Friday, January 27, 2012

Yet another "trigger point" discussion

I've written about so-called "trigger points" before:
1.  Trigger point model deconstruction, models in general
2.  Letter to a biomechanically - minded therapist
3.  Why I don't buy the idea that "trigger points" are in muscle


Lately on Mike Reinold's blog, trigger point true believers and triggerpoint skeptics met and discussed the issue. See "Trigger Point Dry Needling for Lateral Epicondylitis" with over 100 comments, many of them quite passionate, most of the passionate ones from those defending the model of triggerpoints being somehow in muscle, or muscle generated somehow, or being source and/or cause of "pain". And that (for whatever reason) their preferred "treatment", dry needling, was the beall and endall forever amen, instead of just one "treatment", conducted as ritual, no more or less effective than a bunch of other possible choices that would be less invasive. 

Some of the comments were wonderful. One long one was from Nic Lucas, who co-authored a solid systematic review of the papers that have been done about so-called trigger points. In the comment section he said (excerpt):
"As a pain researcher, I am interested in the biochemistry of pain, referred muscle pain, DNIC, sensitisation etc etc – but none of this – even 300 papers on the topic – helps me know if practitioners can reliably and accurately identify trigger points, if they can accurately insert the needle into the trigger point, and if this leads to a superior outcome compared to other interventions."
(See "Reliability of physical examination for diagnosis of myofascial trigger points: a systematic review of the literature." Conclusion: "No study to date has reported the reliability of trigger point diagnosis according to the currently proposed criteria. On the basis of the limited number of studies available, and significant problems with their design, reporting, statistical integrity, and clinical applicability, physical examination cannot currently be recommended as a reliable test for the diagnosis of trigger points. The reliability of trigger point diagnosis needs to be further investigated with studies of high quality that use current diagnostic criteria in clinically relevant patients.")
But back to Mike's blog.
In particular, I want to draw attention to comments made by Jason Silvernail, a fellow moderator at SomaSimple, and very cluey dude.
Excerpts:
"I’d like to say that I don’t do dry needling and I don’t think much of the trigger point conceptual model or the needling approaches now popular in physical therapy. Dr Lucas covered the issues with this theoretical model pretty well. I have no interest in learning dry needling, though I did attend an introductory course by KinetaCore given by the chief instructor Mr Edo Zylstra on the topic so I feel I understand the basics of the rationale and supporting literature. I can imagine wanting to learn dry needling at some future date if there were compelling evidence that this approach could produce better outcomes in my patients than the noninvasive manual therapy and exercise approach I currently use, which is supported by basic science plausibility (a science-based standard) as well as published randomized controlled trials (an evidence-based standard). I’ve seen no indication that such evidence exists, however, to merit the expense of training, the risk (however small) of invasive needling, and the regular use of it to maintain proficiency. Until I have compelling evidence otherwise, it represents in my view a more invasive mode of care that has less research evidence to support it so therefore is of little interest to me personally.
Second, I have every confidence that practitioners such as Ms Wendel or Mr Dommerholt or Dr Reinold have their patients’ interests at heart and strive to provide effective, safe, and appropriate medical care to the best of their ability. I may disagree with some of their methods, but I don’t think there’s any reason to think dry needling as practiced by physical therapists is in any way dangerous or inappropriate. I’m almost certain it compares favorably to the risk/benefit profile of an extended course of NSAIDs for example. I am reasonably sure we agree on most major clinical principles since we share a common profession and treat similar populations of patients. I have no desire to dictate to them how to practice and I’m sure they feel the same way about me, though I do feel we have a responsibility to each other as professionals to question each other closely and challenge our decisions and rationales for doing what we do in clinical medicine. 
Third, dry needling is likely here to stay. Pain treatment continues to suffer from rampant practice variation and the lagging adoption of modern neuroscience. A lack of understanding of modern pain physiology continues to plague good discussions and the understanding of clinical problems. As a result, for example, there is a large amount of literature published on the phenomenon of so-called “muscle pain”. Of course we now know that pain doesn’t come from muscles, it comes from the brain. But we still have a large number of researchers who are very interested in the component of the pain experience that is both nociceptive in nature and arising from the nerve tissue in and around muscles – stating it this way should give you an idea of how incomplete this approach has the potential to be. I suppose they will continue to publish on why they feel nociception from nerve tissue in and around muscle (as opposed to in and around other tissues and as distinct from the many other aspects of the pain experience) is very important. No doubt much of this research advances our understanding, and I don’t begrudge them for publishing in their area of interest. I’m sure if enough people are interested in needling and publish enough studies on various trigger point models and link it somehow in some way to some of the neurophysiology of pain in some patients, there will be a case to be made, whether strong or weak, that dry needling is an option. That’s probably where we are now, from a literature perspective. Certainly these folks are not writing prescriptions for homeopathy (that’s just water) or cutting their patients’ backs open for spinal surgery, or using thrust manipulation of the neck for in a chiropractic subluxation model or telling parents not to vaccinate their children. So, as a Physical Therapist, there are probably larger threats to my patients’ collective health than a group of people in my own profession I probably agree with on 90% of practice issues who happen use needling in their practice alongside manual therapy, exercise, lifestyle changes, and other interventions supported by relevant evidence and provided in a biomedical, non-acupuncture, science-based paradigm. So some perspective on this is helpful in my view. Whether you agree with dry needling or not we are all on the same team, so to speak. Doesn’t mean we shouldn’t argue and push each other, though, more on that later."
My bold.

A bit later, commenting on the discussion itself, how it shaped itself, Jason said (excerpt):

"Having been a regular forum participant in professional venues for physical therapy, strength and conditioning, and medicine since 2002, I’ve seen a wide variety of discussions and responses over the years. I don’t suggest this makes me more qualified necessarily to point out errors in thinking and reasoning other people make, this is just my perspective on this issue and the wider question of online debate within our profession. I think several mistakes were made in the context of this discussion that hampered understanding, and it may be useful to look at them in some detail.
First Mistake: Treating honest questioning of an approach or rationale as an “attack” or that it is “discrediting” or “bashing” a method. Here’s something I’m particularly tired of hearing. Any profession that claims to be based in science should not only encourage rigorous questioning and debate but seek it out as part of our ethical responsibility to each other and to society. Any science-based practitioner should refrain from taking questioning personally and focus on the issue at hand while not confusing what we do with who we are. Someone who questions me closely about what I do is helping me refine my thinking and explore in detail my rationale for my decisions – this is not an attack on me or on my chosen decision but an opportunity for growth and learning.
Second Mistake: Argument from empiricism – “I do what works”. Our personal experience and clinical expertise, while often valuable in clinical care and a consideration in evidence-based medicine, is unreliable and prone to bias. Regression to the mean, placebo, expectancy and multiple other “nonspecific” effects are common in medicine and we need to be aware of them and consider them in our clinical observations. Such a purely empirical approach inevitably ignores much settled science on nonspecific effects, and reveals that such scientific considerations as prior plausibility or relevant basic science have been ignored with little more than a hand wave. As a profession based in science we can do better than this, and we should hold each other to a higher standard.
Third Mistake: Reference bombing, a form of argumentum verbosum or “proof by verbosity”. Mr Dommerholt’s citation of multiple references is, in my opinion, an example of just such a technique. This approach seeks to overwhelm participants or opponents with such a large volume of citations that they cannot challenge the argument since to do so would involve reading through every listed article to attempt to determine if they support the points made. Now, I am sure Mr Dommerholt provided those references in good faith and with the intention of honestly supporting his points. The participants actually did a very good job of reviewing several of his cited references in detail. However, as Dr Lucas pointed out, none of the citations actually supported the key points being made about trigger point diagnosis and reliability. Volume can’t make up for accuracy or applicability. Using references is important but in a discussion like this you should choose them carefully and ensure the point you are making is supported by the citation."
In a third comment, after rebuttal by a prominent triggerpointer/needler defender, Jason says (excerpt):
"My comment on empiricism was also not aimed at you, but was a general statement that applied to the overall discussion. In fact I think Dr Reinhold best exemplified this concept, I hope I’m not out of line saying that on the blog he hosts! I have no problem with empiricism if the concepts and treatments remain firmly grounded in basic science, which is of course the issue several folks have with dry needling in the first place. Sue Blackmore once said something along the lines of “free will is an illusion – doesn’t mean it doesn’t exist, but it doesn’t exist in the way that we thought that it did”. I feel the same way about these clinical concepts. Many people in the manual therapy community have been talking about the importance of “joint pain” for years with all sorts of studies about stiffness of the joint, and innervation for nociception, and the effect of these nociceptors on reflexive nervous system behavior, etc. I don’t deny these facts exist, but I question the relevance of those facts of the “joint dysfunction” construct to clinical treatment. Just as many have published similar background information on “muscle dysfunction”, such as those you helpfully posted for review. I don’t doubt such dysfunction exists, but I question its relevance to clinical treatment and its use to drive our clinical decisions – such as dry needling. It’s not my position that TrPs and joint dysfunction don’t exist – I think they may not exist in the way that we sometimes think they do, and the neurophysiology of pain makes that pretty clear, in my opinion.On whether dry needling works in the clinic- I must say, your seminar anecdotes are disappointing. I would think we can do better in 2012, as I write this entry. I am a manual therapist and if you asked me “does manual therapy work for musculoskeletal conditions” my first move would not be a story at a seminar (of course, I have plenty of those also, don’t we all?),but a very brief citation list of randomized trials and other published evidence to support my position. If you asked me about knee osteoarthritis for example I could cite Deyle 2000 and Deyle 2005 as well as a clinical practice guideline and discuss briefly why, given what we know about the pathophysiology of osteoarthritis (for an excellent review I recommend Brandt 2008) exercise and manual therapy makes sense. If we’ve discussed the scientific rationale of TrPs and dry needling enough already, maybe it’s time we turn to any clinical evidence of efficacy. Do you have a short list of a few randomized trials or other clinical outcome studies on dry needling you could share for consideration? Right now the ratio of anecdote to evidence is a bit high for my comfort level. Peta’s contention that it “worked brilliantly on all” and your above anecdotes are certainly not something we can do much with from a discussion standpoint.I’d also note a book called “Muscle Pain” appears curiously named given what we all should know by now about the neurophysiology of pain. There really isn’t any such thing as “muscle pain”, “joint pain”, “bone pain” etc, since pain a perception in the brain not reliant on any particular connective tissue. These old ways of describing clinical problems are really an obstacle to good understanding of these issues from both the clinician and patient point of view. There really is a difference between nociception and pain and exactly which connective tissue the nociceptive driver of interest resides in and around may not be as important as we imagine it is."
My bold.
Voice of reason.

Be sure to check out the blog of someone long past considering "triggerpoints" or needling or any other "meat" treatment theory, as having any validity whatsoever as they relate to the phenomenon of pain, i.e., Lorimer Mosely, at Body In Mind. As a matter of fact, Jason has been mentioned by name at that blog. See a post from about a year ago, Starting conversations: has Jason hit the Silvernail on the head? about this post in the thread, Enough is enough.
Here is a link to Lorimer's freely available articles. In particular, check out the one titled "Teaching people about pain: why do we keep beating around the bush?" 



Thursday, January 26, 2012

APTA section exposed for including visceral manipulation

In her recent blogpost at Science-based Medicine, Visceral Manipulation Embraced by the APTA, Harriet Hall paraphrased a response by the Director of Education, Carrie Schwoerer, to another member, J.W. Matheson who complained about APTA's inclusion of visceral manipulation, as:


"In other words, “We don’t need no stinkin’ science! We support any treatment that can provide positive anecdotes. We believe the plural of anecdote is data. Instead of offering guidance, we’ll let our members sink or swim: we’ll make them responsible for knowing ahead of time how much evidence supports a treatment and deciding whether they believe it is sufficient to merit a personal decision to study it.”This is beneath contempt. I don’t think I need to elaborate. Another formerly respected organization has drunk the CAM Kool-Aid."


I think she translated correctly.

The comment section went a long way - 93 comments (several from yours truly).
Some of them were memorable: David Gorski replied:
"Ack! I frequently use a line about chiropractors that usually gets a laugh and, as far as I know, I originated, specifically, “Chiropractors are physical therapists with delusions of grandeur.” Inherent in that line is the assumption that physical therapy is science-based, while much of chiropractic is not. After this, I might have to rethink my line. I don’t want to (it’s a great line and physical therapists can do amazing things), but if the APTA keeps this up, I’ll have no choice."

As it turns out, "visceral manipulation" was added to the organization through the "Section of Women's Health". Commentary ensued about how important this was or wasn't to the overall organization.

I lived in a rain forest climate for 25 years. My opinion is, woo is like water: if water finds its way, any way at all, small nail hole even, into your condo building, it will get in and accumulate and rot the walls - eventually the whole building will cave in.

Erik Meira entered the comment section. He is battling from within, has a podcast site, The PT Podcast. He interviewed the same J.W. Matheson who wrote the initial letter to APTA with his concerns, and then sent the reply to Harriet Hall, for comment.

Several comments came from several PTs, and SomaSimple was mentioned. Eric put out a challenge:
"The main thing that I am trying to get across is how muddy the waters get when you try to create a line of demarcation for con ed. Is scientific plausibility enough? Sure, if presented objectively but who does that (even I don’t)? Scientific plausibility is a continuum from “not likely at all” to “almost definite” (no absolutes) so where do you draw the line? The black and white position that I just presented creates such a line, but who would be happy with it? This is the problem we have had trying to create a policy in the past. Every modification we give to that hardline position that I described creates enough of a crack to let a whole lot of things come pouring in. 
I challenge the moderators of SomaSimple (obviously very smart, scientific, and have their heads on straight) to create such a policy (even the “10 steps”). Then see how easily one can make a little tweak to something like MFR to make it fit on a technicality and all of a sudden you need to let them present or face a lawsuit for restraint of trade. Think this won’t happen?" http://en.wikipedia.org/wiki/Wilk_v._American_Medical_Association
So: we have been challenged.
It will take some thinking.
My line in the sand has always been, if it's a mesodermal* derivative you suggest you can alter by using your hands, you're dreaming. If it's an ectodermal* derivative you suggest you can alter by using your hands, we're getting somewhere closer - perhaps. Probably not. A patient's umwelt isn't going to tolerate a therapist as its umfeld, not for long, biopsychosocially speaking, not unless it gets something real (from ITS perspective!) out of the treatment encounter that it can use for becoming more efficient or effective in the world.

*Mesodermal derivative: majority of structural elements and tissue - bone, muscle, connective tissue, tendon, ligament, visceral organs
*Ectodermal derivative: nervous system and neural support tissue (CNS and PNS), skin, teeth, eyes, adrenal medulla, their associated system afferent and efferent functionality

Sunday, January 22, 2012

Is placebo like gravity?

So.. I'm thinking lately that manual therapy will never be able to eliminate placebo from its work. As a commenter (Natalie Shaw) pointed out today on Facebook, it's kinda like gravity. You barely notice it's there. Which made me think about the craziness of a culture demanding that you must take everything out into outer space to weigh it, so that gravity (placebo) is eliminated. How Balnibarian is that? How tooth-fairy supportive is that?

What's worse is a culture that says, OK, if you can't do that, then we accept all sorts of ideas that aren't even plausible. From Science-based Medicine blogpost by Harriet Hall,

Visceral Manipulation Embraced by the APTA




Placebo (in my own humble opinion) is a patient's attitude, readiness: it's in every awake person, every conscious human; it's there all the time, including for something as supposedly as objective as surgery (see comment by ErikMeira in the same SBM thread, Jan 20th).

Viewing it as a confound when building an evidence base for manual treatment (especially for manual treatment of live, conscious, hopeful people) is really counterproductive. I think placebo would be best framed as a match the *patient* might use to ignite his/her own recovery, regardless of treatment.

The corollary of this is that all manual therapy (regardless of kind), or maybe medical treatment too, assists, maybe blows on the flame a bit. Too much is counterproductive, might extinguish it.

Everything a patient needs for combatting nuisance pain is already right there inside their own nervous system. A good human primate social groomer will realize this (however instinctively, non-consciously); he or she will cheerfully step outside his/her own ego to help somebody build whatever fire they need to build to burn off their own pain problem.

Saturday, January 21, 2012

Pain and fire

A stray thought wafted up today, escaping the head hurt brought on by the futile discussions I read everywhere on the topic of placebo.

I've given placebo a lot of thought. I've studied Benedetti's book, The Patient's Brain: The neuroscience behind the doctor-patient relationship, in detail. I think it's great.

Patients with pain are tired of waiting for the medical profession and other health care professions to assimilate pain science. They are banding together into societies and organizations and foundations. They are asking pain researchers to talk directly to them, to explain to them why they hurt so bad, how they might help themselves.

In February Catherine Bushnell is going to do exactly that. She will present a webinar, Out-Thinking Pain: How the Mind can Control Pain. Anyone who wants can register for this. I think it's even free.

I wrote a bit on the topic here, earlier, the confusion that surrounds the idea of placebo.
I just don't think it should be that confusing.
.......

Now, to the topic at hand:

Let's consider a metaphor.

People equate pain with fire. Understandably! Pain is painful. It burns. Burns are painful. They hurt. The fire of burning pain. I get it.

But... but....

What if pain resolution required starting a new fire? A fire of a different kind?
...................



Backfire
The objective would be to turn pain to ashes. Burn up the pain itself. Let a fire roar through the nervous system backwards, and burn pain right out of the humanantigravitysuit, metaphorically speaking. It makes sense to me, now that I've tasted the experience of being in pain, for myself. It didn't feel good. I had to mount an offensive, and fortunately, it was a success. I wrote at length about it in the Killing Pain series.
..........................



Firewood
A fire deliberately set so as to burn off pain needs fuel. Firewood. An intact and hopefully "normal" nervous system has natural capacity. It has descending modulation. This is intrinsic - a whole stack of good seasoned split wood is there in everyone, i.e., central nervous systems know how to make opioids and all sorts of other lovely things that kill pain. All such a fire needs is a light and some kindling, some dry bark or crumpled paper or something.

The way the human brain works, if it is too focused on pain itself, it won't be able to accumulate enough dry kindling. Dry kindling, in this new metaphor, is the ability to distract oneself sufficiently to keep going in spite of having pain.
......



Firepit
A fire can't be started just any old where. You need a place, a context, a shelter from the rain, a hearth. A therapy clinic, and a therapist who knows something about burning off pain, can provide an appropriate context for playing with fire, safely.
.......


Match
Then... then...  you need a match.

Placebo is an expectation, a hope, a connection to something, a drive to seek and find support. In humans, it can be as simple as a phone call to a health care provider. It does not have to be anything fancy, or deceiving. Placebo is a match.

Without the match, nothing else works. It all just sits there.
In fact, if any single thing is not there, resolution won't occur.
All the components of a fire are necessary for it to complete, burn out, and leave behind a pile of ash. A pile of pain relief.

Think about it.
........


Someone to blow the flame to life?
What about manual therapy? I think, for the purpose of this metaphor, manual therapy would be an outside person who physically handles the person in pain, and by so doing, blows gently on the flame to get it going. It isn't always necessary, and sometimes the therapist (depending on what it is they think they're supposed to be doing) might blow too hard and kill the flame instead of helping the flame to kill the pain.

But in small judicious amounts, done carefully in the moment by a therapist skilled in noticing and tracking responses in nervous systems, responding appropriately, willing to take his or her time, manual therapy can help fan the flame so it can take off.




Friday, January 20, 2012

Bio and psycho and social embraidedness

I think "embraidedness" is an actual word. I hope so. Whether it is or isn't, here goes:

The more one reads about the brain the harder it is to maintain any sort of concept that there is NOT almost complete interpenetration of everything. Just yesterday I saw this: Violent homes have the 'same effect on brains of children as combat does on soldiers'
Brain scans were done as children looked at pictures of faces.
"... children who had been exposed to violence at home showed increased brain activity in the anterior insula and amygdala in response to the angry faces."
Both these areas are involved in what Legrain et al. call the salience detection system for the body (as opposed to "pain" matrix.) (Great paper, by the way.)
.....

Over at Edge.org, Andrian Kreye contributed something interesting about "subjective environment":
"Explanations tend to be at their most elegant, when science distills the meanderings of philosophy into fact. I was looking for explanations for an observation, when I came across the theory of "Umwelt" versus "Umfeld" (vaguely environment versus surroundings) by the Estonian biologist and forefather of biosemiotics Jakob von Uexküll. According to his definition "Umwelt" is the subjective environment as perceived and impacted by an organism, while "Umfeld" is the objective environment which encompasses and impacts all organisms in it's realm."

Well, not quite, because the truly objective environment, according to Uexküll is, well, fairly un"know"able:
"These umwelten are distinctive from what Uexküll termed the "umgebung" which would be objective reality should such a reality exist."
But still: Oh. My. That's it. Right there. Trust German to have come up with the perfect word already. I wish I spoke German. It would save me an awful lot of time and energy probably. Oh well..

For a long time I've discussed (with many words and only vague notions and scarce concepts) this very thing: inner and outer environments. The brain has to reconcile them, it has to "embraid" them, in its internal regulation system. Its internal regulation system (according to Mayo Clinic Medical Neurosciences 5th Ed.) is full of opioid receptors, everywhere, and includes the insular cortex and anterior cingulate - part of the salience detection system.

My brain immediately clunked into a new place: I'm pretty sure this is in the ball park:

1. umwelt ("subjective environment as perceived and impacted by an organism"... aka first-person, aka "effective","efferent") 
2. umfeld ("objective environment which encompasses and impacts all organisms in it's realm"...aka, third-person, aka "affective", "afferent").

The brain has to figure out how to intersect itself, coming and going, inner and outer, like a mobius strip, AND still keep itself sorted. Big job. No wonder it is not monolithic.

I find these ideas of umwelt and umfeld to line up fairly well with the ideas of endothermic (warm-blooded) and exothermic. An exothermic creature, like a reptile, loses its heat to the environment. Its environment controls its activity. An endothermic creature, like a mammal, just makes more heat for itself, and goes about its business, doing whatever it wants. Stronger umwelt, completely organic, fights against the umfeld. Even trees push their leaves off when they find them to be a physiological detriment. Their umwelt is better off without them at a certain point. It's all about boundaries, and how to make, then maintain them. Bio or psycho or social.
......

Also, I saw this posted on Facebook yesterday: Cure and Healing by a cancer surgeon, about two patients, both with throat cancer, who to him illustrated the difference:
Patient 1:
"Her surgery and radiation therapy were completely successful and her cancer was controlled.  Nevertheless, she was overwhelmed by depression. She continued to smoke and drink, refused to go out in public, quit her job, and rejected her friends.  She agonized over her appearance and speech. She refused to return for follow-up visits or counseling. I eventually lost track of her."   
Patient 2:
"I received a letter that she had prepared in her own hand prior to her death. “Please don’t feel that you failed me,” she wrote. That message of comfort and gratitude was emotionally wrenching, but nevertheless, welcome and still treasured."   
His conclusion:
"One person was cured but not healed. The other was healed but not cured. We aim for both Cure and Healing, but the difference, I believe, rests in the relationships."  
I agree, it's all in the relationship: but as a therapist, I don't do either. I'm an interactor, not an operator.
I think, rather, with therapeutic contact, both physical and verbal, and by staying well inside my own umwelt, trying hard to not become too much umfeld to the patient, I give his or her brain sufficient and necessary distraction so it can fix itself, sort out its own umwelt and umfeld more optimally. Furthermore, my umwelt does not need to invade anyone elses' umwelt to feel real or validated. It prefers to be left alone, and it assumes everyone elses' likely does too.
....

I have considered my own umwelt quite a lot. It is hypervigilant, like the children mentioned earlier, having been through physical abuse as a young child, before it had any capacity to defend itself. It became obese. Now it is becoming non-obese. It has gained a lot of inner strength and resolve throughout  the entire 20-year process. For whatever reason, it had to expand itself out into the world, and it did it the only way it could - through gaining weight for a time - until it could "feel" itself as "big" as most of those populating its umfeld, and (somehow) gain the idea it was as competent, that it had sufficient agency. At least, that's my story and I'm sticking to it. Now it's ready to change, and it is changing, decluttering, de-hoarding, lightening itself. Pushing off its leaves.
.....

I saw this 4 and a half minute video earlier today, and know it's just the way I'd like to be in another 35 years: My friend Maia, about a 95- year-old ballerina living a beautiful life inside her umwelt. Ah. Nothing about that is the least bit umfeld to my umwelt. In fact I feel like I expand toward, or am drawn toward, her existence, or one similar.

The first I heard of umwelt was in this thread on somasimple.
......

PS: I can't resist - I just saw this gorgeous-looking meaty paper on Facebook all about dopamine, open access, and must link it here: Dopamine, Affordance and Active Inference: 
ABSTRACT: The role of dopamine in behaviour and decision-making is often cast in terms of reinforcement learning and optimal decision theory. Here, we present an alternative view that frames the physiology of dopamine in terms of Bayes-optimal behaviour. In this account, dopamine controls the precision or salience of (external or internal) cues that engender action. In other words, dopamine balances bottom-up sensory information and top-down prior beliefs when making hierarchical inferences (predictions) about cues that have affordance. In this paper, we focus on the consequences of changing tonic levels of dopamine firing using simulations of cued sequential movements. Crucially, the predictions driving movements are based upon a hierarchical generative model that infers the context in which movements are made. This means that we can confuse agents by changing the context (order) in which cues are presented. These simulations provide a (Bayes-optimal) model of contextual uncertainty and set switching that can be quantified in terms of behavioural and electrophysiological responses. Furthermore, one can simulate dopaminergic lesions (by changing the precision of prediction errors) to produce pathological behaviours that are reminiscent of those seen in neurological disorders such as Parkinson's disease. We use these simulations to demonstrate how a single functional role for dopamine at the synaptic level can manifest in different ways at the behavioural level. 

Tuesday, January 17, 2012

Longterm potentiation and nociception

As I scanned through Edge.org's question for 2012, I came upon this: Todd Sacktor's essay on "Elementary Particles of Memory", his contribution to the question,  2012: What is your favorite deep, elegant, or beautiful explanation? 


Excerpt:
The key molecule maintaining LTP is a persistently active enzyme, called PKMzeta. Together with the molecules maintaining LTD that are still being determined, these elementary molecules store most forms of memory. Without the persistent strengthening of synapses by PKMzeta, the ongoing physiological process of LTP at the synapse collapses, and most long-term memories are erased. The animal returns to a "blank slate," with just its genetic inheritance of behavior.
LTP= longterm potentiation. It's a process by which synaptic connections between neurons are strengthened. 
LTP is a persistent strengthening of synaptic connections triggered by a brief episode of high-frequency activity of those connections... The key molecule maintaining LTP is a persistently active enzyme, called PKMzeta... PKMzeta is an unusual form of protein kinase. Once made when LTP is triggered, PKMzeta is active all the time, rather than being turned on and off in response to other molecules. When mutations occur in genes for kinases that render them active all the time, they promote uncontrolled growth in cells, leading to cancer. However, the change in the gene that encodes PKMzeta also restricts the formation of the persistently active kinase to neurons. Because mature neurons are tethered to thousands of other neurons through their synapses, they cannot possibly divide and are remarkably resistant to forming cancers (most brain tumors in adults originate from glial cells, which readily divide). By restriction to cells that communicate but cannot divide, a mutation signaling continual growth, potentially deadly to an organism, was used to maintain long-term memory.
Isn't that remarkable. Here is a paper by him, from 2008: 

PKMzeta, LTP maintenance, and the dynamic molecular biology of memory storage.

ABSTRACT: How memories persist is a fundamental neurobiological question. The most commonly studied physiological model of memory is long-term potentiation (LTP). The molecular mechanisms of LTP can be divided into two phases: induction, triggering the potentiation; and maintenance, sustaining the potentiation over time. Although many molecules participate in induction, very few have been implicated in the mechanism of maintenance. Understanding maintenance, however, is critical for testing the hypothesis that LTP sustains memory storage in the brain. Only a single molecule has been found both necessary and sufficient for maintaining LTP--the brain-specific, atypical PKC isoform, protein kinase Mzeta (PKMzeta). Although full-length PKC isoforms respond to transient second messengers, and are involved in LTP induction, PKMzeta is a second messenger-independent kinase, consisting of the independent catalytic domain of PKCzeta, and is persistently active to sustain LTP maintenance. PKMzeta is produced by a unique PKMzeta mRNA, which is generated by an internal promoter within the PKCzeta gene and transported to the dendrites of neurons. LTP induction increases new PKMzeta synthesis, and the increased level of PKMzeta then enhances synaptic transmission by doubling the number of postsynaptic AMPA receptors (AMPAR) through GluR2 subunit-mediated trafficking of the receptors to the synapse. PKMzeta mediates synaptic potentiation specifically during the late-phase of LTP, as PKMzeta inhibitors can reverse established LTP when applied several hours after tetanization in hippocampal slices or 1 day after tetanization in vivo. These studies set the stage for testing the hypothesis that the mechanism of LTP maintenance sustains memory storage. PKMzeta inhibition in the hippocampus after learning eliminates the retention of spatial memory. Once the PKMzeta inhibitor has been eliminated, the memory is still erased, but new spatial memories can be learned and stored. Similar results are found for conditioned taste aversion when the inhibitor is injected in the insular neocortex. Thus PKMzeta is the first molecule found to be a component of the long-term memory trace.

Hmn. Insular cortex. That little brainpart, important in pain processing, in salience processing, shows up again. 
Anyway.
So... find something that messes with LTP and maybe.. "memory" could be erased? ... but I am way ahead of myself. Let me start again. 

A few days ago, this story came out of Nature | News: High-dose opiates could crack chronic pain. People in Vienna have found a way to reverse longterm potentiation in spinal cord synapses, at least in rat models. Here is the abstract of their paper,  Erasure of a Spinal Memory Trace of Pain by a Brief, High-Dose Opioid Administration:
Painful stimuli activate nociceptive C fibers and induce synaptic long-term potentiation (LTP) at their spinal terminals. LTP at C-fiber synapses represents a cellular model for pain amplification (hyperalgesia) and for a memory trace of pain. μ-Opioid receptor agonists exert a powerful but reversible depression at C-fiber synapses that renders the continuous application of low opioid doses the gold standard in pain therapy. We discovered that brief application of a high opioid dose reversed various forms of activity-dependent LTP at C-fiber synapses. Depotentiation involved Ca2+-dependent signaling and normalization of the phosphorylation state of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors. This also reversed hyperalgesia in behaving animals. Opioids thus not only temporarily dampen pain but may also erase a spinal memory trace of pain.
So, what they did was, took rats, gave them 'chronic pain', i.e., allowed longterm potentiation to develop in their spinal cord synapses such that the second-order neurons conveying nociceptive afferent information to the rats' poor little brains, presumably their insular cortices, along with some other destinations probably, got way better at their jobs. Then, the researchers figured out what dose, and what kind, of opioid it took to reverse all the longterm potentiated changes. It turned out to be something called remifentanil, a "potent ultra short-acting synthetic opioid analgesic drug",  "given to patients during surgery to relieve pain and as an adjunct to anesthetic."

(A bit further down in the Wikipedia link is this interesting comment: 
Doses listed in the package insert from its manufacturer are much higher than those used in actual clinical practice
Huh. Gee, why not use it according to directions?)

Yes, pain would be a good thing to be helped to forget. Great place to start. 

There are only three neurons between anywhere on the surface of a vertebrate (or beneath its surface, I suppose..), and said vertebrate's brain. Clearly the junctions are the right place to target. Clearly opioids can help with pain, both prevention and, apparently, according to this, cure. It looks as though Sacktor may have been looking at the second link in the chain. The Vienna people looked at the first link.

I looked in the Vienna paper to see if PKMzeta figured in at all - the authors say they took a look:
We thus asked whether PKMz in spinal cord also plays a role for the maintenance phase of LTP (22, 23) after LFS. PKMz inhibitor ZIP had, however, no obvious effect on the maintenance of LFS-induced LTP within the observation period of 6 hours (fig. S2D).
22. M. N. Asiedu et al., J. Neurosci. 31, 6646 (2011).
23. T. C. Sacktor, Nat. Rev. Neurosci. 12, 9 (2011).
 It looks like they didn't see what Sactor found, or else they found something else:
Depending on the type of conditioning stimulation, distinct forms of LTP [longterm potentiation] are induced at C-fiber synapses, which affect different groups of postsynaptic neurons (13, 24) and involve signaling pathways that overlap only partially (13, 24, 25). 
We therefore tested whether OID [opioid-induced depotentiation] can also be achieved for other forms of established spinal LTP. We induced LTP by conditioning high-frequency stimulation (HFS, 100 Hz; fig. S3A) of sciatic nerve fibers or by subcutaneous capsaicin injections (fig. S3C). 
The latter selectively activates nociceptive nerve fibers, which express the transient receptor potential channel subfamily V member 1 (TRPV1). Remifentanil also fully reversed these forms of LTP (after HFS,  depotentiation was from 158 ± 8% to 99 ± 9%, n=12,P<0.001; after capsaicin,  depotentiation was from 170 ± 16% to 100 ± 13%, n=5, P<0.001;fig.S3, B and D), demonstrating that OID applies to various forms of activity-dependent LTP at C-fiber synapses.
My comments inside square brackets.

It's probably worth mentioning that if that first synapse, the one in the dorsal horn, can be affected, then the second-order neuron, the one that not only carries the info straight up but can turn into a signal amplifier blasting the info through the thalamus into all the third-order neurons that go to the sensory cortex, insular cortex, anterior cingulate cortex, like a lawn sprinkler on steroids, or a finger over the end of a garden hose increasing the distance and force of the spray, will be diminished to mere leakage. Then the brain will be able to ignore the ordinary light tapping or tinking of rain (nociception) on the roof, instead of a continuous thunderous pounding driving rainstorm day in and day out. Yes, one could still distract oneself (not register it as "pain") but it would probably be a lot harder than if the noise level could just be turned way down again to ordinary levels.


From the Viennese paper:
LTP is a synaptic model for some forms of hyperalgesia (26). We therefore asked whether OID has any relevance for behaving animals. Sub- cutaneous injections of capsaicin quickly led to mechanical hyperalgesia at the injected hindpaw (Fig. 4). The same dosage regimen of remifentanil that caused OID significantly attenuated capsaicin- induced hyperalgesia (Fig. 4A). Not surprisingly, the behavioral hyperalgesia was reversed only partially by the opioid treatment because additional peripheral and central mechanisms contribute to capsaicin-induced hyperalgesia (27, 28). PP1 inhibitor calyculin A fully blocked the attenuation of hyperalgesia by remifentanil (Fig. 4B), suggesting that depotentiation at nociceptive C fibers may erase a memory trace of pain[sic - at this point it's still only nociception]. LTP is expressed in ascending nociceptive pathways, which are relevant for the aversive components of pain. It will thus be interesting to explore whether opioids may also reverse the tonic-aversive state of pain (29). Taken together, the present and our previous data (3) demonstrate that activation of spinal MORs triggers distinct, bidirectional, and state-dependent synaptic plasticity in naïve versus potentiated C-fiber synapses. Remifentanil activates Ca2+-dependent signaling pathways, leading to activation of PP1 and PKC. At potentiated synapses, this normalizes the phosphorylation state [i.e., reverses the energy efficiency gained, makes them work harder again, makes them more "naive" again] of GluR1 at Ser831 and that of GluR2 at Ser880 and thereby depotentiates synaptic strength in C fibers. The presently identified reversal of synaptic LTP in nociceptive pathways provides a rationale for novel therapeutic strategies to cure rather than to temporarily dampen some forms of pain with opioids.
All "synaptic learning" seems to be about, really, in the case of pain, is a ratcheting of energy efficiency, such that the nociceptive neurons take advantage of a chemically altered "gain" in synaptic "strength" so that they can do their job with less fuel, perhaps. Economy of means. The Vienna people have figured out how to reverse that in a rat model, at the first synapse: it seems to me that Sactor's work has had to do with the second synapse upstairs in the brain, that he has not directly involved himself in LTP of the nociceptive system. 


Anyway, those are just some ramblings I've strung together from two recently read pieces of work that sound like maybe they talk about the same thing, LTP, but when I look close, I can't see that they actually do. I need to read the Vienna paper several more times, but so far it still looks like there's a gap between pain science and other neuroscience. It might help if people doing 'pain' science at the first synapse would stop calling it "pain science" and instead would call it "nociception science."



Friday, January 13, 2012

"Robert Trivers: Why do we deceive ourselves?"

Robert Trivers explains deception at many levels, psychosocial and biological. Favorite takeaway line:

"Men tend to be more overconfident than women do. Both of us tend to be overconfident, in various circumstances, but it's more a male disease. So powerful men are both overconfident, and ignorant. That's an unfortunate combination." 

http://fora.tv/2011/10/04/Robert_Trivers_Why_Do_We_Deceive_Ourselves

Sorry, I don't know how to embed this. You will need to copy and paste the url. Please do - it's great, about 16 minutes.

Thursday, January 12, 2012

To be brutally honest..

I'm only 5'2". I gained weight, for years. I did not "feel" too fat.

When I looked at myself objectively, I could "see" that I was "fat".
Deciding to start losing it was a conscious decision. I did not firmly decide to lose weight until I saw I had reached about 190 pounds. The weight of many hefty, bossy, alpha type men. I took some time, but knew that enough was enough, and I'd have to start to rescue myself from the danger of potential deliberately engaged ill-health. Just like I quit smoking at age 30-ish, just because it was time.

I did not weigh myself, almost my whole life. I did not restrict eating. I ate whatever I wanted. Whatever quantity I wanted. Whenever I wanted. I started doing this with no restriction at the end of the eighties, just as I was facing the end of my "youth" and turning 40. Prior to that, I had restricted myself somewhat in order to "look good" (well, as good as it was possible for me to look without trying very hard).

Restricting myself just in order to "look good" began to feel very artificial, very much a constraint I imposed upon myself due to external priorities, only, not because I really wanted to.

I think I must have thought, when I reached midlife, "It doesn't really matter anyway - who do I think I'm trying to impress by being "normal"? "
I deliberately did that socially unacceptable thing called "letting oneself go", and flipped my chin at the whole idea that other peoples' opinion would constrain me: some new part of me started to fight for autonomy: I started gaining weight, dropped external constraint, got to know "me", opened a practice of my own, became an adult, lots of stuff all at once. I went through midlife crisis, menopause, felt awful, felt like I was whitewater rafting almost every day, still functioned in the world.

Getting "big" did not happen overnight. Getting on the internet helped me sit still, which helped a lot. I think I had got my biggest by about 2007.

To be honest, something in me liked weighing a lot. Something about me liked having mass. Something in me liked having gravitas. Something in me definitely liked having a bit of weight to throw around. (See recent blog post about posture and anger and dominance.) Completely subjective of course - I could have been knocked over with a feather, probably. But I felt quite strong, never felt handicapped. I proved many things to myself, by being a fat person for a long time.

1. My weight did not really interfere with my life. It has been a successful life, lived entirely on my own terms.
2. My weight reassured me that I was real. Had substance.
3. My weight never stopped me doing anything I wanted to do. Mind you, nothing I wanted to do was ever particularly physical to begin with.
4. Even though I was never very physical, I was always active; therefore, I think I stayed healthy.

All of this is occurring to me, only now that my weight has dropped by another 20 pounds or so.
Part of me is grieving a bit because it wanted to be "big". But, alas, I can't be "big" and stay healthy in the long term, at the same time. I'm just not tall enough.

To be brutally honest, what I learned from being objectively, medically, dangerously, however-you-want-to-define-it fat, or big, was a new boundary, and some kind of internally derived and sensed power, or sense of self.

Wednesday, January 11, 2012

"It hurts when I do this (or you do that): Posture and pain tolerance"

I linked to this paper earlier this week on Facebook (link to Facebook thread) because something about it made me stop and think.
Abstract: Recent research (Carney, Cuddy, & Yap, 2010) has shown that adopting a powerful pose changes people's hormonal levels and increases their propensity to take risks in the same ways that possessing actual power does. In the current research, we explore whether adopting physical postures associated with power, or simply interacting with others who adopt these postures, can similarly influence sensitivity to pain. We conducted two experiments. In Experiment 1, participants who adopted dominant poses displayed higher pain thresholds than those who adopted submissive or neutral poses. These findings were not explained by semantic priming. In Experiment 2, we manipulated power poses via an interpersonal interaction and found that power posing engendered a complementary (Tiedens & Fragale, 2003) embodied power experience in interaction partners. Participants who interacted with a submissive confederate displayed higher pain thresholds and greater handgrip strength than participants who interacted with a dominant confederate.
My comment there was, "Huh! Non-nociceptive induction of pain. I like the psychosocial angle this paper takes. Strictly visual signaling can sensitize the salience or threat detection system. If this is valid and that's the case, is it any wonder that women seem to have more chronic "pain" than men?"


Chronic pain is experienced by more women than men. Pain is experienced differently by women than it is by men. Pain experienced by people less advantaged socioeconomically is experienced as more disabling. Women are generally less advantaged socio-economically.   


The idea of considering a "salience" system, as opposed to a "pain" system, is important. One of my favorite papers of all time is The pain matrix reloaded: A salience detection system for the body, by Legrain et al, who argue that if a wasp comes toward you and you think it's going to sting you, you will instinctively try to swat it prior to any nociception ever having had to occur. 


Here is the entry for "dominance" in the non-verbal dictionary at Center for non-verbal studies (a great link, by the way - hours of fun and learning.)


An external dominance display travels immediately to the threat detection system via the visual cortex, and the salience network notices. If it's an internally generated dominance display, i.e., one produced by the organism itself, the salience system gets the news via other channels maybe, gets the idea that all is well, I guess. Check out Todd Hargrove's blogpost, Posture and Pain Tolerance, about the same paper. Todd says, 
In the first experiment, participants who assumed a dominant posture displayed higher pain tolerance than those in submissive postures. 
In the second experiment, subjects had differing strength and pain tolerance levels depending on whether they interacted with a partner who used either dominant or submissive posturing. 
For example, if a subject was paired with a partner with dominant body language, this encouraged the subject to adopt a submissive posture in response, which made him weaker and less pain tolerant. 
Remember this next time you hire a buff alpha male as a personal trainer.
My bold.
As a PT, I was taught "good" posture, to be on the lookout for "bad" posture, and to try to "correct" the posture of almost every patient who came to see me. This was going to help them, or so I was led to believe. Not that "poor" posture actually caused, or correction thereof ever really fixed, any actual pain problems. Lots of people with already "good" posture had lots of pain too. To me, this story about psychosocial aspects of posture and pain absolutely destroys "misbehaving meat" heuristic conjecture about posture&pain, entirely.

The whole thing about our being primates is very relevant: as a short female human primate my psychosocial reality is I've been physically subordinate to most people all my life. What I've learned recently about personally inhabiting this kind of humanantigravitysuit, especially as it ages, is that anger is useful against, can even vanquish entirely, pain. (Pain associated with frozen shoulder at least.) Maybe an interoceptive, turned-inward sense of anger naturally builds from frustration of life lived in a world full of taller, and therefore by visual default, more (potentially) dominant people; if extraverted perhaps it turns into short man syndrome, or small dog agression. Perhaps anger is valuable for maintaining a sense of well-being, on an organism level. Clearly subordinate individuals must have to suppress most outward display of any internal anger they may have if they don't want to be killed by the rest of the troop or pack, or in the case of humans, separated from one troop and put in jail with another kind. Clearly humans have to learn how to find inner strength, yet remain humble, remain harmless, remain interactive.  Most figure it out one way or another. 
As a therapist, I never go there. Wading into peoples' feelings. As a therapist, I do not encourage expression of emotion. (I don't suppress it if it comes up, but my kind of therapy has nothing to do with trying to elicit it in others.) I do not want to be in anyone's line of fire; I grew up with a physically abusive (at times) mother, and was attacked once by a very cranky dachshund who dashed out of his yard through his gate at me, while I innocently walked by his house, on the public sidewalk. I've spent a lifetime dealing with, dancing with, trying to understand and harness anger, in myself. I do not want to deal with it in other people in any way whatsoever, especially not as a therapist. Yet, wow. I discovered my own anger to be so extremely useful, so ready to help me, when I had horrid pain. And I found it relatively easy to engage and use effectively in the presence of a therapist, without freaking her out.  So I guess my opinion is, save it til you really need it for something. 


To women, on a biological level, and on much.. OK, most of the human psychosocial level, it's a man's world. Yet.. 
This morning as I rode the elliptical, in front of the movie, Australia, which I've now seen 30-minute chunks of often enough to be able to remember them better, a thought crossed my mind during the scene where Drover arrives unexpectedly to the ball, just as Lady Ashley is right on the brink of signing her cattle ranch over to the appropriately-named robber cattle baron, Carney; "Drover" (the dashing male lead played by flashes-his-12-pack-during-the-movie Hugh Jackman)  who apparently cleans up well, appears at the top of the stair all decked out in a (impossibly!) perfectly tailored suit, just in the nick of time to save the day, the ranch, the lady, and have a bit of inner revenge on the snob bunch by impressing them all with his looks and ability to fox trot after only one drunken lesson out on the range. 
For the one and only time in the whole long movie, he is completely clean-shaven. 
Interesting (I thought as I huffed and puffed): men who shave appear much less dominating to female human primates; men who want to get close to women, without intimidating them by default, shave their faces. They try to make themselves look more like us. I've read there are fish that do the same thing, mimic the appearance of girl fish, and end up mating, having more offspring, or something. It even has a name: inter-sexual mimicry. 






Sunday, January 08, 2012

Yogawareness

Recently NYT published an article to do with yoga: How Yoga Can Wreck Your Body.
Paul Ingraham, at SaveYourself.ca, linked the article on Facebook as did several other people, but somehow Paul's threads always seem to end up being a well-attended party, so here is a link to it: Paul's SaveYourself.ca thread about the yoga article. 

The very first blogpost I ever wrote here was about this very topic: Mourning yoga, October 2005. The tide would seem to not yet have turned, if the New York Times is now feeling obliged to write about yoga injury..

Maybe this will help - a piece from the Guardian sent to me this morning by Ian Stevens, an old online friend who lives in Scotland: Prepare the mind.

It contains five useful preparations:

1. Intention:

"Physical exercise begins before you start moving – with intention. Understanding the function of the exercise, preparing the body, being confident in the required breathing, timing and form, and then committing yourself. After all, if you're not sure where you're going, and how you're going to get there, then you're unlikely to reach your destination. So train smart. Take the time to prepare mentally before each and every exercise. It will ensure a safe, enjoyable, effective workout – maximum benefit, minimum time."
Oh my gosh. Yes. If it's yoga, know that there is no goal at all. None. Just easy expansion, or contraction, in any and all positions, like a sea creature. Working ever so gently toward being able to do that effortlessly. Being able to feel as though gravity is canceled out of your humanantigravitysuit and you are weightless, floating in the universe, physically part of it (you are anyway, whether you acknowledge it or not).

2. Breathing:
"During exercise, the muscles in the body require oxygen to create energy. The breath is crucial in exercising efficiently and effectively. A lack of oxygen will lead to tiredness, tension and even nausea; sufficient oxygen means peak performance and that feeling of being energised. So, take a deep breath at the start of each exercise, then focus on steadily exhaling as you complete the more strenuous phase, and steadily inhaling as you complete the less strenuous phase of the exercise. Whenever possible, avoid holding the breath while exercising. "
I would propose that deep breathing does a LOT more than just "provide the muscles with oxygen." Sure, it does that, but it provides the brain with oxygen too: Furthermore, it expands and contracts the entire trunk, raises and lowers the diaphragm. For sure it will "slide&floss" phrenic nerve roots in the neck, the thoracic spinal nerves within the meat around the ribs, and all the long cutaneous lumbar nerves flowing between and through body wall layers of the low back, pelvis, abdomen, and inguinal fold. Furthermore, deep breathing will change the chemistry of the body a little, which will affect how brainstem nuclei E-ffect E-verything E-lse. Including any sense of anxiety one might start out with. Never ever hold your breath.
3. Timing: 
"Timing in exercise means being fully aware of your rhythm. Each type of exercise has its own natural tempo – some are best performed fast, some slow, steady and deliberate. Timing is often related to the amount of effort we put into the exercise. Try to leave behind robotic, tense movements, and develop a natural, flowing style, like a top tennis player in action. An exercise performed with the right timing will always be more effective than one that is rushed. So focus on the rhythm of each exercise, using the breath to help you."
... And some "exercise", like yoga for example, is best done with no speed whatsoever. It should be done as though you had all the time in the world. It should be done completely outside of mere time.
 4. Form: 
"Good form ensures exercise is done through the entire range of movement, targeting every part of the muscle, in the most efficient way. But good form is rare, because it requires focus, which most of us struggle with, so we forget to check our posture or alignment. For safe and effective exercise, give these your full attention. Think less about getting to the end of the exercise, and instead focus on the moment, bringing your awareness to each and every muscle movement. This is what it means to be mindful of form."
In yoga, people get sidetracked by "form" -  form is gradually accumulated by paying attention over a long period of time to one's own proprioceptive input, and interoceptive input. It doesn't really spring forth fully formed. It's important in yoga to build it oneself, not be externally focused, or let a teacher handle your body for you, or push you into "correct pose" or "proper posture" - if that happens, protest! If you layer in the feeling of improved "form" over time, it will instead become an emergent (inside-out) phenomenon, and not an artificially-imposed-from-without, possibly even nociceptive, externally-corrected constraint on your humanantigravitysuit. Which is, after all, the only place you have to exist. Never let anyone outside you push you around.
5. Recovery:
"Recovery is important between strenuous activity and between different exercises. It requires an awareness of your physical, emotional and mental wellbeing. In the pause between exercises, remain alert and focus on your breath and other sensations. Remember your breath is a barometer to your level of effort. Are you hunching your shoulders, limiting your body's capacity to take in more oxygen? Or even holding your breath? Both will create physical tension and slow your recovery. Good recovery is essential to remain injury-free."
Yoga has a wonderful "pose" called the "corpse pose" (a name that sounds a lot more attractive in its original language). It's my favorite. Basically, it's supine on the floor. On one's back. Flat. Arms and legs full out and relaxed. Still breathing. Deliberately. Fully. Fully inhaling, then exhaling. Not very frequently. It's incredibly relaxing to just lay there, and not do anything except breathe once in awhile, and feel your whole body flatten down onto the floor like the unconstrained water puddle it yearns to become some day, let it practice doing that, even as you're still alive in there and will be for a good long time to come.

Trigger point model deconstruction, models in general

Today I noticed a retweet from a (Spanish, by the look of things) twitterer,  @argoicoechea, who keeps a blog (Goicoechea arturo, his own name, surname first. Here is his bio). 

(Thank you, Chome browser, for making translation so darn simple.) 



What caught my eye about this tweet was that it was about trigger points. So I checked it out. Fibromyalgia, myofascial pain, tender points and trigger points: splitting or lumping?
Open access. I had not seen it yet, when I wrote Why I don't buy the idea that trigger points are in muscle, in July '11. (I don't retract anything I said in that blog post, just in case anyone is thinking I might.)

The paper is co-authored by a pair of researchers, one of whom represents the staunch mesodermalist assertion by the look of it (Bennett), and the other not so much (Goldenberg); it is written in debate-style, point-counterpoint format. 

ABSTRACT: Myofascial trigger points (MTPs) have long been a contentious issue in relation to fibromyalgia, and poorly defined pain complaints in general. Can MTPs be reproducibly identified? Do MTPs have valid objective findings, such as spontaneous electromyographic activity, muscle microdialysis evidence for an inflammatory milieu or visualization with newer ultrasound techniques? Is fibromyalgia a syndrome of multiple MTPs, or is focal muscle tenderness a manifestation of central sensitization? These issues are discussed with relevance to a recent paper reporting that manual palpation of active MTPs elicits the spontaneous pain experienced by fibromyalgia patients.

One of the papers cited by Goldenberg is by a few people I know online.
Lucas N, Macaskill P, Irwig L, Moran R, Bogduk N. Reliability of physical examination for diagnosis of myofascial trigger points: a systematic review of the literature. Clin J Pain.2009;25:80–89. doi: 10.1097/AJP.0b013e31817e13b6. [PubMed] [Cross Ref]

What is a "model"?
I think of a model as a thought bubble. The more variables it can account for, the bigger and shinier will be the bubble, the more opportunities it will provide more people (bigger 'surface area') to see through, to clarify their ideas of physical existence. 
Stephen Hawking, who just celebrated his 70th birthday in spite of having had ALS for decades, is quoted as saying,  “A model is a good model if first it interprets a wide range of observations in terms of a simple and elegant model, and second if the model makes definite predictions that can be tested, and possibly falsified, by observation.”    

So, here's the thing: a model that posits muscles as being bad guys and giving rise to "pain" is a poor model. Problems with the model include:
1. It was built on palpation! 
2. The palpators who push the current muscle (mesodermal derivative) model either deliberately ignored highly innervated custis/subcutis they were palpating through, and therefore didn't explain how they could subtract it as a freakishly unconstrainable confounding variable (bad on them) or else never thought to include it in the first place (still bad on them, but perhaps a bit more forgivable). 
3. Its perpetuators still refuse to consider that the nervous system itself is a probable confounding variable, or how to constrain it (probably because they can't (!) so they keep hoping no one notices. Hey! I notice!) 
4. As Goldenberg points out, interrater reliability is a problem. It stands to reason it would be; unless and until palpators from any school of thought figure out someday how to remove the blubber layer, with all its embedded cutaneous neural structure and unpredictable fractal nervous system qualities which derive from the nervous system's own strong opinions about protecting its organism in each and every moment from exteroceptive environmental threat, models built on palpation only are doomed to be consigned to that category known as belief systems or pseudoscience. The only other way to study sore spots via palpation, in an honest way, would be to include that layer.  
5. Goldenberg: "Just like fibrositis and fibositic nodules have become historical curiosities, MTPs will eventually be discounted as discrete pathologic abnormalities in the muscle." 

I see this image: a triggerpointer injector or investigator who insists trigger points are caused by muscle misbehaviour or pathology sits up on top of a silo, his "model", high and dry, eyes covered by blinkers and ears stuffed by fingers, while a big wet tsunami of neuroscience and biopsychosocial investigation of nociception and pain swells and surges around him. As long as he can artificially control the height of the silo upon which he is perched, by adding more "research" purporting his pet model, the wet won't touch him. But man oh man, that silo will rot away one of these days, and he'll fall in. 

Friday, January 06, 2012

Does this cab make my hippocampus look big?

Lots rattling by today.

1. First, from Deric Bownds Mindblog:


Structural changes in adult brains caused by acquiring knowledge
Excerpt: "We conclude that specific, enduring, structural brain changes in adult humans can be induced by biologically relevant behaviors engaging higher cognitive functions such as spatial memory, with significance for the “nature versus nurture” debate."

OK, so using cognition for spatial memorization will physically bulk up the hippocampus in London taxi drivers. Cool. 




2. Next, from Body in Mind blog:

First impressions do count! Especially if you’re stressed.
          File under, "You never get a second chance to make a first impression."
Kind of important if you're a human primate social groomer, with control only over the context you set for patients. This requires attention to details such as the sensory input your patient's brain will encounter, including noise levels, light, smell, cleanliness  color, temperature, and attention from you. 
It stands to reason that as their brain takes in a new setting, it will be "externally" cognizing. If their bringing you a pain problem to treat (most of them do), they are likely to have found themselves at odds with their own internal cognizing capacity in one way or another. 




3. Which leads me to (open access):

Echoes of the Brain within the Posterior Cingulate Cortex
ABSTRACT: There is considerable uncertainty about the function of the posterior cingulate cortex (PCC). The PCC is a major node within the default mode network (DMN) and has high metabolic activity and dense structural connectivity to widespread brain regions, which suggests it has a role as a cortical hub. The region appears to be involved in internally directed thought, for example, memory recollection. However, recent nonhuman primate work provides evidence for a more active role in the control of cognition, through signaling an environmental change and the need to alter behavior. For an organism to flexibly react to a changing environment, information processed in functionally distinct brain networks needs to be integrated by such a cortical hub. If the PCC is involved in this process, its brain activity should show a complex and dynamic pattern that partially reflects activity in other brain networks. Using fMRI in humans and a multivariate analysis, we demonstrate that the PCC shows this type of complex functional architecture, where echoes of multiple other brain networks are seen in separable yet overlapping subregions. For example, a predominantly ventral region shows strong functional connectivity to the rest of the DMN, whereas two subregions within the dorsal PCC show high connectivity to frontoparietal networks involved in cognitive control. PCC subregions showed distinct patterns of activity modulation during the performance of an attentionally demanding task, suggesting that parts of the dorsal PCC interact with frontoparietal networks to regulate the balance between internally and externally directed cognition.

If what we are about as human primate social groomers, trying to help patients learn to move better, or watching to see if they can move better as a result of our therapeutic interaction with them based on our physical contact with them, or both, it would likely help us to know a bit about how our patient's brain processes internal and external cognition. One already by default is an external distractor for their brain to process. One's goal is to teach them how to focus on themselves, go inside and focus on their own movement, interoception, proprioception, etc., and at the same time use the information you've given them, the ideas you've presented them, about pain, about how the brain descendingly modulates it. For that to happen successfully, as their groomer you have to become unintrusive and invisible so their brains don't have to worry about you anymore.


I am now going to go away, ingest, then digest this delicious-looking paper in a leisurely manner. I'll write any thoughts about it I may have.

Monday, January 02, 2012

Sunday, January 01, 2012

Happy New Year



It's a new dawn, it's a new day, it's a new life



I saw this posted today on Facebook by Alice Sanvito.

Fits me like a glove. Lots of biologic reference in the words, physiology suggested by the blobbishness of the images. Uplifting lyrics sung in a bluesy way. Still not much in the way of colour.

Getting there maybe. Not yet though. Just keep going.

Great song.