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physiology of pain
Helen Godfrey
Abstract
This article is the first in a two-part series which explores pain and its
management from a physiological perspective. Pain is a common experience
which is often inadequately managed in hospital and community settings.
While nurses are in a key position to contribute to successful pain management
there are frequent accounts in the literature that nurses lack knowledge about pain
management. Knowledge of pain physiology is fundamental to its successful
management. This article introduces nurses to the components in the pain
pathway and describes nociceptors which respond to pain stimuli and identifies
pain fibres which carry pain information to the spinal cord. The processing of pain
in the spinal cord is explained and the role of the brain in the manifestation of the
pain experience is also explored. The gate control theory of pain and the more
recent neuromatrix theory are discussed.
Key words: Pain and pain management
Physiology
Cover picture.
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PHYSIOLOGY OF PAIN
professionals who manage pain is required to
elicit improvements in the management of
pain (Stannard and Johnson, 2003).
Nurses are in a unique position to
contribute to successful pain management
since they have many opportunities to identify
patients in pain, assess pain and its effects,
instigate action to control the pain and
evaluate the efficacy of these actions and any
adverse effects. While pain management is an
integral aspect of nursing care it could be
argued that it is often not tangible in terms of
accounting for time spent or in patient
satisfaction (Madjar, 2004).
There is a wealth of literature which suggests
that nurses lack knowledge about pain
management (Clarke et al, 1996; McCaffery
and Ferrell, 1997; Twycross, 2002; Madjar,
2004). To manage pain effectively nurses need
to understand the mechanisms that initiate and
maintain pain. Management of pain by nurses
should be based on current knowledge of pain
physiology as well as understanding the context
and the psychological, social, cultural and
cognitive aspects which contribute to the pain
experience (Clarke et al, 1996;Twycross, 2002).
The concepts introduced in this article reflect
the principles, objectives and content of the pain
curriculum for basic nursing education proposed
by the International Association for the Study of
Pain (IASP), particularly with regard to the
physiological dimension of pain (IASP, 1994).
While pain is much more than a
physiological sensation, effective pain
management depends in part on nurses
having knowledge of the physiological
mechanisms involved in the pain experience.
This article is the first in a two part series and
introduces the key concepts in contemporary
pain physiology and explores the mechanisms
which contribute to pain. The second article
in the series aims to enhance nurses
knowledge by exploring the biological basis
of pain interventions which contribute to
pain management.
Experience of pain
The pain experience varies for different
individuals as a result of a multitude of factors
and circumstances which are difficult to
characterize. Different types of pain can be
experienced; some pain is protective and acts
as an early warning to alert the individual that
tissue damage is occurring or about to occur.
This sort of pain prevents further damage
during healing and repair (Woolf, 1995).
However, pain often outlives its warning role
and becomes persistent and debilitating (Julius
and Basbaum, 2001). Pain can be experienced
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carrying pain information, these are the Aalpha and A-beta fibres (Julius and Basbaum,
2001;Wood et al, 2005).These fibres conduct
impulses more quickly than pain fibres and
can modulate the transmission of pain
information in the spinal cord.
Figure 1. Nociceptors in the skin situated next to a mast cell and capillary loop. Mast cells release their histamine in response to pain
stimuli, the histamine in turn stimulates the nociceptors to secrete neurochemicals including substance P.A cascade of chemicals
ultimately leads to activation of nociceptors and action potentials are generated in the pain fibres and conducted to the spinal cord.
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PHYSIOLOGY OF PAIN
The grey matter in the spinal cord is highly
organized into a number of layers, or laminae:
A-delta fibres terminate in laminae I,V and X,
and C fibres end in laminae I to V (Cross,
1994). Afferent fibres terminating in the
superficial laminae of the dorsal horn are small
and tend to respond only to pain, whereas
neurones in the deeper laminae respond to
noxious and non-noxious input (Barasi, 1991).
The location in the grey matter of the dorsal
horn where the majority of C and A-delta
fibres terminate is called the substantia
gelatinosa (Dickenson, 1995). The substantia
gelatinosa comprises lamina II and III and
represents a system on each side of the spinal
cord of densely interconnecting neurones
which can modulate pain information
(Melzack and Wall, 1965; Melzack, 1973).
Within the spinal cord, each sensory or afferent
fibre is likely to synapse with many small
interneurones located in different regions (or
laminae) of the spinal cord (Barasi, 1991).
Figure 2 Lateral spinothalamic tract.Three sensory neurones carry pain information to the brain in this pathway.
Diameter
Myelination
Conduction
velocity
metres/second
Type of pain
A-delta fibres
Large
Myelinated
525
'First' pain
C fibres
Small
Unmyelinated
12
'Second' pain
Nociceptor
at distal end
High threshold
mechanoreceptor
Polymodal
receptor
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Pain impulse sent to brain
A delta or C pain fibre
Cell body
Axon
Axon terminal
Figure 3 The concept of the gate.The pain fibre (first-order neurone) synapses with the second-order neurone in the
dorsal horn of the spinal cord.These diagrams illustrate the concept of the gate which controls the flow of pain
information to the brain.The arrows represent pain impulses.
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PHYSIOLOGY OF PAIN
by the descending pathway or by sensory
information arriving at the synapse in large
diameter sensory fibres. In both cases, the
second-order neurone will be inhibited by the
natural opioids, sometimes described as
endogenous opioids, secreted from the
inhibitory neurone, and the flow of pain
information up to the brain will be suppressed.
This pain modulation by the bodys own
natural opioids may be described as
endogenous opioid analgesia (Barasi, 1991).
There are a variety of ways in which these
endogenous opioids can inhibit the flow of
pain information. They prevent secretion of
the neurotransmitter, substance P from pain
fibres and compete for substance P receptor
binding sites on the second-order neurone
(Clancy and McVicar, 1998).
Figure 4 Gating mechanism.The gating mechanism in the dorsal horn of the spinal cord relies on a small inhibitory
neurone which when active suppresses the flow of pain information to the brain. Arrows represent nerve impulses.
Sensitization
The neural pathways involved in the
perception and modulation of pain are
plastic, which means they can be modified in
response to a range of stimuli, emotional as
well as physical (Cross, 1994). Neurones
which become used to carrying pain
information can become sensitized. Changes
to the sensitivity of both peripheral and
central neurones are considered central to the
concept of neuroplasticity. Neurones
signalling tissue damage also secrete various
chemicals leading to inflammation and
sustained peripheral activity (Haigh and
Blake, 2001). This leads to changes in
sensitivity of neurones conducting pain
information so that ordinary sensory
information, such as pressure on an injured
foot, becomes transformed into pain
information (allodynia).This helps to explain
why the pain someone feels may be out of
proportion to the tissue damage (Youngson,
1992). The activity of excitatory amino acid
receptors, particularly N-methyl-D-aspartate
receptors on spinal neurones seems to be an
intrinsic aspect of this plasticity (Haigh and
Blake, 2001; Petrenko et al, 2003). The
phenomenon of sensitization illustrates that
pain is an active process rather than just a
relay of noxious information to the brain.
Sensitization occurring in both the periphery
and spinal cord reflects neuronal plasticity
and leads to pain hypersensitivity (Woolf and
Salter, 2000). The phenomenon of wind-up
is associated with C fibres which are
responding to sustained pain stimuli; this
causes a progressive increase (wind-up) in the
response rate of the second-order neurones
(McHugh and McHugh, 2000; Bolay and
Moskowitz, 2002).
Figure 5 Descending inhibitory pathway. Descending pathways can also suppress the flow of pain information
by stimulating the inhibitory neurone.
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Conclusions
Pain is a complex multidimensional experience.
Pain stimuli trigger nociceptors to fire off
impulses along nerve fibres to the spinal cord.Adelta fibres and C fibres carry pain information
to the dorsal horn in the spinal cord. Here the
relative activity of large diameter afferents
carrying sensory information, such as touch or
warmth, modulates the pain signals passing to
KEY POINTS
n Knowledge of the physiological mechanisms involved in the pain experience
is a precondition for effective pain management by nurses.
n Pain producing substances and stimuli in the periphery both activate and sensitize
nociceptors.
n Nociceptors are connected to pain fibres, A-delta and C fibres, which conduct pain impulses
to the gate mechanism in the spinal cord.
n The opening and closing of the gate in the dorsal horn depends on the balance of activity
in pain fibres and the larger diameter sensory fibres carrying non-pain information together
with the activity of the descending inhibitory fibres.
n The descending inhibitory fibres modulate pain by stimulating the inhibitory neurones
in the dorsal horn to secrete endogenous opioids which suppress substance P-mediated
neurotransmission and the flow of pain impulses to the brain.
n A variety of factors and influences are integrated by networks in the brain that form
the neuromatrix and which mediate the pain experience.
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