5. Acute pain
Chronic pain
•Sudden onset
•Temporary (disappears once
stimulus is removed)
•Persistent – usually lasting
more than six months
•can be somatic, visceral,
referred
•Cause unknown – may be due
to neural stimulation
•Physiological responses to
acute pain include increased
RR, HR, BP and reduction in
gastric motility – sympathetic
response)
•Physiological responses are
less obvious especially with
adaptation.
•Psychological responses may
include depression
6. 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…)
7. 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.
8. 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)
9. 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.
10. 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.
11. 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
12. The role of the afferent and efferent pathways in
processing of pain information
Nociceptors: Endings of small unmyelinated and lightly
myelinated afferent neurons.
Stimulators:
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.
Location:
In muscles, tendons, epidermis, subcutanous tissue,
Visceral.
- they are not evenly distributed in the body
(in skin more then in internal structures)
14. Receptors respond to injury
Thermal –excessive heat or cold
Mechanical –tearing, crushing, stretching etc
Chemical
Inflammatory mediators
Lactic acid
ischemia
15. There are four processes in
the pain pathway
1.
transduction
1.
Transmission
1.
Propagation of impulses along spinothalamic pathway.
Modulation
1.
Noxious stimuli translated into electrical activity at sensory nerve
endings
Transmission is modified
Perception
Affective / motivational aspect
Each of these processes present a potential target for analgesic
therapy
16. 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.
17. 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
19. 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 depolarization occurs along these
fibres in the form of action potentials
20. 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. 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 generelated peptide (CGRP).
25. 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 C- fibers
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. 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 is dependent upon:
Cellular damage
Receptor stimulation
Ascending neural pathways
Sensory cortex arousal
Conscious awareness of stimulation of pain
41. 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)
Hinweis der Redaktion
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.
