Wilderman Medical Clinic/Canadian Centre for Clinical Trials/Chronic Pain Clinic
As a pain clinician I use medications such as Gabapentin, Pregabalin, Duloxetine and tricyclics. Often I combine two medications from different classes, i.e. Pregabalin with Duloxetin. Sometimes they help quite well. For people who fail oral medications we use intravenous lidocaine infusion with over 60% success. From non-medication options I use biofeedback and psychotherapy. Interesting results gives musicotherapy. Gentle stretching exercises and aquatherapy program are other useful treatment options.
As a neurologist of many years experience in treating chronic pain, I was extremely frustrated by the low level of remissions from chronic pain with neuropathic etiology. Patients able to overcome this were quite rare. Such phenomena are often driven by glutamatergic excess. What may be needed is a system or drug that down-regulates that over-abundance. The endocannabinoid system inhibits glutamatergic neurons, and is a prime candidate. A preponderance of the long-term improvements and even resolution of such long-standing paint syndromes have come from cannabinoid therapy. I attach two references that may be pertinent to this issue.
I am not a clinician but from research experiences, I think the treatment should consider the etiology of pain and the fact that many mediators are involved in the development of central sensitization. No matter the case, a bi-therapy is highly advised. I believe gabapentin should be used as first line with an anti-oxidant agent.
That is very clear to me, we need glia modulation for that, and there is at least one good glia modulator and non-neuronal cell modulator (eg mast cells) available, palmitoylethanolamide (PEA), a foodsupplement and endogenous lipid signaling compound, shutting off neuro-inflammation and easily to combine with all analgesics and co-analgesics. Shutting down neurons with pregabalin etc only is not enough! I worked with PEA since 2011 and find it a very usefull ajunct in nearly all chronic pain states. PEA is easily avilable via the internet as PeaPure, capsules containing PEA only without any pharmaceutical compound.
It's depend how you consider "central censitization". One of the etiology of "central censitization" is A-beta neurofibers lesions (von Hehn et al. Neuron 2012; Devor Exp Brain Res 2009), than we can follow the clihnicla reasoning of candy MacCabe:
Althought the nerve damage is peripheral the mecanisms for pain sensitization are probably centrally driven with referral back to peripheries where it is perceived as painful. The paradoxical hypo-aesthetic painful to touch territory can be reduced through somatosensory rehabilitation of pain method i.e. Distant Vibrotactile Counter Stimulation (Spicher et al., Somatosens Mot Res 2008; Spicher, 2006; Spicher et al. 2013).
Many clinicians across the US are using a neurostimulation therapy called P-STIM. They are achieving excellent results in most of the patients they are treating. This is applied via the ear and sends minute currents into the brain releasing endorphins. It also apparently affects neuroplasticity.
I recently read 2 articles on the subject of central sensitization: Freeman MD, Nystrom A, and Centeno C. Chronic whiplash and central sensitization; an evaluation of the role of a myofascial trigger points in pain modulation. J Brachial Plexus Peripheral Nerve Inj 2009; 4:2. doi:10.1186/1749-7221-4-2.
Börsbo B, Liedberg GM, Wallin M, Gerdle B. Subgroups based on thermal and pressure pain thresholds in women with chronic whiplash display differences in clinical presentation—an explorative study. J Pain Res 2012; 5:511–521.
Activation of the NMDA receptor is responsible for the development of central sensitization, hyperalgesia, and allodynia and NMDA receptor antagonists are known to be anti-hyperalgesic, thus useful for chronic pain. One such drug would be Amantadine.
Pontifícia Universidade Católica de São Paulo (PUC-SP)
Unfortunately, there is not an ideal medicine to deal with this complex matter. If it is considered just the central sensitization, the most used medicines are the ones to enhance the central inhibitory descending pathways such the triciclics and duals anti-depressives and, on the other way ,the modulatory drugs of the ascending pathways, such the pregabalin and gabapentin. The major problem, in my opinion, is how to control the input of continuous stimulus. For example, osteoarthritis is a major cause of chronic pain and even with a good control of the central mechanisms, the input of stimulus goes on. In this case, the non medicinal treatments, such as exercises and the periphery analgesics are important to maintain musculoskeletal health and with less pain. Even when we discuss the central sensitization, the non medicinal treatments have to be adopted, since there is no treatment that gives full solution for our patients. Other main issue is the association with depression and anxiety that amplifies the symptomatology.
Several authors have discussed central sensitization in OA (Hunter, 2008; Abhishek, 2013; Witt, 2012; McDougall, 2006). Regardless of the source, sensitization perpetuates and amplifies pain in OA. With OA progression, the firing threshold of nociceptors becomes reduced by release of bradykinin, histamine, prostaglandins, lactic acid, vasoactive intestinal peptide, substance P, and CGRP into the joint. As these inflammatory mediators accumulate in the joint, they trigger a self-perpetuating cycle of pain generation. Substance P, in particular, has been implicated in sensitizing nociceptors in OA and appears to have a pivotal role in pain generation. Substance P-staining nerves have been found in the accessory ligaments, synovium, subchondral bone, menisci, and periosteum. Substance P, for instance, is in abundance in the nerves that reinnervate healing tissues after a joint injury involving ligamentous rupture and has been shown to cause peripheral sensitization of nerves in response to normal and noxious joint movements.
National Cancer Institute, Cairo University - Egypt
There is medical treatment and interventional procedures. and this depends on the aetiology and site of the lesion. The commonly used drugs include Gabapentin, Pregabalin, NMDA receptor antagonist (Ketamine) as well as Amitryptilin (Tryptizole)
Interventional procedures include lumbar sympatectomy, Stellate Ganglon block
Spontaneous neuropathic pain and touch-evoked neuropathic pain are not produce by the same neurophysiological mecanisms. The target of Gabapentin, Pregabalin, NMDA receptor antagonist (Ketamine) as well as Amitryptilin (Tryptizole) is the reducation of Spontaneous neuropathic pain Central Senstization is a concept to explain the hypersensibility (Latremoliere A and Woolf CJ, J Pain. 2009 Central sensitization: a generator of pain hypersensitivity by central neural plasticity) [touch-evoked pain i.e. Static mechanical allodynia]: Activation, modulation and modification in the dorsal horn (Woolf & Salter, Science 2000). Unfortunately apart from oxycodone(Watson et al., Pain 2003) we don't know drugs to reduce hypersensibility. A non- pharmacological treatment can help: somatosensory rehabilitation of pain (Spicher et al., Somatosens Mot Res 2008; Spicher, 2006; Spicher et al. 2013).
I do agree with you, but I was writing about human data. I think that the validity of the methods to assess the static mechanical allodynia in the animal models is not exactly the same one than the validity of the allodynography in the humain model.
In patients (this was the question) one of the etiology of "central sensitization" is A-beta neurofibers lesions (Bouhassira and Attal, 2012 Douleurs neuropathiques), and not only C neurofibers.
We have been able to reverse the symptoms of neuropathy, which likely are associated with central sensitization, with our Combined Electrochemical treatment (CET), which is local anesthetic combined with an advanced electromedical device manufactured by Sanexas (Ref Pain Physician, Odell, Sorgnard, Anti-Inflammatory effects of middle frequency current, Nov/Dec 2008). This device functions way beyond TENS. We have also seen reversal of phantom limb pain with evidence of reversal of central sensitization. The early application of this device after injury would like go a long way in reducing central sensitization. I also utilize the device instead of steroids by using caudals to improve patients with post spine fusion syndrome
NMDA antagonist Ketamine is the best and is the most used for reversing sensitisation phenomenon. Check literature and methods on burst ketamine treatment. It is a standard treatment in many countries.
I just found another article in Plos One using a model of OA pain to study the effects on central sensitization by administrating Inhibitory cannabinoid 2 (CB2) receptors: Burston JJ, Sagar DR, Shao P, Bai M, King E, et al. (2013) Cannabinoid CB2 Receptors Regulate Central Sensitization and Pain Responses Associated with
Osteoarthritis of the Knee Joint. PLoS ONE 8(11): e80440. doi:10.1371/journal.pone.00804.
..consider that a gluten-sensitvity with silent inflammation and a leaky gut (which is often accompanied by a leaky blood brain barrier) may be the underlying cause resulting in silent inflammatory process within the pain regulatury centers in the CNS. How to determine this: Use the Cyrex array 3 lab test which gives an answer if gliadins are the cause while other organs are affected being due to the autoimmune antibodies which come from a rampant immune system
Any literature ? Sure, check the book by Perlmutter "Grain Brain" with . refrences
I always target non neuronal cells in these clinical situations and add a glia and mast cell inhibitor to the analgesic regime: 3 times daily 400 mg palmitoylethanolamide for 1 month and in case of too little response I double the dose for the 2nd month. This can create a good response and lower the painscores. We have documented this regime in CIAP patients, neuropathic pain after chemotherapy and diabetic neuropathic pain, as well as nerve compression syndromes.
When CSS disorders include multi-sensory sensitivity [aka MUSES syndrome]
--i.e. when patients are not just hypersensitive to touch and pain but also to all types of other sensory stimuli such as lights, sounds, odors, tastes, movement, hot/cold, etc-- the cause is some prior carbon monoxide poisoning,
and as such, these cases are easily tested, treated and reversed.
Among the specific CSS disorders that commonly match this MUSES profile are fibromyalgia, TMJ, CFS and autism.
How? Because CO poisoning results in elevated levels of CO in tissues, which interferes with the normal functions of endogenous CO, including its role as a gaseous neurotransmitter modulating the nerve action firing potentials of all our sensory nerves. Post poisoning, CO survivors become hypersensitive to even small increases in endogenous CO that are caused by exposure to stressors of all kinds. this is because all types of physiological stressors trigger heme oxygenase-1, the aptly-named universal stress enzyme, to increase the rate at which heme proteins are catabolized, which is the primary pathway by which endogenous CO is produced [along with Fe2+ and biliverdin].
MUSES syndrome is easily established with a few sensory screening questions and 2 blood samples taken from the same elbow: People suffering from chronic endogenous and/or exogenous CO poisoning have venous COHb > arterial COHb. Note the normal a-v gap COHb is not zero but 0 to +1%.
When treated as CO poisoning with supplemental oxygen, this COHb gap gradually normalizes along with sensory sensitivities. But this does not work for people who are only hypersensitive to pain and touch, without any broader MUSES syndrome. Their problem is clearly not CO related and does not resolve with CO treatment.
My protocol for MUSES cases recommends supplemental oxygen at 5 l/m for 2 hours per day via canula, or for those can tolerate it, via a partial non-rebreather mask with one hole closed to increase CO2 rebreathing, which greatly increases minute ventilation and thus the rate of CO exhalation. Hyperbaric is not needed or recommended since it drives more arterial CO into tissues without increasing minute ventilation.
Treatment takes 4 months to complete due to the approximately 120-day lifespan of RBCs in which most circulating CO is bound as COHb. CO in tissues cannot be excreted unless and until it is first released from the many other heme proteins to which it also binds more aggressively than oxygen, including myoglobin in muscles, neuroglobin in the brain, and cytochromes in mitochondria.
After the body's CO burden has returned to normal [with arterial-venous COHb in the range of 0 to +1%], no more oxygen treatment is needed. If any CSS researchers investigate CO testing or oxygen treatment, I'd appreciate hearing the results.
In addition to previous answers: there is a huge difference between patients with nerve damage (like for example in amputees) and patients in which nerve damage is not likely (like in chronic back pain patients).
In the latter case I wonder WHY the cortex might get sensitised. Suppose it is because afferent information is not adequate (a lot of noci info and reduced propriocptive info) for example when patients block their spine (muscular). From this perspective restoring function and normalizing afferent information might do the trick.
I have to agree with you Jan-Paul, although if the changes have been present for a long time it might well be that it can't be reversed/desensitised.
Irene Tracey's work seems to show that there are so many different ways nociception can be amplified and reduced throughout the brain, that targeting change only with pharmaceuticals is surely unlikely to influence.
For example, if a child has a traumatic experience in life, epigenetic changes can occur - this could give rise to ongoing sensitivity to any kind of threatening input. If that child reaches adulthood and an attempt to reverse this tendency is implemented, I wonder how successful it can be?
After all, whatever approach used must address hormonal, neurochemical, biomechanical, contextual, cognitive, emotional and behavioural influences. I don't know of any pharmaceuticals that address all of these factors.
What point reducing central sensitisation if it was an adaptive response for the organism early in life? Wouldn't homeostatic responses then occur to return to what was adaptive early in development?
What point reducing sensitisation if contextual issues such as employment, interpersonal relationships, emotional regulation and so are not also addressed? If we only attempt to change one factor and ignore the remaining influences I don't think we'll be successful at improving the LIFE of the person experiencing the problem.
I always learned that the cognitive and emotional aspects you mention are an integral part of sensitisation. The neuronal changes that are found are a reflexion of what is happening. The process of sensitisation is more than only these changes. So i fully agree: we cant leave them out. Luckily, if we restore normal function, on the same time we might allow the subject to experience to have more controll over his or her body than assumed. This mostly is a positive empowering emotional experience.
For one-sided pain sensitization from old and/or traumatic upper extremity injuries, I have had some success using inhibitory massage and resisted movement techniques applied to the corresponding contralateral sites of the injured or painfully sensitive tissues. It takes multiple sessions to change the neuroplastic maladaptation. Although this answer isn't about psychological approaches, the emotional relief is huge for decreasing TENS unit dependence, reducing pain meds, resuming more normal life activities and finally seeing hope for a future.
The theory is to signal the cortex to increase ipsilateral activation of descending inhibitory pathways through the brainstem, but I've had intermittent to no success with lower body extremities. I have had more limited success with bilateral central sensitization. Then, I have used sustained compressions down the back, which seems to be inhibitory, but doesn't show the dramatic improvements as the contralateral UE work. Would not attempt this approach for OA, or fibromyalgia, as the pain is at multiple sites and it would be hard to activate the descending pathways without increasing the overall pain load.
I am puzzled what is happening when I apply the strategy and it doesn't work. Is it leaky gut? Patient's blocking their awareness of back muscle input? Incorrect diagnosis or application of technique? Great discussion, thank you.
As your research indicates, there are people who are more resilient and continue with life despite chronic pain. Do you consider that it is completely individualized?
Could you define circumstances that give rise to both psychological factors you and others mentioned, and chronic pain/central sensitization, such as a trauma that initiates a sustained feeling of helplessness and suppresses the drive for resuming life as it was before? The U.S. Army is teaching resilience to recruits to encourage post traumatic growth, instead of experiencing PTSD in response to trauma. (http://hbr.org/2011/04/building-resilience/ar/1) Are there parallels with central sensitization and chronic pain? Have you found the resilience that allows people to resume their lives despite pain (not suppression) shows evidence of qualities that can be adapted to train people who are disabled by their pain? Would it diminish central sensitization?
Perhaps several of you have already researched this?
I can provide a small bit of evidence on a small group of patients. Over the years we have treated more than 7000 chronic back pain patients (average of 6 years complaints) of which at least 60% has clinical relevant, significant improvement on functional capacity, but also diminshing of pain. Our conclusion is that if sensitisation plays a role in these patients, at least in some cases this must be reversible (or not be a cause in the first place). Otherwise we could not explain these results.
This therapy focusses on restoration of 'normal function', that is beeing active without compensating muscle activity. Exercises include breathing, muscle relaxing, body-awareness and coordination exercises. This training is not -new age like- but a very down to earth learning process for the patients.
I spent a chapter in my thesis on this treatment. Regrettably getting it published is hard because of the lacking of an adequate controll group.
Regrettably financial and more ethical arguments make it hard to do a true RCT.
It makes me laugh to consider 7000 patients treated as a small sample in terms of evidence! However, I think we need to consider that some kinds of CS might be reversible, and to look for when and how.
If we excluded CS in IBS, migraine, childhood trauma sensitization, post-operative and phantom limb pain, fibromyalgia, and osteoarthritis, could we assume that central sensitization with initially acute peripheral nociceptive input might indeed be reversible under some circumstances? (Baron, Hans, Dickenson: Peripheral input and its importance for central sensitization, 2011. (RG))
Then what is the mechanism for your 60%? Is it related to how breath work, self-awareness, muscle relaxation, and touch contribute to a parasympathetic state, stimulate the release of endorphins and serotonin, decrease cortisol and pain? Does a parasympathetic state also activate the descending inhibitory pathways? Or are there local changes that allow the body to reestablish innocuous sensory pathways for peripheral inputs. Or do you have other hypotheses of the mechanisms involved?
How about the contextual issues Bronnie proposes? They contribute to disempowerment, lack of pleasure in ordinary activities, loss of a sense of independence. Empowerment and resilience, both somatic and psychological in your work and hers, could activate beneficial cofactors, raise the pain threshold, alter synaptic firing away from nociceptive receptivity (http://www.ncbi.nlm.nih.gov/pubmed/19712899), lower the receptive field sizes. Nabb et al’s http://www.ncbi.nlm.nih.gov/pubmed/16835035 shows that repeated massage can raise the pain threshold, presumably by activating oxytocin and opioid neurons.
Bronnie, these methods influence the neurochemical and internal states you suggested. What other nonpharmaceutical interventions could contribute to beneficial outcomes?
This is an exploratory hypothesis about why some interventions seem to work, including mine, Bronnie’s and Jan-Paul’s, and I would be grateful for any additional thoughts. I will be presenting my case report to other providers and am looking to be thorough and to ask the right questions.
We are using a technique termed the Combined Electrochemical Technique (CET), a combination of local anesthetic followed by advanced electronic signaling, to reverse the symptoms of peripheral neuropathy. For the chronic disease of neuropathy we are reversing central sensitization. We also have several cases of phantom limb pain which has been eliminated; any reoccurrence in our patients is always stump pain only; although this data has not yet been published, we believe that is strong evidence of central reorganization. (When the stump pain reoccurs, these patients always respond to electroanalgesia treatment only.) There is literature supporting the CET available; email me at email@example.com
My explanation as to why longlasting pain patients might find relieve, even after years is quite basic. Nociceptic afference is, after all said, still principally a signal that something is not going well in the body and that the owner should take action. All of our patients (100%, because otherwise we do not have a therapeutic entrance) show abbarent motion patterns. Often obvious, sometimes only sleigthly, sometimes spectacular. We consider these motion patterns compensation patterns allowing the person to move and act despite underlying physical problems. In many cases these original problems are long gone, but the subject remains stuck in the compensation pattern. So, compensation patterns allow to move despite problems (this can be considered an evolutionary survival trick, compensation prevents you from beeing eaten if you have only a minor physical problem) However compensation has a cost: it usually uses more muscle activity and so energy. Besides this there is more (continuous) muscle tension leading to malnutritionned and sore muscle. Abbarant traction on ligaments and other tissue also induces irritation and overload.
It is our view that many compliant are not caused by some obscure problem, but by the prolongued compensation itself.
Our treatment focusses on reducing the compensation and allowing the body to function without this overactivated muscle. It is not the learning of new motorpatterns, but more the 'remembering' of already existing, more efficient patterns. (Here is a similarity with 'Hanna Somatics' where they talk about sensomotor amnesia!)
Due to the compensation patterns joints are limited in motion leading to decreased proprioceptive input (and high nociceptive input). What we assume is that this disbalance in input triggers the brain. It wants to know what is happening in the body and becomes alert. This is seen as sensitisation.
As we restore 'normal' motion we assumably also normalize the proprioceptive input and diminish nociceptive input. Now in fantasy: the brain recognizes this normalized input and relaxes again: this input is what it expects and now it can return to life as usual.
Of course psychology is totally interwoven with the above described mechanism. Stress and insecurity stimulate sensitisation, The pressure to perform daily activity causes us to go on using compensation patterns. Daily activities draw our attention away from our bodies, etc etc. But also the other way around: if you can have people focus on what their body is doing and that some activities (like really relaxing muscle) has positive effects on pain (which is a strong positive emotional stimulus) it helps to motivate to continue this path of exercise and training.
From my personal experience and reading of the literature ,
It is not .exposure to stressors of that induces sensitization in term of touch/pain ain or any other sensory response
Chronic exposure usually induces habituation.
It is withdrawal from chronic stressors that brings about sensitization
Think of the hypersensitivity of
ex-alcoholics to alcohol
ex smokers to smoke
ex addicts to their drugs
ex climbers to altitude
ex musicians to loud noise
ex farm workers to heat
ex chemical.workers to.whatever they used to make
(dry cleaner syndrome)
Mammalian responses to sensory stressors including "pain" are mediated in part by CO,
which acts as a gaseous neurotransmitter in modulating the nerve action firing potential of our sensory nerves.
About 75% of endogenous CO comes from the action of Heme Oxygenase-1, which is induced by stressors of alll kinds to catabolize heme proteins that are not fully oxygenated into iron CO and biliverdin.
This stress feedback loop is vulnerable to CO poisoning since our bodies cannot
distinguish inhaled from.endogenous CO.
The subjective hallmark of central sensitization syndromes caused by prior CO poisoning is multi sensory sensitivity (aka MUSES syndrome) affecting at least four of the five basic senses.
Many with this are also hypersensitive to pain, hot or cold weather, vibration, and EMF. They are commonly diagnosed
with CFS, IBS, FM , MCS, TMD etc and in children with sensory integration or processing disorder.
The objective hallmark of chronic unresolved CO poisonig is venous COHb > arterial COHb.
You can also test for.this non-invasivelyby measuring CO in exhaled breath. I have a patent pending breatholding method that can distinguish arterial and venous CO concentrations as well as the CO level in the lungs and in the net of all tissues.
During acute CO exposure, of course, art COHb >> venous, but this usually flips within an hour of leaving any exposure, as more CO diffuses out of tissues than in.
Unless properly treated as CO poisoning, this abmormal COHb gap and the multi-sensory sensitivity that goes with it may take years or even decades to normalize without treatment.
With daily treatment by supplemental oxygen.and/or rebreathing techniques,
it takes.about 4 months to normalize both COHb and sensitization, afer which treatment can be stopped.
I am happy to collaborate with any team that wants to test this.
Breath CO testing tdevices.cost a.few.hundred dollars and my method.of.measuring CO levels in lungs, arteries, veins and tissues takes less than 10 minutes .
I think that if we look to only a few simple mechanisms for both producing or reversing central sensitisation we'll forever miss the mark! The factors I identified in my study were unrelated to modulating pain, and the majority of participants reported NRS scores of between 5 - 8 on a 0 - 10 scale where 0 = no pain and 10 = worst pain. What has emerged is that "making sense of pain" by the individual is a critical part of viewing it as less of a threat, and this is largely a cognitive and social process that results in reduced negative affect. Then having some important valued occupation (as in personally-relevant activities, roles etc) helps drive the development of active coping. Now whether this reduces central sensitisation I have no idea, but it does seem probable that higher cortical processes associated with goal pursuit/motivation, intentional behaviour, and broader self regulation play a role in downregulating ascending neurobiological processes.
I doesn't surprise me that people become far less "sensitive" when movement patterns are normalised - it's getting to the point where an individual is willing to do this, and persist in doing this, that involves those higher cortical processes. And in itself I think this downregulates, as I've just mentioned. People have to have a reason for engaging in things that they're worried about doing - whether it's the promise of reduced pain, or simply engaging in enjoyable occupations.
Chronic pain is a stressor, and Melzack reminds us that along with the neural basis for nociception, we also have hormonal responses - and, thinking from an evolutionary biological perspective - it makes sense to me that the default bias for our protective systems is to increase "alerting" responses to protect the organism (us) from danger. Hence, people are more likely to experience increased pain than reduced pain when the system is threatened during early development.
I think, from my study, that one of the processes we haven't really paid a great deal of attention to is how an individual retains a sense of self in the face of a constant threat. One way we see in people with chronic pain is "self-pain enmeshment", where their identity becomes fused with "being a chronic pain patient' and much of goal-directed behaviour is to remove the pain and return to "normal". People in my study had been informed that removing all pain wasn't going to happen (because their disease process is ankylosing spondylitis or osteoarthritis). This gives certainty - and although it's not pleasant, it does produce some sort of security. Things won't change too much. As a result, people in my study began to integrate the "self-with-pain" into their overall self-concept, aligning who they are with what they want to do and vice versa.
Speculating wildly here, I wonder if this has the effect of reducing stress and therefore reducing the neurobiological processes that underpin stress responses. Along with that, because people are engaged in occupations they enjoy or find valued in, they experience "flow" (Csikszentmihalyi), and their whole biological focus changes from defense to optimising performance.
Does this reduce central sensitisation? I don't have fMRI, so I can't know. What I do know is that these individuals don't find their pain bothers them as much, and this remains evident even in the face of new pains that arise.
NMDA NR2-B selective antagonist has seemed to be most perspective on paper. Ketamine and similar don't appeal, please take the side-effects into account when prescribing them to your patients.
If anyone were interested in doing any kind of research into possible central sensitization & related phenomena, then I would be interested in participating. I have a really unknown situation in where no doctor knows anything what's happening, but very strong sensory dissonance happens is certain specific regions, evolved in certain context, but nothing observable thru EMG etc. I've spent a lot of hours researching that topic etc but nobody knows. I am quite sure that my case is different from most syndromes in some specific manner (I could describe everything about it)
HCG administered in very specific daily low dosing addresses he central sensitization target very effectively with not only remarkable analgesic action, but a marked improvement in the psychosocial component that patients suffering with these disorders are known to struggle with.
Distant Vibrotactile Counter Stimulation is a technique of Somatosensory Rehabilitation of Pain Method. In Static Mechanical Allodyniya condition this technique may reverse Touc-evoked neuropathic pain into tactile hypoaesthesia http://doc.rero.ch/record/9235
Excellent research, dr Spicher! By reading your articles for just 10 minutes, you have already connected the most relevant dots for me. I hope to get in contact with you and find out about the DVCS and allodynography, your research really sounds remarkable! All the best!
We have reversed central sensitization with an advanced Electroanalgesia device manufactured by Sanexas, GmBH. See out publications in PPM. Most recent article shows a clear reversal of phantom limb pain. We also use this device to reverse neuropathies; please see other citations which can be supplied on request - firstname.lastname@example.org
While there are many opinions and research findings, my clinical experience of being a pain psychologist for the past 15 years, coupled with brain science, I have found a three prong approach works best: (1) Knowledge shift (Pain in the Brain); (2) Emotional Regulation (I help my patients with ACT - not having them control or change their thinking about their pain); and (3) Mindful Based Movements (Tai Chi, Yoga, Qi Gong, total body conditioning).
Brain science shows us that, when we are "aware" and not in fight or flight mode (emotionally hijacked), our insula (and other subcoritcal networks) become more active and some studies show growth, which clinically translates to re-processing of the pain networks and less pain intensity and greater functionality.
Central sensitization is a mind-body syndrome that is completely reversible. The pioneer in the field is physician John Sarno, MD, who has written a number of books on the subject. I suggest reading his three most recent books. I developed a case of central sensitization so severe that I was often unable to write, read, watch TV, think at a basic level, speak, exercise, etc. without debilitating nerve pain. It lasted nearly 2.5 years. While there is technically "no cure" for central sensitization because there is nothing wrong, the antidote lies in unlearning unconscious fear (a danger signal) that is triggered in a process whereby pathways are engaged that send pain or other sensations to the body. If you have central sensitization, it is likely that you also have a number of other co-morbidities that can be unlearned, too (ie: Reynaud's, globus pharyngeus, migraine, spasms, burning mouth syndrome, even fibromyalgia, etc.) Pain in central sensitization becomes learned over time. Fortunately it can be unlearned. Patients likely will be embracing a reality, in recovery, in which their senses have been providing them with false information. It is important to consider evidence - does your back hurt all day, but when you are engrossed in a basketball game, it disappears? Look for inconsistencies. Howard Schubiner, MD, and David Schecter, MD, are two other contemporaries with books and information available online. Most physicians are unaware that this is known.
I had my central sensitization successfully treated with low-dose (LD) naltrexone by Dr. Norman Marcus, a pain specialist with expertise in diagnosing and treating Ehlers-Danlos Syndrome (EDS). He has had similar success with LD naltrexone in other patients who have chronic pain and EDS.
The optimal dose is determined through titration until the greatest pain relief is achieved and additional dose increases either do not result in additional improvement of pain levels or a decrease in the benefit achieved at prior doses.
We are using the transcranial Direct Current Stimulation (tDCS) as a complementary non-pharmacological treatment to restore the inhibition pain/vibrotactile sense. One of the target is the modulation of excitability of the Posterior Cingulate Cortex (PCC - BA 23). A meta-analysis of 24 studies: Baptista et al. (2019). Latin American and Caribbean consensus on noninvasive central nervous system neuromodulation for chronic pain management. Pain Rep, 4(e692), 1-20.
Whether or not a person is symptomatic, does the elasticity of a person's skin, (for instance the increased elasticity in the skin of a person with Ehler's Danlos Syndrome,) indicate how much of a "viral load" is able to accumulate in their body? Could the length of time that SARS-COV-2 lingers in the body be correlated with the quality of a person's collagen and elastin? Would there be a positive correlation with more severe cases of SARS-COV-2 and more skin elasticity/joint hypermobility, whether or not diagnosed, especially in younger populations and those who seem otherwise healthy with no risk factors?
What is pain?
The official definition of pain is “an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.” This comes from the International Association for the Study of Pain, the world’s top pain research...
The identification of the source and mechanism of pain is fundamental for the treatment of chronic pain. Chronic pain patients may have multiple sources of pain with an impact on treatment outcomes. (1) These coexisting conditions are more common in women than men. (2) We designed a retrospective study to assess this in patients referred to three c...