Tuesday, June 04, 2013

Melzack and Katz: Part 6e: Ref 4. Pattern theories in History of Pain

The paper, Pain.

Part 1 First two sentences

Part 2 Pain is personal Also Pain is Personal addendum., Neurotags! Pain is Personal, Always.

Part 3a Pain is more than sensation: Backdrop

Part 3b Pain is not receptor stimulation

Part 3c: Pain depends on everything ever experienced by an individual

Part 4: Pain is a multidimensional experience across time

Part 5: Pain and purpose

Part 6a: Descartes and his era; Part 6b: History of pain - what’s in “Ref 4”?; Part 6c: History of pain, Ref 4, cont.. : There is no pain matrix, only a neuromatrix; 

Part 6d: History of Pain: Final takedown


Today, we are still examining the chapter in Challenge of Pain by Melzack and Wall, "Ref. 4" in the new paper, Pain, by Melzack and Katz, in the slow meander through it. (Yes.. some day, we'll arrive back into the paper itself and it will be as though we had never wandered away from it in the first place.)

Anyway: on page 157, we see this:
"As a reaction against the psychological assumption in specificity theory, other theories have been proposed which can be grouped under the general heading of "pattern theory.""
[Melzack is pretty adamant that there be no psychological assumptions, ever.]


The earliest pattern theory developed from Goldscheider (1894), who at first nodded along with von Frey, but later wondered if stimulus intensity and central summation might have anything to do with anything. According to Melzack and Wall he looked carefully at studies of pathological pain, e.g., Naunyn's study in 1889 on tabes dorsalis of late stage syphilis. (See "intensive theory"in wikipedia). Noordenbos in 1959 pointed out that in tabes dorsalis, one of the big symptoms is temporal and spatial summation of input, resulting in pain.
"Successive, brief applications of a warm test tube to the skin of a tabetic patient are at first felt only as warm, but then increasingly hot until the patient cries out in pain as though his skin is being burned." p. 157
Single pinpricks evoke "diffuse, prolonged, burning pain" in someone with tabes. And a pinprick may be felt, but not until as many as 45 seconds later!

Let's hear it again for penicillin!
It made 
syphilis go away for a long long time,
although it 
has crept back lately.

Anyway, thoughtful people wondered about this kind of presentation. They thought, hmmn.. no.... there is more to sensation and pain perception than just a bunch of wires all hooked up.
"Goldscheider.. was compelled to conclude that mechanisms of central summation, probably in the dorsal horns of the spinal cord, were essential for any understanding of pain mechanisms. The long delays and persistent pain observed in pathological pain states, Goldscheider assumed, are due to abnormally long time-periods of summation." p. 158
All other pattern theories derive from Goldsheiber's early recognition that there had to be more going on than met the eye.

1. Peripheral pattern theory: Weddell 1955; Sinclair 1955

  • pain thought to be due to excessive peripheral stimulation
  • still bottom-up
  • theory proposes that all fibre endings (except those found innervating hair cells, in the inner ear I presume) are alike
  • however there is actually quite a lot of receptor specialization, which undermines the theory

2. Central summation theory: Livingston 1943

  • was the first to suggest that remarkable summation phenomena must have a basis in the CNS
  • he conceived of "reverberatory circuits (closed, self-exciting loops of neurons)" existing inside the spinal cord
  • these could be "triggered by normally non-noxious inputs which would be interpreted centrally as pain"
  • this idea is useful for explaining phantom limb pain, sweating and jerking of stump
  • no physiological evidence for functional reverberatory circuits was ever found
  • this theory had an impact however

3. Sensory interaction theory

  • specialized input controlling system normally prevents summation from occurring: if it's destroyed, pathological pain states follow
  • Head, 1920: epicritic and protopathic
  • Bishop 1946: fast and slow
  • Noordenbos 1959: myelinated and unmyelinated
  • fast system usually dominates the slow one: if it fails to do so, the result is protopathic sensation (Head), slow (diffuse, burning) pain (Bishop), or hyperalgesia (Noordenbos)
  • Noordenbos' ideas caught on; idea of a multi-synaptic afferent system in spinal cord contrasts markedly to the idea of a straight-through system, might explain why cordotomy can fail to abolish pain - unless the whole spinal cord is cut, afferent input will find a way in

4. Affect theory

  • older theory (Aristotle) considered pain to be an emotion, opposite pleasure, not a sensation
  • Dallenbach 1939: Von Frey and Goldsheider were battling bitterly about it, and a third figure turned up, H.R. Marshall, who said, "Stop - you're both wrong. Pain is an emotional quality, a quale." 
  • meanwhile progress galloped on and researching 'pain as sensation' gained so much traction that 'pain as affective or motivational' was left behind,  lumped under "reactions to pain" instead of being treated as part of its formation

Next: Evaluation of theories (Hint: they all have something important to contribute)

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