it includes types, theories, pathways, applied aspects everything about pain

1. GOOD MORNING

2. PAIN
ITS PHYSIOLOGY
AND PATHWAYS

3. CONTENTS
• INTRODUCTION
• DEFINITION
• SIGNIFICANCE/BENEFITS OF PAIN
• CLASSIFICATION OF PAIN
• TERMS USED TO DESCRIBE PAIN
• PAIN RECEPTORS
• CLASSIFICATION OF NERVE FIBERS

4. • PATHWAYS OF PAIN
• THEORIES OF PAIN
• APPLIED PHYSIOLOGY
• CONCLUSION
• REFRENCES

5. INTRODUCTION
• Pain is subjective experience
• There are pain receptors they are nerve endings ,present in
most body tissues that only respond on potentially
damaging stimuli
• The messages initiated by these noxious stimuli are
transmitted by specific ,identified nerves to the spinal
cord
• From the spinal cord these stimuli is carried to the brain
in the sensory cortex

6. DEFINITION
PAIN is UNPLEASANT ,SENSORY , and
EMOTIONAL experience associated with actual
or potential tissue damage. (international
association for the study)

7. SIGNIFICANCE OF PAIN
• Pain is an important sensory symptom. Though it is
an unpleasant sensation, it has protective or survival
benefits such as:
• 1. Pain gives warning signal about the existence of a problem or threat.
It also creates awareness of injury
• 2. Pain prevents further damage by causing reflex withdrawal of the
body from the source of injury
• 3. Pain forces the person to rest or to minimize the activities thus
enabling rapid healing of injured part
• 4. Pain urges the person to take required treatment to prevent major
damage

8. TERMS USED TO DESCRIBE PAIN
(1) Burning pain: a connotation of warmth.
(2) Deep pain: from deep visceral or somatic structures, with
the symptoms being generally diffuse, often associated with
symptom referral to other regions and/or muscle spasms.
(3) Itch: a subthreshold pain, which may have a warm or
burning quality, but may become intractable.
(4) Pricking pain: a sharp intermittent character of short
duration

9. .
(5) Stinging pain: a more or less continuous high-intensity
characteristic.
(6) Superficial pain: usually precisely localizable to a superficial
lesion, with the timing, location and intensity of symptoms often
being accurately described by the patient.
(7) Throbbing or pulsatile pain: an intermittent quality coincident
with cardiac systoles.
(8) Tickle: a sensation induced by light superficial movement.

10. CLASSIFICATION OF PAIN
BASED
LOCATION
INTENSITY
DURATION

11. BASED ON INTENSITY
MILD PAIN
MODERATE PAIN
SEVERE PAIN

12. PAIN SCALE
• Given by Wong - Baker

13. • MILD PAIN – PAIN READING FROM 1 - 3
• MODERATE PAIN-PAIN SCALE READING FROM 4-6
• SEVERE PAIN-PAIN SCALE READING FROM 7 -10

14. PAIN
ACUTE PAIN
CHRONIC
PAIN
BASED ON
DURATION

15. ACUTE PAIN / FAST PAIN
Also called as sharp pain, pricking pain, acute pain, and electric pain.
 This type of pain is felt when a needle is stuck into the skin, when the
skin is cut with a knife, or when the skin is acutely burned.
 It is also felt when the skin is subjected to electric shock. Fast-sharp
pain is not felt in most deep tissues of the body

16. CHRONIC PAIN
Also called as slow burning pain, aching pain, throbbing pain,
nauseous pain, and chronic pain.
• This type of pain is usually associated with tissue
destruction. It can lead to prolonged, almost unbearable
suffering.
• Slow pain can occur both in the skin and in almost any deep
tissue or organ

17. BASED ON LOCATION
NEUROPATHIC
PAIN
REFERRED
PAIN
PHANTOM
PAIN
SOMATIC
PAIN
VISCERAL
PAIN

18. • Pain arising from the superficial skin
or subcutaneous tissue caused in
response of noxious stimulus in the
nociceptive nerve fibers of
superficial tissue surface.
• Example superficial cuts and burns
• Usually experienced from muscle
,bone ,periosteum
• Example fracture, arthritis .
Superficial type Deep type

19. VISCERAL PAIN
• Pain from the different viscera of the abdomen
and chest is one of the few criteria that can be
used for diagnosing visceral inflammation,
visceral infectious disease, and other visceral
ailments.
• The viscera have sensory receptors for no other
modalities of sensation besides pain.
• visceral pain differs from surface pain in several
aspect such as visceral pain is that highly
localized

20. NEUROPATHIC PAIN
• Neuropathic pain is caused by damage or disease affecting any part of
the nervous system in the somatosensory system .Neuropathic pain may
be divided into peripheral, central, or mixed (peripheral and central)
neuropathic pain.
• Peripheral neuropathic pain is often described as "burning", "tingling",
"electrical", "stabbing", or "pins and needles".
• Bumping the "funny bone" elicits acute peripheral neuropathic pain.
• Some manifestations of neuropathic pain include: traumatic
neuropathy, tic douloureux, painful diabetic neuropathy, and postherpetic
neuralgia.

21. REFFERED PAIN
DEFINITION
• The disease of a deep organ
gives rise to superficial pain
in some part of the body, not
necessarily overlying the
deep organ.
• Eg . Cardiac pain is felt at inner part
of left arm and left shoulder
• Pain in gallbladder is referred to
epigastric region
• Pain in diaphragm is referred to
shoulder

22. DERMATOME RULE
According to dermatomal rule, pain is referred to a
structure, which is developed from the same dermatome
from which the pain producing structure is developed.
For example, the heart and inner aspect of left arm
originate from the same dermatome.
So, the pain in heart is referred to left arm.

23. MECHANISM OF REFERRED PAIN
• The branches of visceral pain fibers
are shown to synapse in the spinal
cord on the same second-order
neurons that receive pain signals
from the skin.
• When the visceral pain fibers are
stimulated, pain signals from the
viscera are conducted through some
of
the same neurons that conduct pain
signals from the skin, and the person
has the feeling that the sensations
originate in the skin

24. PROJECTED PAIN
If pain fibers are stimulated
mechanically or electrically on their
way to the spinal cord, the brain still
interprets the pain as originating in the
part of the body where the
corresponding nociceptors are located
Example-if the pain fibres travelling in
the ulnar nerve are stimulated at the
elbow, the pain is still perceived to
originate in the hand

25. PHANTOM PAIN
• After the amputation of a limb , the cut ends of
severed nerves innervate the skin covering the
stump. Stimuli existing the nerve fibres at the stump
are interpreted as originating in the limb which does
not exist any more.
• The phantom limb sometimes also experience
pain, which is known as phantom pain

26. PAIN RECEPTORS
• Three Types of Stimuli Excite Pain Receptors:-
Mechanical, Thermal, and Chemical.
• Fast pain is elicited by the mechanical and thermal
types of stimuli,
• Slow pain can be elicitated by the chemicals are
bradykinin, serotonin, histamine, potassium ions,
acids, acetylcholine, and proteolytic enzymes. In
addition, prostaglandins and substance P.

27. Special Importance of Chemical Pain Stimuli During
Tissue Damage.
• Extracts from damaged tissue cause intense pain when injected
beneath the normal skin. One chemical that seems to be more painful
than others is bradykinin.
• The intensity of the pain felt correlates with the local increase in K ion
concentration or the increase in proteolytic enzymes that directly attack
the nerve endings and excite pain by making the nerve membranes
more permeable to ions.

28. CELL MEMBRANE POTENTIAL
A resting neuron cell membrane is polarized
A potential difference is the measure of difference in electrical charge
resting membrane potential is distribution of ions across the membrane
which results the outside of membrane being more positively charged
Normally K+{high inside}
Na+{high outside}
Cl- {high outside}

29. • CHANNEL PROTEINS PUMP IONS
ACROSS THE CELL MEMBRANE
• ACTION POTENTIAL
• NORMALLY IS -70mV
• When a stimulus is applied it
changes into +30mV

30. DEPOLARISATION
• It occurs when Na+ channels
open and Na+ move into the cell
• This causes more positive ion
concentration of the cell
• Thus surface of membrane is more
negatively charged when compared
to inside of axon

31. REPOLARISATION
• Behind the action potential the
potassium channels will open
• Exit of potassium causes membrane to
once again become more positively
charged
• To gain back the resting membrane
potential
• Ion concentration is gained
back by active transport Na K
PUMP
• 3Na+ will be pumped out for every 2 K+
that are pumped in the result is more
positive charge inside

32. CLASSIFICATION OF SENSORY NERVE
FIBERS

33. MYELINATED A delta
FIBERS
• 2-5 MU DIAMETER
• CONDUCTION VELOCITY 12-35 m/s
• Release of glutamate in activation of A delta
responsible of first pain
• Has the ability to localise pain size and its intensity
of noxious stimulus
• LOW stimulation threshold. (TRANSMIT PAIN
DIRECT TO THALAMUS
• Considered to convey impulses conceived as
sharp and penetrating
UNMYELINATED C FIBERS
• 0.4-12 MU DIAMETER
• CONDUCTION VELOCITY 0.5 TO 2 m/s
• Activated by glutamate and substance p =slow
pain
• Pain is dull intense diffuse unpleasant asstd
with noxious stimuli
• high stimulation threshold. ( modulated by
many interneurons bfr reaching the thalamus )
• Transmits impulses which are dull

34. DENTAL PAIN OF PULPAL ORIGIN
 A tooth is primarily innervated from the
maxillary or mandibular division of the
trigeminal nerve that pass essentially
through the apical foramen
 Nerve fibres from this plexus then pass
into the overlying odontoblastic layer,
and comprise both myelinated and
unmyelinated nerve fibres .

35.  Both myelinated (A) and unmyelinated (C)
fibres pass through the apical foramen into
the root canal and generally branch
infrequently until the coronal aspect where
they fan out towards the pulpal dentine
border as Rashkow's plexus.
 some nerves terminate in the pulp proper,
the majority pass towards the coronal
pulpal walls and roof to form the
subodontoblastic nerve plexus

36. • DENTAL SENSITIVITY is a result of direct stimulation of sensory nerve endings
in dentin . The nerves are located in mineralized dentin the most sensitive
area of the tissue is DEJ
• ODONTOBLAST are sensory cells through their processes in the dentinal
tubules , they receive and transfer stimuli to nerve endings in pulp
• DENTINAL SENSITIVITY is aresult of mechanical stimulation of free nerve
endings in pulp caused by rapid flow of the fluid into or out in the dentinal
tubules when stimulated

37. DENTAL PAIN OF PERIODONTAL ORIGIN
 Periodontal ligament capable of transmiting
tactile ,pressure , pain sensation by trigeminal
pathways
 Nerve bundles pass from the pdl from
periapical area and through channels in
alveolar bone along with course of blood
vessels
 Nerve bundles divide myelinated fibers lose
their myelin sheath and end in one of four
neural termination

38.  FREE NERVE ENDING WITH TREE
LIKE RAMIFICATIONS- Terminal
branches of myelinated fibers which
have a tree lik configuration and carry
pain sensation
 RUFFINI LIKE
MECHANORECEPTORS -Located in
apical area near root apex

39.  COILED MEISSENERS
CORPUSCLES
Mechanoreceptors found mainly in mid
root region and spindle like pressure and
vibration endings r surrounded by fibrous
capsule & present in the apex
• ENCAPSULATED SPINDLE TYPE
Found in Root apex are temperature receptors

40. • In periodontal pain can be manifested in two different ways
1. Pain in periapical origin deep somatic pain
2. Pain in gingival tissue superficial somatic pain
 Chronic periodontal disease such as gingivitis and periodontitis r usually painless but
may cause mild episodic or persistent dull pain (low grade infection)
 Sharp periodontal pain asstd with high grade infection and inflammation

41. PATHWAY OF PAIN CONDUCTION
• Transduction of pain As well as normal
sensory receptors which respond to touch,
pressure, stretch, heat, cold etc.,
• The body contains free nerve ending called
nociceptors which activate in response to
noxious stimuli or pain.
• Nociceptors convert noxious stimuli into
nerve impulses that progress centrally to
the spinal cord and then the brain.

42. Transmission
 The activation of the nociceptor
results in a nerve impulse being
transmitted from the site of injury
along the pain fibre or neuron to the
dorsal (rear) horn of the spinal cord
 These are the first order afferent
(upwards) pain fibres. The perception
of pain is the end result of pain
transmission.

43. Relay
The thalamus, which is the sorting centre
for the brain, receives sensory impulses
from various parts of the body
These signals are then passed to the
relevant somatosensory cortex area of the
brain that processes the sensory
information and the perception of pain
takes place

44. • Integration/Interpretation.
The somatosensory cortex identifies
the nature of the stimulus before it
triggers a response, for example,
where the pain is, how strong it is and
what it feels like, whether we need to
‘fight or flight’.

45. Modulation or inhibition of
pain
T Individuals will respond to identical
pain stimulus differently
There are many mechanisms that act to
inhibit pain transmission within the
brain, at spinal cord level and at the
peripheral nociceptors

46. PATHWAY OF FAST PAIN

47. PATHWAY OF SLOW PAIN

48. THEORIES OF PAIN
• Described by DESCARATES IN 1644 PROPOSED AS pain system as a straight
through channel from the skin to the brain
• In early 19th century MULLER postulated as the theory of information
transmission only by the way of sensory nerve
• In late 19th century VON FREY developed the concept of specific cutaneous
receptors for the mediation of touch , heat, cold, pain
SPECIFIC THEORY

49. • Free nerve ending were implicated as pain receptors
• A pain center was thought to exist within the brain which was
responsible for all over manifestations of unpleasant experience
• This theory led to the development of several surgical approaches
in the management of chronic pain by cutting straight through the
tracts

50. PATTERN THEORY
• In 1894 GOLDSCHEIDER was first to propose that stimulus intensity
and central summation are the critical determinants of pain
• The theory suggested that the particular patterns of nerve
impulses that evoke pain are produced by summation of sensory
input within the dorsal of spinal column
• Pain results when the total output of the cells exceeds a critical
level

51. GATE CONTROL THEORY
• Given by Ronald Melzack and Patrick Wall in
1960s
• Gate control theory emphasized modulation of
pain at the spinal cord level by the
simultaneous presence of non-noxious stimuli.
• Suppose a touch(A delta) stimulus is applied
to the same area of skin which has been
subjected to a noxious stimulus(A beta & C).
.

52. • The touch fibre gave a collateral in the
substantia
gelatinosa of the dorsal horn of the spinal
cord which, in turn, inhibited the pain fibre
pre-synaptically through an inhibitory
interneuron That is how a touch stimulus
could reduce the painfulness of a noxious
stimulus.
• The inhibitory interneuron acts as a gate.
When it is activated, the gate is closed, and
pain impulses cannot ascend upwards.

53. • When the gate neuron is inactive, pain
impulses can ascend upwards and
reach the sensory cortex to make us
conscious of the pain
• Example generating a strong
sensation over a painful joint by
application of a counterirritant balm or
cream reduces the pain. In general,
pains are felt more acutely at night
when competing stimuli are absent
than during the day.

54. DRAWBACKS
• . While the gate control theory seems to explain
some of these observations, experimental studies have failed
to find evidence for the type of neuronal circuitry proposed by
the theory.
• However, the theory did stimulate much research
on modulation of pain and contributed to the discovery of an
endogenous pain relief system.

55. • The most important role among these areas
is the PAG. Receptors for morphine and
similar substances (opioid receptors) are
present in all the major relay stations
concerned with pain, i.e. substantia
gelatinosa, reticular formation, PAG as well
as throughout the limbic system, which is
concerned with pain, pleasure and visceral
functions.
ENDOGENOUS PAIN RELIEF
SYSTEM

56. • Further, substances resembling
morphine in their molecular
configuration have been found to
serve as neurotransmitters in areas
of the brain and spinal cord where
opioid receptors are present.
• Endorphins are also released from
the anterior pituitary in response to
stress.

57. • As in other sensory systems, there are descending
fibres which parallel the ascending fibres
• The descending fibres converge in the PAG. Activation
of PAG neurons releases serotonin as a
neurotransmitter in the substantia gelatinosa.
• Serotonin, in turn, activates enkephalinergic
interneurons. The enkephalinergic neurons inhibit the
projection neurons of the pain pathway
• Descending fibres can modulate the intensity of pain.
It seems any form of stress, specially the stress of
pain, activates the analgesic system through the limbic
system

58. GATE CONTROL THEORY REVISITED
• The interneurons which inhibit projection neurons of the
pain system do exist in the spinal cord. But these inhibitory
interneurons are not activated by touch and other primary
afferents , as postulated by the gate control theory.
• Instead, the inhibitory interneurons seem to be activated
by the fibres descending from PAG and related areas.

59. • The dorsal column fibres, while ascending to
the thalamus, give off collaterals to the
reticular formation. These collaterals could
activate the descending fibres of the
endogenous analgesic system.
• Thus a touch stimulus can still close the
gate, although indirectly that dorsal column
stimulation often produces analgesia.

60. APPLIED PHYSIOLOGY
• Hyperalgesia—Hypersensitivity to Pain
A pain nervous pathway sometimes becomes excessively
excitable, which gives rise to hyperalgesia. Possible causes
of hyperalgesia are
• (1) excessive sensitivity of the pain receptors, which is called primary
hyperalgesia
• (2)facilitation of sensory transmission, which is called secondary hyperalgesia.
example
• PRIMARY HYPERALGESIA is the extreme sensitivity of sunburned skin, which
results from sensitization of the skin pain endings by local tissue products from
the burn—perhaps histamine, prostaglandins, and others.
• SECONDARY HYPERALGESIA -results from lesions in the spinal cord or the
thalamus.

61. HERPES ZOSTER (SHINGLES)
• Occasionally herpesvirus infects a dorsal
root ganglion.
This infection causes severe pain in the
dermatomal segment subserved by the
ganglion, thus eliciting a segmental type
of pain that circles halfway around the
body.
• Also called as “shingles,” because of
a skin eruption that often ensues.

62. • The cause of the pain is presumably
infection of the pain neuronal cells in the
dorsal root ganglion by the virus
• The virus is carried by neuronal
cytoplasmic flow outward through the
neuronal peripheral
axons to their cutaneous origins.
• The virus causes a rash that vesiculates
within a few days and then crusts over
within another few days, all of this
occurring within the dermatomal area
served by the infected dorsal root

63. TRIGEMINAL NEURALGIA /
GLOSSOPHARYNGEAL NEURALGIA/TIC
DOULOUREUX
Lancinating or stabbing type of pain occasionally occurs
in some people over one side of the face in the sensory
distribution area of the fifth nerves, this phenomenon is called
tic douloureux
• The pain feels like sudden electrical shocks, and it may
appear for only a few seconds to minutes at a time or may
be almost continuous.
• Often it is set off by exceedingly sensitive trigger areas on
the surface of the face, in the mouth, or inside the throat—
almost always by a mechanoreceptive stimulus rather than
a pain stimulus.

64. • TREATMENT OF The pain of tic douloureux can
usually be blocked by surgically cutting the
peripheral nerve from the hypersensitive area.
• The sensory portion of the fifth nerve is often
sectioned immediately inside the cranium, where
the
motor and sensory roots of the fifth nerve separate
from
each other, so that the motor portions, which are
necessary for many jaw movements, can be spared
while the sensory elements are destroyed.

65. CO-RELATED TERMS IN PAIN
• PARALGESIA- abnormal pain sensation
• THERMIC ANESTHESIA – loss of thermal sensation
• ANALGESIA – loss of pain sensation
• ANESTHESIA –loss of sensation

66. • HYPERSTHESIA – increase sensitivity to sensory
stimuli
• HYPOTHESIA- decrease sensitivity to sensory
stimuli
• HEMITHESIA – loss of sensation to one part of
body

67. • PARESTHIA –abnormal sensation
• GENERAL ANESTHESIA- loss of all sensation with
loss of consciousness produced by anesthetic
agents
• LOCAL ANESTHESIA –LOSS SENSATION IN
RESTRICTED AREA OF BODY

68. CONCLUSION
Pain transmission is a result of complex peripheral and
central processes but by understanding the four steps
of nociception we can begin to understand the complex
process of pain transmission.
This knowledge for the effective assessment of pain
and the selection of appropriate interventions for
managing pain.

69. REFRENCES
• GUYTON AND HALL 13TH EDITION TEXTBOOK OF MEDICAL PHYSIOLOGY,
CHAPTER SOMATIC SENSATION PART 2 ; PAIN, THERMAL SENSATION
• K SEMBULINGUM ESSENTIALS OF MEDICAL PHYSIOLOGY 6TH EDITION ,
CHAPTER PHYSIOLOGY OF PAIN
• TEXTBOOK OF LOCAL ANESTHESIA AND DENTAL PRACTICE BY MONHEIM
CHAPTER PAIN
• UNDERSTANDING MEDICAL PHYSIOLOGY 4TH EDITION BY RL BIJALANI AND
S MANJHUTA CHAPTER PAIN AND RELIEF FROM PAIN
• APPLIED PHYSIOLOGY 2ND EDITION BY CHRISTOPHER

70. •THANK YOU