Pain
The Reverend Dr. David C.M. Taylor
dcmt@liverpool.ac.uk© David Taylor and The University of Liverpool, 1999
Carpenter, RHS, Neurophysiology 3rd Edition 1996, Arnold, pp. 84 - 87
Bray, Cragg, MacKnight, Mills & Taylor, Lecture Notes on Human Physiology 3rd Edition, 1994 Blackwell Scientific Publications, pp. 155 - 158
Kandel, Schwartz & Jessell, Principles of Neural Science 3rd Edition, 1991, Elsevier, chapter 27
and a monograph which is really quite good (!)......
Taylor & Pierau, Nociceptive Afferent Neurones 1991 Manchester University Press
Professor Pat Wall has written a number of good books and articles, you might be able to find a copy of "The Puzzle of Pain" by Melzack and Wall, which was published by Penguin in the early 70's and which started many scientists on the study of the neurophysiology of pain.
The first concept to grasp is that there is more than one kind of pain.
First pain is sharp, precisely located, and produces a reflex phasic contraction.
Second pain is usually intense, poorly located and produces a reflex tonic contraction
|
First pain |
Second pain |
|
|
Adequate stimulus |
Pin prick, heat |
Tissue damage |
|
Sensory unit |
A delta mechanical Mechanical/heat |
C and A delta Polymodal nociceptors |
|
Pathway |
spinothalamic |
Spinoreticular Intralaminar thalamic |
|
Distribution |
Body surface |
Most tissues, superficial and deep |
|
Reflex |
Phasic contraction |
Tonic contraction |
Morphine has little or no effect on first pain, but can be effective against second pain. Although most textbooks emphasise the role of C-fibres in second pain, there is considerable evidence that A delta fibres are very important in humans.
The Gate Control Theory of Pain
was advanced by Melzack and Wall in 1968. It had the great merit of being a testable hypothesis, and prompted huge endeavours in the field of neuroscience. Many of the details in the original model have been questioned, but it remains tremendously influential.
it can explain why rubbing an injured region decreases pain sensation, and has also been invoked to explain the working of acupuncture and TENS (transcutaneous electrical nerve stimulation).
Painful signals pass up the "c-fibre", and are relayed onwards by the pain transmission cell (T). Rubbing the injured region activates the A beta fibre which causes more pain initially, followed by less pain. The decrease in pain sensation is due to the A beta fibre activating a "gate" in the spinal cord. The gate is a cell in the substantia gelatinosa (sg) which inhibits all impulses arriving at the T cell. A really severe pain, will override the A beta activity by inhibiting the sg cell. The other part of the model has now assumed a greater importance, and that is the descending control.
Descending Inhibition
Touch
cortico-thalamic pathways
why we don't feel clothes
Pain
battle and sporting injuries, ecstasy
children, animals, elderly/suffering
Descending control of pain
Evidence in favour:
microinjection of opiates into discrete regions of the CNS (PAG,limbic system,SG) produces analgesia
Microstimulation there also produces analgesia
Opioid peptides are present there
Electrical stimulation of the PAG or NRM produces analgesia
The proposal is that activity in the limbic system, triggered by the mental state, emotion, memories, is passed through the periaqueductal grey to the nucleus raphe magnus, and then on down to interneurones in lamina II of the spinal cord (the sg).
There are two bodies of opinion about the possible mechanism of the inhibition.
Presynaptic inhibition
The descending pathway from the brain releases serotonin (5HT) onto enkephalin containing interneurones, which in turn pre-synaptically inhibit the pain carrying substance P fibre.
This is the currently accepted version of the gate control theory.
The pre-synaptic model is preferred by most pharmacologists, but has not proved particularly useful in designing new drugs. My own preference is for a post-synaptic model, although the model above suffers from the disadvantage that it is difficult to disprove (unlike Wall's gate control hypothesis which was wrong, but a good model because it was falsifiable. Read Popper on what makes a good scientific hypothesis). Try to use your knowledge of synaptic mechanisms to work out the relative effectiveness of pre- and post-synaptic inhibition.
There is a growing body of evidence (Hunt, Duggan, McMahon amongst others) that C-fibres are not important in pain sensation as such - but in signalling to the body that the tissue has been seriously damaged or removed. To really understand this you will need to study this subject at honours level. It relates to the observation that nerve fibres carry chemical as well as electrical information.
