namely the brain stem and limbic system, are responsible for regulation/dysregulation of ANS activation and resulting somatic symptoms.
This is why strictly cognitive (often known as “talk therapy”) and/or emotional therapies fall short; they fail to access the core of the shock trauma. Like reptiles and mammals in our response to threat, we store trauma in the lower cortical structures. Cognitions are limited in their ability to access these areas. Furthermore, it is likely that premature cognitive exploration risks miss-attributions and false memories.
Indeed, clinical experience shows that a high level of activation often compromises the individuals’ capacity to process cognitive and emotional material. Pat Ogden (2000) who also utilizes a somatic approach describes the dynamic: “…clients affective and cognitive information processing may be `driven’ by an underlying dysregulated arousal, causing emotions to escalate and thoughts to revolve around and around in circles”. For similar reasons, SRT typically leans heavily on body-centered processing in the initial part of treatment. This provides a more stable baseline from which to clarify issues related to cognitive-emotional aspects of the trauma.
The `kindled’ limbic amygdala’s (Post, 1995) has frequently been cited as a model to explain the effects of trauma at a micro level. This work is important in illustrating how SRT is believed to be effective. It is worth briefly repeating here:
A small amount of electricity (10th of a millivolt) was delivered to the amygdala of laboratory rats. A typical observation is a spike in the frequency and an immediate return to baseline. Over the course of 6 weeks however this baseline actually rises and is maintained at a higher pre-experimental level. This “kindled” brain provides an excellent illustration of the impact of trauma on the nervous system. Symptoms such as agitation, hyperactivity and `in your face’ sensitivity to stimulation, may be expressions of a `kindled’ brain.
Whether your amygdala has experienced a lot of `stimulation’ may make a difference in the way you respond to trauma. In some instances when the nervous system has been severely compromised by a history of trauma, a “small,” or what would typically be considered an insignificant event, can tip the scales and cause severe symptom presentation. Hence we might see a puzzling array of symptoms in a patient who recently had a 10-km fender bender. Conversely, this model might also explain for instance, the individual who survives a horrific traumatic event with no apparent ill effects.
For the clinical work of SRT, the really exciting work with the `kindled’ amygdala followed when the stimulation was reduced to 1/100th of a millivolt, a process known as quenching. The baseline not only recovers, but remarkably, to pre-kindled levels! Paradoxically further stimulation has led to a reduction in `kindling’. We believe this may provide one explanation for what we are witnessing in our own practices. When later trauma are resolved in a more resourced manner, it has a reparative impact on earlier trauma.
Understanding how the brain stores trauma memories underscores the role of sub-cortical structures and explains the enduring persistence of many trauma symptoms. Acting under the `prime directive’ for survival, the brain is `overdetermined’ to receive and store information from all senses both internally and externally (Perry, 1999). Incoming information is first received by the brain stem and mid brain structures which compares it to previously stored “memories”. This process occurs in a matter of milliseconds often well before cortical centres in the brain have a chance to make interpretations and plan for action. When the threat is perceived, enormous resources are unleashed and immediately this neurochemical mix consolidates—sometimes in one trial learning—somatosensory information and its’ association to danger.
The capacity of the brain to form associations is adaptive, allowing for rapid responding, even though the risk of false positives is increased. The Vietnam vet who jumps at the sound of a car backfiring knows the sound is from a car, but his body has already responded. Often however, these associations may be buried so deeply within lower cortical brain that one may be completely unaware of what triggered a sense of fear or why one feels so badly. Hence it is in the lower brain structures where one senses anxiety; it is within the higher cortical centres wherein interpretation and often false attributions are made. (Perry, 1999).
Even positive activities that trigger a neuronal pattern of arousal are interpreted by the brainstem as signs of danger. A rapid increase in heart rate for the recent heart attack victim is associated with a deadly threat; subsequent increases in heart rates as with intimate relations evokes high activation. Hence trauma sufferers will report difficulties in responding emotionally to their partners; intimate relations serve to retrigger trauma symptoms and evoke avoidance behaviours.
Somatosensory memory also known as procedural memory, which includes memories and associations, is transmitted via the amygdala. It differs from the more widely known declarative, explicit memories which travels via pathways in the hippocampus and the prefrontal cortex. Declarative memory includes facts and events and is notoriously subject to decay. Procedural memory however, includes those enduring habits, emotional associations and conditioned responses that make up the unconscious aspects of behaviour. Procedural memory is a type of implicit memory and is extremely resistant to decay. It is likened to a “body memory” and is one of the reasons for the intractable conditioning that “perpetuates the neural cycle of trauma and dissociation” (Scaer, 2001).
SRT enables access to procedural memory. SRT accesses this information via the language of the lower cortical structures: through kinesthetic, and proprioceptive senses; internally, through respiration, heart rate, temperature, muscular tensing; through image (visual, tactile, auditory, gustatory and olfactory), involuntary movement (including twitches, postural and gestural movements), and the `felt sense’ (Gendlin, 1978) which includes but is greater than affect. Clinical practice shows that a final element, meaning-making follows resolution of the trauma activation. Using sensory modalities also affords the opportunity to work with repressed material only available non-verbally. The process involves those aspects of the traumatic event that has been dissociated and those that have been overcoupled or joined with the experience (Joseph & Zettl, 2001).
That trauma memories are stored in a state-dependent way necessitates that those areas in the brain responsible need to be activated in order for new learning to take place. In the same way that a client who is dealing with acute grief must experience it in order to for to dissipate, unresolved sensorimotor reactions must be experienced for a reintegration to occur. These resolutions include for example defensive maneuvers that, `if given enough time, strength, resources etc.’ the individual would have completed. Because memories are so widely stored from among the brain stem, amygdala and other limbic structures to higher cortical areas, it may only take thinking a thought to trigger patterns of neuronal activation.
The SRT model is also based on an ethological understanding of the mammalian response to threat. SRT is in agreement with Levine (1997) that mammals have an innate capacity to regulate arousal but in humans this process is preempted. When the reticular activating system records the presence of danger, enormous resources are initiated via the sympathetic nervous system in preparation for fight or flight. Defensive maneuvers associated with these survival mechanisms are immediately programmed for completion. Much of this energy is dissipated through successful fight or flight. However, in our modern culture these primeval urges are often blocked by the inhibitory influence of the cerebral cortex. That is, we cannot hurl ourselves from a speeding car (flight) nor maim the individual who merely makes us angry.
When the reptilian brain is waiting to fulfill its fight/flight agenda it is as if the RAS is constantly turned to the `on’ position. Danger is perceived everywhere; there is a scanning the environment to match the undischarged activation in the system. The presentation of hypervigilance and paranoia are recognizable. When you frame symptoms as part of the survival mechanism and examine them in light of an organism continuing to respond to threat, overwhelmed by its environment, they begin to make sense. Frozen in a moment in time, signs of trauma are evident: exothalymic eyes, hyperacousis, photophobia, diaphoresis, muscular bracing, ocular divergence, and/or exaggerated startle.
When fight or flight are not available a third option is automatically operationalized, the freeze or immobility response. As in the case of infants or small children, sometimes this option is the only one implemented. Like the possum playing dead, the freeze response has distinct survival benefits. Most predators will not eat a dead animal as it may be tainted, risking an early death. However an interruption in the natural course of the immobility response to `unwind’ severely compromises the morbidity of animals (Ginsberg, 1974). Baby chicks that are handled and going into shock will live significantly longer than their counterparts who are prematurely awakened.
SRT attempts to facilitate completion of these defensive/motor patterns and extends from the work of Levine (1997). As the client moves closer to the core of the activation, opportunities for an unfreezing of the immobility response occurs. Clients may report coldness turning warm, feeling frozen or stuck. As the immobility response unravels, the client experiences the impulse towards defensive maneuvers, unfinished at the time of the trauma. They will report an urge to `push’, `twist’ or `flee’, for example. When these impulses are allowed expression either actively or through imagination—the same neural pathways are utilized—ANS activation is reduced and symptom relief begins.
While much has yet to be learned on how the immobility response manifests itself in humans, early speculation is generating interesting hypotheses. Levine speculates that a gentle unwinding of the immobility response provides for a discharge of energy associated with trauma. An `unfreezing’ of the immobility response allow the neurological and psychomotor patterns to complete.
Substantial evidence of the degenerative role of the immobility response in humans has come from the work of Stephen Porges (1995). From an exhaustive examination of the neurological correlates of the vagus, the primary nerve of the parasympathetic nervous system, he produced a `Polyvagal Theory of Emotions’. His discovery has made a substantial impact on our understanding of the neurophysiology of emotions. That the `heart’ symbolizes our connection to others is firmly rooted in our biology. Arising from the phylogenetic `layering’ of the vagus his work provides via measurement, the link between psychological and neurophysiological processes.
Porges differentiated the vagus, in two distinct pathways in response to the environment. The primitive `unmylenated’ vegetative vagal system, the `dorsal vagal complex’ is responsible for reducing cardiac output to protect metabolic resources such as digestion. Notably, the immobility response is characterized by an increase in DVC tone and associated with energy conservation: bradycardia, apnea, sphinctor relaxation and lowered gastrointestinal motility. The DVC is very likely the culprit in `Voodoo Death'(in press). The euphemism, “scared to death’ reflects the power behind the DVC in managing intense emotions (terror and helplessness). The DVC, operating alongside sympathetic arousal is like having the foot on the brake with the other on the accelerator (Joseph & Zettl, 2001).
The second, or the `smart’ vagal nerve, developed out of the unique needs of the human species to respond to threat. This latter mylenated vagal system, the ventral vagal, is believed to regulate variability in cardiac output and is the organizing principle for social engagement. It allows for instance sharp changes in responsiveness as we `attend’ and/or engage.
Building on the work of Porges (in press; 1995), Robert Scaer (2001) has named the downregulation of the DVC and the resulting autonomic dysregulation a critical factor in the development of a number of illnesses of unknown origin: asthma, allergies, autoimmune disorders, RSD, fibromyalgia, Whiplash Syndrome and chronic pain. While he acknowledges that the manner in which these illnesses are manifested in the body varies widely, there is an underlying commonality. He notes that these are all problems in regulation and he characterizes them with, “cyclical instability, frequently subtle vasoconstritive/ischemic features, and usually pain”.
The “psychophysical imprint” of traumatic events on brain functioning has shifted the way we define `trauma’. We now include a much wider range of human threat that induces the same characteristic patterns of autonomic arousal. This new paradigm of trauma includes for instance, falls, surgeries, fevers, painful dental procedures and accidents as well as the more traditional forms of trauma such as combat, torture, rape, motor vehicle accidents, and childhood abuse and neglect (Josephs & Zettl, TTB II, 2001).
Increasing evidence supports the idea that the brain is malleable; that new neural pathways can be generated. Researchers in the field of trauma are collecting substantive evidence that clinical intervention can alter brain structure and chemistry in beneficial ways (Schore, 1994). Through a process of empathic attunement and somatic resonance, clinical intervention provides a corrective experience (Perry, 1999; Van der Kolk, 1989). In the same way that a mother’s gaze into her baby’s eyes provides the stimulus for the development of affect regulation, the clinician’s regulatory system is a template for the client (Schore, 1994). In a very dynamic way the client-therapist relationship provides the requisite environment to support growth, particularly in those areas in the brain that mediate arousal. Self-Regulation Therapy is believed to enable this process by tapping into the natural healing abilities of the reptilian brain.
Drawing from a decade of research on the impact of trauma on the neurochemical functioning of the brain, SRT attempts to bridge the gap between scientific research and clinical practice. SRT is hopeful in its conception and while clinical trials have yet to be completed clinical practice is showing promising results.
Writtten by: Dr. Susan LaCombe
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Self Regulation Therapy (SRT) evolved out of the work of Peter Levine and his therapeutic approach called Somatic Experiencing (SE). Since publishing this article research to support the efficacy of SE has been published (access the article via this link):
Brom, D., Stokar Y., Lawi, C., Nuriel-Porat, V., Ziv, Y., Lerner, K., Ross, G. (2017) “Somatic Experiencing for Posttraumatic Stress Disorder: A Randomized Controlled Outcome Study” Journal of Traumatic Stress. 0, 1-9. (https://traumahealing.org/wp-content/uploads/2017/06/Somatic-Experiencing-for-Posttraumatic-Stress-Disorder-2017.pdf)