A more reliable way to extinguish conditioned responses
Historical and theoretical foundation of SDR Therapy
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This article includes a lightly edited extract from a longer paper which detailed an updated understanding of the nature of conditioned responses as an “accidental” neurological pattern which of itself is meaningless, yet which can seriously hobble progress in therapy, as well as comprise the whole of the client’s issue.
How conditioned responses (thoughts, feelings, behaviours) show up in therapy
How conditioned responses form
The myth of “meaning” or “wisdom” of conditioned responses
The futility of inhibition strategies in achieving extinction of conditioned responses
SDR (sensory disruption of reconsolidation) as an extinction strategy
The actual evidence for SDR Therapy as a highly-efficacious extinction strategy
How conditioned responses (thoughts, feelings, behaviours) show up in therapy
It’s possible that the overwhelming majority of problematic thoughts, feelings, and behaviours that comprise most clients’ difficulties or suffering in turn comprise or stem from conditioned processes. Examples are:
Reactivity
Anxiety
Fears, phobias, reluctance
Sequelae of trauma
Jealousy
Anger
Pathological grief
Depression
Compulsions
Some delusions based on flawed perception
Chronic pain that is without sufficient explanatory pathology
Of course other factors can and do contribute, including medical ones (it’s well known that medical conditions can mimic a wide range of psychological disorders) but these conditioned thoughts, feelings and behaviours form a large part of the presenting problem, contribute to resistance, and make it difficult for the client to move forward, slowing progress and delaying the achievement of the client’s desired outcome/s.
How conditioned responses form
Conditioned thoughts, feelings and behaviour are generally extremely useful, and even essential to living as a competent human being. Imagine if we had to think through every single little thing we did or said – life would slow to a snail’s pace and we’d be constantly relearning what is beneficial and what isn’t. Pavlov, after a lifetime of experimentation with conditioning, came to the conclusion that almost everything we think, feel, or do is not actually through cognitive awareness and free will, but is conditioned, with actual awareness following later (which is where we justify what just happened).
American psychologist John Watson took that view to extremes in 1920, saying "Give me a dozen healthy infants, well-formed, and my own specified world to bring them up in and I'll guarantee to take any one at random and train him to become any type of specialist I might select - doctor, lawyer, artist, merchant-chief and, yes, even beggar-man and thief, regardless of his talents, penchants, tendencies, abilities, vocations and the race of his ancestors”, taking no account of what we now recognise as being also related to genetic differences.
But we can all agree that conditioned responses permeate and control our lives to a great extent, and can be useful or can be problematic. So how do they arise?
There are really only two ways that a stimulus can become a conditioned stimulus, leading to a reliable and predictable response each time. The first is repetition (two things consistently paired together sooner or later become an automated neurological process) and the second is via a state of high arousal, which may even be a one-off incident but which could also be experienced as repetition (for example trauma, elation, massive embarrassment/shame).
The myth of “meaning” or “wisdom” of conditioned responses
Regardless of how conditioned thoughts, feelings or behaviours arise, it would be a grave error to regard them as anything other than the brain doing what the brain has evolved to do, that is generally quite helpful but can also be entirely maladaptive. A maladaptive conditioned response is no more significant than picking up a piece of chewing gum on the sole of the shoe, or catching a bug that’s going around.
We do not need to mindfully contemplate it, or worship it as holding some great wisdom. We simply need to get rid of the damn thing.
Some therapists have come to believe that the client needs to “understand” the thought, feeling or behaviour and that somehow this understanding will resolve the issue. Or that we have to understand it prior to resolving this issue. There is no evidence at all for that and in fact that’s not even logical, let alone empirically demonstrated.
On the contrary, with the extinction of the conditioned response, it is common for the client to voice new thoughts and new understanding, of their own volition and clean of therapist input. Extinction followed by discussion is more respectful of the client, and avoids polluting the client’s psychic landscape with the therapist’s own beliefs. It also avoids completely unnecessary angst for the client. Therapy does not have to be like walking over broken glass.
The futility of inhibition strategies in achieving extinction of conditioned responses
Many therapies attempt to moderate or resolve conditioned thoughts, feelings and behaviours via inhibition strategies. Inhibition is at the heart of CBT and its variants, ACT, mindfulness, exposure therapy, EMDR (which is basically just exposure therapy with purple hat protocols added), and others too many to mention here.
Compared to informative controls, all these strategies fail to a very great extent and even if they may appear to be helpful short term, are notorious for failing in the face of stress or threat conditions.
Why do they fail? Because as I’ve said ad nauseum:
“There can be no doubt that under laboratory conditions with animal subjects, inhibition can eventually result in extinction of a formerly conditioned response. Just as with animal studies generally, these studies do not translate to the human experience. Human beings are far more complex psychologically, and do not exist in laboratory conditions. We live in complex environments, which we traverse by means of complex networks of conditioned responses which are being constantly reinforced by that environment, including in ways we are not even consciously aware of. We simply do not have any significant evidence that inhibition is an effective strategy in humans, and reappearance (or relearning) of the unwanted thought, feeling, or behaviour is notorious, particularly under stress or threat conditions.”
So inhibition should not be regarded as in any way effective in resolving maladaptive conditioned responses in humans. It’s not even that great with animals.
SDR Therapy (sensory disruption of reconsolidation) as an extinction strategy
It used to be thought that conditioned responses were challenging to work with and required long, persistent and disciplined efforts to overcome. But it’s turned out this is wrong on all counts and conditioned responses are in fact entirely fragile, and usually quite simple to extinguish. Let me explain.
Conditioned responses are not “stored” anywhere in the mind (or the body for those who’ve been reading vagus nerve BS, or following “energy therapy” BS). Rather than being “stored” the response ”reformulates”, or “reconsolidates” each time a conditioned stimulus is experienced, in a complex interplay primarily between thalamus, amygdala, hippocampus, pituitary, and other structures.
Conditioned responses are fragile because the integrity of a conditioned response is completely and utterly dependent on what could be called “unfettered replay”. Same or similar conditioned stimulus, same response, every time. It’s all over before we have an inkling that the response has occurred in our brain and body and that’s another reason why distraction and inhibition don’t work – they’re way too late to the party.
To effectively extinguish a conditioned response, we need to do more than distract or inhibit: we need to “disrupt”. This means allowing the full effect of the conditioned stimulus (not distracting from it) while simultaneously introducing a very different stimulus.
So how do we do that, because as we see from the work of Libet and others, we only have a maximum of around 0.04 seconds to work with. How do we disrupt the replay in such a minuscule time frame, when we can’t even consciously detect it to start with?
The answer is quite simple: we present the conditioned stimulus in an extended way, simultaneously with a very different but equally intense stimulus or set of stimuli. I write much more about this in other articles right here on Substack, including the free training. I hope you’ll take advantage.
The actual evidence for SDR Therapy as a highly-efficacious extinction strategy
But please stay skeptical! Where is the evidence? Is it purely correlational? Does SDR Therapy look good only when it’s compared to uninformative controls? Is it merely someone’s idea of a whimsical theory or philosophy, not backed by hard science? What do opponents have to say? These are the questions we need to ask.
In the late 1990s/early 2000s, I ran four pilot studies utilising precursors to SDR Therapy for a range of amygdala-mediated disorders: chronic pain (two studies), clinical depression in the moderate-to-severe range, and academic and behavioural performance of children deemed “at risk”. Three of these were written up, but one of the chronic pain studies had an efficacy of 100% and was discounted as an outlier and not written up. The paper on clinical depression was submitted for peer review and published in the journal Frontier Perspectives(1), a journal of Temple University, Philadelphia while my other papers are on Researchgate(2).
All papers demonstrated extremely high efficacy rates for SDR Therapy intervention, in the range of 85-90% (an extreme result not uncommon in tiny groups), although at the time without an overarching or well-developed hypothesis to describe the mechanism more accurately, SDR was referred to somewhat inadequately as “NeuroStim”. Today the word “NeuroStim” is used to describe just one specific SDR extinction technique.
Following these studies, from 2001 to 2003 I developed a theory of chronic pain being in most cases comprised of conditioned neurological activity rather than being nociceptive in nature. Until quite recently this theory had been broadly rejected by the medical community and is still widely regarded as novel, despite the World Health Organisation accepting the IASP’s recommendation of recognising non-nociceptive pain. Today SDR Therapy is still frequently misunderstood as “distraction”, “desensitisation”, “inhibition”, “habituation” or even as “exposure therapy”, all of which are incorrect, inadequate or incomplete explanations of the neurological processes involved and the outcomes obtained.
Prior to the above pilot studies I had for some time been experimentally eliminating chronic pain in the clinic by exposing clients to highly specific conditioned stimuli associated with the pain experience, including very precise and specific idiosyncratic thoughts or perceptions suspected of being associated with (or conditioned to) the pain (being language, metaphor, meaning, beliefs, etc), while simultaneously introducing disruptive sensory stimulation, both real and imagined. You could think of this as incredibly specific and precisely targeted exposure to conditioned stimuli, combined simultaneously with comprehensive arrays of other, disruptive, sensory stimulation (real and/or imagined).
I proposed that chronic pain was largely due to conditioned activity in the brain and nervous system generally, and that this conditioned activity could be extinguished by disrupting the reconsolidation phase of the conditioned response, as described by Soeter et al(3), and also by Phelps and Hofmann(4), whose work will be discussed shortly.
Although excellent results with chronic pain (and other) clients seemed to be achieved, it was appropriate and necessary to put the work to the test in formal trials. After all, it is not unusual for therapists to misinterpret temporary results in the clinic as fantastic and permanent outcomes. Tracey et al(5) found that therapists tend to over-estimate their expertise, and also over-estimate effect size (if any) of the treatments they provide. We humans, eh, at it again with our assumptions.
Due to lack of funding and other resources, those few clinical trials were very small (under powered, ranging from 8 to 25 participants) and not randomised, controlled (except for one), or double-blind, but consisted of treatment groups where participants were taught to self-treat. Approximately 50-60% of the groups eliminated pain entirely almost immediately, and a further 25-50% were able to reduce their pain significantly (ie, reduce their pain level more than 50%). At 2-year follow-up only half of the treatment group were contactable, but in each of those cases the results had been maintained.
Since that time, thanks to the work of many other researchers, some working to investigate the mechanisms of chronic pain, and some working to investigate disruptive (rather than inhibitory) extinction methodology for conditioned responses, my original theory is by now deeply supported by the independent research of many others. My claimed mechanisms and effects have been biologically and empirically verified and can no longer be disputed.
In particular there have been the most exciting advances in extinction of conditioned responses from scientists studying memory and emotion, notably Soeter et al(3) and Phelps and Hofmann(4), whom I mentioned earlier. These researchers have independently identified what they call the “reconsolidation phase” of a conditioned response, and they have shown that where the reconsolidation phase is “disrupted”, there is a failure of the response that is permanent, ie, extinction is achieved quite rapidly and permanently.
Brunet et al(6) also demonstrated that a pharmaceutical agent, in this case the beta blocker propranolol (which blocks physical symptoms of anxiety), given before recall of a traumatic memory, significantly diminished (but did not eliminate) PTSD symptoms over a 6-week period of treatment sessions, with results maintained at 6 month follow up. Brunet currently runs a clinic providing what he calls “reconsolidation therapy” but to my knowledge there has not yet been any long-term follow up, nor a more robust trial.
James et al(7) investigated extinction via disruption of reconsolidation by using traumatic memory activation tasks together with computer game play and found a significant reduction in intrusive memories in the treatment group.
I note that although interesting and significant, the outcomes of Soeter’s and Phelps and Hofmann’s, Brunet’s, and James’ trials of disruption of reconsolidation are not what I would regard as exciting. There are, in my view, major flaws in the methodology of these studies due to a lack of understanding of the nature of extinction of conditioned responses via disruption of reconsolidation that explain the relatively modest outcomes they’ve been able to achieve. These are as follows.
Firstly when we talk about disruption of reconsolidation, this actually only has a useful meaning if we are targeting a very specific conditioned stimulus-response pair. These authors failed to elicit a specific conditioned response and instead instructed participants to merely “think about”, or focus on, or remember a past or current event. None were teasing out the myriad of conditioned stimuli that actually produced the array of symptomatology they sought to resolve. It doesn’t appear that they even made the attempt to fully investigate and identify those stimuli. This approach is too vague to specifically and accurately trigger a single conditioned response and therefore would be expected to result in a statistically and clinically significant but less-than-exciting outcome and that is exactly the type of outcome which has been reported using this poorly-targeted approach. I mean, good on them for having a go – it’s just that the way they’re doing it is pretty half-baked compared to what’s possible.
But this non-specific approach isn’t the only issue – the others are timing, and often the unnecessary use of drugs (which always carries a risk of side effects). Soeter et al and Phelps and Hofmann utilised pharmaceutical disruption, injecting substances into the amygdala region of the brain, or having participants ingest a pharmaceutical preparation (eg before or immediately after recalling a memory). This is also a critical error because the timing of disruption is critical – we must have precision – and it is doubtful that simultaneous, accurate triggering and disruption of the reconsolidation phase of the conditioned response could take place with such an imprecise protocol. The disruptive factor must occur simultaneously with presentation of a precise conditioned stimulus in order to create sufficient disruption (not distraction) specifically during the reconsolidation phase and thereby achieve full extinction of the conditioned response.
To put this as plainly as possible, we cannot disrupt a reconsolidation phase in the absence of that phase, in the same way that we cannot change the volume of a song unless it’s playing. And as these researchers have shown, just because someone has a valid theory in relation to a mechanism doesn’t mean they can apply it in a practical way to achieve a significant outcome.
These researchers are either using the wrong tools, and/or not using them very well. Given these major flaws, the fact that outcomes were statistically and clinically significant in spite of them is indeed grounds for excitement and a very high level of confidence. A proposed larger study of SDR Therapy intends to show what outcomes can be achieved when disruption of reconsolidation is executed with precision. Research partners and sponsors are welcome to get in touch.
In contrast to my and others’ hypotheses, it should be noted that the theory of disruption of reconsolidation does not have consensus even amongst those who study extinction mechanisms, primarily because they see the issue of extinction as being about a chemical process and are focussed on pharmaceutical solutions. Holding a hammer, they see the problem as a nail.
For example Inda et al(8) noted: “…. extinction was also dependent on protein synthesis, following the same temporal course as that followed during acquisition and consolidation. This last fact reinforces the idea that extinction is an active learning process rather than a passive event of forgetting”. I argue against this interpretation by noting that by blocking protein synthesis for a period of time over which a conditioned stimulus was triggered, the extinction of the conditioned stimulus was achieved, so one could equally say that the interference with (read: disruption of) attempted reconsolidation caused extinction. Also I don’t know that one could claim that a response was “forgotten” when it is simply no longer triggered.
Similarly Auchter et al(9) noted: “Fear extinction typically results in the formation of a new inhibitory memory that suppresses the original conditioned response” proposing that it was not so much an extinction of an existing conditioned response, as a learning of a new response which in some way “overwrote” or suppressed the old response. However the “extinction training” which they described as their method in this study would certainly disrupt the reconsolidation phase of the conditioned response and Auchter does not provide evidence of a new memory. In fact they themselves cite earlier studies by Misanin et al(10) (who showed that an electric shock could disrupt reconsolidation and cause extinction), Nader et al(11) (who showed that blocking of protein synthesis during retrieval caused extinction), and Nader and Einarsson(12) who address “reconsolidation, where consolidated memories return to a transient unstable state following their retrieval, from which they must again stabilize in order to persist”.
The theory that “new learning” inhibits an old conditioned response is popular but not demonstrated to date. In the light of the mass of neurological studies around conditioning and extinction it is more logical to consider that the old conditioned response simply fails or no longer exists because reconsolidation was disrupted. It’s not like elimination of a conditioned response creates some vacuum that has to be filled by some new learning! Our brain doesn’t have an “empty bit” just because some old neurological pattern no longer occurs.
Although the theory of “disruption of reconsolidation” is very undeservedly regarded as novel or controversial, Pavlov had already inadvertently discovered it over 100 years ago. In his experiments on salivation rates in dogs, he had set up conditioned responses to electric shocks. In his notes he wrote of his investigation into how far he could stray from the shock site (site of conditioned stimulus) before there was a failure of the response. He found that once he got to the point of failure of response, not only did the response fail at that point, but it was effectively extinguished permanently. Gone. You can imagine my glee at reading this!
Pavlov had inadvertently discovered that if he sufficiently disrupted the conditioned stimulus, he could achieve instant and permanent extinction. Unfortunately, rather than realising the utter enormity of his discovery, he wrote it up simply as a failure of the response, thus delaying an important advance for over 100 years. (See the video “OMG Pavlov”, the permanently-free first unit of the training program attached to this newsletter.)
Another well-accepted theory is the Rescorla-Wagner model(13,14) of conditioning. Part of this model states that there is a specific quantity of conditioned activity that can simultaneously apply to a single conditioned stimulus. If the stimulus is “overloaded” it may collapse, whereupon the response is extinguished. This also fits with the theory of disruption of reconsolidation of conditioned responses.
Crossely et al(15) refers to “cognitive loading” as a method to “unlearn” conditioned neurological processes, but similarly to Soeter et al(3) and other researchers has not extrapolated from this in order to disrupt very specific stimulus-response pairs. I claim that weak, imprecise, or limited disruption of general or vague sets of conditioned responses at play cannot provide optimal outcomes.
Similarly Bouton(16,17) proposed that when a conditioned stimulus is repeatedly paired with stimuli unconnected with the conditioned response, extinction could be achieved. In fact this is a further clear example of disruption of reconsolidation being a highly effective extinction strategy. SDR Therapy strategies do exactly this.
On the basis of in-clinic observation, my own previous trials, and in the light of well-accepted findings of other researchers, I make four claims around a theory of non-malignant chronic pain without explanatory pathology, including a mechanism for the elimination of pain (and other conditioned responses):
1. Non-malignant chronic pain without sufficient explanatory pathology (not pain from acute causes) is almost always non-nociceptive (or nociplastic) and instead is generated by conditioned activity in the brain/nervous system (it’s by now widely accepted that not all pain is nociceptive in nature, and as much as 95% of chronic pain presentations could be non-nociceptive)
2. To permanently extinguish that conditioned activity, we need to identify precise conditioned stimuli, which will always be idiosyncratic to the individual client, and disrupt the reconsolidation phase of each specific, active stimulus-response pair by simultaneously and accurately presenting the stimulus for the unwanted response with other equally (or more) intense sensory stimuli
3. By extending the reconsolidation phase (in order to enable access to it) and simultaneously and repeatedly disrupting that reconsolidation via sensory stimulation, whether external/mechanical or internal/imagined, we achieve extinction of the pain response (or in fact extinction of any conditioned thought, feeling, or behaviour, not just pain)
4. The hyper-sensitivity of the nervous system should be similarly treated, with attention also given to resolution of issues which create or maintain an aroused state, whether negative (such as stress) or positive (such as excitement) so that the system can be given time to return to homeostasis. This includes attending to issues of comorbidity, as well as obvious and critical lifestyle issues such as sleep dysfunction, environmental stress, nutrition/hydration, activity levels, etc.
SDR (Sensory Disruption of Reconsolidation of conditioned responses) Therapy is the name given to specific techniques which have in common an action of rapidly and permanently extinguishing conditioned brain/nervous system activity by accurately disrupting the reconsolidation phase of a conditioned response. Since non-malignant chronic pain without adequate explanatory pathology is generally almost entirely driven by conditioned brain activity, when we extinguish or “switch off” this activity, the pain ceases along with the activity. This can be a highly effective, very rapid and permanent way to eliminate or dramatically reduce chronic pain for most people.
To clarify and emphasise, the claim is that true chronic pain (ie; pain which is without sufficient explanatory pathology) almost always consists of conditioned responses of the brain and central nervous system, and that these conditioned responses can be extinguished very rapidly and permanently using sensory disruption strategies, and that SDR Therapy should be utilised in preference to pharmacological strategies which are so imprecise and which carry a burden of serious side effects, and instead of physiotherapy programs and psychological techniques which are currently not working in any case for the great majority of people.
Note: My comments above in relation to pharmaceutical disruption should not be regarded as anti-medication or anti-psychiatry. I am definitely not saying “don’t medicate”. That would be cruel and irresponsible when people are desperate for “anything, right now!”, and we have many medications that have excellent empirical evidence and are even life saving. But medication alone should never be the whole or even the main focus of treatment for this type of chronic pain (non-malignant, with inadequate explanatory pathology).
Note: All tutorials of the free training program can be found under the menu item “Better Therapy Program” for this Substack publication. These are being uploaded bit by bit, along with ancillary resource material, all at no charge. It is hoped that this open access approach will disseminate knowledge and skills as widely as possible.
References
1. Sutherland C. SDR Treatment for Clinical Depression in the Moderate-to-Severe Range Lifeworks Group Pty Ltd Research Division December 2000. Pre-print. 2000;(December):5-12.
2. Sutherland C. SDR Treatment for Non-malignant Chronic Pain Without Sufficient Explanatory Pathology. 2001;(January):1-6.
3. Soeter M, Kindt M. Disrupting reconsolidation: Pharmacological and behavioral manipulations. Learn Mem. 2011. doi:10.1101/lm.2148511
4. Phelps EA, Hofmann SG. Memory editing from science fiction to clinical practice. Nature. 2019. doi:10.1038/s41586-019-1433-7
5. Tracey TJG, Wampold BE, Lichtenberg JW, Goodyear RK. Expertise in psychotherapy: An elusive goal? Am Psychol. 2014. doi:10.1037/a0035099
6. Brunet A, Saumier D, Liu A, Streiner DL, Tremblay J, Pitman RK. Reduction of PTSD symptoms with Pre-reactivation propranolol therapy: A randomized controlled trial. Am J Psychiatry. 2018. doi:10.1176/appi.ajp.2017.17050481
7. James EL, Bonsall MB, Hoppitt L, et al. Computer Game Play Reduces Intrusive Memories of Experimental Trauma via Reconsolidation-Update Mechanisms. Psychol Sci. 2015;26(8):1201-1215. doi:10.1177/0956797615583071
8. Inda MC. Acquisition, Consolidation, Reconsolidation, and Extinction of Eyelid Conditioning Responses Require De Novo Protein Synthesis. J Neurosci. 2005. doi:10.1523/jneurosci.4163-04.2005
9. Auchter A, Cormack LK, Niv Y, Gonzalez-Lima F, Monfils MH. Reconsolidation-Extinction Interactions in Fear Memory Attenuation: The Role of Inter-Trial Interval Variability. Front Behav Neurosci. 2017. doi:10.3389/fnbeh.2017.00002
10. Misanin JR, Miller RR, Lewis DJ. Retrograde amnesia produced by electroconvulsive shock after reactivation of a consolidated memory trace. Science (80- ). 1968. doi:10.1126/science.160.3827.554
11. Nader K, Schafe GE, Le Doux JE. Fear memories require protein synthesis in the amygdala for reconsolidation after retrieval. Nature. 2000. doi:10.1038/35021052
12. Nader K, Einarsson EÖ. Memory reconsolidation: An update. Ann N Y Acad Sci. 2010. doi:10.1111/j.1749-6632.2010.05443.x
13. Siegel S, Allan LG. The widespread influence of the Rescorla-Wagner model. Psychon Bull Rev. 1996. doi:10.3758/BF03210755
14. Miller RR, Barnet RC, Grahame NJ. Assessment of the Rescorla-Wagner model. Psychol Bull. 1995. doi:10.1037/0033-2909.117.3.363
15. Crossley MJ, Maddox WT, Ashby FG. Increased cognitive load enables unlearning in procedural category learning. J Exp Psychol Learn Mem Cogn. 2018. doi:10.1037/xlm0000554
16. Bouton ME. Context, time, and memory retrieval in the interference paradigms of pavlovian learning. Psychol Bull. 1993. doi:10.1037/0033-2909.114.1.80
17. Bouton ME. Context and behavioral processes in extinction. Learn Mem. 2004. doi:10.1101/lm.78804
Fascinating.