seminar presentation of pain and pain pathways

this is a presentation of pain pathways

1. Pain And Pain Pathways
Viritha
PG 1
Department of oral and maxilla facial surgery
Guide
Dr P SIVA GANESH
Reader
Department of oral and maxilla facial
surgery

2. CONTENTS
•Introduction
•Definition
•classification
•Theories of pain
•Neuroanatomy
•Neurophysiology
•Transduction
•Transmission
•Modulation
•Perception
•Tooth pain
•Diagnosis of pain
•Management of pain
•Conclusion

3. INTRODUCTION
“Pain is not a sensation , it is an experience”.
-Dr Welden E Bell

4. DEFINITION
The International Association for the Study of Pain
Pain is "an unpleasantsensoryand emotional
experience associated with actual or potential tissue
damage, or described in terms of such damage”
(Merskey1986)
Monheim
“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”

6. IASP CLASSIFICATION

7. NEURAL PATHWAYS
Given by Fields-1987

8. NEURAL ANATOMY

9. There is a wide diversity of types of neuron.
TYPES OF NEURON

10. Multipolar neurons are a commonly described type of neuron. One
example is the spinal motor neuron in vertebrates.

11. COMPONENTS OF
NERVOUS SYSTEM

12. FUNCTIONAL
NEUROANATOMY

13. COMPONENTS OF PAIN PATHWAY
Cortex
Thalamus
Medulla
Spinal cord
Receptors
neurons
Higher Centers

14. SENSORY RECEPTORS
GENERAL
SENSES
SPECIAL
SOMATIC VISCERAL
SUPERFICIAL DEEP
Touch-pressure
Thermal
pain
Pain
proprioception
Pain
Baroreceptor
chemoreception
Visual
Audition
Olfaction
gustation

15. SENSORY RECEPTORS
Exteroceptors Proprioceptors Interoceptors
Merkel’s corpuscles
Meissner’s corpuscles
Ruffini’s corpuscles
Krause’s corpuscles
Free nerve endings
Muscle spindles
Golgi tendon organs
Pacinian corpuscles
Periodontal
mechanoreceptors
Free nerve endings
Pacinian corpuscles
Free nerve endings

16. Classification of nociceptors
Mechanical nociceptors
respond to strong pressure
Chemically sensitive nociceptors
respond to chemicals
Thermal nociceptors
respond to temperature
Polymodal nociceptors
respond to combinations

17. NERVE ENDINGS

18. NOCICEPTORS
•A nerve ending that responds to noxious stimuli that can actually
or potentially produce tissue damage.
•Free nerve endings
•Stimulated by:
Thermal
Mechanical
Chemical
Disease

19. •Types of nociceptors
AδMechanical Nociceptors
C Polymodal Nociceptors
C fiber mechanical nociceptors
High threshold cold nociceptors
•Receptor mechanism
Noxious stimuli
Tissue damage chemicals

20. SENSORY NEURONS
First-Order Second-OrderThird-Order
3 Types

21. TYPES OF NOCICEPTIVE AFFERENTS
Mechanothermal afferents
Aδ, 12-18 m/s
Intense thermal & mechical
Polymodal afferents
C, 0.5 m/s
Mech, thermal, chemical stimuli
High-threshold mechanoreceptive
afferents
Aδ
Intense mech, algo genic substances

22. SECOND-ORDER NEURONS
•Low-threshold mechanosensitive neurons (LTM)
Light touch, proprioception, pressure
•Nociceptive-specific neurons(NS)
Noxious stimuli
•Wide dynamic range neurons (WDR)
Noxious, non-noxious

23. LAMINA IN
GREY MATTER
DIFFERENT TRACTS
IN SPINAL CORD

24. •Interneurons
Inhibitory
Excitatory-lamina II & III (Substantia gelatinosa)
Anterolateral
Spinothalamic tract
Dorsal column-Medial
Lemniscal system
Neospinothalamic tract Paleospinothalamic tract
Second-Order neurons

26. HIGHER CENTRES
Brain & Brain stem
Brain stemcerebellum diencephalon cerebrum
medulla pons Midbrain
thalamus hypothalamus
cortex Limbic systemBasal ganglia
Brain & Brain stem

28. MEDULLA OBLONGATA
•White matter-projection
tracts
•White & grey matter-
reticular formation
Vital centres
Nucleus gracilis
Nucleus cuneatus
Olivary nuclei

29. PONS & MIDBRAIN
•PONS
Reticular formation
Reflex centres-5
th
,6
th
, 7
th
,
8
th
•MIDBRAIN
Tracts to cerebrum
Red nucleus
Substantia nigra

30. CEREBELLUM
•2
nd
largest
•Skilled movements
•Equilibrium
•Smooth,
coordinated
movements

31. DIENCEPHALON
•THALAMUS
Relay station between brain
stem, cerebellum &
cerebrum
Directs impulses
•HYPOTHALAMUS
Controls internal body
functions
Nuclei
Upregulates sympathetic
NS

32. CEREBRAL CORTEX
•Thinking, memory
•5 lobes
•Functional areas
Sensory
Motor
Visual
Auditory
Wernicke’s
•Tracts

33. BASAL GANGLIA & LIMBIC SYSTEM
•BASAL GANGLIA
Gross movements
Nuclei
•LIMBIC SYSTEM
Emotional, behavioral activities
Pain/pleasure centre
Basic instinct
Chronic pain
•OTHER AREAS
Ventricles
Periaqueductal Gray
Raphe Magnus nucleus

34. TRIGEMINAL SYSTEM
Thalamus
Second-order neurons
(WDR, NS-Lamina I, II, V, VI)
Trigeminal spinal nucleus
(Medullary dorsal horn)
Gasserianganglion
Sensory input

35. TRIGEMINAL NUCLEUS COMPLEX
SENSORY NUCLEUS SPINAL NUCLEUS
ORALISINTERPOLARIS CAUDALIS

37. AUTONOMIC NERVOUS
SYSTEM
SYMPATHETIC
SYSTEM
T1-L2
PARASYMPATHETIC
SYSTEM
Cranial-III, VII, IX, X
Sacral nerves

38. TRANSDUCTION
Process by which noxious stimuli leads to
electrical activity in the appropriate nerve
endings

40. CHEMICAL MEDIATORS AND FACTORS
Neurotrophins
Vascular
Immune cell
products
Neurogenic
factors
Products of
tissue injury
Sympathetic nerves
Sensory
fibre
NGF, LIF
Cytokines
Endorphins
Enkephalins
Amines
kinins
NO
Neuropeptides
Kinins, 5 HT,
histamine,protons
Amines, NE

41. •Axon transport system-
Subs P, CGRP-
slow neurotransmission
•Neurogenic inflammation-
Axon reflex
•PAIN FEATURES
Allodynia
Hyperalgesia
Pain spread
Spontaneous activity
PERIPHERAL SENSITIZATION

42. TRANSMISSION
•The neural events that carry the nociceptive
input into the CNS for proper processing
•Nerve action potential
•Synapse
•Neurotransmitters
•Ascending tracts

43. NERVE ACTION POTENTIAL

44. ACTION POTENTIAL SEQUENCE
•Involves the action of voltage-gated channels
•Exchanges of ions in and out of the cell

45. ACTION POTENTIAL
SEQUENCE
•Voltage-gated Na+ Channels open and Na+
rushes into the cell

46. ACTION POTENTIAL
SEQUENCE
•At about +40 mV, Sodium channels close, but now,
voltage-gated potassium channels open, causing an outflow
of potassium, down its electrochemical gradient

47. ACTION
POTENTIAL
SEQUENCE
The voltage-gated K+
channels close, so much
Potassium accumulates
outside the cell that
repolarization occurs
so much so that there is
an undershoot at the end
of the AP sequence
equilibrium
potential of
the cell is
restored

48. ACTION POTENTIAL
SEQUENCE
•The Sodium –Potassium Pump is left to
clean up the mess…

49. PROPAGATION OF THE
ACTION POTENTIAL
•Action Potential spreads down the axon in a chain
reaction
•Unidirectional
•it does not spread into the cell body and dendrite due
to absence of voltage-gated channels there
•Refraction prevents spread back across axon

51. SYNAPSE
•Presynaptic terminals
Synaptic vesicles
Mitochondria
Calcium channels
•Receptor proteins
Binding area
Ionophore component
-Ion receptors
-Enzyme receptors

52. SYNAPSE

53. NEUROTRANSMITTERS
•These are neurochemicals that transmit
impulses across the synaptic cleft
Small rapid-acting Large slower-acting
Molecules Molecules

54. RAPID-ACTINGMOLECULES
•Acetylcholine
•Norepinephrine
Glutamate
Aspartame
Serotonin
•Gamma-aminobutyricacid
•Glycine
•Dopamine
•Histamine

55. SLOW-ACTING NEUROTRANSMITTERS
•Substance P
Centrally--excitatory, released from spinal
cord-excites neurons in dorsal horn
Released by unmyelinated afferents--
neurogenic inflammation-wheal, flare
•Endorphins
Neuromodulators of post-synaptic activity
Antinociceptive action
•Bradykinin

56. TRACTS-TRANSMISSION TO CORTEX
•Nociception from orofacial
region-
via trigeminal nerve, VII,
IX, X, 1
st
, 2
nd
, 3
rd
cervical
nerve
•Cross to opposite side-
ANTEROLATERAL
SPINOTHALAMIC TRACT

58. •Neospinothalamic
tract-
Aδ-lamina I-thermal,
mech-fast pain
•Paleospinothalamic
tract-
C-Lamina II, III, V-
modulation-slow pain

59. FAST & SLOW PAIN
•FAST PAIN
Thermal, mech stimuli
Easily localised, sharp, Aδ
Directly to thalamus (ventrobasal
complex)
cortex (somatosensory area) -motor
cortex-muscle action\reflex

60. SLOW PAIN
Chemical stimuli
Difficult to locate
Deep, dull, aching
Suffering
C, Subs P-increase, persistence
Via reticular
formation(bulboreticular
facilitory area/reticular
inhibitory area)
thalamus (intralaminar nuclei)
Frontal cortex, limbic,
hypothalamus-affective

61. MODULATION
•Pain-a sensory experience
19th century (Marshall & Strong):
Perception-reaction hypothesis
Disease &
tissue damage
Pain
Seek care
(pain behavior)
Non-organic
(Psychogenic) pain
Organic pain
Pain
behavior

62. •20
th
century
Pain comprises organic & psychogenic features in a unified sensory &
emotional experience
Alteration/modulationof impulses as they go to higher centers-
FACILITATION & INHIBITION
Perception & reaction-facets of same mechanism NOT separate
components

63. THEORIES OF PAIN
•Specificity theory (Descartes-1644)
•Intensive/Summation theory
•Pattern theory (Goldscheider-1894)
•Sensory interactive theory
•Gate control theory (Melzac & Wall-1965)

64. Specificitytheory(VonFrey(1890))
-Heproposedthatfreenerveendingsgiverisetopain
sensationinbrain.
-Thistheoryisconcernedprimarilywiththesensory
discriminationaspectsofpain,itsquality,locationonskin,
intensityandduration.

65. -Specificitytheorycannotexplain
a)Anypathologicpainproducedbymildnoxiousstimuli.
b)Referredpainthatcanbetriggeredbymildinnocuous
stimulationofnormalskin.
c)Donotexplaintheparoxysmalepisodesofpainproduced
bymildstimulationoftriggerzoneintrigeminalneuralgia.

66. Intensives or Summation theory (Gold Sheider)
•Heproposedthatpainresultsfromover
stimulationofotherprimarysensations.
•Heproposedthatpainresultedwhenactivity
exceededacriticallevelduetoexcessive
activationofreceptorsresultinginconvergence
andsummationofactivity.

67. Noordenbossensory interaction theory
•Heproposedthatrapidlyconductinglargefiber
pathwayinhibitorsuppressesactivityinslowly
conductingsmallfiberpathwaythatconveysnoxious
information.
•Adecreaseintheratiooflargetosmallfiberactivity
resultsincentralsummationandanincreaseinpainand
viseversa.
•Itexplainsdifferentpathologicpainstatus.
•Hyperalgesiafollowingperipheralnerveinjury.

68. MODULATION IN TRIGEMINAL SPINAL
TRACT NUCLEUS
•Revised version of Gate control theory(1987)

69. TRANSCUTANEOUS ELECTRIC NERVE
STIMULATION (TENS)

70. MODULATION IN RETICULAR
FORMATION
•Nuclei-excite/inhibit
•Neurotransmitter-acetylcholine
•Pain signals-increase activity-excite the brain
•Descending impulses excited
•Positive feedback mechanism
•Chronic pain-sleep disruption

71. MODULATION BY THE DESCENDING
INHIBITORY SYSTEM
•Wall & Denvor(1983)-dorsal root ganglion initiate
impulses-arousal, continuous state of pain
•Analgesic system-descending inhibitory system
•3 main sites:
Periaqueductal grey area
Raphe magnus nucleus
Descending neurons in subs gelatinosa
Anterior pretectal nucleus, nucleus coeruleus, parabrachial
area (pons), cortex

72. •Neurochemicals:
Opiods-enkephalins,
endorphins, dynorphins
Serotonin(5-HT)
Noradrenaline
GABA
•Sites for endorphins:
µ, κ, δreceptors
Periaqueductal grey
Limbic structures
Thalamic nuclei
Raphe nuclei
V subnucleus caudalis
Peripheral tissues

73. Inhibition at SG
•Serotonin-chronic pain
•β-endorphins-acute
pain
local effects
of non-noci pri
afferents
descending
inhibitory mech-
NRM
(serotonin),PAG

75. MODULATION BY PSYCHOLOGICAL
FACTORS
excitatory inhibitory
Egocentric conditions
Expectancy
Anxiety
Fear
Depression, despair
Outgoing conditions
Confidence, reassurance
Distraction
Suggestion & hypnosis
Mental absorption
Physical activities

76. OTHER MODULATION FACTORS
physical characteristics of stimulus:
•Modality
•Location
direct bypass to cortex
•Intensity
•Duration

77. CONVERGENCE
•Synapsing of several primary afferent
neurons with 1 second-order neuron
•Summation
•Facilitation/inhibition
•Deeper afferent input
convergence > cutaneous
structures-diffuse, less localized

78. MECHANISMS OF CONVERGENCE
COVERGENCE SUBLIMINAL FRINGE
EFFECT
Convergence-projection theory
Convergence-facilitation theory

79. CENTRAL SENSITIZATION
•Hyperexcitability of the CNS neurons leading to central excitatory
effects i.e. secondary effects of pain
•CAUSES:
Convergence
Neuroplasticity (alteration in impulse processing)
•FACTORS:
Continuous input
Increased duration & intensity of pain

80. MECHANISM OF CENTRAL
SENSITIZATION
•Neuroplastic change-depends on
peripheral noci afferent input for
initiation BUT NOT on it for its
maintenance
Persistent, spontaneous pain

81. SECONDARY EFFECTS OF DEEP PAIN
Afferent
(sensory)
neuron effects
Efferent
(motor)
neuron effects
Autonomic
neuron
effects
“Wind-up”-temporal
summation (pre-
emptive analgesia)
Referred pain
Secondary
hyperalgesia-
features, causes
Muscle co-
contraction
Myofascial trigger
points
Vasomotor
effects
Glandular
effects

82. REFERRED PAIN
•site of pain primary pain
heterotopic pain
•source of pain
•HETEROTOPIC PAIN
Central pain Projected pain Referred pain

83. MECHANISM OF REFERRED PAIN
•CONVERGENCE
•CENTRAL
SENSITIZATION

84. FEATURES OF REFERRED PAIN
Wholly spontaneous
Not accentuated by provocation of site
Ceases immediately if primary pain is arrested
Felt in superficial or deep structures

85. •RULES:
Occurs within single nerve passing from 1 branch to other-follows
dermatome pattern
Rarely crosses midline, unless originates there
If outside the nerve mediating it, felt cephalad to it

86. VISCERAL PAIN
•Receptors only for pain
•Only activated by diffuse stimulus-not localized
•Mainly C fibers-in sympathetic nerves-Chronic-aching-
suffering type of pain
•CAUSES:
Ischemia
Chemical stimuli
Spasm/overdistention of hollow viscus
PULPAL PAIN

87. PERCEPTION
•Final process in the subjective experience of pain.
•Interactions between higher centers determinessuffering &
pain behavior
•Psychological aspect of pain-affects ALL PAINS

88. FACTORS INFLUENCING PAIN
EXPERIENCE
•Level of arousal of brain stem
•Prior experiences
Memory
Autoconditioning
expectancy
•Emotional state
Fear, rage
Helplessness, sadness, depression
Emotional stress-Glaros et al(JADA, Apr 2005)
•Behavioral traits

89. ACUTE PAIN:
Short duration
somatic tissue changes
CHRONIC PAIN:
lasts longer than normal healing time
PSYCHOGENIC INTENSIFICATION

90. CHARACTERISTICS OF PATIENTS WITH
CHRONIC PAIN SYNDROMES (DCNA, 1987)
•Constancy & continuity of peripheral input
•Increased suffering despite therapeutic efforts
•Persistence/prompt relapse of symptoms despite different
treatment
•Increased anxiety
•Obsessive concern with suffering
•Physical & emotional deterioration
•Decreased self-esteem
•Decreased ability to obtain pleasure
•Substance use disorders

91. DIFFERENCE BETWEEN ACUTE & CHRONIC
PAIN(DCNA, 1987)

92. SUMMARY OF TYPES OF PAIN
•Acute or chronic
•Primary or heterotopic
•Inflammatory or non-inflammatory
somatic
neuropathic
musculoskeletal visceral

93. PULPAL PAIN
•TOOTH INNERVATION
Myelinated & unmyelinated-2-4 µm
Extensive branching-ratio 1:3
2 types of pulp axons
Afferent sensory fibers Autonomic efferent
Substance P
acetylcholine
Nor epinephrine
Vasoactive peptide

94. IMPORTANT CLINICAL ASPECTS:
Aδfibrepain-pulpodentinalcomplex intact
Necrotic teeth-(+) vitality, pain -C fibres
“hot teeth”-TTXrsodium channels of C fibres

95. DIFERENTIAL DIAGNOSIS OF
NONODONTOGENIC TOOTHACHE
(DCNA, 1987, 1997)
•Toothache of MYOFASCIAL ORIGIN
Myofascial trigger points
•Toothache of NEUROVASCULAR ORIGIN
Periodic migraine's neuralgia-cluster headache
•Toothaches of CARDIAC ORIGIN
Angina pectoris

96. •Toothaches of NEUROPATHIC ORIGIN
•Toothaches of MAXILLARY SINUS ORIGIN
Acute/chronic sinusitis
•Toothaches of PSYCHOGENIC ORIGIN
Munchausen’s syndrome
Atypical facial pain
episodic continuous
Pre trigeminal neuralgia
Trigeminal neuralgia
Neuritis
Atypical odontalgia
(phantom pain)

97. DENTURE PAIN
•Denture soreness, like all pain, is a complex experience, in which a multitude of
factors interact.
•Pressure is probably the initial cause of irritation to denture bearing tissue. once
the tissue is damaged, substances released by the damaged tissue (histamine and
prostaglandins), and substances released by the nerve endings themselves
(substance P), contribute to causing swelling and increased sensitivity.
•1. UNEVEN DISTRIBUTION; this includes sharp underlying bone, poorly fitting
denture base, excessive vertical height, uneven occlusion.
•2. ABNORMAL FORCE; this includes chewing hard foods and clenching, and the
single denture.
•3. POOR RESISTANCE ; this includes, systemic factors and ageing.

98. TEMPOROMANDIBULAR DISORDER
Definition
•Temporomandibular joint disorder (TMJ) is the
name given to a group of symptoms that cause
painin the head, face, and jaw.
•The symptoms include headaches, soreness in the
chewing muscles, and clicking or stiffness of the
joints.
•They often have psychological as well as physical
causes.
Causes & symptoms
Muscle tension
Injury.
Arthritis.
Internal derangement.
Hypermobility.
Birth abnormalities
Treatment
Medications
Dental occlusal splint therapy
Physical therapy and mechanical devices
Surgery

99. MYOFACIAL PAIN DYSFUNCTION
SYNDROME
It’s a chronic dysfunction where the transition from a functional to a
structural disturbance maybe quite prevalent.
Pain are well localized to the affected joint and provoked by
movement, especially chewing.
Emotional tension, bruxism, lack of occlusion support due to either
unreplaced teeth or old ill fitting dentures may provoke the pain.
Treatment
• Anti-inflammatory analgesics
• Correction of occlusion with adequate denture in those patient
with missing teeth.
• Open surgery –smoothing of the condylar head, repair of
perforated meniscus.

100. Somatopsychic problems
Itsoverreactionofdentalproceduretomoreaggressiveconditions.
Anxious,depressedstateofmindwillamplifythepainandcreate
agitationafterwhatappearstobeanormaldentalprocedures.
Theproceduremaybefittingofnewdenture.
Treatment
Newdenturesmustbecarefullyadjustedreplicasofthepreviousset
orifpossibleofthenaturalteeth.

101. CONTROL OF PAIN
•Removing the cause
•Blocking the pathway of painful impulses
•Raising the pain threshold-NSAIDS, opiods
•Preventing pain reaction by cortical depression-GA
•Using psychosomatic methods-information, assurance
1 and 2 affect pain perception.
4 and 5 affect pain reaction.
3 affect pain perception and pain reaction.

103. ANTI-INFLAMMATORY ANALGESICS

104. PAIN THERAPY

105. CONCLUSION
Pain is a protective mechanism of the body:
it occurs whenever any tissues are being damaged and it
causes the individual to react to remove the stimulus.

106. REFERENCES
•Okeson–Bell’s orofacial pain, fifth edition
•Cohen-Pathways of the pulp
•Guyton –Textbook of Medical Physiology tenth edition
•Chaudhari–Concise Medical Physiology
•Monheim –Local anesthetic and pain control.
•DCNA–Oct 1987, Apr 1997
•JADA –Apr 2005