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An overview of pain pathways, theories of pain control, and methods of pain management. It discusses the role of various systems of the body in pain perception and management, including the opoids system. The document also covers the control of pain perception within the spinal cord and the descending control of pain perception. Additionally, it explores the endogenous opiates theory and the brain's opiate system, as well as the role of endocannabinoids and NSAIDs in pain relief.
Typology: Lecture notes
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review of pain pathways gate theory analgesia opoids system of the body other methods of pain management
Role in Pain
reticular formation
increases level of alertness it is considered the main switch of the cerebral cortex pain pathways terminate in this area and this why persons find it hard to sleep if they are feeling pain
hypothalamus and limbic system
behavioural and emotional responses
thalamus
perception of pain
Pain control theories
gate control theory central biasing theory endogenous opiates theory
Gate control theory
proposed that tha balance of nociceptive and non-nociceptive afferents within the spinal cord determines the transmission of pain information to higher centeres
a gate was postulated at each segmental level of the spinal cord dorsal horn
this gate could be int eh substantia gelatinosa and it allow only one type of impulse
transmission cell (T cell) is involved
if A beta neurons are stimulatde - subtantia gelatinosa closes
transmission of information at the gate
input from large diameter afferents arriving at gate can reduce the pain
eg. rubbing the skin near the site of injury to feel better
transcutaneous electrical nerve stimulation (TENS)
acupuncture (dorsal column stim)
stress induced analegsia
Key
SG - substantia gelatinosa cells T- transmission cels black circle - inhibitory link white circle - excitatory link round knob at end of inhibitory link - pre or postsynaptic link
Central Biasing Theory
descending neurons are activated by: stimulation of A delta and C neurons conginitve processes anxiety depression previous experiences expectations
revised version of gate control model
causes release of enkephalins (PAG) and serotonin (NRM) enkephalin interneuron in area of the SG blocks A-delta and C neurons
Control within the spinal cord
nociceptive tissue damage information reaches the substantia gelatinosa via C fibres
substantia gelatinosa cells are inhibited by:
enkephalinergic interneurons from a delta fibres GABA-ergic interneurons from A beta fibres serotinergic inhibitory fibres descend
Descending control of pain perception
neurones in the cerebral cortex, hypothalamus, amygdala and PAG send descending projections (corticospinal tract) to several brainstem locations:
projections from these brainstem regions can faciliate or inibbit the flow of nociceptive infromatio in the dorsal hon
stimaltion of the PA in the midbrain can cause analgesia
Endogenous opiates theory
least understood of all theories
stimulation of A delta and C fibers causes release of B endorphins from the PAG and NRM
stimulation can also cause ACTH/B-liotropic to be released from the anterior pituitary in response to pain
mechanism of action - similar to enkephalins to block ascending nerve impulses
high concentration in the spinal dorsal horn and medulla - also hypothalamus and peripherally
classes of endogenous opiates:
B-endorphins enkephalins B endorphin, met endorphin
Brain's Opiate System
endogenous opiates (morphine like substances) - inthrececal injection of morphine causes analgesia these can suppress the release of substance P
three classses of opiate receptors:
mu receptors, delta receptors and kappa receptors
widely distributed in the CNS high levels of mu receptors are in the periaqueductal gray region and in the superficial horn activation of mu receptors increases K+ conducance and causes hyperpolarization to prevent depolarization from occuring and prevent AP from passing to the CNS and prevent pain from occuring activation of receptors closes the Ca2+ channels
Endocannabinoids
endocannabinoids can also cause pain relief
eg. anandamide and palmitoyl ethanolamide
Analgesia
NSAIDS inhibits synthesis of prostaglandins in inflammatory pain inhibition of pain transmission by simultaneous tactile sensory signals/ ACUPUNCTURE
mechanism:
Pain relief
aspirin and ibuprofen block sfomratin of prostagnalins novocain block conduction of nerve impulses along pain fibres morphine lesen the perception of pain in the brain by acting on mu receptors
Analgesics
inhibition of COX1 can cause unwanted effects like gastrointestinal bleeding because of ulcers and nephrotoxicity
selective COX 2 inhibitors are now used
Neuropathic pain - treatment
analgesics antidepressants - these work by an action that is poorly understood but it doesnt work the same way as it does to act on deprssion antiepileptic - inhibit excitable neurons in epilepsy and have similar action in neuropathic pain capsaicins
Other methos of controlling
antolateral cordotomy to relieve