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Neuroscience - Control of Pain Perception, Lecture notes of Neuroscience

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

2019/2020

Available from 05/23/2023

janelle-scott
janelle-scott 🇯🇲

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Control of Pain

Perception

Objectives

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

  • broken down into B endorphins and corticosteroids

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