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PAIN
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DEFINITION
IASP defined pain as an unpleasant sensory and
emotional experience associated with actual or
potential tissue damage, or described in terms of
such damage
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Transduction: the conversion of the energyfrom a
noxious thermal, mechanical, or chemical stimulus into
electrical energy (nerve impulses) by sensory receptors
called nociceptors
Transmission: the transmission of these neuralsignals
from the site of transduction (periphery) to the spinal cord
and brain
Perception: the appreciation of signals arrivingin higher
structures as pain
Modulation: descending inhibitory and facilitoryinput
from the brain that influences (modulates) nociceptive
transmission at the level of the spinal cord.
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TRANSDUCTION
Tissue damage release mediators inflammation
nosiseptor (free-nerve ending) peripheral
nervous system
Some analgesics target the inflammatory process
that produces sensitization. For example,
nonsteroidal anti-inflammatory drugs (NSAIDs)
inhibit cyclooxygenase (COX), thus decreasing the
synthesis of prostaglandins.
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TRANSMISSION
Nerve processes primary afferent neurons horn(DH) of the spinal cord
Release of excitatory amino acids (EAAs) (e.g.,glutamate, aspartate) and neuropeptides (e.g.,
substance P) at synapses (connections) betweencells
Some analgesics inhibit nociception in the DH.Example: opioid analgesics bind to opioid receptorson primary afferent and DH neurons and mimic theinhibitory effects of endogenous opioids. 45Baclofen, a GABA agonist, binds to GABABreceptors and mimics the inhibitory effects of GABAon nociceptive transmission
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PERCEPTION
Both cortical and limbic system structures are
involved.
Nociceptive information from some DH projection
neurons travels via the thalamus to the contralateral
somatosensory cortex
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MODULATION
Modulation of nociceptive transmission occurs at
multiple (peripheral, spinal, supraspinal) levels
Models of descending pain systems now include both
inhibitory and facilitory descending pathways.
Nerve fibers from these pathways release inhibitorysubstances (e.g., endogenous opioids, serotonin,
norepinephrine, GABA) at synapses with other neurons
in the DH.
These substances bind to receptors on primary afferentand/or DH neurons and inhibit nociceptive transmission.
Such endogenous modulation may contribute to the
wide variations in pain perception observed among
patients with similar injuries
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Some analgesics enhance the effects of
descending inhibitory input. For example, some
antidepressants interfere with the reuptake of
serotonin and norepinephrine at synapses,
increasing their relative interstitial concentrationavailability)52-53 and the activity of endogenous
pain-modulating pathways.
Thus, some, but not all, antidepressants are used
to treat some types of chronic pain.
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CLASSIFICATION
Nociceptivecaused by the ongoing activation ofA- and C-nociceptors in response to a noxious
stimulus (e.g., injury, disease, inflammation)
Somatic pain
superficial (cutaneous)
deep somatic pain
Visceral
Neuropathiccaused by aberrant signal
processing in the peripheral or central nervoussystem
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CLASSIFICATION
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ASSESMENT
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PHARMACOLOGIC
Non opioid
Opioid
Adjuvan analgesic
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NONPHARMACOLOGIC
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ACUTEVS CHRONICPAIN
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