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Old 27-09-2006, 03:01 PM   #1
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Default Neural Mechanisms of Persistent Pain

HI all ;

I liked this lecture ,here you are :




Neural Mechanisms of Persistent Pain

Professor Marshall Devor


Quote:
Evolution designed the peripheral endings of nociceptive sensory neurons to respond to acute tissue injury and disease with a nociceptive warning signal. Nociceptive signals trigger the experience of pain in a conscious brain. At times of stress and emergency the pain signal might be blunted by the action of supraspinal inhibitory control pathways, but in general, the pain system provides the brain with an accurate report on the state of peripheral tissues. Much is already known about the biology of this system, and we have safe and effective drugs to manipulate it.
The real challenge to today's pain science and medicine is chronic pain, pain with intensity out of proportion to the injury sustained, and that long outlasts any obvious tissue abnormality. Chronic pains frequently occur when there has been direct damage to the pain system itself. Injury to axons in peripheral nerves at least partially blocks the flow of sensory information from the periphery to the central nervous system. This is expected to cause a loss, or at least a blunting, of sensation. Yet, paradoxically, clinical experience shows that neural injury is frequently accompanied by amplified and distorted sensation. This takes the form of allodynia, hyperalgesia, hyperpathia, electric shock-like paroxysms, pain on movement and spontaneous pain. At its most extreme, neural trauma can create elaborate sensations from no input at all (e.g. phantom limb pain). The clinical tools available for managing chronic neuropathic pain are blunt and more often than not, ineffective.
The paradox of chronic pain, and its ultimate clinical solution, lies in the realm of neurobiology. Specifically, we need a better understanding of how neurons respond to injury. Accumulating evidence indicates that axonal injury triggers the generation of abnormal afferent discharge at ectopic sites in the injured primary sensory neuron. This ectopic hyperexcitability is an essential substrate of neuropathic sensation, both spontaneous and stimulus-evoked. Ongoing (spontaneous) neuropathic pain is due to spontaneous ectopic discharge. Since depolarization brings neurons to spike threshold, augmenting ectopic discharge, depolarizing stimuli such as mechanical displacement can augment ectopia. This brings about mechanosensitivity at ectopic pacemaker sites, the basis of pain on movement and on deep palpation. Allodynia and hyperalgesia are due to spinal amplification of sensory input from residual afferents in the injured nerve, and intact afferents in neighboring uninjured nerves. The spinal amplification process, known as "central sensitization", is maintained largely by ongoing ectopic discharge.
Sustained neuropathic discharge appears to be an outcome of intrinsic resonant properties of primary sensory neurons, augmented by axotomy. Recording from primary sensory neurons in excised rat dorsal root ganglia, we found that some cells show subthreshold sinusoidal oscillations in their membrane potential. These oscillations give rise to action potentials when they reach threshold. Neurons without oscillations are incapable of sustained discharge even on deep depolarization. Nerve injury has the effect of increasing the proportion of neurons with subthreshold oscillations, and hence the proportion that generate ectopic spike discharge. Resonance appears to be due to altered trafficking, and altered synthesis, of key molecules of excitability, notably certain voltage sensitive Na+ channels (esp. Nav1.3), and certain K+ channels. Selective pharmacological suppression of subthreshold oscillations may offer a means of controlling neuropathic paraesthesias and pain without blocking afferent nerve conduction.
There is considerable variation in pain threshold and tolerance among individuals, particularly pain associated with nerve injury. Until recently, such variability has been attributed largely to socialization. However, new information based on investigation of animal models of neuropathy suggests that different individuals may have a heritable predisposition to developing chronic pain following neural injury. For example, beginning with a population of rats with heterogeneous and variable pain response in the neuroma model of neuropathic pain, we used selective breeding methods to derived lines that consistently exhibit high versus low levels of symptomatology. This proves that the pain trait is heritable. Subsequent hybridization and backcross experiments indicated that in this model pain response is a Mendelian trait, transmitted primarily by a single autosomal recessive gene with minor modifiers. The gene appears to act by increasing the ectopic discharge generated in injured afferent A-neurons following nerve injury. The ultimate identification of the genetic polymorphisms responsible for phenotypic variability might reveal previously unimagined aspects of pain physiology. But even before specific pain susceptibility genes are identified, the simple knowledge that pain susceptibility has an important heritable component should act to reduce the stigma suffered by individuals in whom pain is extreme through no fault of their own.
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Old 27-09-2006, 03:08 PM   #2
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Very succinct. Where does this lecture come from Emad?
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Old 27-09-2006, 03:15 PM   #3
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Emad,

This paper is talking a lot about ectopic discharges but I do not consider that is a real source of chronic pain. Ectopic discharge is against many physics principles.

An "ectopic" contamination within a nerve is a huge affair that forgets nerves suffer many mechanical stresses without any problem.

IMHO, it doesn't work because the Coulomb law does not let any chance to such a behaviour.
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Old 27-09-2006, 03:33 PM   #4
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Hi Diane & Bernard ;

Well , this lecture comes to me during research to solve my patient with pain attacks ( Neuralgia ) i put a thread here and on NOI , David there responded brought this abstract :

[quote]
Quote:
Some patients with radial nerve problems (eg neurogenic tennis elbow) will report that symptoms worsen during walking and especially fast walking as the elbow is extended forcefully. This suggests a mechanosensitive ectopic impulse generator somewhere along the radial nerve or maybe the musculocutaneous nerve.

I think an “attack” is possible with possible “multiple interacting sites of ectopic spike electrogenesis”. This was the title of the article abstract below. Other papers by these authors may help.

Multiple Interacting Sites of Ectopic Spike Electrogenesis in Primary Sensory Neurons
Ron Amir,1 Jeffery D. Kocsis,2 and Marshall Devor1
1Department of Cell and Animal Biology and the Center for Research on Pain, Institute of Life Sciences, Hebrew University of Jerusalem, Jerusalem 91904, Israel, and 2Department of Neurology, Paralyzed Veterans of America/Eastern Paralyzed Veterans of America Neuroscience and Regeneration Research Center, Yale University School of Medicine, New Haven, Connecticut 06516
Ectopic discharge generated in injured afferent axons and cell somata in vivo contributes significantly to chronic neuropathic dysesthesia and pain after nerve trauma. Progress has been made toward understanding the processes responsible for this discharge using a preparation consisting of whole excised dorsal root ganglia (DRGs) with the cut nerve attached. In the in vitro preparation, however, spike activity originates in the DRG cell soma but rarely in the axon. We have now overcome this impediment to understanding the overall electrogenic processes in soma and axon, including the resulting discharge patterns, by modifying the bath medium in which recordings are made. At both sites, bursts can be triggered by subthreshold oscillations, a phasic stimulus, or spikes arising elsewhere in the neuron. In the soma, once triggered, bursts are maintained by depolarizing afterpotentials, whereas in the axon, an additional process also plays a role, delayed depolarizing potentials. This alternative process appears to be involved in "clock-like" bursting, a discharge pattern much more common in axons than somata. Ectopic spikes arise alternatively in the soma, the injured axon end (neuroma), and the region of the axonal T-junction. Discharge sequences, and even individual multiplet bursts, may be a mosaic of action potentials that originate at these alternative electrogenic sites within the neuron. Correspondingly, discharge generated at these alternative sites may interact, explaining the sometimes-complex firing patterns observed in vivo.
Key words: 4-AP; afterdischarge; ectopic firing; pain; repetitive firing; subthreshold oscillations
[quote]

A link to there ;

http://www.noigroup.com/cgi-bin/ubbc...c;f=5;t=000650

As i tried to search , i found that lecture ,yes Diane seems to be an abstract only , but it is concerning what i discuss. a link to the article ;

http://www.thepainweb.com/doclib/000061.html



Cheers
Emad
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Old 27-09-2006, 03:46 PM   #5
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Thanks Emad..
Bernard, do you assert that nerves cannot form new receptors along their axons and become sensitized?
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Old 27-09-2006, 03:53 PM   #6
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Not at all.

This way makes perfectly sense but a ectopic contamination is not related to ions channels.

Ectopic discharges involve too much things :
  • A poor insulation.
  • A poor noise immunization.
  • A low ionic interaction.
It will be a miracle to have all these ones at once.
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Old 27-09-2006, 03:56 PM   #7
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Bernard, do you not agree that sympathetic fibres are leaky? Their job is to stir axons within the insulation, no?
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Old 27-09-2006, 03:56 PM   #8
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J Neurosci. 2005 Mar 9;25(10):2576-85. Links
Multiple interacting sites of ectopic spike electrogenesis in primary sensory neurons.
Department of Cell and Animal Biology and the Center for Research on Pain, Institute of Life Sciences, Hebrew University of Jerusalem, Jerusalem 91904, Israel. ronamir@pob.huji.ac.il
Ectopic discharge generated in injured afferent axons and cell somata in vivo contributes significantly to chronic neuropathic dysesthesia and pain after nerve trauma. Progress has been made toward understanding the processes responsible for this discharge using a preparation consisting of whole excised dorsal root ganglia (DRGs) with the cut nerve attached. In the in vitro preparation, however, spike activity originates in the DRG cell soma but rarely in the axon. We have now overcome this impediment to understanding the overall electrogenic processes in soma and axon, including the resulting discharge patterns, by modifying the bath medium in which recordings are made. At both sites, bursts can be triggered by subthreshold oscillations, a phasic stimulus, or spikes arising elsewhere in the neuron. In the soma, once triggered, bursts are maintained by depolarizing afterpotentials, whereas in the axon, an additional process also plays a role, delayed depolarizing potentials. This alternative process appears to be involved in "clock-like" bursting, a discharge pattern much more common in axons than somata. Ectopic spikes arise alternatively in the soma, the injured axon end (neuroma), and the region of the axonal T-junction. Discharge sequences, and even individual multiplet bursts, may be a mosaic of action potentials that originate at these alternative electrogenic sites within the neuron. Correspondingly, discharge generated at these alternative sites may interact, explaining the sometimes-complex firing patterns observed in vivo.
PMID: 15758167 [PubMed - indexed for MEDLINE]
Attached Files
File Type: pdf mutiple_interacting.pdf (360.9 KB, 13 views)
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Old 27-09-2006, 04:27 PM   #9
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Quote:
Ectopic spikes arise alternatively in the soma, the injured axon end (neuroma), and the region of the axonal T-junction. Discharge sequences, and even individual multiplet bursts, may be a mosaic of action potentials that originate at these alternative electrogenic sites within the neuron.
OK, so are these what people have referred to as AIGS?
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Old 27-09-2006, 04:31 PM   #10
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Quote:
Originally Posted by Diane View Post
Bernard, do you not agree that sympathetic fibres are leaky? Their job is to stir axons within the insulation, no?
Diane, they are leaky at their endings (peripheral sites). I'm not sure that it will work along the nerve.
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Old 27-09-2006, 04:39 PM   #11
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I'll look up what goes on "along" axons; seems to me I read in one of the Burnstock books on autonomics about the "leaky garden hose" anaology. I'll see if I can find it.
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Old 27-09-2006, 04:49 PM   #12
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Bernard ,thanks for the complete article .

The issue of Ectopic discharges ,polarization and depolarisation is so complex for me ,however i had studied it during my undergarduate study ,but still not clear or shaped in simple language and physics .

The main point is reasoning pain attacks on the Hypothesis of Ectopic discharges ,meaning perpherial hypothesis however is called usually central ,no matter that now perpherial or central ...........
How can we explain pain attacks /dischanges in patients at certain times and after that they are completely free !!

Diane , i think yes AIGS are the source of ectopic discharges !! Seems so !

I agree chronicity has many reasons/grounds more than Ectopic dischagres .

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Old 27-09-2006, 05:16 PM   #13
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Diane and Emad,

I do not discard anyway AIGS but simply its origin.

If a neuron is able to put more ions channels on an axon membrane, it is for an unique interest: a response.

A response to what? Just to solve this complex equation => maintain a transmission of information that is vital for brain.

If you perturb the system in the transmission lines you create of course many problems that seem weird and that we call neuropathic pain.

This kind of behaviour is certainly not designed at first. It comes only with special conditions.

My concern is about the ectopic contamination: an electrical contamination that have few probability to occur.
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Old 27-09-2006, 05:20 PM   #14
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Diane,

Garden hose
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Old 27-09-2006, 05:32 PM   #15
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My understanding of AIGS is that they are more a tissue response, less a firing malfunction, that they tie in with hypoxia. Not that lack of O2"causes" them, but rather that lack of blood flow, creates an undesirable functional ecosystem situation wherein the substances that leak out all the time from the sympathetic outflow axons, onto the inflow sensory axons, anyway, do not get flushed away in a timely manner. That they are like diaper rash, an eruptive response to irritation that has been in place for too long. At least that's how my own simple mind sees things.

If that's true, then the brain has another avenue of sensitization (more peripheral) to deal with, that is outside the DRG's scope. It will be bombarded with more volume of impulses to process.

I think (from Butler, hope I interpreted him correctly) they are extra ion channels that become dismantled once ordinary blood flow is reestablished.
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Old 27-09-2006, 05:41 PM   #16
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Diane,

You're falling in my garden since neuron puts channels only to restore a malfunction.

BTW, a constant leaking site may be a firing site as well.
But a constant leaking site is a tissue injury that doesn't resolve.
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Old 27-09-2006, 05:45 PM   #17
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Quote:
Originally Posted by M Devor
by modifying the bath medium in which recordings are made. At both sites, bursts can be triggered by subthreshold oscillations, a phasic stimulus, or spikes arising elsewhere in the neuron.
That is not natural conditions. Just far away of asymetrical ionic constraints.
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Old 27-09-2006, 05:47 PM   #18
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From this thread, post 31:

Quote:
The sympathetic nervous system is essentially a motor system. To cause pain it must somehow activate the afferent system, especially C and A-delta fibres if the CNS is sensitized. Understanding this pain comes back to receptors. Adrenaline itself does not hurt, it needs receptors attached to nocioceptors to contribute to pain or it must contribute to a chemical soup which activates nocioceptors. Therare thus three places where adrenaline may activate the afferent system. These are contributions to inflammatory soup, contributions to and AIGS or influences due to adrenoreceptor upregulation at the DRG. Adrenaline can act as a central excitatory neurotransmitter, thus it may contribute to the magnification of afferent input. There are more details in chapter 3. Review also figure 3.9.
From post 41, Gray's:
Quote:
Neurotrophins synthesized by target smooth muscle, of which nerve growth factor is the best known example (Levi-Montalcini & Angelletti 1968; Thoenen 1991, p 919), have long been recognized to have trophic influences on sympathetic and sensory nerves of the autonomic nervous system. There is growing evidence that several neurotransmitters, in particular the neuropeptides, which are involved in short-term communication between excitable cells, also have long-term trophic actions on autonomic nerves (Pincus et al 1992). Autonomic neurons are thus continually under the influence of the molecules of their environment, allowing for a considerable degree of plasticity following injury (Hendry & Hill 1992).
From this other thread, post #12:
Quote:
From Butler, p 59 of SNS:
Quote:
MODERN CONCEPTS (of peripheral neurogenic pain)
1. The stability of peripheral nerve function, from nerve terminals to the cortex is incredible. First, consider the encoding, conducting, relay and processing functions and secondly, the mechanical forces being placed upon the system by normal human movement (Butler 1991). An axon can be over a metre long, have differing sources of blood, bend all the time, rub on various tissues and yet it is just one cell. You can read more about the remarkable physical abilities of the nervous system in chapter 5.

2. Axons are designed to be "highways" and transmit impulses raher than generate them. Impulse generation and the transduction processes are feratures of the nerve terminals and perhaps the dorsal root ganglion cells. For persistent nerve pain, impulses need to be somehow modified along the pathway. These modified sites are known as abnormal impulse generating sites (AIGS). Knowledge of AIGS is a key to understanding peripheral nerogenic pain.

3. The subtlety and variety of peripheral nerve contributions to pain states are not appreciated (Sunderland 1978; Loeser 1985; Ochoa 1993; Devor and Seltzer 1999; Serra 1999). Much symptomatology could relate to what Sunderland (1978) referred to as "perversions of function", referring to nerve problems which may not necessarily involve failing conduction and thus rate a diagnoistic category of neuropraxia or Sunderland category 1. Classifications of peripheral neuropathies need updating to include AIGS.

4. The connective tissues of peripheral nerve are innervated and hence capable of causing pain (Hromada 1963; Bove & Light 1997; Sauer et al. 1999). Not much is known about nerve sheath pain, although there is a discussion in Ch. 5. Presumably, the healthier the connective tissues of the sheath then the healthier conduction will be.

5. Despite the existence of many textbooks on focal nerve entrapment, it is unlikely that a focal neuropathy such as nerve compression syndrome will exist on its own. Interactions with nocioceptive pain (via neurogenic inflammation), further changes in peripheral pain (eg. DRG upregulation) and contributions to stress response activation and central sensitisation are likely. A mechanisms approach to pain states is necessary to fully include these components of the pain state

6. A new area of study is the role of the immune system in peripheral neurogenic pain. Pro inflammatory cytokines such as interleukins 1 and 6 and tumor necrosis factor appear far more pain provocative than ever realised. Even undamaged peripheral nerve can become sensitive in the presence of these mediators (Sorkin et al. 1997; Watkins and Maier 2000).
Butler is all about the physiology, the ceaseless drip drip of molecules of leaky this and that onto helpless nerves in certain spots until they begin to signal, a bit more frequently, then a lot more, then in a cacophony and the brain begins to register their plight as a threat.
Certain things are more clear to me as the years go by;
1. The peripheral nervous system is both dependent on and vulnerable to chemistry in its environment. The accompanying blood supply is a friend to it, as long as it stays in its own banks and stays at a steady flow to bath the nerve clear of these cytokines, etc., and bring it the O2 it continuously needs to make its own biochemicals to leak out into other tissues and into the blood stream.

2. Movement keeps the project running optimally. I think one could say that lack of movement = abnormal neurodynamic leading to mechanical pain. It might be a couple orders of magnitude downstream by the time pain is actually registered in conscious awareness, but ignoring those slight signals to move around, shift position, pull back the elbows and yawn, is to ask for trouble later.

3. Mechanical pain has its own "chemistry set" that is not pathological. You could say that all pain is chemical in origin and I don't think that would be wrong.

4. When there is lack of movement/slide in the tunnels, hypoxia builds somewhere in some nerve; Butler mentions the role of the nervous system as an oxygen consumer. He says (p. 40), "The brain is the greediest bodily organ in terms of fuel consumption. It will burn about 10 times as much oxygen and glucose as the other body systems at rest. Although only 2.5% of body weight it will take about 20% of energy consumption. And as we know if it runs out of oxygen, neurones will die very rapidly. It helps to establish how alive the brain is."

OK.. well, if the nervous system is organized to consume that much oxygen perhaps that is why it exists in the first place (Sagan and Schneider, Into the Cool). What if the nervi nervorum's chemo receptor signal about the cytokines was a multi-level message with a subtext? "There's not enough blood flow here to wash off all this cytokine stuff.. we're getting chemical burns down here" could also, I think, be interpreted by an O2 greedy CNS as "O2 levels are down due to lack of blood flow." To me it makes intuitive sense that if motion is lotion for improved perfusion to wash away cytokines, it's just as important for supplying the neuron with adequate groceries/energy for a high rate of metabolism; a well-fed nerve will be a not so cranky nerve. (I thought localized hypoxia specifically as a nocioceptive trigger was in Butler's book but I can't seem to find it at the moment.)
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Old 27-09-2006, 05:49 PM   #19
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constant leaking site is a tissue injury that doesn't resolve
I beg to differ mon ami, the sympathetic axons are leaky, that's how they work, it's perfectly normal physiology.

My point is, that if blood flow is insufficient to keep the leaks diluted, they'll cause trouble.
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Old 27-09-2006, 05:53 PM   #20
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Diane,

I just realize that I took ectopic as synonym of ephactic.
I agree with all the posts.
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Old 27-09-2006, 05:56 PM   #21
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the sympathetic axons are leaky, that's how they work, it's perfectly normal physiology.
If blood flow is insufficient then itis not really a normal condition.
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Old 27-09-2006, 06:19 PM   #22
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If blood flow is insufficient then itis not really a normal condition.
Yes mon ami, that was exactly my point!
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