This document discusses pain, including its definition, characteristics, classification, receptors, mediators, pathways, and theories. It defines pain as an unpleasant sensory experience associated with actual or potential tissue damage. It describes the different types of pain receptors and pathways in the body. Finally, it summarizes several theories that attempt to explain the physiological experience of pain, including the intensity theory, specificity theory, pattern theory, and gate control theory.

1. DR. R.BALAMURUGAN
FIRSTYEAR M.D. PMR

2.  INTRODUCTION
 DEFINITION OF PAIN
 CHARACTERISTICS OF PAIN
 CLASSIFICATIONOF PAIN
 PAIN RECEPTORS
 CHEMICAL MEDIATORS OF PAIN
 PAIN PATHWAYS
 THEORIES OF PAIN

3. • Pain is a sensory experience of special significance.
• Pain is the commonest symptom which physicians are called
upon to treat.
• Pain is an intensely subjective experience, and is therefore
difficult to describe.
• It has two features which are nearly universal. First, it is an
unpleasant experience; and secondly, it is evoked by a
stimulus which is actually or potentially damaging to living
tissues.

4. • That is why, although it is unpleasant, pain serves a protective
function by making us aware of actual or impending damage
to the body.
• Like all sensory experiences, pain has two components
1.Awareness of a painful stimulus
2. Emotional impact (or effect) evoked by the experience.

5. An unpleasant sensation associated with actual or potential
tissue damage and mediated by specific nerve fibres to the
brain, where its conscious appreciation may be modified
by various factors

6.  International Association for the Study of Pain (IASP)
- An unpleasant emotional experience associated with actual or
potential tissue damage or described in terms of such damage.
 BELL
- The subject’s conscious perception of modulated nociceptive
impulses that generate an unpleasant sensory and emotional
experiences associated with actual or potential tissue damage or
described in terms of such damage.
 MONHEIMS
- An unpleasant emotional experience usually initiated by noxious
stimulus and transmitted over a specialized neural network where it is
interpreted as such.

8. 1. Threshold and Intensity
 If the intensity of the stimulus is below the threshold (sub-
threshold) pain is not felt.
 As the intensity increases more and more, pain is felt more
and more .
 as stimulus increases, sense of perception also increases.

9. 2. Pain Tolerance / Response threshold
 If the intensity of the stimulus is increased above the pain
threshold, a level of pain will be reached that the subject can
no longer endure. This is response threshold.
 At this point the individual makes an attempt to withdraw
from the stimulus.
 Range between the pain threshold and response threshold is
termed as Pain Tolerance.

10. 3. Adaptation
 Pain receptors show no adaptation and so the pain continues
as long as receptors continue to be stimulated.
4. Localisation of pain
 Pain sensation is poorly localized. However superficial pain
is comparatively better localized than deep pain.
5. Influence of the rate of damage on intensity of pain
 If the rate of tissue injury (extent of damage per unit time) is
high, intensity of pain is also high.

17. NOCICEPTORS
 free nerve endings (dendrites) in the skin that pick up the
information from the painful stimuli . They are called free
nerve endings as they are not enclosed within a capsule.
 Found almost everywhere: from skin to teeth pulp to joint
membranes to muscles
 The receptors for fast pain are sensitive to mechanical or
thermal stimuli of noxious strength.
 The receptors for slow pain are sensitive not only to noxious
mechanical and thermal stimuli but also to a wide variety of
chemicals associated with inflammation, like, histamine,

18.  Types of nociceptors :
 Aδ (A delta) Mechanical Nociceptors
 C Polymodal Nociceptors
 C fibre mechanical nociceptors
 High threshold cold nociceptors
 Since pain receptors respond to a wide variety of stimuli, they
are called polymodal

19.  These fibres are considered polymodal, as they respond to
mechanical, heat, cold and chemical stimuli.
 Their monotonic increase in activity evokes a burning pain
sensation at the thermal threshold in humans (41–49°C).
 CMH responses are affected by stimuli history and are
subject to fatigue and sensitization modulation.

20.  Activation of these receptors is interpreted as sharp prickling or
aching pain. Owing to their relatively rapid conduction velocities
(5–36 m/s), they are responsible for first pain.
 Two subclasses of AMHs exist: types I and II.
 Type I fibres
- respond to high magnitude heat, mechanical and chemical
stimuli and are termed polymodal AMHs.
- found in both hairy and glabrous skin.
 Type II fibres
- found exclusively in hairy skin.
- mechanically insensitive and respond to thermal stimulation in
much the same way as CMHs (early peak and slowly adapting
response) and are ideally suited to signal the first pain response

21.  Unlike cutaneous pain, deep pain is diffuse and difficult to
localize, with no discernable fast (first pain) and slow (second
pain) components. In many cases deep tissue pain is
associated with autonomic reflexes (e.g. sweating,
hypertension and tachypnoea).
SILENT NOCICEPTORS
 Units that do not respond to mechanical stimuli have been
termed silent nociceptors. Silent nociceptors are also present
within the viscera. Silent visceral afferents fail to respond to
innocuous or noxious stimuli, but become responsive under
inflammatory conditions.

25.  Each sensory receptor is attached to a first order primary
afferent neuron that carries the impulses to the CNS.
 The axons of these first-order neurons are found to have
varying thickness. It has long been known that a relationship
exists between the diameter of nerve fibers and their
conduction velocities. The larger fibers conduct impulses
more rapidly than smaller fibers.

26.  A general classification of neurons divides the larger fibers
from the smaller ones.
Type A fibers
 Alpha fibers: size - 13 to 20 µm, velocity - 70 to 120 m/ s.
 Beta fibers: size – 6 to 13 µm, velocity – 40 to 70 m/s.
 Gamma fibers: size – 3 to 8 µm, velocity – 15 to 40 m/s.
 Delta fibers: size – 1 to 5 µm, velocity – 5 to 15 m/s.
Type C fibers
 Size – 0.5 to 1 µm, velocity – 0.5 to 2 m/s.

27.  The primary afferent neuron carries impulse into the CNS and
synapses with the second-order neuron.
 This second-order neuron is sometimes called a transmission
neuron since it transfers the impulse on to the higher centers.
 The synapse of the primary afferent and the second-order
neuron occurs in the dorsal horn of the spinal cord.

28.  Cell bodies of third order neurons of the nociception-relaying
pathway are housed in: the ventral posterior lateral, the ventral
posterior inferior, and the intralaminar thalamic nuclei
 Third order neuron fibers from the thalamus relay thermal
sensory information to the somesthetic cortex.

30. Neospinothalamic Tract for Fast Pain
 The fast type A(δ) pain fibers transmit mainly mechanical and acute
thermal pain.
 They terminate mainly in lamina I at the dorsal horn and these
excite second order neurons of the neospinothalamic tract.

31. Paleospinothalamic tract for Slow Pain
 This pathway transmits pain mainly from peripheral slow chronic
Type C pain fibers.
 In this pathway, the peripheral fibers terminate almost entirely in
lamina II and III of dorsal horns of spinal cord, together called as
substantia gelatinosa.
 Axons of secondary neurons emerge from the spinal nucleus, cross
the midline and ascend to join fibers of mesencephalic nucleus to
form trigeminal lemniscus or spinothalamic tract of 5th nerve.
 These tracts continue upward and terminate in the postero ventral
nucleus of thalamus. From here it is transmitted to posterocentral
convolutions of cortex.

32.  Various theories being put forward on how
nerve impulses give rise to sensation of pain.

33.  According to this view, pain is produced when any sensory
nerve is stimulated beyond a certain level.
 That is, pain is supposed to be a non-specific sensation and
depends only on high intensity stimulation.
 But the trigeminal system provides an example against this
theory. In case of trigeminal neuralgia the patient can suffer
excruciating pain from a stimulus no greater than a gentle
touch provided it is applied to a trigger zone.
 Although, the intensity theory is not accepted, it remains true
to say that intensity of stimulation is a factor in causing pain.

34.  According to this view, pain is a specific modality equivalent
to vision and hearing etc.
 Just as there are Meissner corpuscles for the sensation of
touch, Ruffini end organs supposedly for warmth and Krause
end organs supposedly for cold, so also pain is mediated by
free nerve endings.
 Certain psychophysical studies have been regarded as
supporting specificity theory. Specialization is known to exist
in nervous system and there are well known tracts.
 But concept of specific nerve ending is no long tenable. The
Krause and Ruffini endings are absent from the dermis of
about all hairy skin, so it is certain that these structures cannot
be receptors for cold and warmth.

35.  Head and Rivers (1908) postulated the existence of two
cutaneous sensory nerves extending from the periphery to the
CNS.
 The protopathic system is primitive, yielding diffuse
impression of pain, including extremes of temperature and is
upgraded.
 The epicritic system is concerned with tough discrimination
and small changes in temperature and is phylogenetically a
more recent acquisition.

36.  This theory states that pain sensation depends upon spatio –
temporal pattern of nerve impulses reaching the brain.
 According to Woddell (1962) warmth, cold and pain are
words used to describe reproducible spatio – temporal pattern,
or codes of neural activity evoked from skin by changes in
environment.
 The precise pattern of nerve impulse entering the CNS will be
different for different regions and will vary from person to
person because of normal anatomical variations.

37.  This theory proposed by Melzack and Wall in 1965 and
recently re-evaluated is receiving considerable attention.
 This theory of pain takes into account the relative in put of
neural impulses along large and small fibers, the small nerve
fibers reach the dorsal horn of spinal cord and relay impulses
to further cells which transmit them to higher levels.
 The large nerve fibers have collateral branches, which carry
impulses to substantia gelatinosa where they stimulate
secondary neurons.

38.  The substantia gelatinosa cells terminate on the smaller nerve
fibers just as the latter are about to synapse, thus reducing
activity, the result is, ongoing activity is reduced or stopped –
gate is closed.
 The theory also proposes that large diameter fiber input has
ability to modulate synaptic transmission of small diameter
fibers within the dorsal horn.
 Large diameter fibers transmit signals that are initiated by
pressure, vibration and temperature; small diameter fibers
transmit painful sensations.
 Activation of large fiber system inhibits small fiber synaptic
transmission, which closes the gate to central progression of
impulse carried by small fibers.