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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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