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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