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What is Pain?Nociception
“defines the processing of information about damaging stimuli by the nervous system to the point where perception occurs at the cerebral cortex and other subcortical structures”
If a damaging stimulus is not perceived, is it pain?
NociceptorsA. Conduct information about noxious events to the dorsal horns
1. have higher activation threshold than most receptors2. somatic: skin, muscles, joints3. visceral: thoracic and abdominal cavities
stretch, chemicals, ischemia
B. Will usually synapse on spinal interneurons
C. Two types of nociceptors1. high-threshold mechanoreceptor (HTM)
a. activated by intense mechanical stimulationb. innervated by thinly myelinated A-delta fibers
- conduct at 5-30 m/sec- sharply localized pain
C. Two types of nociceptors2. polymodal nociceptors (PMN)
a. activated by intense mechanical stimulation, temperatures above 42˚C, and irritant chemicalsb. innervated by unmyelinated C fibers
- conduct at 0.5-2 m/sec- poorly localized pain (dull)
Pain Mediators and Transmitters
A. Can activate or sensitize nociceptors1. ATP2. bradykinin3. histamine4. prostaglandins
B. Substance P1. can be released peripherally at the damage site2. can trigger primary hyperalgesia
- usually short duration
Types of PainA. Secondary hyperalgesia
1. light touch outside immediate area of cutaneous damage causes pain2. not necessarily associated with receptor sensitization
B. Allodynia1. light touch on skin can cause severe pain2. may involve release of substance P in dorsal horns
- increases receptive field sizes and sensitivity- chronic nature may be enhanced by glutamate on NMDA receptors
C. Complex regional pain syndrome (CRPS)1. reflex sympathetic dystrophy (RSD) is one type
2. RSD is an incompletely understood response of the body to an external stimulus, resulting in pain that usually is non-anatomical and disproportionate to the inciting event or expected healing response
Types of Pain
C. Complex regional pain syndrome (CRPS)
3. is clinically defined as an “excessive or exaggerated response to an injury of an extremity, manifested by four somewhat constant characteristics”*
a. intense or unduly prolonged painb. vasomotor disturbancesc. delayed functional recoveryd. various associated trophic changes
*Schutzer SF, Gossling HR. The treatment of reflex sympathetic dystrophy syndrome. J Bone Joint Surg Am. Apr 1984;66(4):625-9.
4. nociceptive nerve endings appear to start expressing adrenergic receptors
Types of Pain
D. Phantom limb pain1. caused by severing a peripheral nerve trunk
a. generates ectopic foci for action potentialsb. sensitive to both mechanical stimulation and SNS activity
2. triggers a neuroma at the stump
Types of Pain
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E. Referred pain
1. visceral nociceptive input carried on ANS fibers2. synapse at their spinal level of origin
Types of Pain
- pain in superficial regions in response to internal damage
A. Mainly project into dorsal root
- spinothalamics- spinoreticulothalamics
Nociceptive Pathways
1. project up via tracts:
- spinomesencephalics2. cross at or just above level
- loss of pain and temperature sensation
Nociceptive Pathways3. will affected by syringomyelia
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syrinx
1. many contain endogenous opioids (enkephalins and endorphins)
Nociceptive PathwaysB. Descending projections
2. many opiate receptor types at these synapses (,,)
1. spinothalamics (localization of pain)
Nociceptive PathwaysB. Ascending projections
2. spinoreticulothalamics (affective component of pain)- refers to the unpleasantness or emotional distress that invariably attends the sensation of physical pain
1. primary sensory cortex (SmI)
Nociceptive PathwaysC. Cortical projections
2. secondary sensory cortex (SmII)3. lesions alter perception but do not necessarily produce analgesia
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4. also some projections to hypothalamus
Nociceptive PathwaysC. Cortical projections
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1. aspirin, paracetamol, ibuprofen, naproxen
Pain ManagementA. NSAIDs
2. inhibit cyclo-oxygenase (COX)- enzyme in production of prostaglandins- PGs potentiate effects of other pain mediators
3. COX-2 inhibitors
- potential GI side effects
valdecoxib (Bextra), celecoxib (Celebrex)
1. based on the gate theory
Pain ManagementB. TENS (transcutaneous nerve stimulation)
2. may also trigger endorphin release
1. active ingredient in red chilis
Pain ManagementC. Capsaicin
2. initially triggers release of substance P3. can topically treat postherpetic neuralgia
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1. good for relieving visceral pain
Pain ManagementD. Opioids
- NSAIDS not so good2. morphine3. heroin (dimorphine)
more lipid soluble than morphinemore rapid onset of activation when injected
4. fentanyl (IV or transdermal)5. methadone - long duration/less sedation (no buzz)6. buprenorphine (Temgesic, Buprenex, Suboxone, Subutex)7. tramadol (Ultram and Ultram® ER)8. codeine (methylmorphine)
analgesic, antitussive and antidiarrheal
Pain ManagementD. Opioids
9. dextropropoxyphene (Darvocet-N and Darvon)10. oxycodone (OxyContin, Percocet, Percodan)11. hydrocodone (dihydrocodone)
- Vicodin, Symtan, Anexsia, Dicodid, Hycodan, Hycomine, Hycet, Lorcet, Lortab, Norco, Novahistex, Hydrovo, Duodin, Kolikodol, Orthoxycol, Mercodinone, Synkonin, Norgan, and Hydrokon
- intermediate-strength analgesic and antitussive- good for those allergic to codeine- stronger than codeine, but about half as potent as morphine
Pain ManagementD. Opioids12. naloxone (Narcan)
opioid receptor antagonist reverses effects of opioids (acute OD treatment)
13. naltrexone (Revia and Depade)opioid receptor antagonistlong-term dependence control (actually better for alcoholism)
Pain ManagementE. Ondansetron (Zofran)
1. relieves opioid withdrawal symptoms without side effects 2. serotonin 5-HT3 receptor antagonist3. primary use is for preventing nausea (chemo, pregnancy)