Pain Syndromes and Chronic Pain Mangement dictated slides 1-18

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Pain Syndromes and Chronic Pain Management:

Pain Syndromes and Chronic Pain Management Maribeth Massie, CRNA, MS, PhD(c) University of New England Master of Science in Nurse Anesthesia Program

Brief review of Pain:

Brief review of Pain Definition of pain: an unpleasant sensory or emotional experience Perception of pain is a product of brain’s abstraction and elaboration of sensory input. Perception of pain varies with individuals and circumstances (soldier injured) Activation of nociceptors does not necessarily lead to experience of pain ( asymbolia for pain; patient under morphine) Pain can be perceived without activation of nociceptors (phantom limb pain, thalamic pain syndrome) Important for survival, protect from damage: congenital and acquired insensitivity (diabetic neuropathy, neurosyphilis ) to pain can lead to permanent damage Pain reflexes can be stopped if not appropriate (step on nail near precipice, burn hands while holding a baby

Pain:

Pain Physiological ( nociceptive ) pain  direct stimulation of nociceptors Superficial somatic pain Deep somatic pain Visceral pain Inflammatory pain Neuropathic (intractable) pain  result from injury to the peripheral or central nervous system that causes permanent changes in circuit sensitivity and CNS connections

Nociceptors (Free nerve ending) :

Nociceptors (Free nerve ending) Thermal nociceptors Activated by noxious heat (temp. above 45 °C), noxious cold (temp. below 5°C), and strong mechanical stimuli  via A-delta fibers Mechanical nociceptors Activated by strong stimuli such as pinch, and sharp objects that penetrate, squeeze, pinch the skin  sharp or pricking pain, via A-delta fibers Polymodal nociceptors : Activated by noxious mechanical stimuli, noxious heat, noxious cold, irritant chemicals  slow dull burning pain or aching pain via non- myelinated C fibers; Persists long after the stimulus is removed

Nociceptors:

Nociceptors Differ in speed of conduction and capacity to be sensitized during inflammation, injury, disease Two main classes: A-delta fiber and C-fiber A-delta fibers Thinly myelinated axons with medium to large cell bodies Conduct impulses at a fast rate and produce sharp, pricking pain C-fibers Unmyelinated axons and cell bodies are small Conduct action potentials slowly resulting in prolonged, burning pain

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Mechanisms associated with peripheral sensitization to pain

Agents that Activate or Sensitize Nociceptors :

Agents that Activate or Sensitize Nociceptors Cell injury  arachidonic acid  prostaglandins   vasc . permeability ( cyclo-oxygenase )  sensitizes nociceptor Cell injury  arachidonic acid  leukotrienes   vasc . permeability ( lipoxygenase )  sensitizes nociceptor Cell injury   tissue acidity   kallikrein   bradykinin   vasc . permeability activates nociceptors   synthesis & release of prostaglandins

Agents that Activate or Sensitize Nociceptors :

Agents that Activate or Sensitize Nociceptors Substance P (released by free nerve endings)  sensitize nociceptors   vasc . perm., plasma extravasation ( neurogenic inflammation)  releases histamine (from mast cells) Calcitonin gene related peptide (free nerve endings)  dilation of peripheral capillaries Serotonin (released from platelets & damaged endothelial cells)  activates nociceptors Cell injury  potassium  activates nociceptors

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Peripheral sensitization to pain: Some definitions: Hyperalgesia  increased sensitivity to an already painful stimulus Allodynia  normally non painful stimuli are felt as painful (i.e .light touch of a sun-burned skin)

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CGRP CGRP Peripheral sensitization to pain:

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To summarize peripheral sensitization to pain: Sensitization results from the release of various chemicals by the damaged cells and tissues ( bradykinin , prostaglandins, leukotrienes ) These chemicals alter the type and number of membrane receptors on free nerve endings, lowering the threshold for nociceptive stimuli Depolarized nociceptive sensory endings release substance P and CGRP along their branches ( axon reflex ) Contribute to spread of edema by producing vasodilation , increase in vascular permeability and plasma transvasation , and the spread of hyperalgesia by leading to the release of histamine from mast cells Aspirin and NSAID block the formation of prostaglandins by inhibiting the enzyme cyclooxygenase Local anesthetic preferentially blocks C fiber conduction, cold decreases firing of C fibers, ischemia blocks first the large myelinated fibers

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Gate Control Theory of Pain:

Pain input to the spinal cord :

A-delta and C fibers release glutamate and peptides on dorsal horn neurons Substance P (SP) is co-released with glutamate and enhances and prolongs the actions of glutamate Glutamate action is confined to nearby neurons but SP can diffuse and affect other populations of neurons because there is no specific reuptake Projecting neurons in lamina I receive A-delta and C fibers info Neurons in lamina II receive input from C fibers and relay it to other laminae Projecting neurons in lamina V ( wide-dynamic range neurons ) receive A-delta, C and A-beta (low threshold mechanoceptors ) fibers information Pain input to the spinal cord

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Ascending Pathways: ->localization, intensity, type of pain stimulus ->arousal, emotion; involves limbic system, amygdala, insula, cingulate cortex, hypothalamus. Mediate descending control of pain (feedback loop)

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Descending pathways regulating the transmission of pain information Intensity of pain varies among individuals and depends on circumstances (i.e. soldier wounded, athlete injured, during stress ) Stimulation of PAG causes analgesia so profound that surgery can be performed PAG stimulation can ameliorate intractable pain. PAG receives pain information via the spinomesencephalic tract and inputs from cortex and hypothalamus related to behavioral states and to whether to activate the pain control system. PAG acts on raphe & locus ceruleus to inhibit dorsal horn neurons via interneurons and morphine receptors . Application : Intrathecal morphine pump s

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Neuropathic (intractable) pain Pain following peripheral nerve injury Greater loss of small fibers than large diameter fibers Axons of surviving A-beta fibers sprout new branches and make connection to neurons vacated by the lost C fibers Nonpainful stimuli become painful. Change from innocuous to noxious sensation is called allodynia Thalamic pain syndrome: usually following stroke in the ventral basal thalamus Rearrangement of local circuit leads to excruciating pain A-beta C fibers Pain Signaling neurons N Phantom limb pain: during amputation under general anesthesia the spinal cord can still “experience” the insult produced by the surgical procedure and central sensitization occurs. To try to prevent it, local infiltration of anesthetics in the site of surgery. But studies show also rearrangement of cortical circuits (cortical region of the missing limb receives afferents from other site of the skin)

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