Pain Descending Pathways: Difference between revisions

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== What is the descending pain modulatory system? ==
== What is the descending pain modulatory system? ==


The ''"top down"'' modulation of pain has been in evidence since the early work of Sherrington<ref name="Sherrington" />&nbsp;showing that nociceptive reflexes were enhanced after transection of the spinal cord. This was further elaborated on by Fields<ref name="Fields">Fields HL. Pain modulation: expectation, opoid analgesia and virtual pain. Prog Brain Res 122:245-253; 2000</ref>&nbsp;and Milan<ref name="Milan">Milan MJ. Descending control of pain. Prog Neurobiology 66:355-474; 2002</ref>&nbsp;who, based upon observations in the 1960's that electrical stimuation of the periaqueductal gray (PAG) area can produce analgesia, demostrated through electrophysiological and pharmacological studies that descending influences on spinal nociceptive processing involves the PAG and the rostral ventronedial medulla (RVM).  
The ''"top down"'' modulation of pain has been in evidence since the early work of Sherrington<ref name="Sherrington" />&nbsp;showing that nociceptive reflexes were enhanced after transection of the spinal cord. This was further elaborated on by Fields<ref name="Fields">Fields HL. Pain modulation: expectation, opoid analgesia and virtual pain. Prog Brain Res 122:245-253; 2000</ref>&nbsp;and Milan<ref name="Milan">Milan MJ. Descending control of pain. Prog Neurobiology 66:355-474; 2002</ref>&nbsp;who, based upon observations in the 1960's that electrical stimuation of the periaqueductal gray (PAG) area can produce analgesia, demostrated through electrophysiological and pharmacological studies that descending influences on spinal nociceptive processing involves the PAG and the rostral ventronedial medulla (RVM).  

Revision as of 14:27, 10 September 2014

Welcome to PPA Pain Project. This page is being developed by participants of a project to populate the Pain section of Physiopedia.  The project is supervised and co-ordinated by the The Physiotherapy Pain Association.
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  • Describe the descending pathways that modulate pain transmission
  • Describe their purpose, how they are activated  and how their actions might impact upon a pain experince

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What is the descending pain modulatory system?[edit | edit source]

The "top down" modulation of pain has been in evidence since the early work of Sherrington[1] showing that nociceptive reflexes were enhanced after transection of the spinal cord. This was further elaborated on by Fields[2] and Milan[3] who, based upon observations in the 1960's that electrical stimuation of the periaqueductal gray (PAG) area can produce analgesia, demostrated through electrophysiological and pharmacological studies that descending influences on spinal nociceptive processing involves the PAG and the rostral ventronedial medulla (RVM).

Work by Hadjipavlou et al[4] used functional and anatomical studies to link the descending pain modulatory system from the brain stem (where the PAG and RVM reside) to a number of higher level brain area including; cingulofrontal regions, the amygdalae and the hypothalamus (figure 1). This may go someway to help explain the role that emotions and cognition have in processing nociceptive information. 


Underpinning the descending pain modulatory system is the endogenous opoid system[5] and according to Willer[6] this system may be activated by a variety of reflex and cognitively trigged states. At the spinal cord (dorsal horn), level the opiod system causes inhibition of substance P from peripheral noxious mechanical stimulation[7] via release of noradrenaline from the dorsalateral PAG (dPAG) and thermal nociceptive stimuli via the release of serotonin from the ventrolateral PAG (vPAG)[8].

How is the system useful?[edit | edit source]

Evidence for pain modulalatory mechanisms were first recorded by Beecher[9]. Beecher, a physician serving the US Army during World War II, oserved as many as three quarters of badly wounded soldiers reported no to only moderate pain and did not require pain relief medication. According to his report the men were alert and responsive and were not trivial, including compound fractures and penetrating wounds. This lead him to the conclusion that "strong emotions" block pain. This clearly opposess the classical Cartesian view where pain was considered to be a hard-wired system that passively transmitted noxious inputs to the brain. It is now generally accepted that the experience of pain does not soley rely on noxious inputs, but many variable interplay with the experience, including memory, mood, environment, attention and expectation. Ultimatley this means the resultant pain experienced to the same sensory input can vary considerably[10]. It is the brain's job to weigh all the information and decide whether creating pain is the most appropraite reponse. This provides a neccesary survival function since it allows the pain experience to be altered according to the situation rather than having pain always dominate[10] 

Why is this useful for physiotherapists?[edit | edit source]

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References[edit | edit source]

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  1. Cite error: Invalid <ref> tag; no text was provided for refs named Sherrington
  2. Fields HL. Pain modulation: expectation, opoid analgesia and virtual pain. Prog Brain Res 122:245-253; 2000
  3. Milan MJ. Descending control of pain. Prog Neurobiology 66:355-474; 2002
  4. Hadjipavlou G, Dunckley P, Behrens TE, Tracey I. Determining anatomical connectives between cortical and brainstem pain processing regions in humans: a diffusion tensor imaging study in healthy controls. Pain 123: 169-178; 2006
  5. Akil H, Watson SJ, Young E, Lewis ME, Khachaturian H, Walker JM. Endogenous opioids: biology and function. Annu Rev Neurosci 7: 223-255; 1984
  6. Willer JC, Dehen H, Cambier J. Stress induced analgesia in humans: endogenous opiods and naloxone-reversible depression of pain reflexes. Science 212:689-691; 1981
  7. Kuraishi, Y. Neuropeptide-mediated transmission of nociceptive information and its regulation. Novel mechanisms of analgesics. Yakugaku Zasshi 2008; 110(10),711-772
  8. Kuraishi Y, Harada Y, Aratani S. Seperate involvement of the spinal noradrenergic and serotonergic systems in morphine analgesia: the differences in mechanical and thermal algesic tests. Brain Res 1983;273, 245-252
  9. Beecher HK. Pain in men wounded in battle. Ann Surg. 1946;123(1):96-105
  10. 10.0 10.1 Bingel U, Tracey I. Imaging CNS modulation of pain in humans. Physiolohy 2008;23:371-380