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primary hyperalgesia
increase of magnitude and duration of response
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secondary hyperalgesia
enlaring of receptor fields of nerves
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allodynia
pain occurring in response to stimuli that doesn't normally cause pain
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transduction
when pain receptors convert pain stimulus into electrical activity
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this fiber is not blocked by opiods
a delta
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a delta properties
- small myelinated
- respond to intense mechanical stimulation and heat or cold
- sharp, stabbing, pricking
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this fiber is blocked by opiods
c fibers
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c fiber properties
- small or unmyelinated
- dull, throbbing, aching, burning, tingling, or tapping
- slow onset
- long lasting
- diffusely localized
- accompanied by sweating, increase HR and BP
- nausea
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this fiber is non painful, related to vibration, stretching, and mechanical pressure, can be involved in abnormal prolonged pain perception
a beta
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this can trigger reflex muscle spasms and are subject to "pain gaiting"
interneurons
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SC pain transmission is dorsal or anterior horn involved
dorsal
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where does conscious perception of pain emerge?
cortex
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gate control theory
pain severity determined by the balance of excitatory and inhibitory inputs in the SC
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nocicpetive pain
clear stimulus response
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neuropathic pain
- usually acommpanied by SnS of neurological dysfxn
- ie paresthesias, itching, anesthesia, weakness
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dysfxnal pain
pain that doesn't serve a protective fxn
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nociceptors
nerve endings contributing to pain sensation
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peripherial sensation
process of releasing chemicals that increase response of nociceptors to noxious stimuli
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central sensitization
CNS adapts nociceptive input and increase magnitude and duration of response to the noxious stimuli
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