Page 11 - BSAVA Guide to Pain Management in Small Animal Practice
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BSAVA Guide to Pain Management in Small Animal Practice
VetBooks.ir initial sharp pain sensations. C bres are small, potentially central sensiti ation. he N A
receptor is therefore a good target for analgesic
unmyelinated slow transmitting nerves, which
selectively carry nociceptive stimuli from
minimi e the development of chronic pain if
the high activation, polymodal nociceptors. drugs such as ketamine, which are thought to
hey are responsible for carrying dull burning used at the time of initial insult.
pain sensations. Modulation is the process of dampening or
he dorsal horn of the spinal cord has been amplifying nociceptive signals. odulation
classi ed into physiological ones or laminae , takes place primarily in the dorsal horn of the
with lamina I being the most super cial. Aδ and spinal cord, but also elsewhere, with input from
C bres terminate predominantly in laminae I II ascending and descending pathways. It is a
but a few terminate deeper, with C bres complex process, and the relationship between
tending to communicate to deeper laminae stimulus intensity and response to pain is not
via interneurons. Interestingly, most touch consistent. he output from the dorsal horn is
a erents also pro ect to deeper laminae and also altered by the interaction of various
this is thought to be the site of pain gating neurotransmitters, all of which are sub ect to
the phenomenon whereby rubbing a painful plasticity and alterations. It is a very labile
area can alleviate some of the acute pain after phenomenon with several distinct components
an in ury. his is thought to occur by activation peripheral sensiti ation, dorsal horn gating ,
of inhibitory interneurons arising from the central sensiti ation wind up, descending
touch receptors. inhibitory pathways and descending facilitatory
ne of three things may happen to the pathways. Peripheral sensiti ation is a form of
a erent signals. irst, a spinal segmental re ex modulation involving local production of
e.g. withdrawal may occur. Secondly, the pro in ammatory mediators contributing to
impulse may be passed on to the brain via hyperalgesia exaggerated response to a
spinoreticular and spinothalamic tracts. hirdly, stimulus that would be expected to be painful
the impulse may be processed modulated, e.g. around damaged tissue. his is in contrast to
gate theory . allodynia, which is a non painful stimulus
he primary a erents synapse on to a eliciting pain, and more likely due to central
variety of di ering postsynaptic cell types. sensiti ation. Non steroidal anti in ammatory
hese include nociceptor speci c NS cells Aδ drugs NSAI s are the analgesic agents of
and C bres only that re in response to painful choice for treatment of peripheral sensiti ation.
stimuli, proprioceptor speci c cells that As previously mentioned, N A activation may
respond to A bres touch , and wide dynamic lead to long term potentiation of the pain
range R cells which respond to all three response via elevated activity of dorsal horn
bres touch to pain. Located deep in lamina V, neurons. his receptor is a target for analgesic
R neurons re in a graded fashion drugs such as ketamine.
depending on stimulus intensity and exhibit escending modulatory pathways have four
wind up synaptic plasticity . tiers but are poorly understood. Inhibition may
here are two ma or postsynaptic receptors arise from the cortex and thalamus, the
involved in spinal cord pain transmission. A PA peria ueductal gray matter PA in the
amino hydroxy methyl 4 mid brain which has a high opioid receptor
isoxa eloproprionic acid receptors are fast concentration and is thought to be important in
activation receptors that set the baseline dorsal opioid mediated analgesia , the nucleus raphe
horn response to noxious and tactile stimuli. magnus NR in the pons and rostral ventral
he second receptor is the N A N methyl medulla RV and nally the medulla
aspartate receptor. Activated by prolonged and oblongata and spinal cord. Although
repetitive C bre stimulation, this receptor descending inhibition is thought to work on
allows calcium ion in ux into the postsynaptic many levels of the CNS, it is considered most
cell and is responsible for wind up and important at the spinal level and can be very
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