B7.005 Prework 1: Pain, Clinical Concepts Flashcards
what is the spinothalamic system
anterolateral system
made up of 1st, 2nd, and 3rd order fibers
moves from periphery through spinal cord, thalamus, and terminates in somatosensory cortex
2 types of pain
fast and slow
parallel paths
fast pain fibers
larger have free nerve endings thermal and mechanical type -A-delta thinly myelinates -sharp pricking pain -accurately localized
slow pain fibers
small
polymodal receptors
-C-fibers unmyelinated and slow
-dull burning pain, poorly localized
contents of dorsal horn of spinal cord
nociceptive fibers
- C fibers to lamina II
- A delta fibers to Lamina I and V
spinothalamic tract
largest tract for pain and temp crosses the midline at level of entry ascends in anterolateral funiculus 2 subdivisions -paleothalamic (slow) -neothalamic (fast)
divisions of the thalamus
medal nuclear group
-wide cortical and basal ganglionic projections
lateral nuclear group
-specific noxious and somatosensory input
-ventrobasal nucleus
description of pain sensation in the cortex
less orderly arrangement of nociceptive inputs to the cortex than tactile inputs
large areas of destruction do not result in loss of pain response
wide cortical association areas involved in emotional response to pain
chemical mediators of sensitization
released by the damaged tissue and nerve endings to decrease the pain threshold
- histamine
- PGE2
- ATP, ACh, 5HT
- bradykinin
- SP
description of visceral pain
similar to slow pain higher proportion of C fibers -2 to 1 in skin -10 to 1 in gut pain often referred to somatic structures
referred pain
pain in deep visceral structures that is felt on the surface of the body
mechanism of referred main
convergence of cutaneous and visceral nociceptors onto the same dorsal horn projection neurons
OR
branching pattern of the sensory nerve
mechanisms of abnormal pain
abnormal... sensitization conduction modulation perceptions
complex regional pain disorder / reflex sympathetic dystrophy
persistent hyperpathia associated with vasomotor changes after an injury
usually after a period of immobilization
extreme abnormal sensitization
signs of complex regional pain disorder
color changes
swelling in limb
treatment of complex regional pain disorder
aggressive mobilization
pain control
sympathetic blockade
neuralgias
abnormal conduction due to nerve damage
focal area of demyelination with cross talk between bare axons (ephaptic transmission)
usually cryptogenic
treatment of neuralgias
carbamezapine
-Na+ channel blocker
surgery
most common neuralga
trigeminal
deafferentation pain
damage to somatosensory symptoms
associated with numbness
presumed secondary to decreased modulation from deafferentation
what is deafferentation
loss of non pain sensory inputs
relative increase of pain: non-pain
pain perceived as a result
when can deafferentation be seen
any lesion affecting non-pain sensory inputs
- peripheral nerves
- dorsal columns
- thalamus
components of the central pain modulation system
*descends* periaqueductal gray -opiate receptors rostroventral medulla -NE, 5HT dorsal horn -enkephalin interneurons
how to eliminate abnormal pain physiology
decrease sensitization
decrease abnormal conduction
increased modulation
change perception
ways to decrease sensitization
early mobility
capsacin (causes substance P release to help deplete it over time)
NSAIDs
steroids
ways to decrease pain conduction
nerve block
spinothalamic tractotomy (only in people w short life spans)
“stabilize” nerve
-anti-epilepsy drugs
ways to increase modulation
increase non-painful input -mechanical stimulation -trans cutaneous stimulator -posterior column stimulator -stimulate periaqueductal grey meds -antidepressants (upregulate descending pathway) -opiates
ways to change pain perception
focus on behavior relaxation therapy biofeedback treat associated psychopathy -anxiety -depression
