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Pain!

Therapeutic Modalities section on pain

QuestionAnswer
PAIN! an unpleasant sensory and emotional experience associated with actual or potential tissue damage Sensory dimension and a Affective-motivational dimension(feelings and emotions)
Mediators of the Response to Injury and Pain Past experience Family experience Culture Expectations Context in which injury occurs or pain is experienced
Pain as a warning or symptom the pain that occurs right after a sprain or fracture or similar injury
Pin as a disease entity When pain restricts you from carrying on with life
Accute Pain protection from injury or signal that something is wrong sudden onset and results in muscle spasm and guarding, corresponds to the events of the accute inflammatory response and usually resolves <6weeks
Persistent Pain Lingering or reoccuring pain symptom of a treatable condition several causative factors
Sources of Persistent Pain Rest-reinjury cycle inaccurate or incomplete diagnosis and evaluation myofaschial pain somatazation
Myofascial pain somatization physical (somatic) manifestation of psychological dysfunction
Chronic Pain Pain lasting beyond usefulness No identifiable and treatable causes Disease entity unto itself Large psychosomatic component
When is pain persistent vs. chronic No clear distinction(chronic) persistent pain is more treatable Chronic pain seems to defy intervention(nothing seems to help)
Referred Pain Pain that is not perceived at the site of trauma or injury
Sources of referred pain Dermatome, Myotome, Scleratome
Scleratome area of bone innervated by a specific nerve root
P,Q,R,S,T (EKG wave) can be used as a guid for the ecaluation of pain
P (EKG wave) provocation-sudden onset or insidious
insidious the cause of w hich is unknown, usually delayed onset
Q (EKG wave) Quatlity- aching, burning, sharp, dull, stabbing
R (EKG wave) where? radiating-dermatome, Pattern?referral-related vicseral pathology (example LBP-colon CA)
S (EKG wave) severity-pain scale
T (EKG wave) timing- when was pain first experienced, is ther a particular activity or time of the day when it is more severe
Free Nerve endings nocieceptors found in deep and superficial tissues responsible for pain sensation
1st order Neurons Motor(efferent)-A alpha Sensory (afferent)-A beta, A-delta, C
SAID sensory afferent in dorsal
MEOV Motor Efferent out ventrial
Primary afferent fibers A-delta, C
A delta as a primary afferent fiber Myelinated Sharp and pricking pain (short duration) Mechanical and temperature sensation Conduction velocities(4-30 m/sec)
C fiber as a primary afferent fiber unmylelinated burning pain(longer duration) mechanical and temperature sensation Dule and diffuse conduction velocities (.5-2 m/sec)
Pain Pathway receptor(nocieceptor), primary afferent(cfiber and adelta), dorsal root ganglia, synapses in dorsal horn then contralaterally forms the lateral spinothalmic tract(second order neuron) synapse in the thalmus(third order neuron) ends in sensory cortex
Gate Theory of Pain components a beta fibers, a delta and c fibers, substantia glelantinosa, transmissioncell, enkephalin interneuron
Substantia glelatenosa influences impulses that are propagated into the 2nd order neuron (T cells) through inhibition Gate keeper!!
Gate theory Concepts perception and alleviation of pain is dependent on interation between larn and small diameter first order afferent input into the dorsal horn Large fiber input excites T cells and SG, resulting in inhibition of noxious out put to t cells
Gate theory small fibers noxious input input inhibitts SG and exvites t cells, resulting in noxious input being transmitted from the t cell to high centers
Gate theory of pain enkephalin interneuron a beta synapse with 2nd order and enkephalin interneuron interneuron synapses at synapse between adelta/cfiber and second order afferent neuron(dorsal root ganglia)
Gate thoery of pain enkephaline interneuron2 Enkephalin is released, blocking substance P and other facilitory transmitter substances from cuasing depolarization of end order neuron "pain message" is blocked befor reaching higher centers(the t cells or the DRG)
Enkephalin an endogenous opiod with a half life of 2 minutes
Descending Inhibition Level II Central biasing pain stimulus to PAG vi second order neurons PAG synapses with raphe nucleus
PAG synapses with raphe nucleus relases enkephiens Pariaqueductal gray area
Desending Inhibition Level II after raphe nucleus from raphe nucleus, axons decsend via dorsolateral pathway to synapse with the enkephalin internuron at segmental level(seratonin is the facilitory transmitter substance in pathway) enkephalin blocks 2nd order receptors for substance P
Level III control of pain betta endorphines input to reticular formations via spinoreticular tract results in RF stimulation of the hypothalmus
beta-endorphins endogenous opiate with half life of 4 hrs large peptide with same structure as morphine 100 times more potent than
Level III pain control after stimulation of hypothalmus projections from the hypothalmus to the raphe nucleus release beta-endorphin, resulting in longer term activation of descending pathway beta-endorphin stimulates raphe nucleus-enkephallin interneuron-analgesia at segmental level system
What decides which level of pain control is used? the more pain you have the high the level is used-you may not have enough pain for your body to activate level III pain control
When are b-endorphins released during exercise
cortizol muscle break down not build up
Created by: jwebst1