S5. pain final

CONTENTS
• INTRODUCTION
• DEFINITION
• TERMINOLOGIES USED
• NEUROANATOMY AND NEUROPHYSIOLOGY OF
PAIN
• PAIN CHARACTERIOSTICS
• DIAGNOSIS
• MANAGEMENT
• CONCLUSION
• REFERENCES
3

INTRODUCTION
• Pain is a sensory experience of special significance to
physicians and basic scientists.
• Pain is the commonest symptom which physicians
are called upon to treat.
• Pain is an intensely subjective experience, and is
therefore difficult to describe.
4

• But 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.
• 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, the first component is the awareness of
a painful stimulus and the second is the emotional
impact (or effect) evoked by the experience.
5

• While the awareness is localized to the area
stimulated, the experience involves the whole being.
• That is why even when only a finger is hurt, the
whole person suffers.
• The two components of pain also imply that the
same painful experience may evoke widely different
degrees of suffering in different persons, and even in
the same person under different circumstances.
6

HISTORY
• Derived from Latin -“Poena” meaning
punishment from God.
• Homer thought pain was due to arrows shot by God.
• Aristotle, who probably was the first to distinguish
five physical senses considered pain to the “passion
of the soul” that somehow resulted from the
intensification of other sensory experience.
7

• Plato contented, pain and pleasure arose from within
the body, an idea that perhaps gave birth to the
concept that pain is an emotional experience more
than a localized body disturbance.
• The Bible makes reference to pain not only in
relationship to injury and illness but also an anguish
of the soul.
8

• Pain is "an unpleasant sensory and emotional
experience associated with actual or potential
tissue damage, or described in terms of such
damage“
• “Pain is an unpleasant emotional experience
usually incited by a noxious stimulus and
transmitted over a specialized neural network to
the central nervous system where it is interpreted
as such”.
 Definition by international association for
study of pain
DEFINITION OF PAIN
9

• “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
• ‘Pain is more or less localized sensation of
discomfort, distress or agony resulting from the
stimulation of specialized nerve endings’.
--Dorland’s Medical Dictionary (1974)
10

• ‘ Pain is an unpleasant sensation that is perceived as
arising from a specific region of the body and is
commonly produced by processes which damage or
are capable of damaging bodily tissue’. In other
words, pain is a somatopsychic phenomenon.
-- Fields (1987)
11

• Allodynia - phenomenon characterised by painful
sensations provoked by non-noxious stimuli
• Hyperesthesia - Increased sensitivity to stimulation,
excluding the special senses.
• Hypoalgesia-Diminished pain in response to a normally
painful stimulus.
• Hyperalgesia – increased the pain sensitivity to noxious
stimuli
• Nociception- The neural process of encoding noxious
stimuli.

PAIN IS MULTI DIMENSIONAL
1. Sensory experience
2. Cognitive– subjects ability to
comprehend and evaluate the
significance of the experience
3. Emotional– represents the
feelings that are generated
4. Motivational– it is the drive
to terminate the pain
13
SENSORY
EXPERIENCE
COGNITIVE
ABILITY
EMOTIONAL

LEVELS OF PAIN PROCESSING
1. Nociception: noxious stimulus originating from sensory
receptor
2. Pain: unpleasant sensation perceived in the cortex as a
result of nociceptive input
3. Suffering: how the being reacts to the perception of
pain
4. Pain behaviour: refers to individuals audible and visual
actions that communicate his suffering to others
14

FOUR DISITINCT PROCESSES INVOLVED
IN EXPERIENCING PAIN
1. Transduction: noxious stimuli lead to electrical activity
in the sensory nerve endings
2. Transmission: refers to neural events that carry the
input into CNS for proper processing
3. Modulation: ability of CNS to control the pain-
transmitting neurons
4. Perception: suffering and pain behavior begin 15

THE NERVOUS SYSTEM AND PAIN
Somatosensory
System
Brain
Somatosensory
Cortex
Thalamus
Spinal Cord
Dorsal Horn
Ventral Root
PNS
Afferent Neuron
Efferent Neuron
A-delta Fibers
C-Fibers
16

SENSORY NEURONS
First Order Second Order Third Order
18
** Interneurons

SENSORY RECEPTORS
• Sensory input from various external stimuli is thought
to be received by specific peripheral receptors that act
as transducers and transmit by nerve action potentials
along specific nerve pathways toward the central
nervous system.
• Termed first–order afferents, these peripheral
terminals of afferent nerve fibers differ in the form of
energy to which they respond at their respective
lowest stimulus intensity, that is, are differentially
sensitive.
20

• The impulse interpreted is nociceptive (causing
pain) if it exceeds the pain threshold, that is, the
intensity of the stimulus is so great that the receptor
is no longer differentially sensitive.
21

SENSORY RECEPTORS
GENERAL
SENSES
SPECIAL
SOMATIC VISCERAL
SUPERFICIAL DEEP
Touch-pressure
Thermal
Pain
Pain
Proprioception
Pain
Baroreception
Chemoreception
Visual
Audition
Olfaction
Gustation
22

• A nerve ending that responds to noxious stimuli that
can actually or potentially produce tissue damage.
• Free nerve endings i.e., they are not enclosed in a
capsule.
• The receptors for fast pain are sensitive to mechanical
or thermal stimuli of noxious strength.
NOCICEPTORS
23

• 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.
• These substances include histamine, serotonin,
bradykinin, acetylcholine, potassium ions and
hydrogen ions.
• It is possible that noxious mechanical and thermal
stimuli also act through the release of some of these
chemicals.
24

• Since pain receptors respond to a wide variety of
stimuli, they are called polymodal.
• Types of nociceptors :
1. C fibre mechano/ heat sensitive nociceptors (CMH)
2. A fiber mechano/ heat sensitive nociceptors (AMH)
25

C – FIBRE MECHANO HEAT SENSITIVE
NOCICEPTORS
• Found in cutaneous tissue.
• When stimulated to sufficient magnitude evokes a
burning pain sensation.
• These fibres are considered polymodal, as they respond
to mechanical, heat, cold and chemical stimuli.
26

A-FIBRE MECHANO-HEAT-SENSITIVE
NOCICEPTORS
• 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.
27

Aδ - fibres C- fibres
Threshold Medium High
Axon diameter 1-6μm 0.2-1μm
Myelination Thinly No
Velocity 5-36 0.2-1
Receptor types Mechano/Nociceptor Nociceptor
Receptive field Small Large
Quality Sharp/first pain Dull/second pain
SUMMARY OF RECEPTOR TYPES
29

FIRST ORDER NEURON
• 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.
30

NERVE FIBERS
Type Diameter
(microns)
Velocity of conduction
(meters/second)
Impulse
A alpha (Ia) 12-24 70-120 Tactile and
proprioceptive
impulses
A beta (II) 6-12 30-70
A gamma 5-6 15-30
A delta (III) 2-5 12-15 pain
B 1-2 3-10
C (IV)--
unmyelinated
<1.5 0.5-2 pain
31

• Two types of cutaneous pain sensation:
1. Pricking pain- felt rapidly—a delta fibers
2. Dull aching pain– delayed– c-fibers
32

• The three types of afferent neurons that provide
nociceptive input to CNS:
1. MECHANOTHERMAL AFFERENTS: primarily A-delta
fibers, respond to thermal and mechanicla stimuli.
2. HIGH THRESHOLD MECHANORECEPTIVE AFFERENTS:
chiefly A-delta fibers, respond to intense mechanical
stimuli, sensitized by algogenic substances, repeated
noxious stimulation.
3. POLYMODAL AFFERENTS: C fibers respond to
mechanical, thermal and chemical stimuli.
33

SECOND ORDER NEURON
• 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.
34

• Three specific types of second-order neurons:
1. The low-threshold mechanosensitive neurons
2. The nociceptive-specific (NS) neurons
3. The wide dynamic range (WDR) neuron
4. Silent nociceptor
** Nociception primarily carried out by the NS and
WDR neurons.
35

• Nociceptive input enters the dorsal horn by way of
NS and WDR neurons in area of lamina I,II and V.
• The LTM neurons not involved in nociception are
more concentrated in lamina III and IV.
• Interneurons- transfer impulses to other
interneurons or to ascending neurons– inhibitory or
excitatory, mostly found in lamina II and III.
• SUBSTANTIA GELATINOSA – comprise area II and III.
38

DORSAL COLUMN LEMNISCAL SYSTEM
• Fibers uncrossed in spinal cord.
• Cross over to opposite side at level of medulla.
• Composed of large, myelinated nerve fibers.
• Transmit signals to brain at velocity of 30-110m/sec.
• Transmits information regarding touch, pressure,
vibration and proprioception.
39

ANTERO-LATERAL SPINOTHALAMIC
TRACT
• Nociceptive input is mostly carried in this area.
• Transmits impulse at slow rate.
• Broad spectrum of sensory information– pain, warmth,
cold, and crude tactile sensation.
• Composed of smaller myelinated nerve fibers.
• Transmit signals to brain at velocities ranging from a few
meters per second to 40meters/second 40

• Divided into:
1. Neospinothalamic tract: Carries A-delta nociceptive
inputs directly to higher centers (thalamus)
2. Paleospinothalamic tract: Carries C-fiber
nociception to higher center through many other
centers ( relay at retcular formation-interneurons)
41

THIRD ORDER NEURON
• 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.
44

BRAINSTEM AND BRAIN
45
Somatosensory
System
Brain
Somatosensory
Cortex
Thalamus
Spinal Cord
Dorsal Horn
Ventral Root
PNS
Afferent Neuron
Efferent Neuron
A-delta Fibers
C-Fibers

THE HIGHER CENTERS OF CNS
46
Brainstem
Medulla
oblongata
Pons
Midbrain
(mesenceph
alon)
Cerebellum Diencephalon
The
thalamus
The
hypothalam
us
Cerebrum
Cerebral
coprtex
Basal
ganglia
The limbic
structures

MEDULLA OBLONGATA
• Also known as medulla.
• An enlarged extension of spinal cord.
• Has several projections or tracts that route impulses
directly to the higher centers.
• Reticular formation: made up of both white and grey
matter, has concentrations of cells or nuclei- centers for
various functions; plays an important role in monitoring
impulses that enter the brainstem
47

PONS
• Located above medulla.
• Composed of both white matter and reticular
formation.
• Fibers run transversely across pons into the
cerebellum.
• Has centers for reflexes mediated by 5th, 6th 7th and
8th cranial nerves.
48

MIDBRAIN/ MESENCEPHALON
• Contain several tracts that relay impulses to
cerebrum.
• Red nucleus and substantia nigra– involved in
muscular control.
49

CEREBELLUM
• 2nd largest part of brain.
• Outer portion is made up of gray matter
• Inner portion-predominantly white matter.
• Controls skeletal muscles
50

DIENCEPHALON
• Links brainstem with cerebrum
• Two major structure: thalamus and hypothalamus
• Two smaller nuclear areas: the epithalamus and
subthalamus
51

THE THALAMUS
• Made up of numerous nuclei that function together
to interupt impulses.
• Is a relay station for most of communication between
the brainstem, the cerebellum and the cerebrum.
52

HYPOTHALAMUS
• Major center in brain for controlling internal body
structures.
• Emotional stress can stimulate the hypothalamus to
upregulate sympatheric nervous system and greatly
influence nociceptive impulse entering the brain.
53

THE CEREBRUM
• Consists of two halves.
• Three major functional units are:
1. The cerebral cortex
2. The basal ganglia
3. The limbic structures
54

CEREBRAL CORTEX
• Made up of predominantly gray matter.
• Associated with thinking process and memory.
• Each cerebral hemisphere is divided into 5 lobes
1. Frontal
2. Parietal
3. Temporal
4. Occipetal
5. Insula
55

• WERNICKE’S AREA: important for sensory
integration, interprets the ultimate meaning of
sensory information;
-- well developed in one of the hemispheres–
prevents confusion of thought processes
56

• Deep within the gray matter of the cerebral cortex lie
tracts made up of white matter
1. Projection tracts: extension of ascending or sensory
spinothalamic tract and descending or motor
corticospinal tract
2. Association tracts: extend from one convolution to
another in same hemisphere
3. Commisural tracts extend from one convolution to a
corresponding convolution in the other hemisphere,
compose the corpus callosum, by which all direct
communication passes between hemispheres. 57

THE BASAL GANGLIA
• Composed of several nuclei that appear to be
intimately involved with coordinating cerebral
activities with other brainstem functions.
• Important in controlling background gross body
movements.
58

THE LIMBIC STRUCTURES
• Comprise the border
structures of the cerebrum
and the diencephalon.
• Control emotional and
behavioral activities.
• Pain/pleasure center- on
indistinctive level drives the
individual towards behaviour
that stimulate the pleasure
side of the center. 59

OTHER IMPORTANT BRAINSTEM
STRUCTURES
1. VENTRICLES: the CSF act as a cushion to brain,
brainstem and spinal cord is confined to certain spaces,
called ventricles.
2. THE PERIAQUEDUCTAL GRAY MATTER: high
concentration of neurons that are capable of producing
powerful neurotransmitters that can greatly modualte
nociceptive impulses
3. THE NUCLEUS RAPHES MAGNUS: function is to
modulate nociceptive input ascending on to the
thalamus. 60

PAIN CLASSIFICATION
1. Pain
2. Acute pain
3. Chronic pain
4. Neuropathic pain
5. Deafferentiation pain
6. Somatic pain
7. Visceral pain
61

PAIN TERMINOLOGIES
1. Pain: An unpleasant sensory and emotional experience
associated with actual or potential tissue damage, or
described in terms of such damage.
2. Allodynia: Pain due to a stimulus that does not
normally provoke pain.
3. Analgesic: Absence of pain in response to stimulation
which would normally be painful.
62
"Part III: Pain Terms, A Current List with Definitions and Notes on Usage" (pp 209-
214) Classification of Chronic Pain, Second Edition, IASP Task Force on Taxonomy, edited by H.
Merskey and N. Bogduk, IASP Press, Seattle, ©1994.

4. Anesthesia dolorosa: Pain in an area or region which
is anesthetic.
5. Causalgia: A syndrome of sustained burning pain,
allodynia, and hyperpathia after a traumatic nerve
lesion, often combined with vasomotor and
sudomotor dysfunction and later trophic changes.
6. Dysesthesia: An unpleasant abnormal sensation,
whether spontaneous or evoked.
63
214) Classification of Chronic Pain, Second Edition, IASP Task Force on Taxonomy, edited
by H. Merskey and N. Bogduk, IASP Press, Seattle, ©1994.

7. Hyperalgesia: Increased pain from a stimulus that
normally provokes pain.
8. Hyperesthesia: Increased sensitivity to stimulation,
9. Hyperpathia: A painful syndrome characterized by an
abnormally painful reaction to a stimulus, especially
a repetitive stimulus, as well as an increased
threshold.
64
214) Classification of Chronic Pain, Second Edition, IASP Task Force on Taxonomy, edited by
H. Merskey and N. Bogduk, IASP Press, Seattle, ©1994.

10. Hypoalgesia: Diminished pain in response to a
normally painful stimulus.
11. Hypoesthesia: Decreased sensitivity to stimulation,
12. Neuralgia: Pain in the distribution of a nerve or
nerves.
13. Neuritis: Inflammation of a nerve or nerves.
65
214) Classification of Chronic Pain, Second Edition, IASP Task Force on Taxonomy, edited by
H. Merskey and N. Bogduk, IASP Press, Seattle, ©1994.

14. Neuropathic pain: Pain caused by a lesion or
disease of the somatosensory nervous system.
15. Central neuropathic pain: Pain caused by a lesion or
disease of the central somatosensory nervous
system.
16. Peripheral neuropathic pain: Pain caused by a lesion
or disease of the peripheral somatosensory nervous
system
66
214) Classification of Chronic Pain, Second Edition, IASP Task Force on Taxonomy,
edited by H. Merskey and N. Bogduk, IASP Press, Seattle, ©1994.

17. Neuropathy: A disturbance of function or
pathological change in a nerve
18. Nociception: The neural process of encoding
noxious stimuli.
19. Nociceptive neuron: A central or peripheral neuron
of the somatosensory nervous system that is capable
of encoding noxious stimuli.
67

20. Nociceptive pain: Pain that arises from actual or
threatened damage to non-neural tissue and is due
to the activation of nociceptors.
21. Nociceptive stimulus: An actually or potentially
tissue-damaging event transduced and encoded by
nociceptors.
22. Nociceptor: A high-threshold sensory receptor of
the peripheral somatosensory nervous system that is
capable of transducing and encoding noxious stimuli.
68

23. Noxious stimulus: A stimulus that is damaging or
threatens damage to normal tissues.
24. Pain threshold: The minimum intensity of a stimulus
that is perceived as painful.
25. Pain tolerance level: The maximum intensity of a pain-
producing stimulus that a subject is willing to accept in a
given situation.
26. Paresthesia: An abnormal sensation, whether
spontaneous or evoked.
69

27. Sensitization: Increased responsiveness of nociceptive
neurons to their normal input, and/or recruitment of a
response to normally subthreshold inputs.
28. Central sensitization: Increased responsiveness of
nociceptive neurons in the central nervous system to
their normal or subthreshold afferent input.
29. Peripheral sensitization: Increased responsiveness and
reduced threshold of nociceptive neurons in the
periphery to the stimulation of their receptive fields.
70

• Suffering: suffering has been defined as including the
experience of pain but also including vulnerability,
dehumanization, a lost sense of self, blocked coping
efforts, a lack of control over time and space, and an
inability to find meaning or purpose in the painful
experience
71

PROPERTIES OF NERVE FIBERS
• Excitability
• Conductivity
• Refractory period
• Summation
• Adaptation
• Infatigability
• All or none law
72

EXCITABILITY OF A NERVE
• Excitability is defined as the physiochemical change that
occurs in a tissue when a stimulus is applied.
• Nerve fibers have low threshold for excitation.
• Depending upon the strength of stimulus two responses
occur:
1. Action potential
2. Electronic potential
73

EXCITABILITY OF A NERVE
NERVE ACTION POTENTIAL
• The resting membrane potential
in the nerve fiber: -70mV.
• Firing is at: -55mV
• Depolarization ends at : +35mV
• Action potential stars at axon
hillock.
• Action potential is propogative ,
biphasic, obeys all or none law
and has refractory period.
ELECTRONIC POTENTIAL
• The subliminal or sub threshold
stimulus does not produce
action potential but it causes
some changes in the resting
membrane potential.
• Slight depolarization of about
7mV.
• It is non- propagative and does
not obey all or none law.
74

CONDUCTIVITY
• The action potential is transmitted through the nerve
fiber as nerve impulse.
• Action potential is transmitted through the nerve
fiber in one direction only.
• The depolarization occurs first on a spot in the nerve
fiber, which causes depolarizes of neighboring areas.
• Depolarization is followed by repolarization
76

• Saltatory conduction- conduction of impulse in myelinated
nerves
77

REFRACTORY PERIOD
• Refractory period is the period in which the nerve does
not give any response to a stimulus. Two types:
1. Absolute refractory period– no response, whatever
may be the strength– corresponds from when firing is
reached to 1/3rd repolarization is complete
2. Relative refractory period– response present– stimulus
strength is increased to maximum– corresponds to
rest of repolarization time.
78

• Summation: when two or more sublimial stimuli are
applied within a short interval of time(0.5m Sec), the
response may be produced.
• Adaptation: the excitability of nerve fiber is
decreased when there is slow increase in strength of
stimulus.
 nerve fiber is continuously stimulated 
continuous depolarization inactivates sodium
pump increase the efflux of potassium ions
79

• Infatigability : a nerve fiber cannot be fatigued, even
if it is stimulated continuously for long time nerve
fiber can conduct only one action potential at a time.
• All or none law: when a nerve is stimulated by a
stimulus with sub-threshold strength, action
potential does not occur.
-- if the strength of stimulus is above the
subthreshold level, whatever may be the strength of
stimulus, the amplitude of action potential remains
the same.
80

SYNAPSE
• The junction between two neurons is called as a
synapse.
• Not an anatomical continuation, but a physiological
continuity between two nerve cells.
81
Anatomical classification Functional classification
1. Axosomatic synapse
2. Axodendritic synapse
3. Axoaxonic synapse
1. Electrical synapse
2. Chemical synapse

ELECTRICAL AND CHEMICAL SYNAPSE
83

STRUCTURE OF A SYNAPSE
(AXOSOMATIC)
• The neuron from which the axon arises is called the
presynaptic neuron and the neuron on which the axon
ends is postsynaptic neuron.
• Presynaptic axon terminals– branches of axon of
presynaptic neuron before forming a synapse
• Terminal knobs enlarged presynaptic terminals
excitatory function of synapse
-- two important structures: mitochondria, synaptic
vesicles 84

• Synaptic cleft: small space in between presynaptic
and postsynaptic membrane
85

FUNCTIONS OF A SYNAPSE
• Main: transmit impulses i.e action potential from one
neuron to another.
• some synapses inhibit transmission of impulses
1. Excitatory synapses
2. Inhibitory synapses
86

SEQUENCE OF EVENTS DURING
SYNAPTIC TRANSMISSION
87

Action potential reaches axon terminal
Opening of voltage gated calcium channels in presynaptic
membrane
Influx of calcium ions from ECF into axon terminal
Opening of vesicles and release of Ach
Passage of Ach through synaptic cleft 88

89
Binding of Ach with receptor and formation of Ach-receptor
complex
Opening of ligand gated sodium channels in post synaptic
membrane and influx of sodium ions from ECF
Development of EPSP
Opening of ligand gated sodium channels in
axon hillock
Influx of sodium ions from ECF into axon hillock and development
of action potential
Spread of action potential through the axon of postsynaptic
neuron

INHIBITORY FUNCTION
1. Postsynaptic inhibition/ direct inhibition: secretion
of inhibitory neurotransmitters GABA and glycine
2. Presynaptic inhibition/ indirect inhibition: failure of
release of excitatory neurotransmitter
3. Renshaw inhibition: occurs in spinal cord
91

PROPERTIES OF A SYNAPSE
1. One way conduction bell-magendie law
2. The synaptic delay
3. Fatigue
4. Summation
5. Electrical property
92

CONVERGENCE AND DIVERGENCE
• Convergence: when many presynaptic neurons
terminate on a single postsynaptic neuron, it is called
convergence
• Divergence: when one presynaptic neuron
terminates on many postsynaptic neuron, it is known
as divergence.
93

NEUROPLASTICITY
• When a postsynaptic neuron is continuously excited
with a particular type of stimulation ( nociception), the
cell itself can activate cellular genes that change its
function to these demands.
• This induction of early genes causes release of proto-
oncogenes called c-fos and c-jun, alters mRNA, which in
turn can change the type and number of receptors that
are formed on the cell membrane.
• As the number and type of receptors change, so also is
the cells function.
94

NEUROTRANSMITTERS
• The chemical mediator substances responsible for
the transmission of impulse through a synapse is
called the neurotransmitter.
95
Rapid acting Slow acting excitatory inhibitory
•Acetyl choline
•Amines-
noradrenaline,
dopamine,
serotonin,
histamine
•Aminoacids-
GABA, glycine,
glutamate,
aspartate
•Substance P
•Enkephalins
•Bradykinin
•Acetylcholine
•noradrenaline
•GABA
•dopamine

ELIMINATION OF THE TRANSMITTER
FROM SYNAPSE
1. Diffusion
2. Enzymatic destruction
3. Reuptake
96

NEUROCHEMISTRY OF NOCICEPTIVE
PAIN
• The peripheral nociceptor can be activated by thermal,
mechanical, and chemicals stimulation.
• When thermal and mechanical stimulation produce
nociceptive input, the reason for the pain is usually
apparent.
• There are a variety of compounds that can accumulate
near the nociceptor following tissue injury that can be
responsible for maintaining nociceptive input.
97

• There are at least three sources of these compounds:
the damaged cells themselves,
secondary to plasma extravasation and lymphocyte
migration
the nociceptor itself.
98

• Damage to tissue cells produces leakage of intracellular
contents.
• Among the substances released by tissue damage are
potassium and histamine, both of which either activate
or sensitize the nociceptor.
• These substances have been documented to excite
polymodal nociceptors and produce pain when
injected into skin.
99

• Other compounds such as acetylcholine, serotonin,
and ATP maybe released by tissue damage and are
known to either activate or sensitize nociceptors.
• Bradykinin one of the most potent pain producing
substances that appears in injured tissue.
• Bradykinin is an endogenous polypeptide consisting
of a chain of nine amino acids.
• Released as part of an inflammatory reaction, it is a
powerful vasodilator and causes increased capillary
permeability.
100

• Polymodal nociceptors can be activated by bradykinin and
they then can become sensitized to thermal stimuli.
• Another group of compounds that synthesize the regions of
tissue damage are the metabolic products of arachidonic
acid.
• These compounds are considered inflammatory mediators
and include both prostaglandins and leukotrienes.
• Prostaglandin E2 is metabolized from arachidonic acid
through the action of cyclo – oxygenase, occurs in
conjunction with an inflammatory process.
101

• Prostaglandins do not seem to be algogenic substances
per se.
• They sensitize nociceptive nerve endings to different
type stimuli, thus lowering their pain thresholds to all
kinds of stimulation.
• Prostaglandins are required for bradykinin to act,
bradykinin in turn stimulates the release of
prostaglandins.
• The two are therefore naturally potentiating.
102

• In addition to the chemical mediators that are released
from damaged cells or synthesized in the region of
damage, the nociceptors themselves can release
substances that enhance nociception.
• One such substance is substance P. and, when
stimulated, can release this potent excitatory
neurotransmitter into the extra cellular space.
• Substance P is a very strong vasodilator and produces
edema. Substance P also causes release of histamine
from mast cells, which is an excitatory neurotransmitter
and also causes vasodilatation and edema.
103

Nociceptive pain:
- mechanisms
involved
in development
104

NEURONAL SENSITIZATION
• When excitatory neurotransmitters are released in the
synaptic cleft, the post synaptic neuron in excited and
an impulse generated.
• If excitatory neurotransmitter remain in the region of
synapse, neuron can be depolarized quickly with the
next release of neurotransmitter.
• This process is known as sensitization.
105

• Sensitization is the result of a lowering of threshold
that causes the depolarization of the primary
afferent neuron.
• Example: sensitivity after several hours in the area
adjacent to receiving a small cut.
106

NEUROGENIC INFLAMMATION
• There is evidence that the axon transport system can
move neurotranmitters in the primary afferent neurons
both centrally (orthodromically) as well as peripherally
(antidromically).
• Antidromic activity of the primary afferent neuron
results in the release of neurotransmitters into the
peripehral terminals leading to sensitization of neurons
in adjacent area neurogenic inflammation.
• Results in local vasodilation (flare) and edema (wheal)
107

INITIATION OF NOCICEPTION AT
BRAINSTEM LEVEL
108
• Tissue injury release bradykinin- potent pain
producing substance
• Tissue injury breakdown of arachidonic acid into
prostaglandin by enzyme cyclooxygenase
• Arachidonic acid leukotrienes by 5-lipoxygenase.
• Activate A-delta and C-fibers

• A-delta quick volley of afferent nociceptive input
into CNS sharp, acute pain.
• Prostaglandins– sensitize the nociceptors to
bradykinin, substance P– cause sensitization of slow
conducting C- fibers dull, aching pain, sometimes
burning sensation.
109

• Tissue injury, originally affect one portion of the
primary afferent neuron, a series of events take place
that lead to expansion of the involved area by
antidromic release of algesic substances.
• Precisely occurs at the branches of a primary afferent
neuron when a single branch is injured.
• With injury , SP and calcitonin gene related peptide are
antidromically released in the other peripheral
branches of the same afferent neuron.
110

• SP then causes mast cells in the area to release
histamine and platelets to release 5HT mediate
swelling, redness and heat+ peripheral sensitivity to
further sensitization=> hyperalgesia.
111

HYPERALGESIA
• Hyperalgesia: increased sensitivity to stimulation at
the site of pain.
1. Primary hyperalgesia: Occurs as a result of lowered
pain the peripheral structures, resulting presumably
from presence of algogenic substances such as
bradykinin, potassium, histamine and 5-HT
112

2. Secondary hyperalgesia: is increased response to
stimulation at the site of pain in the absence of any
local cause; occur with or without accompanying
referred pain.
- secondary hyperalgesia persists for a while after the
primary pain ceases.
- Analgesic blocking of the primary pain site does not
immediately arrest the hyperalgesia as it does for
referred pain.
113

• Two theories to explain secondary hyperalgesia:
1. Sensitization of second order neuron.
2. Neurogenic inflammation.
114

CENTRAL PROCESSING OF NOCICEPTION
• Convergence and divergence
• Spatial and temporal summation
• Facilitation and inhibition
115

SITE OF PAIN AND SOURCE OF PAIN
• Site of pain: location that patient feels the
pain
• Source of pain: area of the body from which
pain actually originates
116

HETEROTROPIC PAIN
Site of pain is not the same location as the source of
pain.
1. Central pain
2. Projected pain
3. Referred pain
117

CENTRAL PAIN
• Pain that emnates from structures of the CNS is felt
peripherally as heterotopic pain.
• Intracranial structures are insensitive to pain.
• Pain emnating from pain sensitive intracranial
structures on or above the tentorium cerebelli is felt
in peripheral distribution of trigeminal nerve.
118

PROJECTED PAIN
• Pain is felt in the peripheral distribution of the same
nerve that mediates the primary nociceptive input.
• Pain resulting from noxious stimulation of a sensory root
or a major nerve trunk is felt in the exact anatomic
distribution of that nerve.
• Projected pain follows dermatomal rule faithfully
• Primarily neurogenous – activation of interneurons,
prolonged firing of injured sensory fibers.
119

• Noxious stimulation of a motor root or a major
motor nerve also induces pain.
• Motor nerve pain is dull, deep somatic pain diffusely
located in the muscles innervated by that nerve.
• Interneurons are involved in a manner similar to that
for projected sensory nerve pain
120

• Pain occurring in a visceral structure is usually not felt
in the viscus itself but on the surface of the body or in
some other somatic structure that may be located
quite some distance away.
• Such type of pain is said to be referred pain.
• It is commonly observed in all type of deep pain both
visceral and somatic pain e.g. the pain of angina
pectoris is often felt in the left arm or the jaw and
diaphragmatic pain is often felt in the shoulder or
neck.
122

• It is not accentuated by provocation of the site where
the pain is felt, it is accentuated only by manipulation of
the primary pain source.
• It is dependent on continuance of the primary initiating
pain, it ceases immediately if the primary pain is
arrested or interrupted.
• Anesthesia of the structure where the referred pain is
felt does not arrest the pain.
• It should be noted that although the primary initiating
pain is of the deep visceral type, the secondary referred
pain may be felt in either deep or superficial structures.
123

The two most popular theories explaining mechanism of
referred pain are
• Convergence Projection Theory
• Convergence Facilitation Theory
124

CONVERGENCE-PROJECTION THEORY
• The sympathetic afferent fibers carrying the pain
sensation emerges from the viscus and via dorsal root
ganglion ends in the posterior horn of the spinal cord.
• Afferent somatic nerve, emerging from the pain receptor,
of the corresponding dermatome of the viscus, enters
the same segment and terminates on the very same cell
where sympathetic nerve is terminating i.e. these two
different neurons converge on the same next order
neuron.
125

• Therefore when the next order neuron is stimulated –
the impulse reaches the brain and person feels pain,
but he feels as if the pain is coming from the
dermatome.
126

CONVERGENCE FACILITATION
THEORY
• According to this theory, nociceptive input from the
deeper structure causes the resting activity of the
second order neurons pain transmission in the spinal
cord to increase or be facilitated.
• The resting activity is normally created by impulses
from the cutaneous afferents, facilitation from deeper
nociceptors causes the pain to perceived in the area
that creates the normal, resting background activity.
127

• The theory tries to incorporate the clinical
observation that blocking sensory input from the
reference area with either L.A. or cold, can sometimes
reduce the perceived pain e.g. in myofacial pain,
application of a vapocoolant spray is actually a popular
and effective modality used for pain control.
128

SUBLIMINAL FRINGE EFFECT
• The afferent sympathetic nerve bringing pain sensation
from the viscus terminate on the second order neuron,
but at the same time it also via collateral, stimulate
another second order neuron.
• This second order neuron is synapsed with somatic
neuron of the corresponding dermatome.
• Therefore, when the pain is felt by the patient, he feel as
if the pain is coming from the corresponding
dermatome.
129

• When pain is referred, it is usually to a structure that
developed from the same embryonic segment or
dermatome as the structure in which the pain
originate.
• This is called dermatome rule e.g. during embryonic
development the diaphragm migrates from neck
region to the adult location between the chest and
abdomen and take its nerve supply, the phrenic nerve
with it.
DERMATOME RULE
130

• One third of the fibers in the phrenic nerve are
afferent and they enter the spinal cord at the level of
II to IV the cervical segments, the same location at
which afferents from the tip of the shoulder enter.
131

• Referred pain does not occur haphazardly but in fact
follows three clinical rules:
1) Referred pain frequently occurs within a single nerve
root, passing from one branch to another.
E.g.. Mandibular molar presenting with a source of pain
will commonly refer pain to a maxillary molar. This is
fairly common occurrence with dental pain.
 Generally, if the pain is referred to another
distribution of the same nerve, it does so in a
laminated manner; This lamination follows
dermatomes. 132

 Trigeminal lamination patterns are determined by the
manner in which the primary afferent neurons enter in
the spinal tract nucleus.
 According to Kunc, the location of the trigeminal
nociceptive terminals within the nucleus caudalis is as
follows:
a) Fibers from parts near the saggital midline of the face
terminate highest in the nucleus (cephlad).
b) Fibers from parts located more laterally terminate
lowest in the nucleus (cauded).
c) The intermediate fibers terminate intermediately in
the nucleus.
133

• This grouping of the terminals of the primary trigeminal
neurons should influence the location of clinical effects of
central excitation, a molar tooth projects dorsal to canine
projects dorsal to an incisor, which confirms the vertical
lamination just cited.
• This means incisors refer to incisors, premolars to
premolars, and molars to molars on the same side of the
mouth.
• In other words, molars do not refer pain to incisors or
incisors to molars.
134

2) The referred pain in the trigeminal area rarely
crosses the midline unless, it originates at the midline.
 For example, pain in the right temporomandibular
joint will not likely cross over to the left side of the face
nor will right molar pain refer to a left molar.
 This is not true in the cervicospinal region or below,
cervicospinal pain can be referred across the midline,
although it normally stays on the same side as the
source.
135

3) If referred pain is felt outside the nerve that mediates
the pain, it is generally felt cephlad to the nerve
(upward, toward the head) and not caudally.
 Clinically this means that deep pain felt in the sacral
area maybe referred to the lumbar area, as well as
lumbar to thoracic, thoracic to cervical, and cervical to
trigeminal.
136

CENTRAL SENSITIZATION
• Describes changes occurring at a cellular level to
support the process of neuronal plasticity that occurs
in nociceptive system neurons in spinal cord and in
supraspinal centers, as a result of activation of
nociceptive system.
• Excitatory amino acid receptors, particularly those of
N-methyl-d-aspartate subtype, have been strongly
implicated in the generation of central sensitization.
137
A. Wright. Recent concepts in the neurophysiology of pain; manual therapy (1999)
4(4)196-202

138
Release of EAA at presynaptic terminal
G-protein mediated activation of phospholipase C in
postsynaptic terminal
Release of calcium from intracellular compartment +
production of diacyl glycerol
Modulate ion channel activity
Upregulate NMDA receptor
Enhance the neurons responsiveness to subsequent
EAA release

• The development of tenderness, the spread of pain
from a primary location, increased guarding of an
affected area and alteration in skin temperature are
some clinical characteristics which may be
manifestations of neuroplasticity due to central
sensitization.
139
A. Wright. Recent concepts in the neurophysiology of pain; manual therapy (1999)
4(4)196-202

EXPERIENCE OF PAIN
• PERCEPTION- REACTION HYPOTHESIS:
 Given by Marshall and Strong in 19th century.
 Pain not only a sensory experience but involves
dominant features on a mental level, such as prior
conditioning, evaluative significance, memory and
emotional response
140

• PSYCHONEUROTIC PAIN:
 Maurice concluded the exaggerated reaction is
due to psychic factors and termed psychoneurotic
pain
• ORGANIC PAIN:
 Pain behaviour that could be accounted for on the
basis of structural changes
• PSYCHOGENIC PAIN:
 No structural changes could be found to explain
the pain.
141

• Noxious stimuli of comparable intensity may produce
varying degrees of pain in the same individual under
different circumstances.
• For example, an injury acquired by an athlete in the
sports field or by a soldier in the battlefield is less
painful than a comparable injury suffered in a road
accident.
• In other words, pain can be modulated.
143

• In the 1960s neurophysiological studies provided
evidence that the ascending output from the DH of the
spinal cord following somatosensory stimulation
depended on the pattern of activity in different classes
of 1° sensory neurons.
• Melzack and Wall proposed the ‘gate control’ theory of
pain.
• It suggested that activity in low-threshold, myelinated
1° afferents would decrease the response of DH
projection neurones to nociceptive input (from
unmyelinated afferents).
144

• Although there has been controversy over the exact
neural substrates involved, the ‘gate control’ theory
revolutionized thinking regarding pain mechanisms.
• Pain is not the inevitable consequence of activation
of a specific pain pathway beginning at the C-fibre
and ending at the cerebral cortex.
• Its perception is a result of the complex processing
of patterns of activity within the somatosensory
system.
145

PAIN MODUALTION IN TRIGEMINAL SPINAL
TRACT NUCLEUS
• As trigeminal spinal tract nucleus is the brainstem
extension of the spinal dorsal horn, it is assumed that
the same discussion ( gate control theory) holds good
for trigeminal nerve input.
• The gate control theory suggested that both myelinated
and unmyelinated primary afferent neurons converge to
synapse with both second order neurons as well as
interneurons in the substantia gelatinosa (lamina II).
146

• The neurons have a direct excitatory effect on the
second-order neuron- transmission cell (T cell).
• The substantia gelatinosa neurons were proposed to
inhibit neurotransmitter release from both primary
afferent neurons, thus inhibiting the impulse carried
by the primary afferent neuron.
• The myelinated afferents were proposed to excite
the inhibitory interneurons, which in turn would
reduce the activity of pain transmission neuron.
147

• Selective stimulation of large diameter myelinated fibers
produce analgesia; activity of unmyelinated nociceptive
neurons inhibit substantia gelatinosa cells and enhance
transmission of primary afferent to T-cell increase
nociceptive transmission to higher centers
• Clinical relevance of gate control theory:
Touch hot stove : pain
Immediately wave hand: no pain
Stop waving: pain returns
Implies c-fiber input carrying nocicpetion is inhibited by
a-beta fiber associated with motion
148

PAIN MODULATION IN RETICULAR
FORMATION
• Reticular formation is the portion of brainstem that
contains a number of nuclei that can either excite or
inhibit incoming impulses.
• Pain signals in particular increase the activity in this
area and strongly excite the brain to attention.
149

There are certain areas of the reticular formation that
have concentrated cells(nuclei) that produce certain
neurotransmitters, influence the neural activity in the
area.
• Locus ceruleus – produce norepinephrine– excite brain
activity
• Nucleus raphe produces serotonin—inhibits brain activity
• Substantia nigra– produces dopamine– dual role
• Gigantocellular nucleus– acetylcholine- excite neural
activity 150

• Not only does the reticular formation influence
ascending impulses onto the thalamus and cortex,
return impulses/ descending impulses are also
enhanced.
• Anytime the cerebral cortex becomes activated by
either thinking or motor processes, reverse signals are
sent back to the brainstem excitatory area, increasing
the impulses
• Provide a positive feedback system—allows beginning
activity in cerebrum to support still more activity,
leading to an awake mind.
151

PAIN MODUALTION IN DESCENDING
INHIBITORY SYSTEM
• In1983, Wall and Denvor made a significant discovery
while studying nerve injury in rats.
• They determined that peripheral receptor is not the
only region of the neuron that can initiate afferent
impulses.
152

• The dorsal root ganglion cells also initiate sensory
impulse as – tonic, low-level, spontaneous
background discharge that is propagated
orthodromically into the root and antidromically into
peripheral nerve persistence of nociceptive
impulse after peripheral anesthesia.
• This ongoing sensory input from the dorsal ganglia
participates in the arousal system, which if not
countermanded would tend to prevent sleep and
induce a continuous state of pain.
153

• The neural mechanism in the brainstem that appears
to balance this continuous barrage of sensory
input descending inhibitory system.
• A balance between ongoing sensory barrage and
descending inhibitory system needs to be maintained
for normal functional activities, allowing for proper
rest and sleep.
• 5HT is one of the most important neurotransmitter in
the descending inhibitory system
154

• The descending inhibitory system is thought to affect all
sensory input ascending into brainstem.
• The portion of this system that affects nociceptive
inputs is– analgesic system, consists of three major
components:
1. Peri-aqueductal grey matter
2. The nucleus raphes magnus
3. A group of descending neurons that terminate in the
substantia gelatinosa of spinal tract nucleus and dorsal
horn.
** Electrical stimulation of NRM and PAG can almost
completely suppress strong nociceptive impulses
155

• Recent studies have demonstrated that a pain- provoked
stimulus in one area of the body can actually raise the
pain threshold in another part of the body.
• This explains the phenomenon called DIFFUSE NOXIOUS
INHIBITORY CONTROL
• Suggests that when a painful stimulus is felt in one
portion of the body, CNS activates a widespread or
diffuse system that seems to reduce the transmission of
noxious stimuli from other areas of the body
156

• Represents a protective control of the human that
enables the individual to focus and respond to one
important area of tissue injury, even when multiple
sites exist
157

PAIN MODULATION BY PSYCHOLOGIC
FACTORS
• EXCITATORY MODUALTING FACTORS:
 egocentric psychologic conditions that center the
subjects attention toward oneself have an excitatory
effect on pain.
Wall and Melzack determined that the level of pain
due to injury was directly related to the degree of
attention directed toward the injury at the time.
158

• The more one is absorbed with one’s suffering, the
more intense it becomes.
• Expectancy is an important factor due to memory,
anticipation or prior conditioning, whatever one expects
in the way of pain is likely to be what one experiences.
• ** the real potent excitatory modulators : ANXIETY AND
FEAR—produces the consequence of pain experience.
• As maladaptive behavior ensues , depression and
despair flourish– chronicity associated with depletion of
endorphins sets in
159

INHIBITORY NEUROMODULATORS
• Outgoing psychologic conditions that direct one’s
attention to energies away from the self have favorable
modulating effect on pain.
• A feeling of serenity born of confidence and assurance
has a marked inhibitory influence.
• Distraction is inhibitory.
• Overcoming maladaptive behavior by constructively
coping with the painful situation has a very favorable
modulating influence.
160

• It is often assumed that pain is a warning that damage
has occurred. But this is not strictly true.
• Because pain may occur when there is no obvious
disease as in primary neuralgias and many diseases
does not cause pain, at least in the early stages.
• So these are various theories being put forward on
how nerve impulses give rise to sensation of pain.
162

INTENSITY THEORY
• According to this view, pain is produced when any
sensory nerve is stimulated beyond a certain level.
• In other words 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.
163

• 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.
164

 Specificity Theory (Johannes Muller, 1842):
• 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.
165

• 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.
166

 Protopathic and Epicritic theory:
• 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.
167

Pattern theory (Goldscheider, 1894):
• 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. 168

 Gate Control Theory
• 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.
169

• The large nerve fibers have collateral branches,
which carry impulses to substantia gelatinosa where
they stimulate secondary neurons.
• 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.
170

• 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.
171

FAST PAIN & SLOW PAIN
 Fast Pain
• Also known as Sharp pain, pricking pain or acute pain.
• Easily localized.
• Not felt in the deep visceral organs.
 Slow Pain
• Also known throbbing pain, aching pain or chronic pain.
• Poorly localized
• It can occur both in skin and in almost any deep tissue or
organ.
176

1. Emotional status:
• The pain threshold depends greatly on attitude
towards the procedure. In case of emotionally unstable
and anxiety patient the pain threshold is low but
reaction is high.
2. Fatigue:
• Pain reaction threshold is high in subjects who has
good night sleep and relaxed, then those persons who
are tired.
178

3. Age :
• Older individuals tend to tolerate pain and thus have
higher pain reaction threshold than young
individuals. Perhaps their philosophy of living or the
realization that unpleasant experiences are a part of
life may account for this fact.
179

4. Racial and nationally characteristics:
• The Caucasian and Negro races have little or no variation
in the pain reaction threshold.
• The Latin Americans and Southern Europeans are more
emotional than North Americans or Northern Europeans
may be in warmer climates tend to have lower pain
reaction threshold.
5. Sex :
• Men have higher pain threshold than women. This may be
a reflection of man’s desire to maintain his feeling of
superiority and this is exhibited in his pre determined
effort to tolerate pain.
180

6. Fear and apprehension:
• Most cases pain threshold is lowered as fear and
apprehension increases. Individuals who are
extremely fearful tend to magnify their experiences.
181

DIAGNOSIS BASED ON SPECIFIC
QUESTIONS AND TESTS
184

 Questions asked-two type
• General questions
• Specific questions
RECORDING THE HISTORY
185

• Some general questions are-
• What can I do for you?
• Pt give response in three ways-
Historical, Diagnostic & Factual
• What sort of pain are you having ?
• Varied response affected by
Physical, psychological, social factors
186

SPECIFIC QUESTIONS
• Anatomical location where the pain is felt
• Origin and mode of onset
• Intensity of pain
• Nature of pain
• Progression of pain
187

• Duration of pain
• Movement of pain
• Localization behavior
• Effect of functional activities
• Concomitant neurological signs
• Temporal behavior
• Previous treatments and their effects.
188

PAIN SCALES
• Visual Analog Scale
• Locate area of pain on a picture
• McGill pain questionnaire
– Evaluate sensory, evaluative, & affective components
of pain
• 20 subcategories, 78 words
None Severe
0 10

Scoring
• Add up the total number of words chosen, up to the
maximum of 20 words (one for each category)
– The level of intensity of pain is determined by the
value assigned to each word.
• 1st word = 1 point
• 2nd word = 2 point
• And so on
– Pt could have a high score of 20, but have a low-
intensity score by selecting the 1st word in each
category.

• Pain sensations may be controlled by interrupting the
pain impulse between receptor and interpretation
centers of brain.
• This may be done chemically, surgically or by other
means.
• Most pain sensations respond to pain reducing
drugs/analgesics which in general act to inhibit nerve
impulse conduction at synapses.
194

• Occasionally however, pain may be controlled only by
surgery.
• The purpose of surgical treatment is to interrupt the
pain impulse somewhere between receptors and
innervation centers of brain, by severing the sensory
nerve, its spinal root or certain tracts in spinal cord
or brain.
195

TENS- TRANSCUTANEOUS ELECTRIC
NERVE STIMULATION
• Byproduct of gate control theory.
• Therapeutic modality
• Rationale: anti-nociceptive effect of stimulating
sensory nerves.
196

• An interrupted faradic current of very low intensity at
a frequency of 50-100hz is used.
• Stimulation of a-beta fibers
• Stimulation is below what is required to activate a-
delta and c nociceptive fibers.
• Tingling or vibratory sensation is felt.
• Immediate effect, disappears rapidly.
197

ACUPUNCTURE
• ACUS = NEEDLE, PUNGERE = STING
• Method of inhibiting pain impulses.
• Acupuncture theory is based on an invisible system of
communication between various organs of the body
that is distinct from circulatory, nervous and endocrine
system.
198

• Needles are inserted through selected areas of skin
and then twirled.
• After 20-30 minutes, pain is deadened for 6-8 hours
• Location of needle insertion depends on part of body
acupuncturist wishes to anesthetize.
• Example : to pull a tooth – a needle is inserted in the
web between thumb and index finger.
199

• Pain Inhibiting Mechanism
It can be -
• Endogenous
• Exogenous
200

• Endogenous Method of Controlling Pain Includes -
1) Removing the cause:
 It is a desirable methods.
 It is imperative that any removal leave no permanent
environmental changes in tissue, since this condition
would then be able to create the impulse, even though
the original causative factor had been eliminated.
201

2) Blocking the pathways of painful Impulses
• This can be done by injecting drug possessing local
analgesic property in proximity to the nerve involved.
• Thus preventing those particular fibers from
conducting any impulses centrally beyond that point.
These two method act by altering pain perception.
202

3) Raising the pain threshold :
• Raising pain threshold depends on the pharmacological
activity of drugs possessing analgesic properties.
• These drugs raise pain threshold and therefore alter pain
reaction, conceptually there are two components of pain
(a) Nociceptive
(b) Affective component.
• The path of nociceptive component is spinothalamic tract
 Thalamus. This component is purely physical component
of pain.
203

4) Affective Component
• It is the psychological component associated with pain.
The path is that some fibers from STT to thalamus
terminate in some intermediate stations in the reticular
formation of brain stem and are called spinoreticular
thalamic system.
• Non-narcotic analgesic like aspirin can inhibit the
nociceptive but not the affective component of pain
whereas opioid (Morphine) inhibit affective as well as
nociceptive components of the pain. They act centrally
at cortical and sub cortical centers, to change patient
mind and his reaction towards pain 204

5) Preventing pain reaction by cortical depression
• Eliminating pain by cortical depression is by the use of
general anesthesia.
6) Using Psychosomatic Method
• This method affects both pain perception and pain
reaction. It include audio analgesia
205

PAIN PATHWAYS AND
MEDICATIONS
207

208
Pain Pathways Medications
Peripherally (at the nociceptor) Cannabinoids, NSAIDs, Opioids,
Tramadol, Vanilloid receptor antagonists
(i.e., capsaicin)
Peripherally
(along the nociceptive nerve)
Local anaesthetics, Anticonvulsants (except
the gabapentinoids)
Centrally
(various parts of the brain)
Acetaminophen, Anticonvulsants (except
the gabapentinoids), Cannabinoids,
Opioids, Tramadol
Descending inhibitory pathway
in the spinal cord
Cannabinoids, Opioids, Tramadol,
Tricyclic antidepressants, SNRIs
Dorsal horn of the spinal cord Anticonvulsants, Cannabinoids,
Gabapentinoids, NMDA receptor
antagonists, Opioids, Tramadol, Tricyclic
antidepressants, SNRIs

CONCLUSION
• Pain is bad, but not feeling pain can be worse.
• Individuals with a congenital absence of pain receptors
are extremely rare but not unknown.
•Such individuals are very poor at avoiding accidental
injuries, and often inflict mutilating injuries on
themselves.
• As a result, their life span is usually short.
209

• Thus pain, although unpleasant, is a protective
sensation with enormous survival value.
• Pain is a multidimensional experience involving both
the sensation evolved by noxious stimuli but also the
relation to it.
• The sensation of pain therefore depends in part on the
patient past experience, personality and level of
anxiety.
210

• Every day patient seeks care for the reduction or
elimination of pain.
• Nothing is more satisfying to the clinician than the
successful elimination of pain.
• The most important part of managing pain is
understanding the problem and cause of pain.
• It is only through proper diagnosis that appropriate
therapy can be selected.
211

1. Jeffrey P. Okeson.Bell`s ‘Orofacial pain’, 5th edition.
2. Text book of Medical Physiology, 2nd edition, Chaudhari.
3. Text book of Medical Physiology, 10th edition, Arther C Gyton.
4. Textbook of medical physology, sembulingam
5. Text book of ‘Oral medicine’- 10th edition, Burkett’s.
6. Gray's Anatomy – 38th Edition, Churchill Eivingstone.
7. Textbook of neuroanatomy-1st, 2nd edition, vishram singh
8. Textbook of anesthesia- monheims
213

214
9. Pain – Wikipedia, the free encyclopedia
10. Rolf-Detlef Treede. Neurophysiological studies of pain pathways in
peripheral and central nervous system disorders. J Neurol (2003) 250 : 1152–
1161.
11. A. Wright. Recent concepts in the neurophysiology of pain. Manual
therpy 1999;4;196-202
12. "Part III: Pain Terms, A Current List with Definitions and Notes on Usage"
(pp 209-214) Classification of Chronic Pain, Second Edition, IASP Task Force
on Taxonomy, edited by H. Merskey and N. Bogduk, IASP Press, Seattle,
©1994.
13. Joseph F Audette, Alison BaileyIntegrative pain and medicine: the
science and practice of complementary and alternative medicine in pain
management.

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