DR.CHAITHRASHREE

1. Physiology of pain, pain
control & anxiety management

2. Contents
 Introduction
 Definition
 History
 Neurophysiology of pain
 Classification of pain
 Factors affecting pain
 Neural anatomy of pain
 Etiology
 Theories of pain

3. INTRODUCTION:
•Pain - commonly experienced symptoms in dentistry.
•Pain - not a simple sensation but rather a complex
neurobehavioral event involving at least two components.
•Pain perception
•Pain behavior

4.  Derived from Latin “Poena”; meaning punishment from
God
• PAIN
• Pain - indispensable for normal life.
• provides information about tissue damaging (noxious)
stimuli and helps us to protect ourselves from greater
damage.

5. DEFINITION
o Pain - An unpleasant emotional experience usually initiated
by a noxious stimulus and transmitted over a specialized
neural network to the central nervous system where it is
interpreted as such.- Monheim’s
 Pain is defined as “a more or less localized sensation of
discomfort, distress or agony resulting from the stimulation
of specialized nerve endings”.- Dorland’s Medical
Dictionary

6. HISTORICAL NOTE:
o Aristotle was the first to distinguish the five physical senses and
considered pain to be a “passion of the soul”.
 Plato contended that pain & pleasure arose from within the body. That gave birth
to the concept that pain is an emotional experience more than a localized body
disturbance.
 Freud developed the idea that physical symptoms could result from the thought
processes. He considered that symptoms such as pain could develop as a solution to
emotional conflicts (psychosomatic pain)

7.  During the 19th century, the developing knowledge of
neurology fostered the concept that pain was mediated by
specific pain pathways & was not simply a result of
excessive stimulation of the special senses
 In recent years, specialization of nociceptive pathways has
been identified

8. The neural
anatomy of pain

9. NEURON
• structural and functional unit
• 10 billion neurons
STRUCTURE:
 Nerve cell body(soma)-
 Axon
 Nerve endings

10. CLASSIFICATION OF NEURONS
Multipolar
Bipolar
Unipolar
Based on structure

11. Sensory neuron
Interneurons
Motor neuron
FUNCTION OF NEURONS

12.  Nerve is a bundle of axons
Epineurium
Perineurium
Endoneurium
NERVE

13. Types of nerve
fibers
1.Depending upon
structure
Myelinated
fibers
Unmyelinat
ed fibers

14. 2.Depending upon function
•Motor or efferent:
• Sensory or afferent:

15. SENSORY NEURONS:
 FIRST ORDER NEURONS
 SECOND ORDER NEURONS
 THIRD ORDER NEURONS

17. 3.Based on conduction velocities
Erlanger-gasser classification
 GROUPS OF NERVE FIBERS:
 A GROUP
 B GROUP
 C GROUP

18. PROPERTIES CORELATED WITH DIAMETER :
• As Diameter increases
• Velocity of conduction increases.
• Magnitude of electrical response increases.
• Threshold of excitation decreases.
• Duration of response decreases.
• Refractory period decreases
FIBRES DIAMETER CONDUCTION VELOCITY
A FIBRES 3-20micra 100 m/s
B FIBRES Upto 3 micra 3-14 m/s
C FIBRES 0.5- 1 micron .05-2 m/s

20. A GROUP
 largest fibers.
 myelinated.
 sensory and motor in function.
 It is further classified into 4 sub groups.
 Aα (afferent and efferent fibers)
 Aβ (afferent and efferent fibers)
 Aγ (efferent fibers)
 Aδ (afferent fibers)

21. B GROUP
 myelinated.
 preganglionic autonomic nerve.
C GROUP
 smallest fibers.
 unmyelinated.
 They have high threshold i.e. 30 folds that of A group.
 postganglionic sympathetic nerve.

23. Innervations of human teeth
 Initial innervation begins – crown formation
 6 stages includes:
 Neurogenesis
 Cell migration
 Cell differentiation
 Synaptogenesis
 Apoptosis
 Synaptic re-arrangement

24.  Nerve enters dental papilla – bell stage
 Cell bodies – sensory neurons of pulp – trigeminal ganglion
 Thousands of axons enters pulp – apical foramen.
 There are 2 types of sensory nerve fibres in pulp
 Myelinated- A- fibres
 Unmyelinated – C- fibres
 A-delta fibres- first to form and degenerate.
 Larger fibres – branch – cell rich zone – plexus of raschkow.
 90% of a – delta fibres – located – pulpo-dentinal junction and coronal portion
of pulp.
 C – fibres – located – cell free zone and core of pulp.

25.  According to Johnsen et.al human premolars received 2300 axons at apex.
 Where:
 20% - myelinated fibres.( A- fibres)
 13%- A- delta fibres
 7% - A- beta fibres
 80% - unmyelinated fibres ( C- fibres)
 Myelinated axons- 312 +/- 149
 Unmyelinated axons – 2000 +/- 1023

26. Stimulus to fibres:
 A- fibres – stimulus – probing, drilling, hypertonic solutions and heat
application
 C fibres- cold application and chemical mediators
 Stimulus is due to hydrodynamic effect.
 Application of heat: Application of cold:
Vasoconstriction
Prolonged effect
Anoxia of A- fibres
vasodilation
Increased intra-
pulpal pressure
C- fibres are
affected
pain

27. Pulpal innervation changes in response
to dental caries:
Dental caries progressing towards dentin
Moderate caries –
forms reactionary
dentin & localized
sprouting of nerve
endings
Deep dental caries
Damage of nerve endings, glial cells and dendritic
cells – dentin-pulp interface
Impaired modulation of NGF
Nerve apoptosis
Pulpal inflammtion

28. Neuro- transmitters of pulp
Pulpal insult due to trauma , caries etc
Vasodilation and increased pulpal pressure –
Pulpal inflammation
Release of substance-p and glutamate and crgp
Inflammatory response
Histamine &
bradykinins
seratonin
C-fibresA-delta -fibres

29. Pulpal innervation changes in response
to physiological root resorption:
Physiological root resorption is an asymptomatic
process
Degradation of nerve plexus precedes root
resorption
Wallerian- axonal degradation
Decreased number of fibrils and bundles
Demyelination of damaged axon – myelin debris
Debris- obstacle for regeneration and contribute for
inflammatory response

30. RECEPTORS ENDINGS
FIVE BASIC FUNCTIONAL TYPES OF RECEPTORS
•Mechano receptors:
•Thermoreceptors:
•Nociceptors :
•Electromagnetic receptors or photoreceptors:
•Chemoreceptors :

31. Receptors
• Cutaneous receptors :
– Touch receptors : meissners corpuscle merkels discs
– Pressure receptors : pacinian corpuscles
– Temperature or thermoreceptors
– Pain or nociceptors : free nerve ending
Exteroceptors:

32. • Chemoreceptors :
– Taste: taste buds
– Smell : olfactory receptors
• Telereceptors :
– Hearing
– Vision

33. • visceroreceptors :
– streachreceptors, baroreceptors,
– chemoreceptors, osmoreceptors
• proprioreceptors :
– muscle spindle, golgi tendon organ,
– pacinian corpuscle and free nerve ending
Interoceptors :

34. o Three types of stimuli that excite pain receptors.
 Mechanical
 Thermal
 Chemical
o Chemicals that excite type of pain are
o - Bradykinin
o - Potassium ions
o - Serotonin
o - Acids
o - Histamine
o - Acetyl choline
STIMULUS :

35. Nerve impulse
 It is the mechanism of development of receptor potential and
generation of action potential in the nerve fiber.

36. Nerve conduction
1.Generation of action potential
2.Impulse spread
3.Synapse

37. 1. Generation of action potential:
• Nerve is polarized at rest
• Conduction of impulse depends on electrical potential that exists across the nerve membrane
• Sodium and chloride outside the membrane
• Potassium ions inside the membrane
• Potential inside of the nerve is negative and outside is positive

38. 2. Depolarization(reduction of memberane potential from –ve
value towards zero)
Alteration in permeability
 Increased Na diffusion into the nerve cell due to opening of voltage gated Na+ channels.
 Depolarization from resting to firing threshold -50 to -60mv.
 Marked increase in memberane permiability to Na+
 Outside becomes negative relative to the inside
 Electrical potential of 40 mV exists on the interior of the nerve cell at the end of
depolarization

39. Repolarization
• Permeability to Na+ decreases resuling in decrease Na+
influx..
• Rapid efflux of Potassium, restores original
electrochemical equilibrium and resting potential

41. 2.Impulse propagation:
A. Unmyelinated axons:
B. Myelinated axons: Saltatory conduction

42. SYNAPSE
 junction between the 2 neurons .
 not the anatomical continuation .
 physiological continuity between 2 nerve cells.

43. SYNAPSE
 CLASSIFICATION
ANATOMICAL CLASSIFICATION :
 Axo-somatic synapse
 Axo-dendritic synapse
 Axo-axonic synapse
Functional classification
 Electrical synapse
 Chemical synapse

45. Passage of Ach through synaptic cleft
SEQUENCE OF EVENTS DURING SYNAPTIC
TRANSMISSION
• Arrival of action potential in the axon terminal
• Opening of calcium channels in presynaptic
membrane
• Influx of calcium ions from ECF into the axon
terminal
• Opening of the vesicles and release of Ach
• Formation of Ach –receptor complex
•Opening of sodium channels and influx of sodium ions
From ECF.
•increased Na+ permeability causes depolarization of post
synaptic membrane
•Action potential

46. PROCESSING OF PAIN:
Pain Pathway :
Fields divided the processing of pain from stimulation of
primary afferent nociceptors to the subjective experience of
pain in 4 steps :
Transduction : It is the process by which noxious stimuli leads
to electrical activity in the appropriate sensory nerve ending.
Transmission : It refers to neural event that carry the
nociceptive input into the central nervous system for proper
processing.
Modulation : the neural impulse (nociceptive) are changed or
altered before reaching the higher centers (Cortex).
Perception : It determined by interaction of the (cortex,
thalamus, and limbic system) higher centers.

47. Transduction:
It is the activation of the primary afferent nociceptor.
 Primary afferent nociceptors can be activated by various stimuli.
 Primary afferent nociceptors can be activated by intense thermal, mechanical
and noxious chemical stimuli.
 They are also activated by stimulation from inflammatory mediators produced
by body in response to tissue injury.

48. 2. Transmission
 Refers to the process by which peripheral nociceptive information is
relayed to the central nervous system.
 The primary afferent nociceptors synapses with a second order pain
transmitting neuron in the dorsal horn of the spinal cord where a new
action potential heads towards higher brain structures.

50.  Dual pain pathways in spinal cord and brain stem
 On entering the spinal cord, the pain signals take two
different pathways to brain, through:
 Neospinothalamic tract
 Paleospinothalamic tract.

51. Neospinothalamic pathway for fast pain:
A-DELTA fibres are stimulated by thermal & mechanical stimulus
Free receptors of 1st order Neurons picks up the stimulus
1st order neurons, terminate in Lamina-1
1st order neurons excite the 2nd order neurons of Neospinothalamic tract
Fibres cross opposite side through anterior commissure and pass
upwards to the brain stem in anterolateral column
Few fibres – terminate – reticular area in brain.
Majority fibres terminate – thalamus (VPL Nucleus)
Remaining fibres terminate – Posterior gyrus of thalamus
3rd order neuron – terminate – basal brain area & somato sensory
cortex

52. Paleospinothalamic pathway for slow pain:
C fibres are stimulated by chemical stimulus
Free receptors of 1st order Neurons picks up the stimulus
1st order neurons, terminate in Lamina-2, 3 & 5 (substancia gelatinosa & Rolandi
1st order neurons excite the 2nd order neurons of Neospinothalamic tract
Here the last neuron in the series gives rise to long axons that mostly join
the fibers from the fast pain pathway, passing through the ant. commisure
to opposite side of cord. Then upwards to brain in anterolateral pathway.
Few fibres – terminate – reticular area of medulla,pons &
mesencephalon
periaquaductal gray
1/10th – 1/4th - terminate –Thalamus
3rd order neuron – terminate – basal brain area & somato sensory
cortex

55. 3. Modulation:
 Refers to mechanisms by which the transmission of noxious
information to the brain is reduced.
 The endogenous pain inhibiting system consists of 3 major
components and other accessory components.
 Periaquaductal Gray Area (PGA) – release enkephalins (medulla)
 Nucleus Raphe Magnus (NRM) – release serotonin (mid-brain)
 The release of these neurotransmitters inhibit ascending neurons
 A pain-inhibiting complex is located in the dorsal horns of the
spinal cord.
 At this point the analgesia signals can block the pain before it is
relayed on to the brain.

57. DESCENDING PAIN CONNECTIONS
 the descending pathways are fibres that descend from
brainstem to spinal cord to modulate the incoming signals.
 Notable neurotransmitters mediating this anti-nociceptive
effect include noradrenaline (norepinephrine), and
serotonin in the raphe nuclei.
 Opioid receptors are prevalent here.

58. 4. Perception:
 The final step in the subjective experience of pain is perception.
 When nociceptive impulse reaches the cortex, perception occurs.
 It is at this point that suffering may occur.
 Suffering refers to the manner in which the patient responds to pain.

59. Classification of Pain:
1) According to Site:
SOMATIC PAIN: Pain due to noxious stimuli from :
 Superficial
 Deep

60. According to Type:
Nociceptive Pain
 Caused by irritation to special nerve endings (nociceptors).
 Associated with events such as burning the hand, twisting the ankle etc.
 Felt as dull or sharp aching pain and mild to severe in nature.
Typically controlled by removing the irritation or medical treatment. Responds
well to mild pain medications like NSAIDs or other drug therapies.
E.g. Sprained ankle (temporary) cancer or arthritis – chronic.
Neuropathic Pain
 Caused by dysfunction or damage to the nervous system.
 Associated with events such as injury, disease, or trauma confined to a small
area due to an infection or a surgery.
 Felt as sharp, intense and constant in nature.
 Responds poorly to standard pain therapies such as mild analgesics and other
pain medications.
 Trigeminal neuralgia.

62. 1. ACUTE PAIN:
It arises in about 0.1 sec., usually pricking, sharp fast nature,
short duration and pain is closely related to somatic tissue
changes – trauma / disease.
Fast Pain:
Stimulation of A fibres are felt earlier due to myelinated
thick and faster rate of conduction.
2. CHRONIC PAIN:
chronic pain is pain of long duration history, frequently
associated with irritability and depression.
Second / Slow pain:
Stimulation of ‘c’ fibres are felt after longer interval due
to non-myelinated thin and slower rate of conduction.

63. 3. Inflammatory pain:
Tissue injury causes release of Prostaglandins and bradykinin
which results in local vasodilation and increase in capillary
permeability and then the stimulation of pain receptors
(Noxious) occurs.
4. Non -Inflammatory Pain:
Poorly understood, chronic type, no obvious tissues
changes and may originate from somatic or neurogenous
structures or may be psychic .

64. 5.MUSCULO SKELETAL PAIN
Deep somatic pain originating from skeletal muscles,
facial sheath and tendons, bone and periosteum.
6.NEUROPATHIC PAIN;
Generated within Nervous system due to some
abnormality of neural structures.
7.ODONTOGENIC PAIN:
Deep somatic pain originating in dental structures and
periodontium.
8.VASCULAR PAIN :
Deep somatic type of pain of visceral origin that emanates
from the afferent nerve that innervates blood vessels.

65. 9.PRIMARY PAIN
Pain that identifies the true source of nociceptive input.
10.HETEROTROPIC PAIN
Heterotopic pain that is felt in an area that is innervated
by a nerve different from the one that mediates the
primary pain.
11.REFERRED PAIN
Pain felt in an area other than its true source.

66. ETIOLOGY OF PAIN
Pain has a multi modal etiology, but some specific pathological processes are commonly associated
with pain.
 INFLAMMATION:
Tissue injury: Chemical inflammatory mediators (bradykumin, Prostaglandins)
Vasodiliation & Pain
 Muscle pain
 Vascular pain: Vasodilation & Vascular permeability
 Neural pain : Neurectomy, Compression, Myelin degeneration, trauma, bacterial infection etc
 Allergic & Toxic conditions.
 Direct noxious chemical, mechanical or thermal .

67. FACTORS AFFECTING PAIN :
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.
2.Fatigue :
Pain reaction threshold is high in subjects who has good
night sleep and relaxed, then those persons who are tired.

68. 3.Age :
Children and young adults have high threshold of pain
compared to adults.
4. Fear and apprehension :
Most cases pain threshold is lowered as fear and
apprehension increases. Individuals who are extremely
fearful tend to magnify their experiences.

69. 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.
.

70. THEORIES OF PAIN

71.  This theory defines pain, not as a unique sensory experience but
rather, as an emotion that occurs when a stimulus is stronger than
usual.
 This theory is based on Aristotle’s concept that pain resulted from
excessive stimulation of the sense of touch.
 Goldscheider further advanced the Intensity Theory, and showed that
repeated tactile stimulation (below the threshold for tactile perception)
produced pain in patients with syphilis who had degenerating dorsal
columns. When this stimulus was presented to patients 60–600 times/s,
they rapidly developed what they described as unbearable pain.

72.  Draw Backs:
 The trigeminal neuragia cases : In this condition patient can suffer excrauating
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.

73. • Rene Descartes (1664) • Pain occurs due to
stimulation of specific pain
receptors (nociceptors) with
transmission by nerves
directly to the brain
• “intensity of pain is directly
related to the amount of
associated tissue injury”.

74.  Specificity theory is one of the first modern therioes
for pain.
 It holds that specific pain receptors transmit signals
to a pain centre in the brain that produces the
perception of pain.
 Von frey argued that the body has a separate sensory
system for perceiving pain – just as it does for hearing
and vision .
 This theory consider pain as an independent sensation
with specialised peripheral sensory receptors which
respond to damage and send signals through pathways
to target centres in the brain .
 Thus , it is based on the assumption that the free nerve
ending are pain receptors and that the other three types
are specific to a sensory experience

75.  Draw Backs:
 It is accepted that C fibers convey impulses mediating
pain. But some ‘C’ fibers will respond to mechanical
stimuli of only a few milligrams of skin pressure which
does not cause pain [Iggo, 1960].
 In other words they are not specific for Nociceptive stimuli

76.  Strong investigated physical pain, particularly that felt through
the skin.
 He proposed that pain was an experience based on both the
noxious stimulus and the psychic reaction or displeasure
provoked by the sensation.
 Strong concluded that pain is the sensation. The first sensation
was the experience of heat and then came the sensation of pain.

77. • Goldscheider proposed that
there is no separate system for
perceiving pain , and the
receptors for pain are shared
with other senses ,such as
touch.
• This theory considers that
peripheral sensory receptors,
responding to touch warmth
other non damaging and
damaging stimuli gives rise to
non painful or painful
experience as a result of
difference in the pattern of the
signals sent through the
nervous system.

78.  It proposed that the intense stimulation resulting from
the nerve and tissue damage activates fibers within
the spinal cord creating abnormal reverberating
circuits with self-activating neurons.
 Prolonged abnormal activity bombards cells in the spinal
cord, and information is projected to the brain for pain
perception.

79.  Hardy , wolff , and goodell, 1940s
 It stated that pain was composed of two components : The
perception of pain and the reaction one has towards it.
 The reaction was described as a complex , past experiences , and
various psychological factors which influence pain perception

80.  It describes two systems involving transmission of pain ; fast and slow system.

81. :

82.  According to this theory an alteration in the local pH in a nerve or in the
vicinity of nerve is the cause for pain.
 Eg. The pain due to an abscess can be reduced by making the area alkaline.
 ACIDITY CAUSES PAIN
 ALKALINE REDUCES PAIN

83. Ronald Melzack
Patrick D. Wall

84. • It explains how pain can be modulated in the spinal
cord.
• This theory embraces the interaction of the
physiological, psychological and socio-cultural factors
which lead to pain perception and response.

85.  The most renowned Pain theory is the Gate
Control Theory (GCT)
 First proposed in 1962, & again in 1965 by
Ronald Melzack(a Canadian psychologist ) and
Patrick david Wall(a British physician )
 Idea that the perception of physical pain is not
a direct result of activation of nociceptive, but
instead is modulated by interaction between
different neurons, both pain-transmitting and
non-pain-transmitting.

86. 1. No input -- the inhibitory neuron prevents the
projection neuron from sending signals to the brain --
gate is closed.
2.Normal somatosensory input -- large-fiber stimulation
-- Both the inhibitory neuron and the projection neuron
are stimulated -- inhibitory neuron prevents the
projection neuron from sending signals to the brain --
gate is closed.
3.Nociception (pain reception) -- small-fiber stimulation
-- inactivates the inhibitory neuron, and the projection
neuron sends signals to the brain informing it of pain ---
gate is open.

87. Conditions that close
the 'Gate'
Physical
Medication
Counter-stimulation
Emotional
Positive Emotions
Relaxation
Rest
Mental
Intense concentration or
distraction
Involvement and
interest in life activities
Conditions that open
the 'Gate'
Physical
Extent of the Injury
Inappropriate activity
level
Emotional
Anxiety or worry
Tension
Depression
Mental
Focusing on the Pain

88. To be continued…

89. Thank you