PAIN

Submitted by: Group 74

Submitted to:
Mrs. Mary Jeannie Patrimonio
Pathophysiology
of Pain
Transmission of Pain:
 Transduction
 Transmission

 Perception

 Modulation
 Transduction
 Begins when the free nerve endings (nociceptors)
of C fibers and A-delta fibers of primary afferent
neurons respond to noxious stimuli. Nociceptors
are exposed to noxious stimuli when tissue
damage and inflammation occurs as a result of,
for example, trauma, surgery, inflammation,
infection, and ischemia.
 Noxious stimuli (with potential to injure tissue)
trigger the release of biochemical mediators (e.g.
prostaglandin, bradykinin, serotonin, histamine,
substance P) that sensitize nociceptors.
 Transduction
The nociceptors are distributed in
the:
 somatic structures (skin, muscles,

connective tissue, bones, joints);

 visceral structures (visceral organs

such as liver, gastro-intestinal tract).

 Transmission
 The perception of pain occurs when the nociceptors
are stimulated and transmit signals through sensory
neurons in the spinal cord. These neurons release
glutamate, a major exicitory neurotransmitter that
relays signals from one neuron to another. The
signals are sent to the thalamus, in which pain
perception occurs. From the thalamus, the signal
travels to the somatosensory cortex in the cerebrum,
at which point the individual becomes fully aware of
the pain.
 Transmission
 There are 2 pathways for
transmission of pain in the CNS.
These are the neospinothalamic tract
(for fast pain) and the
paleospinothalamic tract (for slow
pain).
 Transmission
 Fast pain travels via type Aδ fibres to terminate on
lamina I (lamina marginalis) of the dorsal horn.
Second order neurons of the neospinothalamic tract
then take off and give rise to long fibres which cross
the midline through the anterior commisure and pass
upwards in the contralateral anterolateral columns.
These fibres then terminate on the Ventrobasal
Complex (VBC) of the thalamus. From here, third
order neurons communicate with the somatosensory
cortex. Fast pain can be localised easily if Aδ fibres
are stimulated together with tactile receptors.
 Transmission
 Slow pain is transmitted via slower type C fibres to
laminae II and III of the dorsa horns, together known
as the substantia gelatinosa. Second order neurons
take off and terminate in lamina V, also in the dorsal
horn. Third order neurons then join fibres from the
fast pathway, crossing to the opposite side via the
anterior commisure, and travelling upwards through
the anterolateral pathway. These neurons terminate
widely in the brain stem, with one tenth of fibres
stopping in the thalamus, and the rest stopping in the
medulla, pons and mesencephalon. Slow pain is
poorly localized.
 Perception
 Perception of pain is the awareness—typically
an uncomfortable awareness—associated with
a specific area of the body. It depends on the
transmission of pain signals through the
thalamus to the cortex and limbic system. At
this point in pain processing, perception of the
pain experience is influenced by social and
environmental cues, as well as by cultural
conditioning and past personal experiences.
 Perception
 The perception of pain is clearly a complex
process. It usually acts to tells us when we are
potentially damaging our bodies (acute), but
sometimes it serves no purpose (chronic). We can
share one another’s pain, but we cannot quantify for
sure the degree to which another is in pain, making
pain a very difficult phenomenon to research and
understand. The experience of acute pain is often
easier to understand than that of chronic pain because
we can imagine our own sensation of pain associated
with the given pain-inducing situation.
 Modulation
 The major brainstem regions that produce this
effect are located in poorly defined nuclei in
the periaqueductal gray matter and the rostral
medulla. Electrical stimulation at each of these
sites in experimental animals not only
produces analgesia by behavioral criteria, but
also demonstrably inhibits the activity of
nociceptive projection neurons in the dorsal
horn of the spinal cord.
 Modulation
 Understanding the central modulation of pain
perception (on which the placebo effect is
presumably based) was greatly advanced by the
finding that electrical or pharmacological stimulation
of certain regions of the midbrain produces relief of
pain . This analgesic effect arises from activation of
descending pain-modulating pathways that project,
via the medulla, to neurons in the dorsal horn—
particularly in Rexed's lamina II—that control the
ascending information in the nociceptive system.
 Theories of Pain
 Affect Theory
 Pattern Theory

 Specificity Theory

 Gate Control theory

 Affect Theory
 In psychology, affect is an emotion or subjectively
experienced feeling. Affect theory is a branch of
psychoanalysis that attempts to organize affects into
discrete categories and connect each one with its
typical response. So, for example, the affect of joy is
observed through the reaction of smiling. These
affects can be identified through immediate facial
reactions that people have to a stimulus, typically
well before they could process any real response to
the stimulus.
 Affect Theory
 Tomkins (1962) stressed that each affect
functions as an amplifier that calls attention to
anything with which it becomes associated or
"coassembled." There are nine of these
nonspecific amplifiers, and therefore nine
different ways that affect can, by this
amplification, increase the likelihood that the
information with which it has been assembled
will be used by the organism.
 Affect Theory
 Interest-excitement and enjoyment-joy, the two
positive affects, are counterbalanced by six decidedly
negative affects (fear-terror, distress-anguish, anger-
rage, dissmell, disgust, and shame-humiliation), all of
which may be halted instantly by surprise-startle, an
affect that is too brief to have either a positive or a
negative flavor. By their effects on bodily structures
that evolved for other reasons (heart rate, voice, facial
musculature, sweat, etc.) these nine innate affects call
attention to their triggering source in nine quite
different ways.
 Affect Theory
 All of these sites of action for innate affect are
quite ordinary biological mechanisms set off
by well known groups of neurotransmitters.
Since these sites of action can be set off under
the control of affect programs, we infer that
one of the properties of the affect system is to
direct the release of neurotransmitters.
 Affect Theory
 If some aberration of neurotransmitter
metabolism causes things to happen at the sites
of action normally associated with one or
another innate affect, we humans are likely to
mistake the pattern of actions so released as
the gestalt normally associated with a normal
affect.
 Pattern Theory
 Pattern theories consider that peripheral
sensory receptors, responding to touch,
warmth and other non-damaging as well as to
damaging stimuli, give rise to non-painful or
painful experiences as a result of differences in
the patterns [in time] of the signals sent
through the nervous system.
 Pattern Theory
 Goldschneider (1920) proposed that there is no
separate system for perceiving pain, and the
receptors for pain are shared with other senses,
such as of touch. According to this view,
people feel pain when certain patterns of
neural activity occur, such as when appropriate
types of activity reach excessively high levels
in the brain.
 Pattern Theory
 These patterns occur only with intense
stimulation. Because strong and mild stimuli
of the same sense modality produce different
patterns of neural activity, being hit hard feels
painful, but being caressed does not.
 Specificity Theory
 There is a special system of nerves which carries
messaged from pain receptors in the skin to a pain
centre in the brain.

 One points of favour is that there are specialized

receptors in the skin for different sensations like heat
and touch.

 Specific stimulus has a specific receptor which goes

to a location in the brain
 Specificity Theory
 The specific location identifies the pain’s
quality

 Psychological pain : Phantom Limb Pain

 Gate Control theory
 To explain why thoughts and emotions
influence pain perception, Ronald Melzack and
Patrick Wall proposed that a gating mechanism
exists within the dorsal horn of the spinal cord.
Small nerve fibers (pain receptors) and large
nerve fibers ("normal" receptors) synapse on
projection cells (P), which go up the
spinothalamic tract to the brain, and inhibitory
interneurons (I) within the dorsal horn.
 Gate Control Theory
 The interplay among these connections
determines when painful stimuli go to the
brain:
 When no input comes in, the inhibitory neuron
prevents the projection neuron from sending
signals to the brain (gate is closed).
 Gate Control Theory
 Normal somatosensory input happens when
there is more large-fiber stimulation (or only
large-fiber stimulation). Both the inhibitory
neuron and the projection neuron are
stimulated, but the inhibitory neuron prevents
the projection neuron from sending signals to
the brain (gate is closed).
 Gate Control Theory
 Nociception (pain reception) happens when
there is more small-fiber stimulation or only
small-fiber stimulation. This inactivates the
inhibitory neuron, and the projection neuron
sends signals to the brain informing it of pain
(gate is open).
Gate Control Theory
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SALAMAT SA PAKIKINIG!!!

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