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This description began as a paper presented at the Ontario Inter-Urban Pain Conference, held in
Waterloo 29/11/1996, by Don Ranney, MD, FRCS, Founder and at that time Head of the School of
Anatomy, University of Waterloo; Consultant, Orthopaedic Medicine and President, Disability
Assessment Services, Inc.
This was tho opening presentation at a conference on Mind-Body Pain and has been updated many
times since then as new information was discovered.
What is Pain?
Four centuries ago Descarte described pain in terms of an alarm bell ringing in a bell tower. From this
came the concept that there can be false alarms and we have therefore come to distinguish
"psychogenic pain" from "real pain". This is now known to be a false distinction, but still we hear today
the concept of hurt being not the same thing as harm, with the implication that much that hurts may be
ignored. The International Association for the Study of Pain has published the following definition of
pain which reflects what has been learned about pain in the last four centuries, and primarily in the
past half century.
Pain is "an unpleasant sensory and emotional experience associated with actual or potential tissue
damage, or described in terms of such damage" (Merskey, 1986).
From this definition we see that pain is a perception in the same way that vision and hearing are. By
this I mean that its significance is determined by the cerebral cortex in the light of other activity there.
It involves sensitivity to chemical changes in the tissues and then interpretation that such changes
are, or may be harmful. This perception is real, whether or not harm has occurred or is occurring.
Cognition is involved in the formulation of this perception. There are emotional consequences, and
behavioral responses to the cognitive and emotional aspects of pain.
Nociceptive pain is pain in which normal nerves transmit information to the central nervous
system about trauma to tissues (nocere = to injure, Latin).
Neuropathic pain is pain in which there are structural and/or functional nervous system
adaptations secondary to injury, that take place either centrally or peripherally (Jensen, 1996).
Much of what has previously been considered psychogenic pain is now better understood as
neuropathic pain of central origin. The IASP defines central pain as "pain initiated or caused
by a primary lesion or dysfunction in the central nervous system" (Merskey, and Bogduk,
1994). "Neuropathic" should not be confused with "neurogenic", a term used to describe pain
resulting from injury to a peripheral nerve but without necessarily implying any "neuropathy".
The persistent pain often experienced in chronic work-related musculoskeletal injuries, as well as in
those with long continued pain for other reasons, may persist because of a Central Nervous System
dysfunction. But this is a CNS dysfunction secondary to long continued peripheral pain.
With this introduction we can now begin to follow the pathways by which information is transmitted
centrally and is ultimately perceived as pain. It travels to the spinal cord or brainstem as a train of
electrical impulses in C fibres or A delta fibres of spinal or certain cranial nerves. After crossing the
synaptic junction through an extremely complex series of chemical interactions the, signal passes
once more electrically to higher CNS levels in Nociceptive Specific, or less pain specific Wide
Dynamic Range neurons.
We shall examine in turn peripheral nerve sensitivity, dorsal horn transmission, dorsal horn
pathophysiology, supraspinal modulation of the nociceptive signal, ascending pathways, and cortical
reception areas involved in pain perception. While doing so we should keep in mind an expression of
Dr Ken Casey, "Nociception is born in the dorsal horn, but we don't call it pain till it reaches the brain"
(IASP Conference, Vancouver, August 1996).
all six layers of the dorsal horn (primarily layers one, two, and five)
influx of sodium and calcium ions from the interstitial spaces and outflow of potassium ions
from within the nerve cell.
temporal summation. If a stimulus arrives at the synapse in the dorsal horn more frequently
than once every 3 seconds, the post-synaptic electrical discharge becomes more prolonged,
with consequent increase in the severity of the pain.This temporal summation is termed
"windup". To explore further the relationship between windup and central sensitization see
Price (1999), p.90-96.
Central sensitization is characteristic of chronic pain. With long continued stimulation, there
are physiological changes.But many are structural in nature. For example, changes in
expression of genes (e.g.,c-fos and c-jun) occurs within the secondary (e.g., spinothalamic or
spinoreticular) neurons that arise in the dorsal horn. These genetic changes affect the volume
and type of enzymes and neuropeptides produced. Thereby they induce long term changes in
these post-synaptic cells. One of these changes is that nerve growth factor begins to be
produced in sufficient quantities as to promote alteration in patterns of nerve connections in
the dorsal horn of the spinal cord at or about the level of incoming pain fibres. This structural
reorganization in the spinal cord's dorsal horn is one factor that can explain "abnormal"
spread of pain that is still referred to as "psychogenic" by those who, nearly four centuries
later, continue to view pain as Descarte did. Incoming fibres from a particular area are able to
gain access to neurons ascending to conciousness that normally just carry information from
areas some distance away, involving different levels of the spinal cord (Jensen, 1996). For
example, after crushing the sciatic nerve in rats there is initially hyperalgesia (an exaggerated
response to painful stimuli) in the skin supplied by the sciatic nerve. After a few days, there is
hyperalgesia well beyond this area, even in the area supplied by the femoral nerve. Hoheisal
et al (1994) and Mense et al (1997), members of the same team, have shown similar effects
when the sciatic nerve is stimulated after the gastrocnemius-soleus muscle in rats has
become inflammed.
Dorsal ganglion reflexes may be generated. Under certain conditions there can be reflex
activation of the incoming sensory fibre. This not only reinforces the incoming stimulus; it also
sends a retrograde electrical impulse which discharges substance P peripherally into the
tissues, with consequent increase in inflammation.
Volume transmission is the extrasynaptic spread of neuroactive molecules well beyond their
target sites. These substances may lead to long term potentiation of primary afferent
neurotransmission and lasting changes in both neuronal excitability and gene expression.
This mechanism may also be involved in the spread of pain perception beyond the area of
injury.
Several supraspinal pain modulating loops exist. These can increase or decrease the amount
of pain.
Other descending anatomical pathways exist that are primarily inhibitory, but some may
facilitate pain perception. These and the supraspinal modulating loops will now be briefly
described. Much less is known about them than about lower level CNS changes, but research
continues daily to bring us more information.
It has been known for some time that the reticular formation of the brain stem is involved in either
facilitation or inhibition of perception of pain under the influence of cortico-reticular signals. It was
assumed there was one spinoreticular/reticulospinal loop on each side of the body. It is now known
there are at least five on each side, that these pass information in both directions, and may be
inhibitory or facilitatory. They connect the spinal cord to the following areas of the brainstem:
1. the dorsolateral pontine tegmentum
2. the rostral ventral medulla
3. the dorsal medulla
4. the caudal medulla
5. the lateral hypothalamus
The effect of stimulating some of these centres can last from an hour to several days. There are
pharmacological as well as anatomical distinctions between them.
reticular formation
thalamus
2. The spinoreticular pathway ascends on both sides of the spinal cord to the intralaminar
nuclei of both the right and left thalamus. From there the next neuron in the chain takes the
information to many areas of the brain, e.g., the anterior part of the cingulate gyrus
( emotion ), the amygdala ( memory and emotion ), and hypothalamus ( emotion and the
vascular response to emotion ). Unofficially I like to call it the "suffering" pathway.
3. The dorsal column pathway has long been suspected of transmitting visceral nociception to
the thalamus (as well as somatic touch and position sense). Now this is known to be so
(Hirshberg, et al, 1996 ).
4. The spinomesencephalic tract has been described travelling with the spinotectal tract to the
periacqueductal grey matter and superior colliculus of the midbrain. This may be the same as,
or related to, the pathway travelling to the parabrachial nucleus in the brainstem -- which in
turn projects to the amygdala, hypothalamus, and other limbic system stuctures in the
forebrain.
5. The spinohypothalamic pathway is a very recently described route which does not synapse
in the reticular formation. It carries information of emotional significance from the skin, lips,
sex organs, gastrointestinal tract, intracranial blood vessel tongue and cornea directly to the
hypothalamus.
Clearly there is one pathway that is concerned with a discriminative analysis of pain, but many others
that concern our reactions to it, and feelings about it. One, we could say, engages "the mind", while
the others involve the whole person.
Dr. Eldon Tunks, Director of the McMaster Chronic Pain Clinic, after reading my article offered this
information:
"There are treatments that may actually aggravate central sensitization pains--oxycodone
working on kappa receptors, prolonged high dose opiod metabolites...excessive triptans or
ergotamine for migraines, and untreated pain itself. It is also becoming clear there are some
kinds of treatment that may have more specific advantages in treating central sensitization:
gabapentin, pregabalin, tramadol, amitriptyline, buprenorphine, (and) ketamine, for
example."
Non-anatomical pain is one of the features Gordon Waddell noted in his 1978 paper that
would make such a candidate unlikely to have a beneficial result from surgery for a herniated
lumbar disc. But his findings have been improperly used to suggest malingering. He himself
said so.
Because there seems to be a feeling that Waddell's Signs indicate a non-physical problem, I wrote the
paper published in AJPMR in 2010 refrred to above. But as the journal now holds the copyright of my
intellectual property, I cannot reproduce it here. But you can read a modified copy.
As I understand better how the mind thinks, I think I can understand the mind of my dog and so wrote
a book about him "I'm a Bear: Autobiography of a Golden Doodle as told to Don Ranney." You can
read about it
here.
References
Boivie J, Central pain syndromes. In Campell JN (ed) Pain 1996 - An Updated Review , IASP Press,
Seattle, p.23-29.
Dubner R, Basbaum A, Spinal dorsal horn plasticity following tissue or nerve injury. Chapter 11 in
Walls PD and Melzack R (eds) Textbook of Pain, 3rd ed., 1994, Churchill Livingstone, Edinburgh,
p.225-241.
Fitzgerald M, Woolf CJ, Axon transport and sensory C fibre function. In Chahl LA, Szolcsanyi J,
Lembeck F (eds) Antidromic Vasodilation and Neurogenic Inflammation, 1984, Akademiai Kiado,
Budapest, p.119-140.
Hirshberg RM, Al-Chaer ED, Lawand NB, Westlund KN, Willis WD, Is there a pathway in the posterior
funiculus that signals visceral pain? Pain 1996; 67: 291-305.
Hoheisel V, Koch K, Mense S, Functional reoorganization in rat dorsal horn during experimental
myositis. Pain 1994; 59: 111-118.
Jensen TS, Mechanisms of neuropathic pain. In Campbell JN (ed) Pain 1996 - An Updated Review,
IASP Press, Seattle, p.77-86.
Mense S, Hoheisel V, Kaske A, Reinert A, Muscle pain: Basic mechanisms and clinical correllates.
Chapter 32 in Jensen TS, Turner JA, Wiesenfeld-Hallin Z (eds) Proceedings of the 8th World
Congress in Pain Research and Management, 1997; 8: 479-496.
Merskey HM, Pain terms. Pain 1986; suppl. 3: S 215- S 221.
Merskey HM, Bogduk N, Classification of Chronic Pain , 2nd ed., 1994, IASP Press, Seattle, p.211.
Price DD, Psychological Mechanisms of Pain and Analgesia, 1999, IASP Press, Seattle.
Wall PD, The mechanisms by which tissue damage and pain are related. In Campbell JN (ed) Pain
1996 - An Updated Review, IASP Press, Seattle, p.123-126.
Fitzgerald M, The development of pain mechanisims, pain effects and pain expetiences in infants and
children. Chapter 38 in Mogil J (ed) Pain 2010 - An Updated Review, Refresher Course Syllabus,
IASP Press. Seattle, p.383-289.
Ranney D: A proposed neuroanatomical basis of Waddell's nonorganic signs. American Journal of
Physical Medicine and Rehabilitation, 2010;89: 1036-1042.
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Created by: ranney@hsfx.ca 1997/04/14
Revised by: ranney@hsfx.ca 2014/02/17