Centralization
"The key feature of the nervous system is centralization. It offers few circuits for local interactions of body parts. The CNS is almost always involved even if the distance, as from thumb to index finger, is slight. Intercession of the brain and spinal cord ensures integrated and coordinated activity.
Exceptions are instructive. The local cutaneous response to irritating stimuli (raking a blunt probe over the skin) has three components: local reddening (vasodilation from injury), wheal formation (transient edema from tissue fluid extrusion), and ensuing vasodilation (flare) with lowered thresholds and increased sensitivity to pain (pinprick). The flare and hyperalgesia represent an axon reflex. Nociceptive (pain) nerve endings are activated by substances released by injured tissue cells, and nerve impulses are conducted a short way centrally along nociceptive axons and then distally over branches of these axons to nearby arterioles, causing them to dilate. Advanced or primitive (it is sluggish, starting in about 20 sec. and developing fully in around 3 min), this reflex involves local nerve fibers only, not the CNS.
The "triple response" illustrates three concepts. Pain receptors sense chemical, as well as mechanical and thermal stimuli. Their sensitivity is increased by substances accumulating in the damaged area. Their response includes a neuroeffector component. They release substances (peptides) that initiate further events, providing further protection and favoring local tissue repair.
Studies in invertebrate neural systems show extensive local control of visceral function. Exceptions to central control are also found in the mammalian ANS. Near-normal interaction of bowel segments persists in the absence of CNS innervation. Sensory fibers from the gut exert feedback in intramural autonomic ganglia on visceral motor neurons regulating smooth muscle in the intestinal wall. The nervous system has pattern generators, both central and peripheral: systems with cellular, synaptic, and network properties (cyclic firing rhythms, reciprocal inhibition of cell pairs, leader and follower cells) that provide automated mechanisms for generating rhythmic movements (breathing, walking) or periodic activities (sleeping, waking). Regulated by neural (sensory feedback, volitional override) or neuroendocrine influences, pattern generators are pithy examples of neural endogenous activity."
This is a very instructive passage, particularly in its clear explanation of the peripherality of the axon reflex, but I would be so bold as to quibble with Angevine over his use of the term, "pain receptors." Some pain researchers part company with this terminology, preferring instead to refer to peripheral receptors that register chemical, mechanical and temperature stimuli which could be harmful (but aren't necessarily), as nociceptors, not "pain receptors." They are quite clear that strictly speaking, incoming information to the CNS is not "pain" until the brain decides it is, at which point it will make it so. It may seem a small point, but depending on context, the brain may choose to ignore nociception entirely to deal with a completely different, but from its perspective, more pertinent or immediate threat. Numerous examples of this are in the pain literature dating back to the Civil War. Also, the brain is capable of making "pain" in the absence of any noxious input (Derbyshire 2004).
Additional reading
For axon reflex:
1. Axon Reflex (3-page pdf)
2. Excerpts from book, Clinical Motor Electroneurography: Evoked Responses Beyond the M-wave on axon reflex
3. Axon reflex as discussed in book, Biology of Skin
4. Caselli A; Validation of the nerve axon reflex for the assessment of small fibre dysfunction JNNP 2006 (abstract)
For pain without nociception:
5. Derbyshire SW Cerebral activation during hypnotically induced and imagined pain 2004 (10-page pdf)
For pattern generators:
6. Hooper, SL Central pattern generators, 2000: 16-page pdf
2 comments:
This statement in your post:
"...refer to peripheral receptors that register chemical, mechanical and temperature stimuli which could be harmful (but aren't necessarily), as nociceptors, not "pain receptors." They are quite clear that strictly speaking, incoming information to the CNS is not "pain" until the brain decides it is, at which point it will make it so."
Is vastly more important than just a quibble :-) It encapsulates one of the fundamental insights that I have gained from your blogs and related writings. It is a concept that most physicians (especially surgeons) seem completely unaware of.
The idea that there is "real pain" and then "pain that is just in your head" seems to be dying harder than the idea that the sun and stars orbit around the earth.
Hi Kent,
You said, "It is a concept that most physicians (especially surgeons) seem completely unaware of."
I concur completely.
"The idea that there is "real pain" and then "pain that is just in your head" seems to be dying harder than the idea that the sun and stars orbit around the earth."
Yes, I agree, but there is hope, in dribs and drabs, from several switched-on researchers/physicians/surgeons. It will probably take even longer for this (by now, at least two decades-old)information to trickle through the manual therapy community and change the thinking and practice patterns significantly.
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