Neural internet

Let's pretend for a moment that the body is completely democratic, that electrical signaling does not exist. Each cell can communicate with every other cell adjacent to it. Let's say we're manual therapists, working on somebody's toe. Let's say the cells in the patient's toe can "feel" us just fine, and they want to tell all their little friends about our contact. They do this through squirting molecules out into their extracellular environment, hoping that one or more of the molecules will land in an appropriately shaped pocket on some other cell's membrane, that the recipient cell will pick up the phone (accept the molecule), receive the news, be perturbed about it enough to care, and respond somehow, maybe by passing the message on.

Let's pretend this happens from cell to cell. But like one of those games where messages are passed around a room, by whispering in the next person's ear, the message soon becomes garbled and by the time it gets all the way around the room it's often not the same as when it started out.

In the body, the message gets passed along for a few cells out, maybe, but it will degrade, fade, dilute. We're talking chemistry in an ocean, really..

So, neurons evolved! Problem solved! Message stays crisp, each neuron responds to a particular sort of stimulus. Hi-fidelity occurs. There are only three cells between anywhere on the surface of the body, and a part of the same body which can protect its organism! The ENTIRE organism! How cool is that!?

Some of the neurons that evolved, and live up in ganglia by the spine, grew two enormously long arms, one of which monitors the skin on the outside of the toe, and the other goes right into then up a pathway at the back of the spinal cord - right up to inside the medulla! [dorsal column nucleus] Which makes these the longest cells in the entire vertebrate body!

There are still places where molecules have to swim across oceans, but only two places, and they are special enclosed places called synapses, with lots of helpers available called synaptic proteins, to help the message remain non-degraded. Yeah, sometimes problems happen and messages go astray or maybe the organism hasn't got quite a full complement of messenger molecules, or is lacking a particular dock shape.. but on the whole, information is greatly sped up, and action can be taken well ahead of danger to the organism, usually.

Single cell organisms still have to do everything on their own, with only a membrane between them and the rest of the entire world; some multicell creatures without neurons still have to rely on cell to cell communication. Life is way better (at least faster in lots of ways) than it used to be, since evolution came up with the neural internet.

Traits and continuums

Trying to gather a few thoughts together into some kind of bundle..

1. Recent blogpost from Fred Wolfe on Fibromyalgia Perplex,  Fibromyalgia as a Trait (and a Continuum) Disorder

Delicious post: 
Fibromyalgia is a symptom based disorder, not a sign based (therefore categorical) "disease." And may never become one. Certainly Fred Wolfe, himself, backed away from his original  attempts to do just that. (See this link, in this post.)

"Pain, fatigue and sleep problems affect all people at some time, and some people are afflicted more than others. Fibromyalgia can be diagnosed by criteria when all of these symptoms are continuous (chronic) and bothersome (severe)."

 "When people with fibromyalgia were followed for an average of 4 years, it was found that patients switched between criteria-positive and criteria-negative states frequently, with 44.0% failing to meet criteria at least once during follow-up." 

 So, people can fade in and out of "having" it, and some who may "have" it, don't even know it. 

Definition of "trait: 

"Applied to fibromyalgia, trait means the tendency of those with fibromyalgia to respond to physical or mental stress in a stereotyped way—by increasing pain, fatigue and the other symptoms of fibromyalgia."

OK, sounds like their brains have learned to respond that way. 
.......
The way brains learn to deal with all sorts of things in life. 
Which brings me to the next thought I want to bundle in, somehow:

2. A poster on SomaSimple, MaxG, picked up on the notion of Trait and continuum:

"Last year I read Oliver Sacks great book on migraines (called, well, "Migraine").In some parts, he takes an almost philosophical look at migraine headache as a sort of forced withdrawal response of an organism to a stressor. 

Sacks incorporates migraines into several "frames" in the book:

1.) in a continuum of allied "neurological disorders" (epilepsy, narcolepsy, vagal attacks, catatonic reactions, etc.), where the differentiato between each "disease" is the duration of symptoms and the "Jacksonian level" (functional level of neural integration).2.) in a "disease cycle" where the sufferer alternates between bouts of, say, migraines, ulcers and psoriasis as a response to particular stressors, being symptom free of one while suffering from the other, etc.3.) migraines as a continuum itself; where it is implied that amny people suffer from subclinical bouts of migraines (with or without aura, with or without vagal symptoms, with or without headaches) and the clinical cases simply represent one "extreme" of this continuum.

I hope I'm not the only one seeing a similar line of thinking in the above quoted article on FM.
I find this concept of exaggerated stress responses fascinating.Viewing the human organism as a "complex dynamical system" that is hardly in a simple equilibrium but more in a state of constant "circling" around one "chaotic attractor" (maybe a "normal" state") and thinking of "diseases" like migraines or FM as a jump to a different "chaotic attractor"; this makes a lot of sense, in my opinion of "spectrum" disorders like FM and migraines."

3. Then he posted a wonderful image that looks a bit like this, but not this exact one: 

Loenz attractor image from wagner.nyu.edu

Here is the one he shared:

http://www.stsci.edu/~lbradley/seminar/images/lorenz3d.gif

4. His picture reminded me of this blogpost from the Dana foundation:  Unlocking the Mystery of Consciousness,  by Lauren Ware:

Excerpt: 

..... "Information doesn't just flow through a brain like cars down a highway," says Brown. "It creates all kinds of loops, some excitatory, some inhibitory, some that amplify, down-regulate or modify other circuits."

5. His post reminded me of a couple items (see REFERENCES) discussed in the March issue of Nature Reviews Neuroscience, blogged about here: Moving your mind instead of your body. 

6. Anyway.. here's to rostral control of descending modulation of all manner of afferent input, sensory-discriminative exteroceptive and afferent-motivational interoceptive input, be it nociceptive or non-nociceptive. The only way to know if it is or isn't nociceptive, for real, is to examine it, and decide. If it vanishes, great - you managed to help your own brain descendingly modulate it favourably. If it didn't vanish, you might want to hire a careful human primate social groomer to add a bit or even more than just a bit of exteroceptive contact, so your brain has a chance to get a better fix on it, then try again. But realize this: only you will be able to change it, from the inside, by building pathways, so, best get started. 

REFERENCES
1. Artur Luczak,  Peter Bartho,  and Kenneth D. Harris;  Gating of Sensory Input by Spontaneous Cortical Activity. The Journal of Neuroscience, 23 January 2013, 33(4): 1684-1695

2. Kenneth D. Harris & Alexander Thiele; Cortical state and attention. Nature Reviews Neuroscience 12, 509-523 (September 2011)

Moving your mind instead of your body

I found this paper earlier today, Mindfulness starts with the body: somatosensory attention and top-down modulation of cortical alpha rhythms in mindfulness meditation, and planned to comment on it a bit, but became sidetracked by the CRPS paper.

Serendipitously Todd Hargrove beat me to it, and produced this wonderful blogpost! Meditation and Pain. Thank you Todd - you saved me piles of time!

What I thought might be fun would be to compare and contrast, speculate a bit on the possibilities presented by this new (unrelated) paper by Luczak et al. from NatureReviewsNeuroscience, Gating of Sensory Input by Spontaneous Cortical Activity, which proposes a mechanism by which rostral centers might "control" sensory input. It was about auditory input, but I'm thinking, this could maybe be extrapolated to other kinds of sensory input. Nature Reviews Neuroscience commented and suggested reading this paper as well, from a few years ago, Cortical state and attention, (Harris et al) in which the authors describe how selective attention can affect input into cortical columns. This sentence from the abstract is particularly delicious: 

"We suggest that selective attention involves processes that are similar to state change, and that operate at a local columnar level to enhance the representation of otherwise non-salient features while suppressing internally generated activity patterns."

The NRN post about these two papers, titled "A gate for sensory responses," and behind a paywall, says, "In a new study, Harris and colleagues show that one role for irregular spontaneous activity may be to allow higher-order structures to control the representation of sensory stimuli... Harris and colleagues show that one role for irregular spontaneous activity may be to allow higher-order structures to control the representation of sensory stimuli." There are references to brain neuronal functions called "activity packets," (which are spontaneous) , and "Population activity fluctuations were strong in synchronized states — that is, there were clear activity packets — whereas population activity seemed more evenly distributed in desynchronized states..  both during silent periods and during sustained tone presentation, suggesting that cortical state influences the structure of activity packets more than does an auditory stimulus... [in that] activity packets are triggered by corticocortical rather than thalamocortical connections, the authors propose that activity packets in primary auditory cortex reflect the top-down opening of a ‘gate’ that allows input from lower auditory regions to be processed by primary auditory cortex." (My bold)

OK, that's a bit dense, but I think it means that the cortex has final call on what goes on in the brain, or at least where to put a boundary between itself and what it has to sift from its inner and outer environments somewhere in the cortical columns (processors) of the brain. And I think that sifts right back to the paper from PLoS1 that Todd blogged about, an excerpt from which is here: 

"Using a common set of mindfulness exercises, mindfulness based stress reduction (MBSR) and mindfulness based cognitive therapy (MBCT) have been shown to reduce distress in chronic pain and decrease risk of depression relapse.

Paying attention to interoception in a safe context might be all it takes. Really, it's looking that way. 
Last word to Todd: 

"Meditation seems like powerful medicine indeed, perhaps second only to general exercise in its health benefits. I find it fascinating that this all purpose mental muscle can be developed by something as simple as focusing attention on bodily sensations.So don’t just sit there!Pay attention to just sitting there! You might get better at playing the mental movies you want to watch."

CRPS: A review, by J Field

I found this paper as I rolled around on the internet yesterday:

J Field; Complex Regional Pain Syndrome: a review

J Hand Surg Eur Vol. 2013 Jan 22

"Abstract 

Complex regional pain syndrome, formally known as reflex sympathetic dystrophy, is a poorly understood condition that describes a collection of clinical symptoms and signs occurring in the peripheries most commonly after trauma. Pain is the main problem. It is generally out of proportion to the degree of injury and can be unresponsive to narcotics. In addition joint stiffness, temperature and colour changes, and swelling occur. The diagnosis and treatment are challenging for any clinician and a multidisciplinary approach is often necessary with physiotherapy, occupational therapy, and the pain team. The hand surgeon is involved for two reasons, firstly as the upper limb is the most frequently involved, and secondly because the condition may be a complication of the patient's surgery and result in a much prolonged recovery. This review elucidates the recent advances in the knowledge of the aetiology, classification and treatment of this fascinating condition."

J. Field of Cheltenham General Hospital is listed here as Mr. Jeremy Field, one of the ortho surgeons. 

Here is his CV. Looks like he specializes in hand surgery and has a special interest in CRPS.

I have treated at least three patients that I know of, in my whole life, who I'm pretty sure had this condition, all women, all post-wrist fracture. The first two I encountered as a young hospital therapist, decades ago. I barely knew what I was doing. If they got better it was in spite of me, not because I was able to help them very well. 

The last one was just a few years ago, long after I had established my own practice and knew a great deal more about pain science. She did very well in an outpatient setting. 

Anyway - to the paper, and some delicious excerpts. 

1. "International Association for the Study of Pain (IASP) in 1994 coined the term complex regional pain syndrome (CRPS). CRPS is divided into two types: CRPS type I where there is no obvious nerve damage and CRPS type II where there is identifiable nerve damage (causalgia) (Stanton-Hicks et al., 1995).
"Using the IASP criteria, patients must have con- tinued disproportionate pain and one symptom in three of four categories (sensory, vasomotor, sudomotor, and motor), and one sign in two of the same categories. There must be no other diagnosis that better explains the symptoms and signs." (p.1)

2. "As the symptoms and signs of both types of CRPS are similar the use of the terms ‘high flow’ CRPS (or warm CRPS) and ‘low flow’ (or cold CRPS ) are being used more often. High flow CRPS, describing the hot, painful oedematous extremity, and low flow CRPS the cool, atrophic limb." (p. 2)

Field says, pain is the biggest problem. Described as burning, nagging and throbbing, it combines three categories into one horrible sensory soup: 

"1. hyperalgesia – increased sensitivity to noxious stimuli – i.e. a pin prick causing very severe pain. 2. allodynia – pain provoked by non noxious stimuli– i.e. stroking the skin causing pain. 3. hyperpathia – temporal summation of allodynia – i.e. repeated stroking causing increased pain." (p.2)

Additionally, it is non-dermatomal, unresponsive to narcotics, "out of proportion to the degree of preciptating injury," severe to the point where active movement is avoided and so is contact. Synchiria ("touching the affected limb hurts the other limb"),  hyperacusis (intolerance of ordinary sound levels),

more generally, smudging of somatosensory representational maps, are common features. Vasomotor instability, swelling, and stiffness are big problems. 

"In CRPS even thinking about moving (motor imagery) can itself cause pain and potentially hinder movement (Moseley, 2004, Moseley et al., 2008)."(p.4)

There does not exist any diagnostic test - diagnosis is clinical.

The juiciest part is the aetiology. I love it when people who write papers actually stick their necks out a little bit, dare to say out loud what everyone already thinks anyway, and sign their name to it. 

Field runs through all the precipitating factors that have been identified: trauma, especially fracture, strokes, heart attacks, smoking, hereditary factors, and even no cause. It can occur following surgery for carpal tunnel or Dupuytren's contracture, so patients undergoing these procedures should be made aware of the risk, however slight it may be. 

Altered limb awareness, opposite limb symptoms, symptoms in face or jaw, do NOT mean the condition is caused psychologically. 

Field thinks there are two main causes, inflammatory and neurological, likely related.

"In the early phase of the condition the clinical features of rubor, tumor, calor, dolor and function laesa certainly point towards an inflammatory response." (p.5)

Presence of inflammatory mediators such as tumour necrosis factor, CGRP, interleukin2, and Substance P, might be the result of neurogenic dysregulation, which leads us to the neurologic points he makes, next (the juciest of the juiciness in this paper): 

"The theory of a neurological abnormality in CRPS type I is the more compelling for two reasons. Firstly the symptoms experienced are so like those in CRPS type II, where there is a specific nerve injury. Secondly the bizarre symptoms associated with pain being experienced in other parts of the body are best explained by cortical reorganisation."

"Neuralgic pain associated with CRPS may be explained by damage to small fibre neurons. These thinly myelinated (A-delta) and unmyelinated (C-fibre and sympathetic axons) transmit afferent information from mechanical, thermal and chemical stimuli. They are also responsible for release of vasoactive peptides such as CGRP and substance P, which are present in CRPS. These small fibres are particularly sensitive to injury, and their degeneration often results in pain (Llewelyn et al., 1991). Nerve conduction studies are not sensitive enough to pick up these abnormalities. Histological examination has found C-fibre degeneration, but no myelinated axon damage in limbs amputated for CRPS (Van der Laan et al., 1998). Immunological labelling of axonal markers has confirmed small fibre nerve damage in CRPS (Oaklander et al., 2006). With this small fibre nerve damage come the trophic changes in the skin seen in CRPS (Figure 2). Very similar skin, nail and hair changes occur in small fibre peripheral neuropathies (SFPN)." (p. 5) (my bold.)

There we are, back to C-fibres and all their weird efferent function, trophic supply to tissue being among them. Without the C-fibres, mesodermal targets don't know what to do with themselves. Without C-fibres, blood supply to everything - including nerves themselves, hello? - becomes a bit of a dysregulated mess. 

He goes on to include bone changes as being the plausible result of small fibre damage.

"Bone scan and radiographic changes are attributed to increased osteoclastic activity. Osteoclasts are only bone resorbing at low ph which is when small fibre nociceptors will fire. Small fibre secretions are critical for bone formation and maintenance and bone is significantly influenced by small fibre axonal degeneration (Hukkanen et al., 1993). The pain in long standing or chronic CRPS could be explained by some form of nerve damage as occurs in the long standing pain experienced in post herpetic neuralgia." (p.5) (my bold.)

He goes on to describe various cortical changes that occur due to CRPS, mapping changes chief among them. 

"There is definitely an alteration of perception of the limb in CRPS. Patients pay less attention to the affected limb, have peculiar desires to amputate, and have a mismatch between sensation of the limb and how it looks." (p.6)

Most of the time symptoms resolve but it can take years, and sometimes... the symptoms do not resolve. 

It might recur, but whether it will or won't is kind of debatable. There isn't enough evidence to suggest it's preventable. Treatment is confusing but the best kind is interdisciplinary. Hand therapy is essential. Mirror therapy can be helpful. DMSO cream might be helpful but evidence is small. Oral medication doesn't seem to help a whole lot. Injections don't seem to work. Don't resort to amputating. Watch out for signs: 

"1. pain, but particularly allodynia and hyperalgesia that can be demonstrated. The temporal summa- tion of hyperalgesia is difficult to feign. 

2. trophic changes in skin and nails. 

3. wasting of muscles. 

4. fixed joint contractures. 

5. radiographs showing periarticular osteopaenia –
although not diagnostic a radiograph showing changes is significant." (p.8)

Red flags include: 

"1. excessive swelling – check for excessively tight cuffs or ligature marks further up the limb. 

2. wrapped-up limbs – these may be to accentuate temperature or colour differences, and bad cases of CRPS would never let anything touch the hand. 

3. flexed posture of fingers with no fixed contracture. 

4. Alterations of colour and temperature can be achieved from dependency and immobilisation of
the hand (Singh and Davis, 2006). 

5. Inconsistency of timing and degree of tremors." (p.8)

Reference:

1. M J M de Klaver, M A van Rijn, J Marinus, W Soede, J A P M de Laat, and J J van Hilten; Hyperacusis in patients with complex regional pain syndrome related dystonia. J Neurol Neurosurg Psychiatry. 2007 December; 78(12): 1310–1313.

Juxtapositions on afferent input

I love when a bunch of papers come flying out together, or else sequentially but close enough together that they seem related, that all seem to relate favourably to human primate social grooming. 

Here they are:

Hao Wu, John Williams, Jeremy Nathans; Morphologic diversity of cutaneous sensory afferents revealed by genetically directed sparse labeling. eLife 2012;1:e00181  (Written about here)

Vrontou, S. et al. Genetic identification of C fibres that detect massage-like stroking of hairy skin in vivo. Nature 493, 669–673 (2013) (abstract only)

Tajerian M, Alvarado S, Millecamps M, Vachon P, Crosby C, et al. (2013) Peripheral Nerve Injury Is Associated with Chronic, Reversible Changes in Global DNA Methylation in the Mouse Prefrontal Cortex. PLoS ONE 8(1): e55259. (Open access)


What do all these papers say?

The first one has mapped the surface of skin. In rats.. but still. Surface of skin. Humans have surface of skin too. Probably we still have pretty axons trailing around, even though we lost most of our fur long ago. Whatever, we still have lots of Ruffini endings in any case. They'll do.

The second one is just the latest in a string of papers, going back years, about how there are afferent neurons that specifically code for pleasurable sensation.

The third one actually tries to measure what goes up in the brain in peripheral nerve injury (code for nociceptive input/neuropathic "pain" in a mouse model), and how it can be reversed "environmentally" - which is to say, from "outside" the organism, by environmental "enrichment." Which likely involved more pleasurable distraction, interaction with other mice (including contact), and more movement in general. Although the authors didn't say that specifically.

Fred Wolfe, trigger points, fibro

Today I was very pleased to read a blogpost from a blog that is new to me - The Fibromyalgia Perplex, by Fred Wolfe:

Travell, Simons and Cargo Cult Science, Feb 14 2013:

An excerpt:

"David Simons, who with Janet Travell were the authors of Myofascial Pain and Dysfunction: The Trigger Point Manual (TPM),²was a remarkable physician. At his death in 2010, he was memorialized in a long New York Times obituary that included this: ` David G. Simons, whose ascent more than 19 miles above the Earth in an aluminum capsule suspended from a helium balloon set an altitude record in 1957 and helped put the United States on the road to manned space flight died April 5 at his home in Covington, GA’ [a record that still stands (FW)]. Janet Travell was equally famous. President Kennedy’s physician, the first woman physician at the New York Hospital, she was also the author of an illuminating autobiography. If trigger points needed a mother, she was it. In fact, the Travell and Simons drawing of trigger points and their radiations began as a poster presentation at an American Medical Association meeting that was later published as an ‘exhibit.’³ 

But if there ever was need for examples of PP-EBM, these authors provided it. In a book that was filled with extraordinary anatomic drawings, Travell and Simons provided figures of locations of trigger points, radiation of pain, injection and `spray and stretch’ techniques.  In one 61-page chapter, the authors provided detailed information about perpetuating factors for myofascial pain (MFP) and trigger points, including 317 references. The book was an enormous success—a bible of trigger points. It found it way into academic libraries and practitioner’s offices through several editions. In a perfect example of science by citation and PP-EBM, it was repeatedly cited as an authoritative reference. Many, like me, trying to understand trigger points, read deeply in the book. But the more I read the more I doubted. The book represented opinion, not science. None of the trigger points or their treatments were validated; none were tested for reliability. There were almost no studies in the Travell-Simons book, just testaments. Most of the perpetuating factors were plain wrong, and represented outdated, overthrown junk science."

1. Dr. Frederick Wolfe, his picture, profile. 

2. He is named as author or co-author in 400 papers.

3. He came up with the idea of treating fibromyalgia as a disease, then later regretted doing so.

From Drug Approved. Is Disease Real? in the NYT, 2008: 

"Dr. Frederick Wolfe, the director of the National Databank for Rheumatic Diseases and the lead author of the 1990 paper that first defined the diagnostic guidelines for fibromyalgia, says he has become cynical and discouraged about the diagnosis. He now considers the condition a physical response to stress, depression, and economic and social anxiety.
“Some of us in those days thought that we had actually identified a disease, which this clearly is not,” Dr. Wolfe said. “To make people ill, to give them an illness, was the wrong thing.”"

And to make such a big deal out of imaginary nouns called "trigger points" was clearly the wrong thing in the first place. People have been gouging away at them ever since, with needles, with elbows, with thumbs.

Previous posts by me about so-called "trigger points"
1.Yet another "trigger point" discussion Jan 27/2012
2.Trigger point model deconstruction, models in general Jan 8/2012
3. Why I don't buy the idea that "trigger points" are in muscle  July 4/2011
4. Letter to a biomechanically-minded therapist July 9/2011

I want to stand up and clap my hands off. I really do. Thank you for this, Dr. Wolfe.

Where is the therapeutic boundary?

Today I spotted this link posted to FaceBook: A good pain. 

The tagline reads, "Returning to action, safely, is paramount to junior hockey players who want to help the club and impress scouts"

I facepalmed through the entire news story, and I'll explain why.

At first glance, it seems like a nice story - PT helping an athlete with some shoulder pain - one of those feel good stories that promotes the profession and reminds everyone about athletes and how hard they work and what a great thing sports are, etc., etc. 

John Beesley is probably a fine, well-intentioned PT, who bought the idea and sincerely believes the delusion that his magic hands are physically rootling out and attacking knotted up muscle tissue. However, imposing his own mesodermalist belief system on a patient during treatment, or worse, reinforcing an existing mesodermalist belief system the patient might have about why they have pain, coupling it to what they feel from the therapist while being treated, and removing the patient's locus of control from them, over-riding their nociceptive threshold, is truly cringe-worthy. 

Some other cringeworthy points:

1. That athletes are somehow "special" people. 

"[Cooper]Rush, a six-foot-seven defenceman likely to be drafted in this summer's National Hockey League entry draft - isn't your average physiotherapy patient."

Well, no - he's 6 foot 7 inches and plays hockey. Other than that, he has a nervous system that could become sensitized, just like anybody else's. 
Furthermore [lest we forget..], Lance Armstrong, Oscar Pistorius. Athletes are not exactly the paragons they are made into by adoring fans. They are still human - the bigger they are, the harder they fall, in both the physical and theatrical sense.

2. That the thing they really-really "need" from physiotherapists is even more nociceptive input, inflicted by a professional, because it will "speed healing": 

"... it's hardly comfortable. 

"Is that tolerable?" Beesley asks Rush as he pushes into his shoulder."Pretty painful," comes the reply.
"Then I'll keep going," the physiotherapist says. "This is a good pain."

Major facepalm. 

... 

As someone who has never liked this entrenched set of ideas, ideas that not only still circulate around in our profession but actually find traction in news stories, and are stirred, promoted by physiotherapy organizations linking them on Facebook, as though this nociception-inflicting and -accepting behaviour were something to be proud of.. it's really, really hard for me to get my face unstuck from my palms. As a PT who does not concur, I mean. 

I doubt the PT in the story understands the first thing about pain science. He probably still views pain as 'weakness leaving the body' (said in a deep, slow, gravelly, macho voice). He likely assumes pain is a signal sent up to the brain a la Descartes. He probably never heard of Clifford Wolfe or of central sensitization. If he had, he may have chosen different words to use, or may have realized he really didn't need to inflict more nociceptive input on his patient in order to help his shoulder; just rule out red flags, give him some novel input through manual therapy staying well INside the comfort range of the patient, leaving the patient with locus of control, put some strips of bright coloured tape on him until movement felt comfortable, encourage normal movement, prescribe a firm timeframe, and not hurt him. 

Why not? Athletes love pain don't they? 
They probably don't like the kind that can arrive seemingly out of the blue when the second order nociceptive ascending neurons figure out how to get better at their job, more efficient at doing it, so they can handle more traffic. Yes, it can happen, if the genetics are favourable for it, and a trigger exists. Not a great situation for any brain to have to unpredictably, and suddenly, face a tsunami of chronic pain to deal with. It's hard to know in advance who could end up becoming a chronic pain patient, even with the best of screening tools. Even if somebody who is young and an athlete used to taking a pounding isn't the likeliest candidate for such a fate, do we really want our profession to contribute support to a set of memes that is unsustainable and counterproductive for anyone who does have the potential to develop chronic pain? Do we really want PTs out there who are more physical than therapist? 

Suggested reading: 

1. Clifford Woolf, 2011. Central sensitization: Implications for the diagnosis and treatment of pain.  Pain. 2011 Mar;152(3 Suppl):S2-15 (open access)

2. Latremoliere A, Woolf C. Central sensitization: A generator of pain hypersensitivity by central neural plasticity. J Pain. 2009;10(9):895-926 (open access)

3. Costigan M, Scholz J, Woolf CJ;  Neuropathic pain: a maladaptive response of the nervous system to damage. Annu Rev Neurosci. 2009;32:1-32 (open access)

4.  Ji RR, Kohno T, Moore KA, Woolf CJ.; Central sensitization and LTP: do pain and memory share similar mechanisms? Trends Neurosci. 2003 Dec;26(12):696-705.

Peripheral nerves and gorillas 2

Peripheral nerves and gorillas 1.

Today I spotted what I think might be a gorilla. Inattentional blindness. So I edited my first wikipedia page. More about that later.

Over at SomaSimple Barrett started yet another thread on his favorite topic, ideomotor movement: Revealing the Shadow II.  You can read it there if you wish. He asked what the difference was between his baby, simple contact, and my baby, dermoneuromodulation.

There is so much we agree on, except for one thing - he doesn't see the outer layer of the body as being very consequential [which may be because he is so tired (as am I) of all the operator nonsense that has grown up over the years that has to do with this layer].

What layer am I talking about? The epidermis/dermis/hypodermis layer. The blubber layer.

The nonsense we agree on has to do with people imagining that they are stretching the fascia inside it, instead of realizing they are setting into motion all sorts of motor output by the nervous system, a clear sign of the nervous system responding to outside exteroceptive input.

We both agree on that, and it's a huge overlap, almost entire. However, his stance is that ALL movement in response to treatment is outward from the brain, is ideomotor, from the brain, linked to some kind of idea or thought, conscious or unconscious.

This I cannot agree with. I think at first there is reflexive movement. A whole lot of reflexive movement. No thinking required. 

Can hypodermis "move"?
The blubber layer in question has no motor volition within itself*, other than autonomic. That is its only motor business. [And, just for the record, as a therapist I'm only interested in neural structure within that layer, and the vessels that feed it. There is only so much life left, and I'm spending mine studying that which has agency in the daily normal pain free life of the entire human organism. I could not care less about adipocytes etc..]

To me, this means that any "movement" that's palpable, by me as therapist, especially the small stuff, is likely to be of the fluid kind; one can sense pulsing or whooshing just below the skin, sometimes. I am pretty sure by now this is reflexive response, only.

A quick and dirty look at the peripheral nervous system
Mesodermalists ALWAYS think about muscle first. They can't help themselves. It's how they learned the body. When they learn nervous system, they ALWAYS learn the motor output system. That is to say, the corticospinal paths and the corticobulbar paths, the paths the brain uses to send commands to muscle. Striated muscle. The red stuff in pictures of the body. The meat. They are muscleheads. They want to relate everything, everything to movement, to motor control. When they treat, they imagine they are stretching muscle. They want to stretch it, knead it, strengthen it, lengthen it, soften it, harden it, get rid of what they think are its trigger points, whatever. They imagine if they can corral this misbehaving mesoderm somehow, all will be well.

When musclehead mesodermalists think of the PNS, they think only of motor nerves that go to muscle. But seriously folks, motor neurons are CNS, not true PNS, and muscles are just meat puppets at their ends.

I look at the peripheral nervous system differently, because although it has the same mommy, ectoderm, it has a different daddy - instead of being made out of neural tube, it's made out of neural crest.

Motor neurons that have their cell bodies inside the spinal cord, have neural tube daddies, go out to muscle targets, and have hitched a ride with their siblings, the rest of the peripheral nerves, which contain a variety of other kinds of neurons, all of which have neural crest as their daddy.

They might all travel together, but they have very different roles, and destinations. Some are bringing in information to tell the brain, and some are taking information from the brain or at least from the CNS, out to the muscles. Muscles are puppets of the nervous system. They do not have any volition of their own. Not that the spinal cord can't affect them if it wants to. I do not dispute that.

The autonomic system takes care of daily business "locally" which is to say, more peripherally, outside the spinal cord, with cell bodies in ganglia that live near to, but not within, the spinal cord. Not that they don't communicate with the spinal cord. They do. The peripheral nervous system, made from neural crest, and its sibling, the central nervous system, made from neural tube, talk to each other all the time and like conjoined twins born of the mother, ectoderm, share a lot of information of the signaling sort about the body they share.

But they can also operate - a little bit - autonomously from each other. What I'm saying is that although the central nervous system has evolved capacities that are light years more sophisticated than anything the PNS can do by ITself, like think, the PNS was running organisms all by itself very well before vertebrates came along about 500 million years ago, whose fish ancestors organized a CNS into a little something called a "spinal cord" with a little "brain" on one end. I call that, collectively, the critter brain. It's been busy running physicalities of various shapes and sizes and species way longer than the more sophisticated bits of CNS have, which, in humans, are only a couple hundred thousand years old. It developed "automaticity", auto-nimity, autono-mousness, autonomy, in that length of time. Little by little, as the brain (in the beginning just the critter brain only) grew bigger through evolutionary time, it developed more capacity to inhibit the peripheral nervous system. The critter brain and the PNS have had a lot longer together to figure each other out and learn how to work together. The human CNS, nice and fluffy though it is, is really new, only a couple hundred thousand years old; the old CNS has no problem at all knocking it offline in order to deal with itself, particularly if it senses any threat to itself coming in from the PNS.

Some of the different neurons in the PNS include sympathetic, parasympathetic (but not out to skin in humans, except lips, as I recall), and weird things called visceral afferents that do not belong to the first two categories, which are afferent, but do have efferent function anyway, sort of. The other big class of neurons are exteroceptive sensory neurons, which include big fast fibres that are well-connected to the primary sensory cortex of the brain, and lots of interoceptive neurons which also report to the brain but more slowly and through slower pathways.  They have cell bodies in prevertebral ganglia, sympathetic chain ganglia, and dorsal root ganglia. Each ganglia is like a little brain. It can make certain programed decisions by itself. As long as everything is going along in a fairly ordinary way.

A quick and dirty look at visceral afferents
See "visceral afferent neurons" (VANs), notes from Chapter 2 in Jänig's huge book, Integrative Action of the Autonomic Nervous System: Neurobiology of Homeostasis. VANs come in two main flavours, spinal visceral (SVANs) and vagal visceral (VVANs).

Here is a slide that lays out the intricacies of what visceral afferents do.

If you happened to miss it, here it is again, spelled out:

1. They report to CNS

2. They modify regulation of viscera by extracentral reflexes in prevertebral ganglia (NOTE: extracentral - outside the CNS. They have some autonomy. And some agency. But I doubt they can "think".)

3. They "release neuropeptides from peripheral endings, e.g., CGRP and Substance P - these travel both ways in neuron" (so presumably they could secrete them at both ends?)

4. Through their trophic capacity they might "influence synaptic connectivity in spinal cord with second-order neurons." (We know how well this goes, when it comes to situations like central sensitization - the brain doesn't like this a whole lot usually..)

They are not "efferent" in that they can't "move" anything - their business is reported to the older parts of CNS like crazy though. Which is why they are deemed to be "afferent" - they hang out with the sympathetic efferent fibres but are neither sympathetic nor parasympathetic - they are their own kind of unclassifiable neuron. See Is there anything “autonomous” in the nervous system?

The only thing they can do is squirt stuff out onto their target organ, which, of interest to us, in the outer layer, is the wall of blood vessel. Why? Because hypodermis contains so freaking much vasculature! Why? Because it's a cooling organ for all the heat we make as a) mammals, and b) mammals with freakishly huge brains that are only 2% of our body but use 20% of all the fuel! We run hot! No wonder we lost our fur.. 

Our hypodermis/dermis contains 10 times more blood than it needs for its own maintenance. Our nervous system keeps itself cool by running huge amounts of blood out toward the environment to cool it off. Sweating helps. It's hugely important, and requires a huge amount of finely controlled vasculature. Controlled by the PNS, monitored and regulated by the CNS, as long as things are going along normally.. 

Think of the effort involved in driving a car. Not much, right? Just enough steering to keep the car on the road between the ditches. 

Some visceral afferents are mechanoreceptive with high threshold, and others are mechanoinsensitive/chemoreceptive. 

If we skip through to notes on section 2.4.2, we meet up with the spinal kind, out in skin. 

The rest is a very detailed examination of all the reflexive connections between visceral afferent ascending pathways, and descending critter brain pathways which can be up to 5 times more powerful. [Anyway, the chapter is intense, but I made VERY careful notes, so if you're interested, go to the link and download the pdf directly.] 

My contention is that until and unless the critter brain gets this force of nature, this visceral afferent "behaviour", subdued, the human part of the brain won't be able to access the motor output part of itself very readily. 

Inner jellyfish?

It's all well and good, but no movement of this kind (to my knowledge) involves any "thought" - it seems all still pretty reflexive at this stage. Might as well be jellyfish neurology, this part is so old. Jelly fish are not noted for having much in the way of intellect. They can move in the wild, but if we were to consider visceral afferents as a trapped inner jellyfish, they can't go anywhere anymore - all they can do is squirt potentially irritating, annoying juice on their surroundings. 

Maybe it all works like a mirroring of evolutionary history of nervous system formation: visceral afferents are the inner jellyfish to the critter brain (fish onward) which came along and learned how to deal with the inner jelly fish just fine, long before humans came along with our big fat socially responsive neocortices.  Manual therapy soothes the critter brain AND human brain in a manner just sufficient and necessary to help the three nervous system aspects sort themselves out, and especially to help the critter brain to subdue the nasty sensations the jellyfish have created, and then the human brain makes friends once again with the critter brain. Ah sweet relief. THEN movement can happen unimpeded, and will feel good. Nociception will have changed to yes-ciception. The critter brain will relax/stretch its limbs, the human brain will stand up, bend its spine, twist its torso freely all around. 

Wikipedia

When I went to look up hypodermis in Wikipedia, I realized they listed all the contents of hypodermis with out mentioning cutaneous nerve. So I made an edit to include a short point on them, with a link to Wikipedia's own page on cutaneous nerves. 

Seriously, how could I let that stand uncorrected? 

Cutaneous nerves

If I have anything that remotely resembles an obsession, this is it. And I really despair that no one but me, apparently sees the importance of these, how superficial they lie, especially their rami, all the way out to skin [scroll down for pictures], and how easy they are to construct new treatment models around. See Nash et al 2004 for a description of the skin ligaments that form neural tunnels for rami to branch out to innervate the outermost layer of skin.  

The cutaneous nerves are the nervous system's, the nervous systems', own feelers, out into the passive, heavy, thick skin organ all round the outside of the body, which is laced with all those spinal visceral afferents which can leak all those annoying substances on them not only from vessels on the outside of them but also on the inside of them, and woe betide any cutaneous nerve or ramus thereof which happens to be a bit entrapped somehow, because its neurons' membrane permeability will be adversely affected by compression or tension, and some of that nasty business will get straight on them and may well bug the heck out of them. Once that happens it's like being in a bank as it is being robbed. Bam! lockdown. No one can leave until after the police have arrived and have interviewed everyone in turn. In the body, movement can't happen until the neurology straightens itself back out again [or a bigger threat looms..]. I don't really care what kind of movement it is or it isn't - I think motor output phenomena happen very close together, but sequentially. This is the way I like to splice together the story of what happens to the nervous system as it resets its function to being "normal" again, able to move. I don't think movement requires much "thought", conscious or unconscious. I think once it turns back on, it's turned back on, period. Just like the doors are unlocked at the bank, once everyone has been interviewed by the police and the teller hits the switch. Then everyone is free to move again. Home. 

To sum up:

We humans love our illusion that we are in the driver's seat, that we "own" our bodies, that our nervous systems are under our control. 

Heck no. 

Our nervous system is the boss of us, not the other way round. It keeps us alive [whatever "us" is..]. It puts us to sleep at night so it can fix itself, restore dopamine stores, glutamate, whatever, keep us breathing, our hearts pumping, make us roll over without waking us all the way up. In the morning, our nervous system wakes "us" up, because its bladder needs to be emptied, and it's hungry and wants "us" to go get it something to eat. Nervous systems were around long before one end got very fluffy and decided to call itself "human." Once our nervous system shuts off, so do we. That's it. 

It can be a bit disconcerting, I realize, to face the fact that the "we" we think we are, is mostly just a projection out to the world, produced and directed by a nervous system that has been continuously evolving throughout evolutionary time, isn't finished, that needed a social module. But that still has bits of itself that are still a lot like the first bits to ever have evolved. 

"We" float from day to day embedded in a living ecosystem we recognize as "our" physicality, a bunch of cells made from atoms that came from stardust that stay organized as a "body" because a tiny percent of all the cells making it up are really long, skinny and can talk really-really fast to each other. And burn up a huge amount of oxygen and glucose in the process. 

Imagine three concentric spheres, one inside the other like Russian nesting dolls: 

1. Innermost sphere = peripheral nervous system (minus motor neurons) and visceral afferent system, or jelly fish brain. It can sting! And it does, all the time. As long as blood flow is sufficient, its annoying secretions do their immediately local task and are quickly washed away before they bother any other neurons. No prob. PNS looks after itself, plus a whole lot of circulatory issues, reflexively. Axon reflex, etc. It talks to itself through its ganglia. The central nervous system listens in, offers its opinion, keeps the car (the body) on the road (of homeostasis).   

2. Next sphere out = critter brain. This is the spinal cord and brainstem, and hypothalamus, a few bits of ancient cortex - insular cortex, anterior cingulate, limbic; also motor output but not very sophisticated, mostly there to approach mates or prey or escape being somebody else's lunch  ... Invented by fish ancestors, we have all of this in common with every other vertebrate species on the planet. Its job is to monitor and regulate, guard the boundaries of organismic existence. Social grooming evolved at this stage though, so there was some social connecting, within and between species. Food was usually involved, at first..  

3. Third and outermost sphere = human brain. Voluntary control of striated muscle. Shares motor control with critter brain. Can interrupt critter brain control for short periods of time, like not blinking, like not breathing. But can't keep it up for long. Has sensory afferent "spies" all the way out to skin. Needs to know what's out there in the environment, so if it sits on a thorn, for example, it can know to move. And when, depending on context. Needs to make contact with other creatures to feel safe, succored, socially accepted, mandatory while still an infant, finds pleasant even as adult. Loves to pretend, then believe, that it has dominion over self and even over others and over imaginary domains it has invented, like social structures. Even over other peoples' body structures. See operator models.

All three share the same peripheral nerve trunks.  

If the sk-input isn't right, the output will falter. People come to manual therapists because they want their skin organ, loaded with those visceral afferents, held in various directions, or moved certain ways so their nervous system can get a fix on the problem and solve it, so they can move freely once again. The only system that can "move" anything in the skin layer is the sympathetic NS (smooth muscle, vascular constriction, sweating) and visceral afferents through vasodilation. Those are cellular "movements" - but they can add up, I suppose... reflexively. The human brain can drag its hurting physicality off to a therapist and together they can work out what the system might need to get it rebooted so that it will hurt less. We hope. 

When we put our hands on somebody's skin surface we are NOT touching muscle directly. Muscle does NOT respond immediately, usually, unless someone flinches away because of expectation, because you haven't created a safe context, because you are creating some nociceptive input for them to deal with. But if all is set up to transpire smoothly, the autonomics start up right away, and the critter brain comes over to check you out. There isn't any thought to any of this - it's all hard-wired and normal. After the first two systems have checked you out, done their job, are satisfied, the critter brain can relax, because it managed to finally squirt the right stuff from the drug cabinet in the brain stem down the spinal cord: then - and only then, in my opinion [and I'll go to my grave being pretty sure about this], the critter brain will let the human brain move the body again - no problem. 

I do not think it's appropriate to skip over any of this information, or assert that one or more of these steps don't matter, or leave them entirely out of an explanatory model, or mistake an explanatory model for a treatment model. 

I would assert that understanding how the system works, how its parts work and what they need, is important, so that you can move ever further away from the possibility of creating any chronic pain patients. The world does not need more of these, especially when there are scads of human primate social groomers around, and all they need in order to work more intelligently, is to take on more and better information. 

We can do better. So much better. 

.................................

*There isn't any somatic motor output of the striate muscle persuasion anywhere in the hypodermis layer except for in the face and front of neck, as far as I have learned, to date. Please tell me if I'm mistaken on that. Striated muscle is found throughout the hypodermis layer there. Why? Because the face and front of neck are built from neural crest, and neural crest is very, VERY weird. It can build ANYthing. But it's still ectoderm, not mesoderm.  

Alberto A. Rasia-Filho; Is there anything “autonomous” in the nervous system?

Adv Physiol Educ March 2006 vol. 30 no. 1 9-12