Delayed onset and resolution of Pain

[nari]

This paper appeared in BRAIN (2001), 124,1067-1076
Author: G D Schott, national hospital for Neurology and Neurosurgery.

It is a bit old, but useful reading. There is no URL and it is rather long, but some of you may be able to access it.

BERNARD:

In the introduction there is a quote in French which is not translated. It seems pivotal to the paper, so could you translate. please?

Here it is without the accents:

Les cicatrices nerveuses gardent une potentialite evolutive.
Pour elles, la notion de temps ne compte pas......Le calme clinique ne signifie pas que tout est fini. Le temps n'existe pas pour nos tissus.

Leriche 1951.


Merci

Nari

[bernard]

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11353723

Brain. 2001 Jun;124(Pt 6):1067-76.
Delayed onset and resolution of pain: some observations and implications.

Schott GD.

The National Hospital for Neurology and Neurosurgery, Queen Square, London WC1N 3BG, UK.

Occasionally, pain after disease or trauma develops only after a prolonged interval. Examples include late-onset pains which first occur months or years following a stroke, spinal cord lesion or amputation of a limb; a previously experienced pain that is recalled years later; and latent pain triggered for the first time by a further insult in the same area. Late-onset pains may develop gradually or suddenly, and may be brief or long standing. Pains which develop after an innocuous insult may be associated with slowly evolving sensory changes. However, even long-standing pains, particularly those of nociceptive origin, may resolve sometimes after many years. Resolution, which again can occur gradually or suddenly, may be spontaneous or follow development of another disorder or after therapeutic intervention. The duration of this pain relief can range from minutes to an indefinite period. These clinical phenomena, and the mechanisms, including genetic factors, subserving them, have been little studied. It is postulated that mechanisms implicated in acute pain may not be the same as those that subserve pain that develops after a long interval. Those late-onset pains which develop slowly after innocuous lesions may be associated with a variety of slow anatomical, physiological and biochemical changes. In late-onset pains that follow a painful insult, however, memory of the former pain and threshold triggering factors may be particularly important. Further studies of these neglected conditions may lead to understanding of as yet unknown processes subserving pain and to novel approaches to treatment.

Publication Types:
·Review
·Review, Tutorial

PMID: 11353723 [PubMed - indexed for MEDLINE]

[nari]

Bernard

Thank you.

I think it is amazing that this fellow was thinking along modern lines of thought half a century ago!!

Nari

[Diane]

Hi Nari, Bernard,
What a good article and how good that it is fully accessible. I've decided to add the link to my website. Thanks to you both for providing that.
Further down in the article, at the end almost, is the author's translation of the sentence in question:
"The skin does not quickly forget its previous injuries, no matter how normal it looks. Skin `memory' may last a lifetime' (Wolf et al., 1995)"

Hmmmnnn....skin. One of my favorite topics.
Cheers,
Diane

[bernard]

Hi Diane,

It's sure, you've got the patients "under their skin". (Hope my joke works? :oops: , it has for me two senses!)

[Diane]

Hi All,
Bernard, I'm sure it could be taken lots of ways...
Here is a paper that I found awhile ago, from Aus of course, that I quite like. It supports the contention that pain comes not from tissue or joints but from nerves. I thought I'd post it for your viewing pleasure:

http://websites.golden-orb.com/pain-education/100137.php
Cheers,
Diane

[nari]

Thanks Diane, that is a worthwhile article on pain.

Actually, your last sentence has me really intrigued.
..'pain comes not from tissues or joints but from nerves'..

As pain is transmitted only by nerves and nothing else that I have heard of; is the conclusion such a new one?

Comments happily received!


Nari

[Diane]

Hi there,
Nari, about this sentence,"It supports the contention that pain comes not from tissue or joints but from nerves."
Lots of practitioners still think pain comes from joints, or that joints are the only places that nerves get pinched, or that the structures around the joints, the capsule, ligaments, synovium etc are the first things they think of to rule out when someone has a pain, ache, or lack of range. Lots still think that muscles directly hurt from lactic acid etc. ( I think that idea was laid to rest lately..) I recall Butler always reacting to what I presume he thought was sloppy language or thinking in this regard, and insisting time and again, "we don't treat anatomy."
Well.. actually I still do, (treat contractile structures or at least the skin over them, usually where I guesstimate nerve exit points are located subcutaneously) or at least refer to muscles as culprits squeezing nerve tunnels within themselves, but I long ago moved past the idea that the muscles were painful in and of themselves. Dysfunctional maybe but not painful.. Ditto joints.
Cheers,
Diane

[rolf]

Hi Diane!
I do agree that all pain is neurogenic,(nociceptive or neurophatic),but dont you consider that its possibble that muscles in cramp/increased tension is able to pinch the peripher nerv and then give a neuropathic pain senssation?Espessialy through muscular tunnels.(scaleneii,,pec minor,pronto teres ,supinator etc)(irritation of the" nevri nevroum")
What to treat?Muscle or nerve?What abouy both?In my clinical pracsis i try to deactivate the increased musculat tone,triggerpoint needeling maual streching,dynamic, which might be pinching the nerv and at the same time activate nerve gides,(mob.)We cant forget pousture ,ergonomics,etc etc-
RIN

[Diane]

Hi Rolf,
I am guessing that your comment/question might have more to do with intent rather than reality... visualizing that you are treating muscle as you work on a neck... I agree that neural tunnels can get squeezed or distorted by dysfunctional muscle tightness. Likewise I think cranky neural structures can cause the brain to tighten up muscles.. It can be quite circular at times. What is really going on in there (?)....

I try to remember that all I can really get my hands on with hands-on...is skin. I can get my fingerprints stuck to it and slide it this way and that, and below the skin it feels as though tension relaxes. The only thing that makes sense is reflex action. But yes, I absolutely do visualize where the muscles are and how they "feel" and how they "lengthen" and how contractile tissue "opens"... I feel stuff and those images are the movies my brain makes to go with the sensations. Sometimes I wish I had "fingercams." (All I can really "see" is the increased range people demonstrate after, and the widened pupils as they realize they just did a movement, like look over their shoulder, and can see way more than they could before when their neck only rotated 30 degrees.. that sort of thing.)
Cheers,
Diane

[bernard]

Hi Somasimplers,

Skin or muscle. Muscle or skin. I love all my family. 8) 8)

When I had headaches (a long time ago), skin was ever thicker and tender and painful, muscle was tight (but I cannot say if painful without touching the skin) and motion painful.

Acting on the skin helped to bring some relief and muscle relaxation.
But relaxing actively the muscle, relieves the pain and skin is supple and painfree!

Choose the family?:wink:

[rolf]

HI all!
Hers agood one from Mense S.
Journal Neurol. 2004 feb.251
"Neurobiological basis for the use of botulinum toxin in pain therapy."
RIN

[bernard]

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=14991335

J Neurol. 2004 Feb;251 Suppl 1:1-7.

Neurobiological basis for the use of botulinum toxin in pain therapy.

Mense S.

Institut fur Anatomie und Zellbiologie III, Universitat Heidelberg, Im Neuenheimer Feld 307, 69120 Heidelberg, Germany. mense@urz.uni-heidelberg.de

The various serotypes of botulinum toxin (BoNT) exert their action by inhibiting the exocytosis of acetylcholine (ACh) on cholinergic nerve endings. BoNT cleaves proteins (e.g. SNAP-25 or VAMP) that are necessary for the docking of the ACh vesicle to the presynaptic membrane. Without docking, no ACh can be released into the synaptic cleft and the innervated structure is paralyzed. This article focuses on the neuromuscular endplate. The main targets of BoNT therapy are states of muscle hyperactivity such as contractures (in the physiological sense), or spasm and focal dystonias. CONTRACTURES: The "integrated hypothesis" of the formation of myofascial trigger points suggests that a lesion of a muscle damages the endplate so that excessive ACh is released. This causes a local contracture (partial contraction of a muscle fiber) underneath the endplate. The contracture compresses small blood vessels, and the tissue becomes ischemic. Ischemia leads to the release of bradykinin (BKN) and sensitization or excitation of nociceptors. BoNT is a causal therapy in these cases, because it stops the excessive ACh release. SPASM: Reflex spasm in a given muscle can be induced by nociceptive input from neighboring joints or muscles. If the force generated by a spasm is relatively high, it will compress the large blood vessels supplying the muscle. The final effect again is ischemia. In this case a drop in pH may accompany the ischemia and BKN are known to be effective stimulants for muscle nociceptors. DYSTONIA: In cases of weak dystonias, a compression of blood vessels is unlikely. However, the tonic contraction will cause a lowering of pH and a release of ATP. Muscle cells contain ATP at concentrations sufficient to excite muscle nociceptors. In cases of spasm and dystonia, BoNT can abolish the pain by relaxing the muscle. Since many patients report alleviation of their pain before the muscle relaxing effect of BoNT has set in, a direct analgesic action of BoNT is being discussed. Most hypotheses rest on the assumption that BoNT inhibits not only the exocytosis of ACh but also of their neurotransmitters. Such an action could be analgesic if the release of neuropeptides from nociceptive nerve endings is prevented. This way, BoNT could alleviate the pain of neuropathies and various types of headache where neurogenic inflammation plays a role. Another site of an analgesic action could be the postganglionic sympathetic nerve ending that uses norepinephrine and ATP as transmitters. Norepinephrine is known to increase cases of chronic pain, and ATP is a stimulant of muscle nociceptors. If BoNT inhibits the release of these transmitters, it could be analgesic in cases of sympathetically maintained pain including the complex regional pain syndrome.

PMID: 14991335 [PubMed - in process]

[nari]

Good article, Bernard.

Is anyone aware of any proof that a tense muscle causes pain?
I had understood that muscles cannot be shown to 'produce' pain of themselves. The lactic acidosis build-up is not proven to cause pain of itself.

Any comments?
(I expect a flood of surprised denials!)

Nari :wink:

[bernard]

Nari,

The same old problem! What does hurt us? Muscle, nerves, skin? :?:
I put a topic about some explanation? But had no reply! :(
http://www.somasimple.com/forums3/viewtopic.php?t=71

What are your thoughts before trying to accuse and execute the guilty one? :wink:

[nari]

Bernard

Ah-ha....the neural factor raises its gargoyles, once more.

The list of involvement of nerves in all sorts of conditions,along with other factors is growing.

Ischaemic nerves can complain as loudly as the rest.


Nari :P

[Diane]

Just to be clear, Bernard, by a 'bad venous system' I'm going to assume you mean bad circulation, both incoming and outgoing. Not enough oxygen getting to the nerves and not enough drainage of deoxygenated blood away from nerves. There can be a couple possibilities for such a state.
1. Faulty circulatory "plumbing": eg: AV malformations , growth defects in it, that sort of thing. Might be OK for awhile with collaterals but as demand of the body grows through time and size of body increase, circulation is structurally deficient...
2. Presuming the plumbing was built OK in the first place, not enough exercise leads to not enough demand for O2 by tissues leads to tightness based on SM amnesia.. leads to mechanical stress on nerves and further annoyance/O2 deprivation to them when exercise demand increases
3. Tight skin? (My own idea.., sympathetics overactive, semi-permanent 'gooseflesh') Tension patterns that are psychologic in origin making one's skin literally thicken.. OK...by nanometers probably, but a motor output that could be enough to force changes in sensory input and lead to pain states. Lots of nerves in skin. Lots of blood is shuttled through skin on its way around the body, more than necessary for O2 delivery, body needs to push off waste heat etc. Skin tightens and body can't get deeper agenda met via circulation through skin, nerves in skin signal O2 distress, brain throws up its hands in despair and issues a pain state...
Diane

[nari]

Diane

I like your post, especially the last sentence where the brain "gives up" and "turns on" pain! it could be said that it makes a Pain Statement... :roll:

I have wondered about patency of veins at times; and people with veins (in the extremities) that look like mountain ranges and which rise in size under physical stress. I am one of them; and nurses used to stare at my hands and glaze over at the thought of accessing with their needles.

I wonder about varicose veins (which physios used to treat for some reason) and the pain they sometimes seem to cause in people. Pain only sometimes occurs, apparently, and its origin might fit your proposal well.


Nari

[Diane]

I think the reason vasculature hurts is easy, it is highly innervated. Not with sensory nerves like in our skin, that we can consciously be aware of, but the silent free ending sort of sensory nerve (strewn everywhere, throughout all tissue) that is always reporting back to the brain what's going on in the body. Seems to me I remember reading that free nerve endings are 'silent' when firing normally, but if their firing pattern changes beyond "normal" parameters the brain will register/impart "pain", maybe at the site, maybe referred.

Arterial vasculature has motor innervation to regulate its size, control blood pressure locally depending on what's needed at the moment. Sensory feedback can tell the brain, or maybe a ganglion (mini brain) somewhere, that an artery is being kinked by a normal movement, and the ganglion will tell some other vessel to relax so that sufficient blood flow will get to the foot (or whatever) by collateral means. All innervation has feedback so the main system can know the moment to moment state of affairs. Especially something as vital as blood supply. Feedback equipment is 'sensory'...

Retinaculum over tendons is a great place for venous return to get backed up.

I'm glad others can see skin like I do, as the outside of the sensory cortex.
:)
Diane

[bernard]

Hi All,

The paper is now available in full text and pdf format.
I uploaded a copy for our collection.

Delayed Onset and Resolution of Pain (http://www.somasimple.com/pdf_files/delayed_onset.pdf)