4. Types of pain
•
•
•
•
•
Acute versus chronic
Nociceptive versus Neuropathic
Somatic versus visceral
Referred versus non referred pain
Somatogenic versus psychogenic
6. Acute pain
Chronic pain
•Sudden onset
•Persistent – usually lasting
more than six months
•Temporary (disappears once
stimulus is removed)
•can be somatic, visceral,
referred
•Physiological responses to
acute pain include increased
RR, HR, BP and reduction in
gastric motility – sympathetic
response)
•Cause unknown – may be
due to neural stimulation
•Physiological responses are
less obvious especially with
adaptation.
•Psychological responses may
include depression
7. Nociceptive v Neuropathic
• Nociceptive pains result from activation of
nociceptors (Pain receptors)
• Neuropathic pain result from direct injury
to nerves in the peripheral nervous
system. (Alcoholism, diabetic neuropathy,
post-herpetic neuralgia, etc…)
8. Somatic v Visceral
• Somatic pain
– Superficial: stimulation of receptors in skin
– Deep: stimulation of receptors in muscles, joints and
tendons
• Visceral pain
– Stimulation of receptors in internal organs, abdomen
and skeleton
– Often poorly localised as fewer receptors located in
viscera
– Visceral pain can be referred.
9. Referred pain
• Pain experienced at a point distant to its point of
origin
• Area of referred pain is supplied by same spinal
segment as actual site of pain
• Brain misinterprets signals as coming from
somatic regions
• Knowledge of different types of referred pain is
important in clinical diagnosis because in many
visceral ailments the only clinical signs is
referred pain.
• Good section on referred pain can be found in
Guyton and Hall (2006)
10. Somatogenic versus psychogenic
• Somatogenic pain is a pain originating from an actual
physical cause e.g. trauma, ischaemia etc
• Psychogenic pain is pain for which there is no
physical cause. It is not however imaginary pain and
can be as intense as somatic pain.
11. Pain threshold
The pain threshold is the point at which a stimulus is perceived as pain.
A patient who is hyper-reactive is considered to have a low pain threshold.
On the other hand a patient with a high pain threshold can tolerate pain.
The pain threshold is affected by:
•Emotional status.
•Fatigue.
•Age.
•Sex
•Fear and Apprehension.
12. Neuroanatomy of pain
The portions of the nervous system responsible for the
sensation and perception of pain may be divided into three
areas:
1. afferent pathways
2. CNS
3. efferent pathways
The afferent portion is composed of:
a) nociceptors (pain receptors)
b) afferent nerve fibres
c) spinal cord network
13. The role of the afferent and efferent pathways in
processing of pain information
Nociceptors: Endings of small unmyelinated and lightly
myelinated afferent neurons.
Stimulators:
Location:
Chemical, mechanical and thermal stimuli
Mild stimulation → positive, pleasurable sensation
(e.g. tickling)
Strong stimulation → pain
These differences are a result of the frequency
and amplitude of the afferent signal transmitted
from the nerve endings to the CNS.
In muscles, tendons, epidermis, subcutanous tissue,
Visceral.
- they are not evenly distributed in the body
(in skin more then in internal structures)
15. Types of stimuli
• Receptors respond to injury
– Thermal –excessive heat or cold
– Mechanical –tearing, crushing, stretching etc
– Chemical
• Inflammatory mediators
• Lactic acid
• ischemia
16. Pain pathway
There are four processes in
the pain pathway
1. transduction
–
2.
Noxious stimuli translated into electrical activity at sensory
nerve endings
Transmission
–
3.
Propagation of impulses along spinothalamic pathway.
Modulation
–
4.
Transmission is modified
Perception
–
Affective / motivational aspect
Each of these processes present a potential target for
analgesic therapy
17. 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:
– Unimodal – respond to only one type of stimulus
– Polymodal – respond to more than one type of
stimuli.
18. Transduction -Receptor
activation
• When cellular damage occurs, tissues release
chemicals that stimulate nociceptors
–
–
–
–
–
Bradykinin
- Histamine
Serotonin
- Acetylcholine
Potassium ions
Prostaglandins (PGE2, PGI2)
Substance P
• The activity and sensitivity of nociceptors is
profoundly altered by such mediators (enhances
receptor response to noxious stimuli).
• See article by Kelly et al ( 2001) for interesting
information on this aspect
20. Transduction
A delta fibres and C fibres
• Nociceptors respond to noxious stimuli and
covert energy at the site of the stimulus into
neural impulses
• Nociceptors are terminal endings of primary
afferent fibres. These can be classed into two
main types
– myelinated A-delta fibres
– non-myelinated C fibres
• When the threshold level of the stimulus is
reached, then depolarisation occurs along these
fibres in the form of action potentials
21. Transduction - A delta fibres and C fibres
A-Delta fibres
C- fibres
myelinated
unmyelinated
fast ( first) pain -conduct at 535m/sec
Slow (second) pain – conduct at
0.5-2.0m/sec
Associated with Sharp, brief,
prinking pain
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
24. Pain Transmission Pathway
• Both A delta and C nociceptor fibres synapse in the
dorsal horn of the spinal cord
• Evidence suggests that neurotransmitters released at
this point include substance P, glutamate, calcitonin
gene-related peptide (CGRP).
25. Pain Transmission Pathway
• Secondary neurones cross the cord and
ascend through the antero-lateral
spinothalamic tract to the thalamus where
they synapse with tertiary neurones
• These tertiary neurones ascend from the
thalamus to somatosensory cortex.
28. • • nociceptors →
transmitted by small Adelta fibers and Cfibers to the spinal cord
→ form synapses with
neurons in the dorsal
horn(DH)
•
From DH →
transmitted to higher
parts of the spinal cord
and to the rest of the
CNS by spinothalamic
tracts
31. Perception
• Transduction, transmission, modulation
interact to create subjective emotional
experience of pain.
• The portion of CNS involved in the
interpretation of the pain signals are
the limbic system, reticular formation,
thalamus, hypothalamus and cortex
32. The brain first perceives the sensation of pain
• The thalamus, sensitive cortex :
perceiving
describing
localising
of pain
• Parts of thalamus, brainstem and reticular formation:
- identify dull longer-lasting, and diffuse pain
• The reticular formation and limbic system:
- control the emotional and affective response to pain
Because the cortex, thalamus and brainstem are
interconnected with the hypothalamus and autonomic
nervous system, the perception of pain is associated with an
autonomic response
33. Theory of pain production and modulation
• Most rational explanation of pain production and modulation
is based on gate control theory (created by Melzack and Wall)
• According to this theory, nociceptive impulses are
transmitted to the spinal cord through large A- delta and
small C- fibers
• These fibers create synapses in the SG
• The cells in this structure function as a gate, regulating
transmission of impulses to CNS
34. Stimulation of larger nerve fibers (A-alfa, A-beta) causes the cells in SG to "close the
gate".
A closed gate decreases stimulation of T-cells (the 2nd
afferent neuron), which decreases transmission of impulses,
and diminishes pain perception
Stimulation of small fiber input inhibits cells in SG and
"open the gate".
An open gate increases the stimulation of T-cells →
→↑ transmission of impulses → enhances pain perception
• In addition to gate control through large and small fibers
stimulation, the central nervous system, through efferent
pathways, may close, partially close, or open gate.
Cognitive functioning may thus modulate pain perception
35.
36. 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
41. ’WHO Analgesic ‘Ladder
Severe
Moderate
Mild
Step 3
Strong opioids (e.g., morphine)
with or without non-opioids
Step 2
Weak opioids (e.g., codeine)
with or without non-opioids
Step 1
Non-opioids (e.g., NSAIDs,
acetaminophen = paracetamol)
Notes de l'éditeur
Hyperlink – reference McCance and Heuther chapter 14 p402.
e.g. post therpetic neuralgia – after shingles, anaesthesia dolorosa can follow therapeuic transection of sensory nerves
Central sensitization can develop from many chronic painful conditions. Continued stimulation by peripheral afferent nerves leads to distinct biochemical and physiologic changes. For example, nerve growth factor (NGF) begins to be produced in quantities sufficient to alter the nerve connections within the dorsal horn of the spinal cord. The number and types of receptors that respond to excitatory stimulation increase, resulting in heightened postsynaptic responsiveness to what would normally be perceived as mildly painful stimulus.
