A New Hypothesis of Chronic Pain

[101N]

http://www.ncbi.nlm.nih.gov/pubmed/26965423

A New Hypothesis of Chronic Pain

In accordance with these recent advances, we propose a novel definition of chronic pain. Rather than defining pain by its sensations, we propose a definition that emphasizes the neurobiological mechanisms that control behavioral adaptations, and we hypothesize that persistence of pain is likely mediated through the reorganization of the cortex by corticolimbic learning mechanisms. We therefore posit that chronic pain is a complex web of sensory and emotional experiences, coupled with behavioral adaptations. Specifically, we posit that the chronic pain state is a consequence of a change in value related to nociceptive afferent information impinging on the cortex, with limbic emotional learning mechanisms underlying this shift in value and with little opportunity to extinguish these emotional memories. Subconscious changes in contextual salience and the value of nociceptive inputs are signals that drive cortical reorganization, given that they render the pain more emotional and modify decision making and selection of behaviors. The net outcome is a brain that has learned to filter emotions, actions, and reward through the lens of pain, rendering the brain addicted to pain.

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[deleted185747]

BRAVO! Very well stated!

 

[lobelsteve]

SO a hypothesis that states pain is all in your head. Is this anything new? Can anyone propose a treatment? CBT? ECT?

Baby steps.

 

[freddydpt]

http://www.ncbi.nlm.nih.gov/pubmed/11749873

I'd be curious to read this article but can't get access.

 

[Papa Lou]

Jeez why do you have to try soooo hard to sound intelligent? All the verbiage is superfluous (doth thou think not?)

 

[LizzyBusyBee]

The Emotional Brain as a Predictor and Amplifier of Chronic Pain. - PubMed - NCBI

A New Hypothesis of Chronic Pain

In accordance with these recent advances, we propose a novel definition of chronic pain. Rather than defining pain by its sensations, we propose a definition that emphasizes the neurobiological mechanisms that control behavioral adaptations, and we hypothesize that persistence of pain is likely mediated through the reorganization of the cortex by corticolimbic learning mechanisms. We therefore posit that chronic pain is a complex web of sensory and emotional experiences, coupled with behavioral adaptations. Specifically, we posit that the chronic pain state is a consequence of a change in value related to nociceptive afferent information impinging on the cortex, with limbic emotional learning mechanisms underlying this shift in value and with little opportunity to extinguish these emotional memories. Subconscious changes in contextual salience and the value of nociceptive inputs are signals that drive cortical reorganization, given that they render the pain more emotional and modify decision making and selection of behaviors. The net outcome is a brain that has learned to filter emotions, actions, and reward through the lens of pain, rendering the brain addicted to pain.

I am willing to try it

 

[freddydpt]

Sounds like neuroplasticity to me.

 

[powermd]

Sounds like neuroplasticity to me.

What gets fired, gets wired.

Addicted to pain, I like it.

 

[Aether2000]

Sooooo..... L-DOPA plus NSAIDS given acutely can attenuate the development of allodynia and in chronic pain situations may also reduce allodynia? Is that the takeaway? Of course there is the long list of side effects.....

 

[DrCommonSense]

The Emotional Brain as a Predictor and Amplifier of Chronic Pain. - PubMed - NCBI

A New Hypothesis of Chronic Pain

In accordance with these recent advances, we propose a novel definition of chronic pain. Rather than defining pain by its sensations, we propose a definition that emphasizes the neurobiological mechanisms that control behavioral adaptations, and we hypothesize that persistence of pain is likely mediated through the reorganization of the cortex by corticolimbic learning mechanisms. We therefore posit that chronic pain is a complex web of sensory and emotional experiences, coupled with behavioral adaptations. Specifically, we posit that the chronic pain state is a consequence of a change in value related to nociceptive afferent information impinging on the cortex, with limbic emotional learning mechanisms underlying this shift in value and with little opportunity to extinguish these emotional memories. Subconscious changes in contextual salience and the value of nociceptive inputs are signals that drive cortical reorganization, given that they render the pain more emotional and modify decision making and selection of behaviors. The net outcome is a brain that has learned to filter emotions, actions, and reward through the lens of pain, rendering the brain addicted to pain.

Solution: Suboxone

 

[101N]

Neither suboxone or IPM.

 

[painj]

Not a doctor-but extremely interested-
With this synopsis-all patients with pain should have psychiatric counseling prior to forming any type of treatment plan-long or short-in order for the brain to allow the body to heal from this treatment? Or would the brain need to refocus it's "muscle memory" through treatment to then allow the body to benefit from the treatment?

 

[drusso]

https://www.regenexx.com/pne-chronic-pain-denier-movement/

 

[101N]

Regenexx the new Purdue

 

[drusso]

Regenexx the new Purdue

Hardly...

https://www.regenexx.com/high-dose-narcotics-for-moderate-osteoarthitis/

https://www.regenexx.com/avoid-drug-reps-office-like-plague/

It's just not that "new." It's so 1990's...

Pain and the neuromatrix in the brain.
Melzack R1.
Author information

Abstract
The neuromatrix theory of pain proposes that pain is a multidimensional experience produced by characteristic "neurosignature" patterns of nerve impulses generated by a widely distributed neural network-the "body-self neuromatrix"-in the brain. These neurosignature patterns may be triggered by sensory inputs, but they may also be generated independently of them. Acute pains evoked by brief noxious inputs have been meticulously investigated by neuroscientists, and their sensory transmission mechanisms are generally well understood. In contrast, chronic pain syndromes, which are often characterized by severe pain associated with little or no discernible injury or pathology, remain a mystery. Furthermore, chronic psychological or physical stress is often associated with chronic pain, but the relationship is poorly understood. The neuromatrix theory of pain provides a new conceptual framework to examine these problems. It proposes that the output patterns of the body-self neuromatrix activate perceptual, homeostatic, and behavioral programs after injury, pathology, or chronic stress. Pain, then, is produced by the output of a widely distributed neural network in the brain rather than directly by sensory input evoked by injury, inflammation, or other pathology. The neuromatrix, which is genetically determined and modified by sensory experience, is the primary mechanism that generates the neural pattern that produces pain. Its output pattern is determined by multiple influences, of which the somatic sensory input is only a part, that converge on the neuromatrix.


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Pain. 1999 Aug;Suppl 6:S121-6.
From the gate to the neuromatrix.
Melzack R1.
Author information

Abstract
The gate control theory's most important contribution to understanding pain was its emphasis on central neural mechanisms. The theory forced the medical and biological sciences to accept the brain as an active system that filters, selects and modulates inputs. The dorsal horns, too, were not merely passive transmission stations but sites at which dynamic activities (inhibition, excitation and modulation) occurred. The great challenge ahead of us is to understand brain function. I have therefore proposed that the brain possesses a neural network--the body-self neuromatrix--which integrates multiple inputs to produce the output pattern that evokes pain. The body-self neuromatrix comprises a widely distributed neural network that includes parallel somatosensory, limbic and thalamocortical components that subserve the sensory-discriminative. affective-motivational and evaluative-cognitive dimensions of pain experience. The synaptic architecture of the neuromatrix is determined by genetic and sensory influences. The 'neurosignature' output of the neuromatrix--patterns of nerve impulses of varying temporal and spatial dimensions--is produced by neural programs genetically build into the neuromatrix and determines the particular qualities and other properties of the pain experience and behavior. Multiple inputs that act on the neuromatrix programs and contribute to the output neurosignature include. (1) sensory inputs (cutaneous, visceral and other somatic receptors); (2) visual and other sensory inputs that influence the cognitive interpretation of the situation; (3) phasic and tonic cognitive and emotional inputs from other areas of the brain; (4) intrinsic neural inhibitory modulation inherent in all brain function; (5) the activity of the body's stress-regulation systems, including cytokines as well as the endocrine, autonomic, immune and opioid systems. We have traveled a long way from the psychophysical concept that seeks a simple one-to-one relationship between injury and pain. We now have a theoretical framework in which a genetically determined template for the body-self is modulated by the powerful stress system and the cognitive functions of the brain, in addition to the traditional sensory inputs.