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PAIN PATHWAYS
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PAIN PATHWAYS
History
Definition
classification
Theories of pain
Neuroanatomy
Neurophysiology
Transduction
Transmission
Modulation
Perception
Tooth pain
Diagnosis of pain
Management of pain
Conclusion
MEANING OF PAIN
Derived from Greek - “Poin”
Derived from Latin - “Poena”
HISTORY
Homer - arrows shot by the gods
Aristotle - “passion of the soul”
Plato - emotional experience
Bible - anguish of the soul
Freud - solution to emotional conflicts
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DEFINITIONS
Butterworth’s Medical dictionary
International Association for the Study
of Pain (IASP)-
“an unpleasant sensory and emotional
experience associated with actual or
potential tissue damage or described in
terms of such damage”
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”
Multi-dimensional experience:
Sensory-discriminatory
Cognitive
Emotional
motivational
CLASSIFICATION
Duration
Fast/slow pain
Region affected
Etiology
Pain mechanisms
Clinical perspective
IASP CLASSIFICATION
OROFACIAL PAIN
CLASSIFICATION
(Bell’s)
THEORIES OF PAIN
Specificity theory (Descartes-1644)
Intensive/Summation theory
Pattern theory (Goldscheider-1894)
Sensory interactive theory
Gate control theory (Melzac & Wall-
1965)
NEURAL PATHWAYS
Given by Fields-1987
Transduction
Transmission
Modulation
Perception
NEURAL ANATOMY OF
OROFACIAL REGION
“ perhaps the capacity of the human brain
falls short of the ability to understand
its own complexity”
- Thibodeau
NERVE NEURONS
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COMPONENTS OF NERVOUS SYSTEM
FUNCTIONAL
NEUROANATOMY
COMPONENTS OF PAIN PATHWAY
Receptors
Spinal cord
Medulla neurons
Higher
Centres Thalamus
cortex
SENSORY RECEPTORS
GENERAL
SENSES
SPECIAL
SOMATIC VISCERAL
SUPERFICIAL DEEP
Touch-pressure
Thermal
pain
Pain
proprioception
Pain
Baroreception
chemoreception
Visual
Audition
Olfaction
gustation
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
NERVE ENDINGS
NOCICEPTORS
A nerve ending that responds to noxious
stimuli that can actually or potentially produce
tissue damage.
Free nerve endings
By:
thermal
mechanical
chemical
disease
FREE NERVE ENDING
Types of nociceptors
Aδ Mechanical Nociceptors
C Polymodal Nociceptors
C fibre mechanical nociceptors
High threshold cold nociceptors
Receptor mechanism
Noxious stimuli
Tissue damage chemicals
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SENSORY NEURONS
3 types
First-Order Second-Order Third-Order
FIRST-ORDER NEURONS
Classified by Gasser & Erlanger
Classified by Guyton
Classification by Gasser & Erlanger
Classification by Guyton
Group Ia-muscle spindles
Group Ib-golgi tendons
Group II-discrete tactile
Group III-pricking pain,
temp, crude touch
Group IV-burning pain,
itch, temp, crude touch
TYPES OF NOCICEPTIVE AFFERENTS
Mechanothermal afferents
Aδ, 12-18 m/s
Intense thermal & mech
Polymodal afferents
C, 0.5 m/s
Mech, thermal, chemical
stimuli
High-threshold
mechanoreceptive afferents
Aδ
Intense mech, algogenic
substances
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
LAMINA IN
GREY MATTER
DIFFERENT
TRACTS IN
SPINAL CORD
Interneurons
Inhibitory
Excitatory- lamina II & III (Substantia
gelatinosa)
Second-Order neurons
Anterolateral
Spinothalamic tract
Dorsal column-Medial
Lemniscal system
Neospinothalamic tract Paleospinothalamic tract
HIGHER CENTRES
Brain & Brain stem
Brain stem cerebellum diencephalon cerebrum
medulla pons Midbrain
thalamus hypothalamus
cortex Limbic systemBasal ganglia
MEDULLA OBLONGATA
White matter-
projection tracts
White & grey matter-
reticular formation
Vital centres
Nucleus gracilis
Nucleus cuneatus
Olivary nuclei
PONS & MIDBRAIN
PONS
Reticular formation
Reflex centres-5th
,6th
, 7th
,
8th
MIDBRAIN
Tracts to cerebrum
Red nucleus
Substantia nigra
CEREBELLUM
2nd
largest
Skilled movements
Equilibrium
Smooth, coordinated
movements
DIENCEPHALON
THALAMUS
Relay station
between brain stem,
cerebellum &
cerebrum
Directs impulses
HYPOTHALAMUS
Controls internal
body functions
Nuclei
 Upregulates sym NS
CEREBRAL CORTEX
Thinking, memory
5 lobes
Functional areas
Sensory
Motor
Visual
Auditory
Wernicke’s
Tracts
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
TRIGEMINAL SYSTEM
Sensory input
Gasserian ganglion
Trigeminal spinal nucleus
(Medullary dorsal horn)
Second-order neurons
(WDR, NS-Lamina I, II, V,
VI)
thalamus
AUTONOMIC NERVOUS SYSTEM
SYMPATHETIC
SYSTEM
T1-L2
PARASYMPATH
ETIC SYSTEM
Cranial-III, VII,
IX, X
Sacral nerves
TRANSDUCTION
Process by which noxious
stimuli leads to electrical
activity in the appropriate
nerve endings
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
PERIPHERAL SENSITIZATION
Axon transport
system-Subs P,
CGRP-
slow
neurotransmission
Neurogenic
inflammation- Axon
reflex
PAIN FEATURES
Allodynia
Hyperalgesia
Pain spread
Spontaneous activity
TRANSMISSION
The neural events that carry the nociceptive input
into the CNS for proper processing
Nerve action potential
Synapse
Neurotransmitters
 Ascending tracts
NERVE ACTION POTENTIAL
SYNAPSE-INTERNEURONAL JUNCTION
Presynaptic terminals
Synaptic vesicles
Mitochondria
Calcium channels
Receptor proteins
Binding area
Ionophore component
-Ion receptors
-Enzyme receptors
SYNAPSE
NEUROTRANSMITTERS
These are neurochemicals that transmit
impulses across the synaptic cleft
Small rapid-acting Large slower-acting
Molecules Molecules
RAPID-ACTING MOLECULES
Acetylcholine
Norepinephrine
 Glutamate
Aspartame
 Serotonin
• Gamma-aminobutyric acid
• Glycine
• Dopamine
• Histamine
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
TRACTS-TRANSMISSION TO CORTEX
Nociception from
orofacial region-
via trigeminal nerve,
VII, IX, X, 1st
, 2nd
, 3rd
cervical nerve
Cross to opp side-
ANTEROLATERAL
SPINOTHALAMIC
TRACT
Neospinothalamic tract-
Aδ-lamina I-thermal,
mech- fast pain
Paleospinothalamic
tract-
C-Lamina II, III, V-
modulation-slow pain
FAST & SLOW PAIN
FAST PAIN
Thermal, mech stimuli
Easily localised, sharp, Aδ
Directly to thalamus
(ventrobasal complex)
cortex (somatosensory
area) -motor cortex-
muscle actionreflex
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
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
20th
century
Pain comprises organic & psychogenic features in
a unified sensory & emotional experience
Alteration/modulation of impulses as they go to
higher centres-FACILITATION & INHIBITION
Perception & reaction-facets of same mechanism
NOT separate components
GATE-CONTROL THEORY
Melzac & Wall (1965)
Conceptual model of sensory, motivational,
central control determinants of pain(1967)
MODULATION IN TRIGEMINAL
SPINAL TRACT NUCLEUS
Revised version of Gate control theory(1987)
TRANSCUTANEOUS ELECTRIC
NERVE STIMULATION (TENS)
MODULATION IN RETICULAR
FORMATION
Nuclei-excite/inhibit
Neurotransmitter-acetylcholine
Pain signals-increase activity-excite the brain
Descending impulses excited
Positive feedback mech
Chronic pain-sleep disruption
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
Neurochemicals:
Opiods-enkephalins,
endorphins, dynorphins
Serotonin(5-HT)
Noradrenaline
GABA
Sites for endorphins:
µ, κ, δ receptors
Periaqueductal grey
Limbic structures
Thalamic nuclei
Raphe nuclei
V subnucleus caudalis
Peripheral tissues
Inhibition at SG
Serotonin-chronic
pain
β-endorphins-acute
pain
local effects
of non-noci
pri afferents
descending
inhibitory mech-
NRM
(serotonin),PAG
CLINICAL APPLICATIONS
TENS-DIS-serotonin (brain), dynorphin (spinal cord)
ACUPUNCTURE & ELECTROACUPUNCTURE-endogenous
antinociceptive system-enkephalins, β-endorphin
 HOKU POINT
HYPNOSIS-endogenous opiods
DIFFUSE NOXIOUS INHIBITORY CONTROLS (DNIC)
MECHANISMS-counter-irritation
MODULATION BY PSYCHOLOGICAL
FACTORS
excitatory inhibitory
Egocentric conditions
Expectancy
Anxiety
Fear
Depression, despair
Outgoing conditions
Confidence, reassurance
Distraction
Suggestion & hypnosis
Mental absorption
Physical activities
OTHER MODULATION FACTORS
physical characteristics of stimulus:
Modality
Location direct bypass to cortex
Intensity
Duration
CONVERGENCE
Synapsing of several
primary afferent neurons
with 1 second-order
neuron
Summation
Facilitation/inhibition
Deeper afferent input
convergence > cutaneous
structures- diffuse, less
localized
MECHANISMS OF CONVERGENCE
COVERGENCE SUBLIMINAL FRINGE
EFFECT
Convergence-projection theory
Convergence-facilitation theory
CONVERGENCE IN TRIGEMINAL SYSTEM
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
MECHANISM OF CENTRAL SENSITIZATION
Neuroplastic change-
depends on peripheral noci
afferent input for initiation
BUT NOT on it for its
maintainance
 Persistent, spontaneous
pain
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-
Muscle co-
contraction
Myofascial
trigger points
Vasomotor
effects
Glandular
effects
CO-CONTRACTION
REFERRED PAIN
site of pain primary pain
heterotopic pain
source of pain
HETEROTOPIC PAIN
Central pain Projected pain Referred pain
MECHANISM OF REFERRED PAIN
CONVERGENCE
CENTRAL
SENSITIZATION
FEATURES OF REFERRED PAIN
FEATURES:
Wholly spontaneous
Not accentuated by provocation of site
Ceases immediately if primary pain is
arrested
Felt in superficial or deep structures
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
CLINICAL CORRELATES FOR PULPAL PAIN
VISCERAL PAIN
Receptors only for pain
Only activated by diffuse stimulus-not localized
Mainly C fibres-in sympathetic nerves-Chronic-
aching-suffering type of pain
CAUSES:
Ischaemia
Chemical stimuli
Spasm/overdistention of hollow viscus
 PULPAL PAIN
SUMMARY OF PATHWAY
PERCEPTION
Final process in the subjective
experience of pain.
Interactions between higher centres
determines suffering & pain behavior
Psychological aspect of pain-affects ALL
PAINS
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
MECHANISTIC MODEL vs.
BIOPSYCHOSOCIAL MODEL
“BIO”-nociceptive
input from somatic
tissues
“PSYCHOSOCIAL”-
interaction between
thalamus, cortex,
limbic system
CHRONIC PAIN
ACUTE PAIN:
Short duration
somatic tissue changes
CHRONIC PAIN:
lasts longer than normal healing time
 PSYCHOGENIC INTENSIFICATION
MECHANISMS MODIFYING CHRONIC PAIN
PHYSIOLOGICAL MECHANISMS:
Sensitization
Spreading muscle spasm
Autonomic factors
PSYCHOLOGICAL FACTORS:
Cognitive & affective factors
Behavioral factors-secondary gains
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 diff treatment
Increased anxiety
Obsessive concern with suffering
Physical & emotional deterioration
Decreased self-esteem
Decreased ability to obtain pleasure
Substance use disorders
DIFFERENCE BETWEEN ACUTE &
CHRONIC PAIN(DCNA, 1987)
PSYCHOGENIC PAIN
Unpleasant sensation that has no organic
basis-“Rare” diagnosis!!
Present if psychopahology is revealed
Chronic pain-pain behavior
Hypochondriasis
Somatization
Malingering
Munchausen syndrome
Management-antidepressants, antipsychotics
SUMMARY OF TYPES OF PAIN
Acute or chronic
Primary or heterotopic
Inflammatory or non-inflammatory
somatic neuropathic
musculoskeletal visceral
PULPAL PAIN
TOOTH INNERVATION:
Myelinated & unmyelinated-2-4 µm
Extensive branching- ratio 1:3
2 types of pulp axons
Afferent sensory fibres Autonomic efferent
Substance P
CGRP
acetylcholine
Norepinephrine
Vasoactive peptide
SIGNIFICANCE OF EXTENSIVE BRANCHING
Various levels of branching:
Large no. of dentinal tubules
Accessory foramina
Multiple teeth
Significance:
Poor localization of tooth ache
Lack of paraesthesia
Reinnervation and regeneration
INTRADENTAL RECEPTORS
RECEP
TOR
SITE ACTIVATOR SENSATION
FELT
P2X3 Subodontoblas
t plexus
Drilling, mech
stimulus, air-blast
Sharp pain
TRPV1 Pulp-Aδ, C
fibre
Polymodal-low pH,
intense heat (>45°),
inflam
Dull pain
TRPV2 Pulp-Aδ, Aβ
fibres
Mech,
High heat (>50°)
Pain
ASIC pulp inflam Pain
Opiod -µ pulp Attenuating
pain
SENSORY AFFRENT FIBRES
Aβ Aδ Aδ C FIBRE
LOCATIO
N
dentin dentin
(pulpodentinal
complex)
pulp Central part of
pulp
RESPOND
S TO
Vibration,
purely
mechanorec
eptive (non-
nociceptive)
Probing, drilling,
air-drying, mech
irritation,
hyperosmotic
solution
Polymodal:algoge
nic chemicals,
intense heat/cold,
mech stimulation
(deep cavity)
PAIN
QUALITY
Pre-pain,
Sharp, well
localized
dentinal pain
Sharp, well
localized,
momentary,
dentinal pain
unclear Poorly-localised
dull pain, radiating
pain
HYDROD
YNAMIC
Yes Yes No No
PEPTIDE CGRP CGRP CGRP CGRP, Subs P
DENTINAL SENSITIVITY
IMPORTANT CLINICAL ASPECTS:
Aδ fibre pain- pulpodentinal complex intact
Necrotic teeth-(+) vitality, pain - C fibres
“hot teeth”-TTXr sodium channels of C fibres
PERIPHERAL MECHANISMS--NEUROGENIC
INFLAMMATION
Nociceptors-Subs P, CGRP
Cracks/injury-sprouting of nerves
-hypersensitivity
Branching of fibres
-poor localization of pain
-peripheral sensitization of adjacent teeth
CENTRAL NEURAL MECHANISMS
“onion-skin” pattern of organisation- referred pain
Convergence-poor localization, referred pain
Neuroplasticity & central sensitization
-spontaneous pain
-allodynia
-hyperalgesia
-Spread & referral of pain
Thus, IRREVERSIBLE PULPITIS
ACUTE CHRONIC PAIN
 Endodontic treatment/extraction-rarely cause
neuropathic pain due to neuroplastic changes
CLINCAL CORRELATES-TOOTHACHE
Pre-pain: electric stimulation
Mech stimulation: discomfort to patient
REVERSIBLE PULPITIS:
Peripheral sensitization
sharp, short-lasting, intense
IRREVERSIBLE PULPITIS:
Central sensitization
Dull, long-lasting, radiating
PAIN IN ENDODONTICS
Usually due to periapical inflammatory reaction
NO. OF HYPOTHESES (SELTZER):
Effect of chemical mediators
Alteration of local adaptation syndrome (Selye, 1953)
Changes in periapical tissue pressure (Mohorn et al,
1971)
Microbial factors (Sundqvist, 1976)
Changes in cyclic nucleotides (Sproles et al, 1979;
Bolanos & seltzer, 1981)
cAMP
cGMP
Imunological phenomena
Humoral immunity- Johannessen et al (1986)
Cell-mediated immunity- Cymerman et al (1984)
Psychological factors
(Scott & Hirschman, 1982; Berggen & Meynert, 1984)
DIFFERENTIAL DIAGNOSIS
“What you don’t know-
you won’t diagnose”
- Sir William Osler
DIFFERENTIAL DIAGNOSIS FOR
PULP PAIN
Hyperreactive pulpalgia
Dentinal hypersensitivity
Hyperaemia
Acute pulpalgia
Incipient
Moderate
Advanced
Chronic pulpalgia
Barodontalgia
Hyperplastic pulpitis
Necrotic pulp
Internal resorption
Traumatic occlusion
Incomplete fracture
DIFERENTIAL DIAGNOSIS OF
NONODONTOGENIC TOOTHACHE
(DCNA, 1987, 1997)
Toothache of MYOFASCIAL ORIGIN
Myofascial trigger points
Toothache of NEUROVASCULAR ORIGIN
Periodic migrainous neuralgia-cluster headache
Toothaches of CARDIAC ORIGIN
Angina pectoris
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)
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.
ANTI-INFLAMMATORY ANALGESICSANTI-INFLAMMATORY ANALGESICS
PAIN THERAPY
CONCLUSION
“Pain is not a sensation,
it is an experience”.
-Dr Welden. E.Bell
REFERENCES
Okeson - Bells orofacial pains
Timothy Miles – Clinical Oral Physiology
Malcolm Harris – Clinical Oral Science
Bradley - Essentials of oral physiology
Ingle - Endodontics
Seltzer-Endodontology
Cohen- Pathways of the pulp
Guyton – Textbook of Medical Physiology
Chaudhari – Concise Medical Physiology
Monheim – Local anesthetic and pain control.
DCNA – Oct 1987, Apr 1997
JADA –Apr 2005
Seeley- Anatomy & Physiology
De Graaff, Ira Fox-Concepts of Human Anatomy
& Physiology
Sherwood- Human Physiology from Cells to
Systems
Malvin Ring- Dentistry, an Illustrated History

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