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The peripheral nerves show a decrease in the density of both myelinated and, particularly,
unmyelinated peripheral nerve fibres, an increase in the number of fibres with signs of
damage or degeneration and a slowing of the conduction velocity; in rats, reductions in
substance P, calcitonin gene‐related peptide (CGRP) and somatostatin levels have been
reported.
Similar structural and neurochemical changes have been noted in the CNS. In older humans
there are sensory neuron degenerative changes and loss of myelin in the dorsal horn of the
spinal cord as well as reductions in substance P, CGRP and somatostatin levels. Decreases in
noradrenergic and serotonergic neurons may contribute to the impairment of descending
inhibitory mechanisms and may underlie the decrease in pain tolerance seen in the older
person (see below). Age‐related loss of neurons and dendritic connections is seen in the
human brain, particularly in the cerebral cortex including those areas involved in nociceptive
processing; synthesis, axonal transport and receptor binding of neurotransmitters also change.
Opioid receptor density is decreased in the brain but not in the spinal cord, and there may be
decreases in endogenous opioids. However, the functional consequences of such age‐related
changes remains a subject of debate and recent functional MRI (fMRI) studies show more
similarities than differences in the magnitude of activation in the brain response to acute
noxious stimulation (Cole et al, 2008).
Variations in pain perception are best determined in controlled situations where severity of
the noxious stimulus is standardised and mood is not an active variable. This can be done with
experimental pain stimuli, or to a lesser extent, with standard medical procedures such as
venipuncture and wound dressings.
The results of studies looking at the effects of experimental pain stimuli (brief noxious stimuli
that do not result in tissue injury) on pain thresholds are conflicting and seem to depend on
the type of stimulus used. In general, older people tend to have higher thresholds for thermal
stimuli while results from mechanical stimulation are equivocal and there may be no change
over the age groups with electrical stimuli (Gibson, 2003 Level I). The significance of these
observations in the clinical setting, where pain is associated with tissue injury, remains
uncertain although they could indicate some deficit in the early warning function of pain and
narrow the gap between identification of the pain stimulus and recognition of a stimulus that
might cause tissue injury (Gibson, 2006). For example, in patients with an acute myocardial
infarction, greater intensity of chest pain was inversely correlated with lower pain threshold
(Granot et al, 2007 Level IV); presentation and treatment of those patients with less pain may
therefore be delayed.
Studies looking at age‐related changes in pain tolerance are limited but, in general and using
a variety of experimental pain stimuli, there is a reduced ability in older people to endure or
tolerate strong pain (Gibson, 2003 Level I). This could mean that severe pain may have a greater CHAPTER 11
impact on the more vulnerable older person.
Also noted have been significantly smaller increases in pain threshold following prolonged
noxious stimulation and prolonged recovery from hyperalgesia (Zheng et al, 2000 Level III‐2;
Gibson, 2006). Using experimental pain stimuli it can be shown that the threshold for temporal
summation is lower in the elderly (Gibson & Farrell, 2004). In subjects given trains of brief
electrical stimuli of varying frequency, older subjects showed temporal summation at all
frequencies of stimulation whereas summation was not seen at the lower frequencies in
younger subjects (Farrell & Gibson, 2007 Level III‐2). Temporal summation of thermal stimuli was
increased in the older compared with younger subjects (Edwards & Fillingim, 2001 Level III‐2;
Lautenbacher et al, 2005 Level III‐2) and more prolonged (Edwards & Fillingim, 2001 Level III‐2), but
temporal summation of pressure pain showed no age‐related effects (Lautenbacher et al, 2005
Acute pain management: scientific evidence 399
