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american pain society definition
unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage
Margo McCaffery definition of pain as a nurse
whatever the experiencing person says it is, existing whenever he says it does.
is pain single or multi dimensional
multi dimensional components of pain
-temporal (acute, chronic)
-etiology (cancer, non-malignant)
-pathophysiological (nociceptive, neuropathic)
-pain appears in distress
-temporally related to noxious stimuli
-signs are mainly SNS mediated
signs of acute pain
-inc or labile BP, HR
-release of Epi, cortisol
-pt may not appear to be uncomfortable
-pain extending beyond expected time course of painful syndrome
-no obvious signs
consequences of inadequately treated acute pain
-Post-surgical: impaired respiratory and GI function
-Prolonged return to function, decreased ability to participate in rehab activities
-Risk of pain becoming chronic
consequences of inadequately treated chronic pain
-disability, inability to work
primary somatosensory cortex
-In postcentral gyrus of parietal lobe
-Receives sensory and proprioceptive info from skin, muscles, joints and tendons.
somatosensory association cortex
-Posterior to primary somatosensory cortex
-Interprets / understands pain
why can pain be localized
-because nociceptor pathways are kept in a specific anatomical order in the spinal cord
-somatosensory cortex → dermatomes and the somatosensory "homunculus"
dorsal horn of the spinal cord
-Grey matter; located dorsally
-Receives sensory information
-Sensory neurons that transmit impulses from skin or internal organs toward the CNS.
-Primary afferent neuron: The first neuron in the somatosensory pathway.
dorsal root ganglion
An enlarged area of the dorsal root where the cell bodies of afferent neurons are located.
-connector neurons between sensory and motor neurons
-Some can also inhibit transmission of the pain signal at the level of the dorsal horn.
-sensory receptors in the skin, muscle, joints, connective tissue and some viscera that selectively respond to noxious or potentially tissue-damaging stimuli.
-Are free (non-encapsulated) nerve endings of primary afferent nerve fibers (axons) in peripheral tissues
important property of nociceptors
they can be sensitized -> their excitability can be increased as a result of tissue damage and inflammation
a reduction in the threshold at which the nociceptor responds to a noxious stimulus and an increase in the magnitude of that response
nociceptive pain results from
tissue damage or potentially tissue-damaging stimuli
pain signal starts in
types of nociceptive pain
somatic nociceptive pain
-originates from receptors in skin, muscles, etc.
visceral nociceptive pain
-when internal organs swell, stretch or become damaged
what is nociception
-Refers to the process by which information about tissue damage is conveyed to the central nervous system (CNS)
-Direct stimulation of afferent neurons due to tissue injury, or stimuli indicating potential injury or tumor infiltration of skin, soft tissue or viscera
nociception is proportional to
stimulation of the nociceptor, so: more tissue damage -> more pain
4 basic processes of nociception
-Process of converting painful stimuli to neuronal action potentials
-Noxious stimuli → tissue damage or potential tissue damage
process of transduction
-Nociceptors transduce noxious stimuli into action potentials and are sensitized.
-Chemical mediators alter the membrane potential of the nociceptor → increased sensitivity (and reactivity) of nociceptor to noxious stimuli.
-Once released, these chemicals bind and activate specific receptors on the nociceptor, increase the excitability of the neuronal cell membrane and lead to generation of an AP.
chemicals released =
-Chemical mediators released include K+, H+, serotonin, bradykinins, norepinephrine, prostaglandins, others
-Certain prostaglandins, including PGE2, increase nociceptor sensitivity
internal or external substances
Stimulated nociceptors transmit impulses to the CNS by means of specialized sensory fibers
primary sensory fibers for transmission
Aδ fibers, C fibers
-large, myelinated fibers
-involved in fast transmission of sharp, stinging, and highly localized pain
-small, unmyelinated fibers
-involved in slower transmission of dull, aching, and poorly localized pain that lingers
transmission more info
-Most sensory afferent pain fibers enter the spinal cord by way of the posterior nerve roots
-Cell bodies of pain neurons located in the dorsal root ganglion of the spine.
-Pain signals transmitted by afferent fibers enter the spinal cord through the dorsal horn, synapse on second order neurons, and then cross the cord (decussate) and project centrally in the anterolateral tract
-Neurotransmitters that bind N-methyl-D-aspartate (NMDA), AMPA receptors in spinal cord are released.
-Signal terminates in thalamus, which acts as relay station to cortical regions.
ascending sensory pathways involve how many neurons that communicate serially?
what are they?
first order, second order, and third order neurons
the primary afferent neuron. Synapses with the → second order neuron
at the dorsal horn.
This neuron decussates and travels via the anterolateral tract to the thalamus, where it synapses with the → third order neuron
relays pain signal to the somatosensory cortex, which will localize and interpret the pain.
transmission pain travel
1. 1st order neuron (primary afferent) with cell body in the dorsal root ganglion, carries pain signal from the site of injury to the dorsal horn.
2. Synapse of 1st order neuron with 2nd order neuron in the dorsal horn of the spine.
3. 2nd order neuron decussates, travels up the anterolateral tract to the thalamus
4. Synapse of 2nd order neuron with 3rd order neuron in the thalamus.
5. 3rd order neuron in the thalamus relays pain signal to somatosensory cortex.
substance P, glutamate
-calcitonin gene-related peptide (CGRP), others - all involved in transmission of pain signal.
-Substance P is a peptide neurotransmitter
-contributes to nociceptor excitation and sensitization and also contributes to inflammatory pain by inducing release of histamine from mast cells.
without ? pain signals wouldn't be transmitted to CNS
key role in generation and propagation of an action potential
-When brain interprets pain as "painful", unpleasant
-Impulse becomes a conscious perception of pain
likely brain structures involved in perception
-Reticular system - autonomic response
-Somatosensory cortex- localization and interpretation/characterization
-Limbic system - emotional and behavioral
level of pain stimulation required to be perceived
-degree of pain an individual is willing to bear before seeking relief
-Varies among individuals
-Descending pathway from the brain to the dorsal horn of the spine.
-Complex mechanism whereby synaptic transmission of pain signals is changed; may be inhibited or amplified.
key players in inhibiting pain signals
-endogenous opioids (enkephalins, endorphins and dynorphins): block release of neurotransmitters, like glutamate and Substance P
big difference between transduction vs. modulation
transduction: serotonin and NE can INCREASE pain
modulation: serotonin and NE can reduce pain
"Rub it, it will feel better!": Rubbing activates non-nociceptive A-beta fibers which inhibit the transmission of nociceptive information.
Known as the "gate control theory of pain".
gate control theory of pain
-A-beta fibers normally carry information about touch, vibration or pressure, NOT pain.
-Inhibitory interneurons in the dorsal horn inhibit 2nd order neurons that transmit pain.
-C-fibers normally inhibit these interneurons, allowing the pain signal continue its journey.
-But A-beta fibers stimulate interneurons that in turn inhibit 2nd order pain-transmitting neurons.
-Hence, non-painful mechanical stimuli decreases pain transmission.
transduction in a nutshell
Noxious stimuli converted to impulses, AP generated
transmission in a nutshell
Movement of impulses ascending from the periphery to the spine and then to the brain
perception in a nutshell
Recognizing, defining and responding to the pain
modulation in a nutshell
Descending pathways exert inhibition or amplification on pain transmission.
reduced perception of pain stimuli
reduced perception of all sensation
abnormal sensation; not unpleasant
abnormal sensation; not pleasant
Pain response to normally non-painful stimuli
extreme pain response to painful stimuli (i.e., stimulus is expected to be painful, but response is extreme)
spread of sensitivity to noninjured areas
-Adaptive mechanism that facilitates healing of injured tissues: ensures that contact with the injured tissue is minimized until repair is complete
-Usually abates and resolves with healing
-Increases sensitivity to stimuli in affected area
-Role in peripheral sensitization and central sensitization
-"Inflammatory Soup": Substance P, histamine, 5-HT, NE, prostaglandins, H+ ions.
-Combined effect is to lower threshold for neuronal activation and increased rate of firing (generating APs)
-Plays a role in allodynia, hyperalgesia and in central sensitization
-Increased excitability of neurons within the CNS.
-Ongoing nociceptive input from periphery causes gradual increase in dorsal horn (DH) neuron firing known as "wind up"
-Prolongation of this input results in longer-lasting DH excitability, due to changes in expression of genes via activation of transcription factors.
-Although the pain feels as if it originates in the periphery, it is actually a manifestation of abnormal sensory processing within the CNS
inc excitability is triggered by
a burst of activity in nociceptors (after injury) which alter the strength of synaptic connections between the nociceptor and the neurons of the spinal cord
-an increase in NMDA receptors in the DH which have enhanced responsiveness to glutamate. -This increase in receptors can last long after the peripheral stimulus has ceased
-The NMDA receptor switches a low level of pain perception to a high level and perpetuates the pain state
-Wind up shows clinically as a progressive increase in pain over the course of a repeated stimulus
central sensitization manifests as
-Hyperalgesia (extending beyond region of injury)
-Prolonged pain after transient stimulus (persistent pain)
-Spread of pain to uninjured tissue (referred pain)
~Can persist long after healing of the injury in chronic pain states. Maladaptive.
~May result from inadequately-treated acute pain.
neuropathic pain originates from
direct injury or irritation of nerves, resulting in disturbance of function or pathologic change
neuropathic pain described as
burning, stinging, numbing, tingling, electric, shock-like
neuropathic peripheral vs. central
depends on where lesion occurs
mechanisms of neuropathic pain
-Nerve regeneration results in sprouts and neuromas that fire spontaneously
-Peaks several weeks after injury
-Changes in expression of Na+/K+ channels
-Low-threshold sensory fibers terminate in areas where nociceptive neurons usually terminate
-Associated allodynia and hyperalgesia
examples of central neuropathic pain
poststroke pain, pain associated with multiple sclerosis or Parkinson's disease, spinal cord injury
examples of peripheral neuropathic pain
post-herpetic neuralgia, diabetic neuropathy, chemotherapy-induced neuropathy, HIV sensory neuropathy, phantom limb pain
assessment of pain
don't need to know
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