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To Pain
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Content
Instructions
definitions of pain
Types of pain
Pain Transmission pathwa
y
Analgesic drugs
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What is pain?
Many definitions..
pain is whatever the experiencing
person says it is, existing when he
says it does (McCaffery, 1980)
Pain is an unpleasant sensory or
emotional experience associated
with actual or potential tissue
damage (International Association
for the study of pain 1986)
Complex warning sign. Difficult to
measure as peoples perception of
pain varies
Perception of Pain?
Perception of pain is
dependent upon:
Cellular damage
Receptor stimulation
Ascending neural pathways
Sensory cortex arousal
Conscious awareness of
stimulation of pain
Types of pain
Acute v chronic
Acute pain
Chronic pain
Sudden onset
Temporary
(disappears once
stimulus is
removed)
can be somatic,
visceral, referred
Associated anxiety
Physiological
responses to acute
pain include
increased RR, HR,
BP and reduction in
gastric motility
sympathetic
response)
Persistent
usually lasting more
than six months
Cause unknown
may be due to
neural stimulation
or a decrease in
endorphins
Physiological
responses are less
obvious especially
with adaptation.
Psychological
responses may
include depression
Nociceptive v
neuropathic
Somatic v Visceral
Somatic pain
Visceral pain
Referred pain
Somatogenic versus
psychogenic
Pain pathway
There are four processes in
the pain pathway
1.
transduction
Transmission
2.
Modulation
3.
Transmission is modified
Perception
4.
Transduction receptors
Pain is detected by
nociceptors (noci = harmful)
Free nerve endings of
sensory neurones
Found in all tissues and
organs (except brain)
Can be classified as either:
Transduction
-Receptor activation
Bradykinin
Histamine
Serotonin
Acetylcholine
Potassium ions
Prostaglandins (PGE2, PGI2)
Substance P
Transduction
TRAUMA
Mechanical
Thermal
chemical
Overall effect is
increased nociceptor
activation
noc
r
o
t
p
ice
Mediators
Bradykinin Histamine
Serotonin Acetylcholine
Potassium ions
Prostaglandins (PGE2,
PGI2)
Substance P
Types of stimuli
Inflammatory mediators
Lactic acid
ischemia
Transduction - A delta
fibres and C fibres
or
non-myelinated C fibres
Transduction - A delta
fibres and C fibres
A-Delta fibres
C- fibres
myelinated
unmyelinated
Associated with
dull,burning, aching,
prolonged pain
Well localised
More diffuse
Elicited by mechanical
or thermal stimuli
Elicited mainly by
chemical stimuli or
persisting mechanical
or thermal stimuli
Transmission
Transmission by
primary A-delta and Cfibres
a
Grey
matter of
Dorsal
horn
Secondary neuron
in
m
I A-Delta or
la
II
III
C fibre
IV
V
Pain Transmission
Pathway
Pain Transmission
Pathway
Somatosensory cortex
Perception
Transduction, transmission,
modulation interact to create
subjective emotional
experience of pain.
Modulation of Pain
interneuron
Pain
transmission
blocked by
release of
opiates
opioid
opioid
recepto
t
n
re ay
e
Af thw
pa
Primary
neurone
To thalamus
Secondar
y neuron
Interneuron
(releases
endogenous
opiates
e.g.endorphins)
Primary
neuron
(nociceptor)
Modulation of Pain
Action of opioids
Modulation of Pain
Interneurons in the
Substantia gelatinosa cells
respond to the activity of :
Descending pathways
Endogenous analgesic
pathway. Norepinephrine,
serotonin and opioids are
involved in brainstem inhibitory
pathways that modulate pain
in the spinal cord.
Modulation of Pain
descending pathways
The periaqueductal grey matter (PAG)
in the midbrain has a role in
analgesia and is rich is opioid
receptors
PAG receives impulses from many
brain regions inc. hypothalamus,
cortex and thalamus. Stimuli include
stress, exercise, acupuncture.
Main neuronal pathway activated by
PAG stimulation extends first to
nucleus raphe magnus (NRM) in
the medulla and then to dorsal horn
interneurones. Enkephalins are
released at these synapses and
inhibit nociceptor NT release
Periaqueductal grey
matter
Medial lemniscus
Red nucleus
Corticospinal tract
MEDULLA
Nucleus Raphe
magnus
Medial lemniscus
Corticospinal tract
To thalamus
interneuron
SPINAL CORD
Spinothalamic
tract
nociceptor
Substanti
a
gelatinosa
in spinal
cord
Pain
transmissio
n
Opens
pain
gate
Small
Adelta / C
fibres
Actions
and
response
s
Analgesic drugs
Opioid drugs
Respiratory Depression
Bradycardia / Hypotension
Nausea
Pupillary constriction
Constipation
Decreases motility of gut
Euphoria
endogenous
opioid
binds to
receptor
receptor
antagonists
such
as naloxone
bind to
receptors
and block
action
of
endogenous
and
exogenous
opioids
produces reaction
in cell
antagonist produces
no reaction in cell
NSAIDS
Action of cyclooxygenase
Constitutive
pathway
(stable conc)
Induced
pathway
phospholipid
phospholipid
Arachidonic acid
COX 1
enzyme
Prostaglandins
associated with
normal body
functions
e.g. prostaglandin
E2 (for kidney
function),
prostaglandin I2
(for stomach
protection)
Arachidonic acid
COX-2
enzyme
Inflammatory
prostaglandins
NSAIDS: mode of
action
Side effects of
NSAIDs
Linked to inhibition of
prostaglandins
Paracetamol
Anaesthetics
Local : block
neurotransmission by
blocking sodium transport
Local anaesthetics
Epidurals administered to
epidural space
Spinal anaethesia
Administered in intrathecal
(subarachnoid) space
Local Anaesthetics
nervous impulses
depend on Na+ ions
entering axons of
neurons via Na+
gates
Na
Na+
nervou
s
impuls
e
axon of
pain
neuron
Na+ gates
local anaesthetics
block Na+ gates so
nervous impulse are
not transmitted
Epidurals / spinal
anaethesias
Amitriptyline
Anti-convulsants
References
Web sites
http://www.cs.uta.fi/~jh/homunculus.html
http://faculty.washington.edu/chudler/flash/hom.html
http://www.elfstrom.com/arthritis/nsaids/actions.html
http://www.painresearch.utah.edu/crc/CRCpage/defi
nit.html
END OF
SESSION
We hope that this has been a useful
resource in preparing for the pain
seminar