Dysponesis
by Siegfried Othmer | August 5th, 2010
The Dysponesis Hypothesis
We are always casting about for better ways to frame the work that we do in order to make it comprehensible to other professionals and lay persons. Sometime it helps to dip into past history to see how others wrestled with the same issue. One notion that has threaded its way through is that of simple inefficiency in brain regulatory function, which naturally leads to the suggestion that our training improves regulatory effectiveness through promoting higher efficiency in the regulatory mechanisms. It’s a simple concept with a certain amount of face validity, and also offers the virtue of vagueness where we are still uncertain about the details. Another slightly different theme is that the brain sometimes works against itself, that its efforts to right the ship are sometimes counter-productive.
The term dysponesis encompasses a variety of dysfunctions in which the CNS operates counter to the desired end-result. In considering the possible utility of this term in modern parlance, I am going back to an article written by George Whatmore and Daniel Kohli back in 1968 (Behavioral Science, 13(2), 102-124, (1968)), and reprinted as a book chapter in the text Mind/Body Integration (Erik Peper, Sonia Ancoli, and Michelle Quinn, editors), which was first published in 1979. The authors were two physicians in private practice.
The authors refer to “errors in energy expenditure that interfere with nervous system function,” i.e. the notion of inefficiency, resulting in “reduction of the organism’s productivity and disturbance of its emotional reactivity, ideation, and central regulation of various organs of the body.” The term dysponesis is a conjoining of “dys” with “ponos,” for effort, work, or energy—dysfunctional efforting, basically. But the consequences are seen as quite broad, with altered nervous system functioning “affecting the regulation and organ function of just about any system of the body.”
Dysponesis can affect emotional reactivity; it can disturb autonomic function, not only via the emotions but by direct influence on the autonomic centers. It is able to alter primary sensation; it is able to affect ideation; and it can affect endocrine function. Basic research was brought to bear on behalf of each of these propositions.
“Treatment is a form of neurophysiologic engineering wherein basic principles of neurophysiology are used to carry on a retraining within the nervous system.” The authors appear to be foreshadowing what has emerged as neurofeedback specifically, and the neuromodulation technologies generally. Unfortunately, the authors had to prove their theory with the clinical tools at hand, and the relatively poor outcomes at the time (in the modern perspective) probably doomed their hypothesis to practical irrelevance.
Steeped as we are currently in the remediation of trauma syndromes, including PTSD and Attachment Disorder, the dysponesis hypothesis struck me as particularly relevant to PTSD, which was not yet an established category in 1968, nor even in 1979. The authors in fact cite the example of flight from a dangerous animal, resulting in “bracing” responses that later may be carried over into social situations where these are dysfunctional. Dysponesis is thought to be most relevant to the etiology of acute or chronic anxiety. Bracing against a threat raises the arousal level and increases the excitability of the limbic system. Increased efforting is thought to be a causative agent in hyperventilation syndromes, which all by themselves can kindle a more pervasive disregulation cascade.
Inappropriate bracing was thought to keep the reticular activation system engaged even as the person retires for the night, precipitating insomnia. Unproductive persistent efforting precipitates fatigue and exhaustion. By extension it plays a role in depressive syndromes as well. Further, it is deemed to play a primary role in headache and backache syndromes, mediated by dysfunctional bracing and in the case of migraine, by disturbance of autonomic nervous system function, leading in turn to the cascade of vasoconstriction and —dilation. Dysponesis was even thought to be capable of kindling obsessive and compulsive states, as well as hypochondriasis. It was argued that it might even contribute to the onset of schizophrenia.
On the larger scene, dysponesis was also proffered as a mechanism for more far-reaching somatic functional disturbances, including digestive distress (irritable bowel, etc.), impotence and diminished libido, cardiovascular dysfunctions (tachycardia and hypertension), eczema and neurodermatitis, and even myocardial infarction.
It was this extrapolation of the dysponesis model to implicate apparently minor dysfunctions in the etiology of even major medical issues downstream that I found particularly insightful. This is specifically relevant to PTSD, where similarly pervasively degenerative trajectories are kindled by “mere” psychological trauma. A unitary perspective on PTSD which considers physiology as primary is badly needed.
The relevance of dysponesis to PTSD has in fact been recognized in a publication by Martin R. Smith, who used to be associated with the Biofeedback Institute of Los Angeles, with Marjorie and Hershel Toomim. His article dates back to 1993, and is accessible on the web. (Reference 3). A second, more recent article is available in the biofeedback literature, by Elizabeth Stroebel. The focus is on application to children, in that they readily understand the concepts involved. (Reference 4)
Primacy of the Motor System
While the authors were indeed farsighted in the generality and inclusiveness of their conception, it was also rooted in the psychology of the day. The notion of efforting was very much tied to the motor system. But then everything else seemed to be tied to the motor system as well. “…minute eye efforts participate in the production of visual images.” “Without eye effort there is no visual image.” The authors speak of covert motor activity. “Tongue, throat, and other speech region efforts participate in the auditory images of words.” The Watsonian understanding that without speech there can be no thought seemed to be alive and well. One is reminded of the controversy as to whether anxiety gives rise to flight, or whether it is the act of recoiling from a presumptive snake, or of running from a threat, that infuses the visceral experience of fear.
While we may reject the postulated primacy of the motor system in this formulation, the rather deeper truth alluded to here is the connectedness of things within the CNS, and that notion is certainly very current. When the circuit diagram is drawn for dysponesis, it is a model for the “systems perspective” on our physiology. We may simply have to jettison a notion or two to bring things up to date. One is the idea of sequencing, that one system is prescriptive for another in a uni-directional manner. An analogy here might be to something like bowling, where the causal chain of events is unambiguous. The second is the notion of the primacy of the motor system.
The motor system is indeed primary from the perspective of the outside observer, because its activities are readily observable. And it is primary in terms of cortical organization of output because there is such a large commitment of cortical real estate to the motor system and its associated pre-motor region. This becomes even more obvious when one also includes the somatosensory cortex, with which it is strongly inter-leaved, and the motor planning function of the pre-frontal executive. But the motor system is not in charge. It should not be talked about as if it possessed any sort of autonomous agency that somehow determines the state of the limbic system, for example.
The modern systems perspective compels the view that matters are much more mutually interactive. There is no autonomy anywhere in the system. Everything is in the act of communication, and communication intrinsically exercises a measure of control. The vector diagram of A controlling B, which in turn controls C, is no longer availing. Matters are under each other’s mutual, reciprocal and contemporaneous influence. The arrow of time and the chain of causality get lost in a teeming swamp of mutuality and interactivity.
On the other hand, the authors are really interested in making the case that appealing to the motor system is effective in restoring function in the presence of dysponesis. It does not require the primacy of the motor system for this proposition to be valid. There simply needs to be a mutual interaction between the systems, and the data supporting that hypothesis were plentiful even in the sixties. For example, curarized cats exhibit diminished emotional reactivity and decreased hypothalamic excitability.
Most recently, it has been observed that botox injections to inhibit frown muscles in the forehead had the effect of delaying the recognition of negative emotions. This could be seen as confirming the older understanding that facial expressions serve to augment, not merely reflect, the emotions they represent. Rather than interpreting this as giving the motor system a controlling role, however, one might now say that the network representation of a particular emotional state carries with it the expectation that the motor system should be syntonic with the experience. It should be part of the dance. When it is not, a different balance point is reached within the whole system. The emotional state is governed by a complex voting scheme in which the state of the motor system plays a part.
The focus on the motor system was also reflected in the early work of Barry Sterman and Joel Lubar. The sensorimotor rhythm was associated strictly with the sensorimotor cortical region, and early on Sterman assumed that SMR reinforcement would have benefit only for motor seizures. Lubar initially targeted hyperkinesis specifically, the defining condition of what was called ADHD only some years later. The subsequent extension of neurofeedback to other conditions was motivated on our part by the conception that organismic arousal was strongly represented in the activation of the motor system that was being targeted explicitly in the training. The operative principle was one first articulated by Sherrington: “The motor act is the cradle of the mind.” We thought that the motor system would give us access to the whole regulatory machinery, and of course at some level it did.
Diagnosis and Treatment of Dysponesis
So how is the dysponetic status determined, and how is the therapy administered? Here matters are more obscure. The authors talk of relying on a special type of electromyography (EMG). Inappropriate bracing is identified by means of an electromyometrogram (EMMG), and training procedures are instituted to effect normalization. This involves what we would now call biofeedback, but this article was written before the Biofeedback Research Society was organized in 1969, where the word biofeedback was first coined.
Before going on to describe the results of their training procedure, the authors assure the reader that “(P)sychotherapy appears to have no correcting effect on dysponesis.” On the other hand, “(P)harmacologic agents likewise fail to correct dysponesis because they cannot teach.” And there we have it. The authors have laid out a domain of dysfunction in which the individual circuit elements actually work as designed, but which at a higher organizational level do not serve the organism well. Motor neurons fire as they should, and sensory neurons inform as they should. The regulatory architecture is intact. Hence pharmacology could play only a minor role at best. At the same time, the dysponetic responses can be considered as autonomic in character, in that they are not under the normal, direct control of our pre-frontal executive even if they are part of the voluntary nervous system. So they are not very accessible to psychotherapy. We are confronted here with functional disorders that derive from learned responses that are being inappropriately reinforced.
The salient point is that retraining of the system is called for, a kind of physical therapy for the nervous system. With the perspective of hindsight, it now appears that the concept of retraining the motor system for better function might have had a better shot at acceptance within the health care field than the term biofeedback. In that regard, it might be recalled that the term biofeedback was controversial even at the outset, with Barry Sterman among others cautioning against its adoption. By gaining a beachhead with Joe Kamiya’s alpha training, the mystical elements associated with that work also came through the door. This observation is not to be taken as a criticism of such mystical elements. It was just that the sober world of academic research was not prepared to entertain them. And so the whole thing was happily tossed out of the window and dismissed. By the time that EMG and other peripheral biofeedback was nudged to the forefront of the field, the whole concept of biofeedback already had acquired some baggage, and found itself fighting uphill all the way.
It’s just retraining, and since we are retraining system function, feedback to that system about its own state of functioning at that instant ought to be helpful, particularly since the whole system architecture is based on feedback, both internal and external. How is it that the biofeedback critics did not get this? How is it that they insisted upon the most impeccable of scientific evidence, derived from the most unassailable of study designs, to be persuaded of such a foundational principle that feedback-aided learning works with respect to regulation of our own states? The neurofeedback deniers these days are like polar bears drifting out to sea on a rapidly shrinking ice floe. How will they ever explain their perennial obtuseness to their grandchildren?
The authors go on to say that “(T)he possible origin of the dysponesis in a given patient is not considered important for treatment purposes.” It is unhelpful to go back to what may have triggered the development of the dysponetic response at the outset. It now exists as a disruptive entity that must be dealt with in its own terms. The relevance to trauma syndromes such as PTSD comes to mind immediately in this context. The original trauma, whatever it may have been, is secondary in clinical relevance to the physiological disruption it has given rise to, and revisiting the trauma is no longer curative.
Of course there are many examples of exposure therapy being very helpful; there is no denying it. But it is a bit like picking up a lizard by the tail. Matters are really not under control, and one is interacting with a highly reactive subject. The lizard may even escape, leaving behind nothing more than its wriggling tail. The therapist may continue his exertions, but the subject of interest is unavailable. If, on the other hand, one grasps the lizard by the neck and simply turns him over belly-up, the animal will go into “play-dead” mode and becomes manageable immediately. Similarly, physiological self-regulation should be the first objective with PTSD. By the time PTSD is encountered clinically, it can no longer be regarded as primarily a psychological issue. Matters have metastasized into the physiology, and that is the triage issue requiring immediate attention.
The authors go on to describe their learning procedure. The description is somewhat vague because different detection methods are appropriate for the various manifestations of the dysponetic response. The client must learn to recognize these responses, and unfortunately “(T)here is no way of conveying to the patient by words alone what he is to be observing.” Covert bracing efforts have to be brought “into the realm of observable phenomena.” “Once a person has learned to observe a given effort, that effort comes directly under his control…and he can diminish it to whatever degree he chooses.” This is a description of a biofeedback procedure, and it is one that merely demands demonstration in order to show that learned control can be achieved.
Clinical Results with the Targeting of Dysponesis
Unfortunately, what may work well in microcosm may still falter in the face of actual clinical complexities. The cases described in this paper, which date back to the fifties, uniformly took many sessions to achieve resolution. An engineer with intractable headaches received some 97 training sessions before finding relief. A patient with intractable back pain received over 200 training sessions, and improvement was a gradual process covering some five years. That will hardly make the papers. A person hospitalized repeatedly for depression and anxiety had a total of 188 training sessions. However, she never had to be hospitalized again from the time the training began.
Obviously there were inefficiencies here in the procedure, just as there were inefficiencies in the functioning of the client. That is where the greatest change has occurred over the intervening four decades. With the above as a backdrop, let us now consider just how far we have come using a very similar treatment model but with better procedures. It is routinely possible to bring relief for the cardinal symptoms of PTSD in a matter of some 20 neurofeedback training sessions. Restoring a high level of function, on the other hand, will require additional training. Even the most intractable migraine cases can now typically be brought under control in twenty to forty sessions of neurofeedback. Anxiety and depression syndromes are much more easily dealt with than before. Conditions of chronic pain are being helped much more effectively.
A Current Perspective on Dysponesis
The primary difference between the early historical roots of biofeedback and current approaches is that presently attention is being devoted to the central mechanisms where the disregulation is first lodged. Failures at the macro level as subsumed in the dysponesis model are ultimately traceable to failures at the micro level that are now directly accessible to reinforcement strategies for resolution.
But all of the prior principles of biofeedback carry over. One must make the behavior visible to the person so that it can be acted upon in a reinforcement paradigm, and the burden largely falls on the individual’s engagement to effect recovery. The learning process is progressive and cumulative, and one must train to the point of mastery. There is one salient difference, however, from the prior work: Currently the focus is on function rather than on dysfunction. It is the restoration of function that is called upon to banish dysfunction. The brain is only too eager to engage with such a process. Function is its charter. Challenges demand mastery.
Further, over time the process has burrowed deep into the mechanisms by which the brain organizes its hierarchy of control. We are now affecting the quality of the brain’s internal control system at its most foundational level. The adequacy of regulatory function is largely a matter of the quality of communication within the cerebral networks, which in turn is a matter of exquisite control of timing relationships. These are best represented in dynamic phase relationships among neuronal assemblies.
Unsurprisingly, this should then allow therapies to proceed with greater dispatch. And thus it is possible to report that in one instance a Vietnam veteran with an abysmal forty-year history of PTSD was able to shed the cardinal symptoms within a mere three sessions—-although he went on to benefit from more than sixty sessions. It was possible for a migraineur with a multi-decadal history of frequent, intractable migraines to resolve this condition in forty sessions of neurofeedback, over which time no full-blown migraine was ever again experienced, and none have been experienced since. It was possible for an anorexic pre-teen, untreatable at UCLA, to recover fully with about 24 training sessions. It was possible for an anorexic adult with daily panic attacks to announce that from the first session on she had no more panic attacks. And it was possible for three contemporaneous clients with nearly continuous migraines over extended periods to become substantially migraine-free within a couple of weeks. Controlled studies, anyone?
On the other hand, when we survey entire training histories, we too find that the most challenging clients often stay with us for many sessions, many months, and sometimes years. Progress will have been made all the while, and we are typically no longer gnawing at the original conundrums that brought the client to us in the first place. But good function remains more a goal than the reality. A compromised brain may continue to benefit from long-term training, and we should arrange ourselves to provide it affordably. Unfortunately, no third-party reimbursement scheme can accommodate that level of demand. Ultimately, neurofeedback has to be offered in a continuum from a clinic-based to a self-care-based model, the latter with only minimal clinical supervision, and it all has to be done on an affordable basis as well.
A Synthesis in the Disregulation Model
It is frankly difficult for me to read this paper and not lament the four decades the field of mental health has wandered in the wilderness, all the while neglecting the most potent hypothesis underlying mental dysfunction: Disregulation is the issue, and self-regulation constitutes the remedy. This disregulation is lodged in dysfunctional patterns adopted within neural networks as learned responses, albeit conditioned by genetic, epigenetic, and developmental contingencies. The Dysponesis Model was sufficiently robust that it could organize the information available at the time into a coherent whole with broad clinical reach. In the meantime, psychopharmacology has been just successful enough in psychiatry to take up all the oxygen at the National Institutes of Health, and cognitively mediated psychotherapy has been just successful enough to keep alternative therapies at bay within the field of psychology. Now even autistic children have behavioral techniques inflicted on them, electric shock therapy among them. And they are continually experimented upon with inappropriate medications. Meanwhile the evidence for what actually works is never given its due. Only in the world of religion and of the social sciences are efforts so assiduously mounted to guard settled belief against the corrosive onslaught of disagreeable facts.
References
1. Whatmore, G.B., & Kohli, D.R. (1968) Dysponesis. A neurophysiologic factor in functional disorders, Behavioral Science, 13(2), 102-124.
www3.interscience.wiley.com/journal/114032528/abstract
2. Whatmore, G.B., & Kohli, D.R. (1979). Dysponesis. A neurophysiologic factor in functional disorders, Chapter 33 in Mind/Body Integration, Essential Readings in Biofeedback
Eric Peper, Sonia Ancoli, and Michelle Quinn, editors, Plenum Press, New York
3. Smith, Martin R. (1993) Dysponesis. An Important Factor in PTSD.
http://responsesidetherapy.com/pdf/Dysponesis.pdf
4. Stroebel, Elizabeth L. (2005), Dysponesis hits the spot: A translation for and by children, Biofeedback, Winter 2005, pp. 135-138
http://www.aapb.org/tl_files/AAPB/files/BIOF3304-Stroebel.pdf
Hello -I’m a Chiropractor and worked with Drs. Annette Long and Alvah Byers in Colorado, on the effects of the Chiropractic adjustment to alter brain wave patterns. Over 300 case studies with interesting results. We began to realize that the chiropractic adjustment acted as a neurological pattern interrupt. We noted that we were seeing changes in brain activity in one adjustment that would take 40 to 60 session of neurofeedback. (Dr Byers’ statement, not mine) When we added NFB after the adjustment, we saw even better responses. Dysponesis is basically what Chiropractic has been talking about for 115 years. I don’t see dysponesis stating that the motor system is primary but that the “errors in energy expenditure (Chiropractic subluxation – not bony displacement) are expressed by the motor system. – Bad message – inappropriate actions – Would love to talk to you about a common direction – love your work!!!
Richard
I am fascinated by your report, and also happy to hear that Alvah Byers is still active professionally. Many years ago a chiropractor came up to me excitedly after I had given a talk and told me of the significant overlap between his work and what I was reporting. This triggered my thinking about possible common mechanisms. At the time, the more dramatic, impulse chiropractic was still in vogue. It occurred to me that what might be involved in any sudden realignment was a volley of synchronous afferent inputs to the thalamus, which would have the effect of resetting the ambient set-point of thalamic function. The problem, of course, is that the technique is so variable and unpredictable in its outcome, and it is not readily steerable. You get what you get. Perhaps that has changed with subsequent refinements. This is where neurofeedback may have a significant advantage. We can tailor our training exquisitely to the situation. So first of all it seems obvious that neurofeedback should be of interest to chiropractors as a complement to their existing methods. And secondly, the implications for mechanisms should be further pursued from both perspectives.
I think dysponesis is an explanatory term that still applies to nearly all of what we do in behavioral health care. I first came across the term circa 1980 in “The Physiopathology of Functional Disorders” by Whatmore and Kohli, 1974 and have since used that concept to understand and explain what I do. It seems to me that the idea functional disorders develop as a result of prolonged misplaced effort to cope applies equally well to disorders of the central and autonomic nervous systems as it does to the sensory-motor nervous system. In fact, 80 to 90 percent of the reasons patients consult their primary care providers are stress-related. Hyper or hypo-arousal, instabilities, disinhibitions, hyperventilation, guarding and bracing, cognitive distortions, self-defeating beliefs, etc, etc can all be seen as manifestations of misplaced effort and therefore dysponesis. I say “Hurray” for the concept of dysponesis and a hearty “thanks” to Siegfried Othmer for refreshing our awareness of it. May this very useful concept that explains the cause and remedy (learn self-regulation skills that remove dysponesis) of so many functional disorders live on.
Having long experience with an array of PTSD treatments let me give this the old college try.
i agree with Dr. Othmer that the term “dysponesis” is suitably vague enough to serve as a kind of learning tool. i also agree that it suffers from an outdated allegiance to single-line theory. the underlying problems appear to be reticulated, networked and circular.
But there are other reasons to disagree with this concept than single-line theory. the sense i get from “bracing” is not what I get from “flight”, as in fight or flight. Flight is part of the sympathetic (SNS) dominated energy expenditure system. Bracing is not. Bracing seems much more like a freeze response. a freeze response is a parasympathetic (PSNS) modulated energy conservation tactic.
this is what I think Dr. Othmer is driving at when he criticizes the idea that the motor system is tied into effort, cognitive sorting and realistic perception. I believe the phrase he was looking for is, “Do we run because w e feel fear or do we feel fear because we run?” the answer is the latter.
I remember Bessel van der Kolk kicking up a lot of dust among trauma therapists when he suggested he didn”t think very much trauma would emerge from the 9/11 attack. As I’m sure we all remember too well, multitudes were able to effectively mobilize their flight system by running away.
When fight or flight cannot be activated, THEN bracing occurs. this means, effectively, that the external threat becomes internalized. the threat is now an embodied representation and if the trauma is developmental, it is embodied again, it would seem, at the developmental level at which it occurred.
All of which makes a cognitivist, realist interpretation of these matters useless. Because the representation is embedded, a person is not seeing fear or even reacting to it. he is reacting to the fear of fear. So, characterizing these issues as physioneurotic realities as opposed to psychosomatic distortions looks better and better.
The second reason to disagree with dysponesis (and much of the thinking in trauma theory and therapy) allows us to get a better look at real psychobiological processes. Stephen Porges” polyvagal theory, for example, shows that it is a mistake to assume that the stress system is a single, one-size-fits-all process. Instead, the stress system is phylogenetically evolved: we have three stress responses that recapitulate our reptilian – mammallian – human heritage.
the freeze response, according to Porges, is associated with the evolutionarily older part of the vagal nerve called the dorsal vagal and is a healthy response in reptiles and mammals. E.g., a reptile has no circulatory system, so as it heats up with energy expenditure, it needs a way to rapidly cool down. A dorsal vagal response rapidly decreases its metabolic output (decreased oxygen needs, e.g.) and the lizard acquires that rigid, mask-like appearance one often sees as it sits motionless on a rock.
What’s healthy in animals though may not be healthy in humans because polyvagla theory holds that we have recourse to all three levels of response. the human stress response, then, can be unpacked at any of those levels.
another related factor to consider is the affect regulation (AR) concept of decoupling in Allan Schore’s work. In PTSD the entire ANS is decoupled. It loses not only reciprocity as might occur only at chronic or acute levels of stress, but the ability of each branch to effectively communicate with the other.
this is why PTSD is not simply a large-scale excitatory response as so much of trauma theory assumes (as does the DSM-IV). When decoupled the nervous system is susceptible to a freeze response, perhaps thought of as the third component of the ANS.
Also, one autonomic signature (AS) shows only how someone, say, with PTSD “presents”. I.e., a person whose AS is PSNS dominant is fatigued, withdrawn, with a globalized confusion (that is not depression) and is probably low immune. But that does not mean he is without anxiety. His anxiety is just blanketed by the massive numbing. Obversely, a person whose AS is SNS dominant is excitable, visibly unstable, phasing in and out of strong emotions, has a lot of intrusiveness and is probably high immune. But similarly, that does not mean he is without and ever-increasing quotient of numbing and withdrawl. It’s just not “in relief”; this person would be all figure with less awareness of ground.
All of this should be of increased interest to anyone who is looking for further evidence of the actual neurobiological processes involved since Schore cites a lot of research delineating the pathways in the limbic system across which both the SNS and PSNS dominated disregulated responses travel.
One main reason why this whole array of responses (freezing, internalization, decoupling, somatoform, emotional and mental dissociation, unpacking) bypasses single-line thery is due to a major feature of Schore’s AR take on PTSD: right-side significance over against left-side dominance.
Schore is the farthest thing from a polemicist but in his work the idea of left-side dominance would probably invoke a lot of laughter. AR is sometimes called developmental neurobiology because, as above, the instantiation of these disregulated responses occurs at the developmental level involved. It’s the job of the right side to create effective, EMOTIONAL modulatory patterns in the top-down, bottom-up circuits that traverse from the pre-frontal, to the limbic to the brainstem. The left side does not have those kind of connec tions.
To accept the idea of left-side dominance, in my view, is to buy a top-heavy package deal of social constructions that covertly valorize, 1) science itself (paradoxically) in the form of rigid attachments to “mirror of nature” observation and communication styles, 2)male identity and 3)adult identity.
the last of these is particularly important for anyone in NFB who wants to get at the root of emotional problems with a new scientific psychology. Wouldn’t practitioners want , at least theoretically, to approach the clients psychobiology in the COMPLETE terms of that psychobiology? If the kinds of psychobiological issues in PTSD (and others) are instantiated at developmental levels, then any kind of NFB that wants to do full justice to the client, will have to look at AR.
Dysponesis (especially “b racing”) is about both anxiety and fatigue. But in a way that tragically divides what should be a unitary, self-regulating response.