2. Contents
Definition of Pain
Types
Pain Receptors
Dual Nature of Pain
Factors Affecting Pain Tolerance
Pain Theories
Processing of Pain
Control of Pain
Conclusion
References
3. Definition of pain
International Association for the Study of
Pain has defined pain as
“an unpleasant sensory and emotional
experience associated with actual or
potential tissue damage; or described in
terms of such damage.”
4. “An unpleasant emotional experience
usually initiated by noxious stimulus
and transmitted over a specialized
neural network to the CNS where it
is interpreted as such”- MONHEIM
5. HISTORY
PAIN - Derived from french word “peine”
Aristotle—a “quale :passion of the soul”
1644 - Descrates - “Specificity theory”,
1894-Goldscheider-Pattern theory
19th century -1906- Sherrington-specialized
nociceptors
1943 –Livingston- “Pain mechanism”
1965-Melzack & Wall “GATE CONTROL
THEORY”
1969-Reynolds- Opioid receptor-mediated
analgesia
6. PAIN - GLOSSARY OF TERMS
ALLODYNIA –Pain caused by a stimulus that does not
normally provoke pain.
ANALGESIA- Absence of pain in response to
stimulation that would normally be painful
DYSESTHESIA- Unpleasant abnormal sensation,
whether spontaneous or evoked.
NEURALGIA- Pain in the distribution of a nerve or
nerves
NEUROPATHY- Disturbance of function or pathologic
change in a nerve.
PARESTHESIA- Abnormal sensation, whether
spontaneous or evoked
7. ALGESIA- any pain experience following
a stimulus
CAUSALGIA- pain after trauma to a
nerve that maybe associated with
vasomotor dysfunction.
HYPOALGESIA-a diminished pain
response to a noxious stimulus in an
affected area
HYPERALGESIA- an increased pain
response to a noxious stimulus in an
affected area
10. ROLE OF
NEUROTRANSMITTERS
Nerve signal transmitted
from one neuron to next
through inter neuronal
junctions –SYNAPSE
Neuro chemicals
transmitting impulses
across the synaptic cleft –
neurotransmitters
16. Pain receptors
A receptor is a transducer, that converts
one form of energy (Heat, Mechanical,
Chemical) in the environment into electric
energy( i.e action potential) in the neuron.
The receptors which mediate pain are
called NOCICEPTORS.
17. free nerve endings.
small unmyelinated ‘C’ fibres or
myelinated ‘A δ’ afferent neurons.
widespread in superficial layers of
the skin as well as in periosteum, the
arterial walls, the joint surfaces, & the
falx & tentorium of the cranial vault.
Deeper tissues - sparsely supplied.
18.
19. Fiber Diameter
(µ)
Conduction
velocity (m/s)
Function
A-alpha
A- beta
A-delta
A-
gamma
B
C
6-20
5-12
1-4
3-6
< 3
0.4-1.0
30-120
(myelinated)
30-120
5-25
15-35
3-15 (myelinated)
0.7-2.0
(unmyelinated)
Motor, perception
Motor, perception
Pain, temperature, touch
Muscle tone
Various autonomic
functions
Various autonomic
functions; pain
temperature, touch
20. Types of pain (Acc. to Guyton)
FAST PAIN SLOW PAIN
A∂ fibers
Velocity between 6 and
30m/sec.
Sharp pain, pricking pain, acute pain
and electric pain
Eg. type of pain felt when
a needle is stuck to the
skin
C fibers
Velocity between 0.5-
2m/sec.
Slow burning pain, aching
pain, throbbing pain,
nauseous pain and chronic
pain
Usually associated with
tissue destruction
21. Types of pain (Acc. to Guyton)
FAST PAIN SLOW PAIN
Not felt in deeper
tissues
generally elicited by
mechanical & thermal
types of stimuli.
It can lead to
prolonged,
unbearable suffering.
It can occur both in
the skin and in almost
any deep tissue or
organ
generally elicited by
chemical types of
stimuli
22. Stimuli that excite the receptors
Thermal stimulation- Raising skin temperature
above 45ºC or exposure to cold (0ºC) is painful.
Mechanical stimulation due to:
Excessive pressure or tension on nerves.
Eg- a blow on the head, pulling of hair etc.
Compression of nerves by tumour, a prolapsed
intervertebral disc.
Chemical stimulation by irritant chemicals such
as histamine, kinins & prostaglandins released
from damaged tissue.
23. Chemical pain mediators
A substance to be classified as chemical pain
mediator should follow following criteria
General accessibility and activation as a
consequence of injury, infection or mechanical
tissue damage.
Suppression of mediator formation should result
in prevention of pain fiber activation.
25. One chemical that seems to be more painful than others is
bradykinin.
Increase in potassium ion concentration and proteolytic
enzymes that directly attack the nerve endings and excite pain
by making the nerve membranes more permeable to ions.
Prostaglandins and substance P enhance the sensitivity of
pain endings but do not directly excite them.
26.
27. Tissue ischemia as a cause of pain
When blood flow to a tissue is blocked, tissue becomes
painful within minutes.
Accumulation of large amounts of lactic acid in the tissue
as a consequence of anaerobic metabolism.
It is also probable that other chemical agents, such as
bradykinin and proteolytic enzymes, are formed in the
tissues.
28. Muscle spasm as a cause of pain
Partially from the direct effect of muscle spasm in
stimulating mechano-sensitive pain receptors
Also result from the indirect effect of muscle spasm to
compress the blood vessels and cause ischemia.
30. THEORIES OF PAIN MECHANISM
(A) Specificity theory:
1980’s von Frey advocated the concept specific
cutaneous receptors pain, touch, cold, pressure and heat.
- He proposed that free nerve endings gave rise to pain
sensation in brain.
- This theory is concerned primarily with the sensory
discrimination aspects of pain, its quality, location on
skin, intensity and duration.
31. Major deficits of specificity theory:
- Specificity theory cannot explain
a)Any pathologic pain produced by mild noxious
stimuli.
b)Referred pain that can be triggered by mild
innocuous stimulation of normal skin.
c)Do not explain the paroxysmal episodes of pain
produced by mild stimulation of trigger zone in
trigeminal neuralgia.
32.
33. B) Pattern theory
Goldschieder 1894
He proposed that pain results from over stimulation of
other primary sensations.
He proposed that pain resulted when activity exceeded a
critical level due to excessive activation of receptors
resulting in convergence and summation of activity.
34. Major deficit:
The theory did not recognize the importance of
receptor specialization to noxious stimuli.
35.
36. C) Gate Control Theory
Melzack & Wall 1965
Combined the strengths of previous theories
and added some of its own.
multidimensionality of the pain experience.
37. The term “gate” only refers to the
relative amount of inhibition or
facilitation that modulates the
activity of the transmission cells
carrying information about noxious
stimuli.
38. Information about the presence of injury is transmitted
to the central nervous system by small peripheral
nerves.
Cells in the spinal cord which are excited by these
injury signals, are also facilitated or inhibited by other
large peripheral nerves that also carry information
about innocuous events ( temperature or pressure).
Descending control systems originating in the brain
modulate the excitability of cells that transmit
information about injury
39. Activity in large fibers tends to inhibit transmission
(close the gate)
Small fiber activity tends to facilitate transmission
(open the gate).
Thus the theory recognizes receptor specificity and
mechanisms of convergence, summation and inhibition.
41. CLINICAL APPLICATIONS OF THE GATE
CONTROL THEORY OF PAIN
Dentists regularly experience the distraught patient with
a tooth ache.
Such emotional stress may enhance the pain as a result of
influence of central control on the gate.
In this, the higher centers may be influencing the
gating mechanism.
42.
43.
44.
45. A may be the larger fibers of the pulp. If A - fibers
are not stimulated, pain is a result of C fiber and A -
fiber activity.
If cavity preparation is cut, these smaller fibers produce
the painful response because there are few A - fibers at
the periphery.
If there is a pulpitis & A - fibers deeper in pulp are
stimulated, they close the gate to pain from C fiber
activity.
46. Conversely, if A - fibers are not activated
by inflammatory process, C fiber
summation can cause pain.
Alternate A - & C fiber stimulation as a
result of pulp inflammation closes & opens
the gate resulting in intermittent and
spontaneous pain
48. Dual Nature of Pain
Pain has two components:
Pain perception
Pain reaction
49. PAIN PERCEPTION PAIN REACTION
Objective component
of pain.
Physio-anatomic
process
similar in all healthy
individuals and varies
little from day to day
Stimulus intensity and
duration are uniform
Emotional experience to
the perceived injury.
Psycho physiological
process involves the
cortex, limbic system,
hypothalamus &
thalamus.
Varies from individual to
individual and also from
day to day in the same
person.
Inversely proportional to
pain thshold
50. SENSORY THRESHOLD- defined as the lowest
level of stimuli that will cause any sensation-the
summation of large sensory fibres from
receptors for touch, temperature & vibration.
PAIN THRESHOLD – As the stimulus is
increased, the sensation becomes stronger until
pain is perceived. This is pain threshold.
Fairly constant among individuals.
51. PAIN TOLERANCE / RESPONSE THRESHOLD
If the intensity of the stimulus is increased above
pain threshold, a level of pain will be reached
that the subject can no longer endure.
This is pain tolerance or the response threshold.
At this point the individual makes an attempt to
withdraw from the stimulus.
Range between the pain threshold and the
response threshold is termed as a person’s
tolerance to pain.
52. FACTORS WHICH ALTER THE
PAIN TOLERANCE
Physiological factors
Psychological factors
Other factors-age, sex, fatigue
54. Psychological factors
Attention-paying too much attention to stimulus
inc. intensity of pain
Expectation-one encounter with a specific
source of discomfort can dramatically affect thre
reaction to the same exposure in th future
Emotions- fear anxiety and distress elevate pain
Coping strategies-many want other than
medicine can help in reducing pain. Eg:-
distraction , positive affirmations
55. OTHER FACTORS
1. Emotional status
emotionally unstable patients have a low pain threshold
2. Fatigue
patients who are tired have low pain threshold
patients rested , had a good night sleep have high threshold
3. Age
older individual tend to tolerate pain hence have higher pain
threshold than younger
in cases of extreme age pain perception is affected
4. Sex
males have higher pain threshold than females
56. Nature of pain
Intermittent short duration separated by pain free
periods
Continous long duration , variable intensity
Recurrent two or more similar painful episodes
Remission Recurrent pain with intermittent pain free
intervals
Periodic pain regular recuring episodes
58. Processing of pain from the stimulation of primary
afferent nociceptors to the subjective experience of
pain can be divided into 4 steps
1) Transduction
2)Transmission
3) Modulation
4) Perception
59.
60. TRANSDUCTION
is the process by which the
noxious stimuli lead to electrical
activity in appropriate sensory
nerve endings
61. activation of the primary afferent
nociceptor.
can be activated by intense thermal
& mechanical stimuli, noxious
chemicals and noxious cold.
also activated by stimulation from
endogenous algesic chemical
substances.
62. Bradykinin- inflammatory mediator
Increase plasma extravasation & produce
edema.
Replenished supply of
inflammatory mediators
Causes sympathetic nerve terminal to release
a prostaglandin.
68. Neospinothalamic tract
The fast type A pain fibers -- mechanical and
acute thermal pain.
Terminate mainly Lamina I (Lamina marginalis)
Excites 2nd order neurons of the
Neospinothalamic tract.
fibers --cross -- opposite side of the cord
through ant.commisure --pass upward to the
brain stem in the anterolateral column
69.
70.
71.
72.
73.
74. Termination of Neospinothalamic tract in Brain
stem and Thalamus :
A few fibers terminate --- reticular areas.
most pass ---- thalamus--- terminate--- ventral
posteolateral nucleus (VPL).
A few fibers terminate -- post. Nucleas of thalamus
(PO)
THALAMUS
3rd neurons
basal areas of the brain somatosensory cortex.
(Post central gyrus)
75. Capability of Nervous system to localize fast pain
in the body :
localizes much more exactly than slow chr.
pain.
If pain receptors stimulated without
simultaneously stimulating tactile receptors,
even fast pain may still be poorly localized,
often within loom of stimulated area.
76. PALEOSPINOTHALAMIC TRACT :
Transmits pain by C fibers -terminate --
laminae II & III of the dorsal horns,
(SUBSTANTIA GELATINOSA).
Here the last neuron in the series gives rise to
long axons that mostly join the fibers from the
fast pain pathway, passing through the ant.
commisure to opposite side of cord. Then
upwards to brain in anterolateral pathway.
77.
78.
79. Termination of Paleospinothalamic tract in CNS :
they terminate principally in
1.Reticular nuclei of medulla, pons,
mesencephalon.
2.Tectal area of mesencephalon deep to the sup.
and inf. colliculi.
3. Periaqueductal gray.
4. Some fibers may terminate in Hypothalamus
and Limbic system.
Only 1/10th to 1/4th of the fibers pass all the
way to thalamus - Medial and intralaminar
thalamic nucleus (MIT).
Thalamus 3rd neuron
Somatosensory cortex.
81. Very poor capability of the nervous system to
localize precisely the source of pain transmitted
in the slow-chronic pathway
poor localization of pain .
can be localized to a major part of body eg
one arm or leg but not a specific point.
82. SUBSTANCE P, THE PROABLE SLOW-
CHRONIC NEUROTRANSMITTER OF
TYPE C NERVE ENDINGS
C pain fiber terminals entering the spinal cord
secrete both glutamate transmitter and substance P
transmitter.
The glutamate transmitter acts instantaneously and
lasts for only a few milliseconds. Substance P is
released much more slowly, building up in
concentration over a period of seconds or even
minutes.
83. FUNCTION OF THE RETICULAR
FORMATION, THALAMUS AND CEREBRAL
CORTEX IN THE APPRECIATION OF PAIN
It is believed that cortex plays an important
role in interpreting the quality of pain
Pain perception might be a function of lower
centers
85. THE PAIN SUPPRESSION (ANALGESIA)
SYSTEM IN THE BRAIN AND SPINAL CORD:
The degree to which each person reacts to pain
varies tremendously.
This results partly from the capability of the brain
itself to control the degree of input of pain signals
to nervous system by activating of a pain control
system called an analgesia system
(descending inhibitory systems)
86. Inhibitory Transmitter substances - Enkephalins &
Serotonin.
An endogenous opioid system for pain modulation
also exists.
87. Endogenous opioid peptides are naturally
occurring pain-dampening neurotransmitters and
neuromodulators that are implicated in pain
suppression and modulation because they are
present in large quantities in the area of the brain
associated with there activities .
89. MECHANISM OF REFFERED PAIN
Reffered pain originates at one site (e.g.
mandibular first molar) and is experienced
at another site (e.g. the ear).
The two most popular theories to explain
the mechanism of referred pain are;
convergence-projection
convergence-facilitation
90. Convergence-projection theory:
Most popular theory
Primary afferent nociceptors from both visceral
and cutaneous neurons often converge onto the
same second order pain transmission neuron in
the spinal cord
The brain, having more awareness of cutaneous
than of visceral structures through past
experience, interprets the pain as coming from
the regions subserved by the cutaneous afferent
fibers.
91.
92. Convergence-facilitation theory
Similar to the theory above, except that the
nociceptive input from the deeper structures
causes the resting activity of the second order
pain transmission neuron in the spinal cord to
increase or be “facilitated”
The resting activity is normally created by impulse
from the cutaneous afferents.
“facilitation” from the deeper nociceptive impulses
causes the pain to be perceived in the area that
creates the normal, resting background activity.
95. Control of Pain
Methods:
Removing the Cause
Blocking the pathway of painful stimulus
Raising the Pain Threshold
Preventing the pain reaction by Cortical
Suppression
Using Psychosomatic methods
96. Conclusion
Pain is a unpleasant sensation but it is a protective
mechanism that prevents the tissue damage and
aware individual about future harm.
97. References
GUYTON . Textbook of Medical Physiology. 11th
edition :
Pg no. 588-606
MONHEIMS local anasthesia and pain control 7th
edition
MALAMED. Local anaesthesia. 5th ed.
