Page 30 - BSAVA Guide to Pain Management in Small Animal Practice
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4 | Chronic and osteoarthritic pain
VetBooks.ir nociceptive transmissions are integrated to Facilitation of nociceptive
generate perception of the nature, location and
transmission
intensity of the pain.
Increased facilitation of nociceptive impulses
within ascending neurones can be produced by
Actual tissue damage, such as may be repeated C bre stimulation, as may be present
during in ammatory states. ne mechanism
encountered within in amed synovial oints, through which facilitation occurs involves the
results in the liberation of in ammatory N-methyl- aspartate N A receptor. uring
molecules from damaged cells, which may normal states, the in ux of calcium to
produce a state of peripheral sensitization, postsynaptic neurones caused by the binding of
in which the altered cellular environment glutamate to the NMDA receptor (calcium
results in the recruitment of ‘silent’ (high channel is reduced by the presence of a
threshold, inactive in unin ured tissue magnesium ion within the channel pore.
nociceptors, augmented action potential Ongoing depolarization of the postsynaptic
generation in response to the application of membrane e.g. fre uent C bre action
suprathreshold stimuli (producing potentials results in removal of the magnesium
, and generation of spontaneous blockade, and greatly increased calcium in ux
action potentials causing spontaneous pain . in response to glutamate binding (Nowak et al.,
ngoing in ammatory processes, such as 1984 . Postsynaptic facilitation has also been
OA, will maintain nociceptors in a state ascribed to synaptic release of substance P,
of hyperexcitability. tumour necrosis factor alpha, and
prostaglandins. Increased central transmission in
Neuropathic pain response to nociceptive stimulation contributes
Pain arising as a direct consequence of a to the clinical phenomenon of hyperalgesia.
lesion or disease a ecting the somatosensory Access of non-nociceptive
system is termed neuropathic pain reede et
al., 8 and may arise from lesions in either
the peripheral or central nervous system CNS . horn cells
Common examples of neuropathic pain Non-nociceptive information, such as touching
producing pathologies in small animals include or stroking of the skin, is conveyed to the CNS
syringomyelia and spinal cord compressive via A a erent bres. Similar to nociceptive
disc lesions. It is important to note that a erents, these bres synapse with modali-
neuropathic pain is not synonymous with ty speci c ascending pro ection neurones;
central sensitization, the latter (described however, the speci city of sensory transfer is
below may result from high intensity of reliant on e ective inhibitory interneurones,
sustained nociceptive input owing to which prevent cross-talk between low
nociceptive, in ammatory or neuropathic threshold A bres and ascending nociceptive
sources of pain. neurones Scho negger et al., 8;
Sandkuhler, 9 . A failure of inhibitory
interneurone activity permits innocuous
Central sensitization sensations to be misinterpreted as painful, a
phenomenon termed .
he propensity of ascending neurones to relay
nociceptive information to higher structures
within the CNS is governed by the net e ect of inhibition of nociceptive
opposing facilitatory and inhibitory mechanisms,
which act to regulate the excitability of spinal information
cord neurones. A number of these mechanisms C bre nociceptive a erent input provokes a
are described here. spino bulbar spinal re ex termed descending
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