Pain pathway theories of pain

Pain pathway gate control theory
Pain management
An unpleasant emotional experience usually initiated by noxious stimulus and transmitted over a specialized neural network to CNS where it is interpreted as such.
1. Exteroceptors: arising from receptors from skin & mucosa. sensed at conscious level
E.g. Merkel corpuscles : Tactile receptors.
Free Nerve ending :Perceive superficial pain.
2. Proprioceptors : From musculoskeletal structures.
The presence , positions & movement of body. below conscious levels.
E.g. 1) Muscle spindles : Skeletal muscle fibers. Mechanoreceptors.
2) Free nerve ending : Perceive deep somatic pain & other sensations.
3. Interoceptors : From viscera of body below conscious level.
E.g. Pacinian corpuscles : perception of touch-pressure.
Free nerve ending : Perceive visceral pain & other sensations.

1. Presented By:
Dr. KaminiDadsena

2. Outline :

3. Introduction

4. Pain
International association for
the study of pain (IASP) (WHO)

5. Pain
Bell

6. Pain
Monheim

7. Changing concepts of pain :
1.protective mechanism
2.localized sensation as a result of noxious
stimulation.

8. Changing concepts of pain :
1.Cognitive
2.Emotional
3.Motivational

9. Types of pain
1)Experimental
2)Transient
3)Acute pathological pain
4)Chronic pathological pain

10. Types of pain
1.somatic
a.Superficial
b.Deep
2.visceral

11. Types of pain
1.Referred pain
2.Phantom pain

12. Classification of oro-facial pain:
A.Somatic Pain
a)Superficial Pain
i.cutaneouspain
ii.mucogingivalpain
b)Deep Pain
i.musculoskeletal pain
ii.visceral pain
B.Neuropathic Pain
a)Episodic Pain
i.paroxymalneurologic
ii.neurovascular
b)Continuous Pain
i.Central mediating
ii.Peripheral mediating
iii.Metabolic poly neuropathies
•Mood disorders
•Anxiety disorders
•Somatoform disorders
•Malingering
•Psychological factors affecting
a medical condition
•Any other mental disorders

13. Classification of oro-facial pain:
1.Inflammatory Pain
2.Non Inflammatory Pain –
poorly understood , psychic, chronic
Tissue injury
Prostaglandin&
Bradiyinin
Local vasodialation&
capillary permeability
Receptors Noxious
Stimuli
pain

14. 1. Exteroceptors
i.Merkel corpuscles
ii.Free Nerve ending
2. Proprioceptors
i.Muscle spindles
ii.Free nerve
3. Interoceptors
i.Paciniancorpuscles
ii.Free nerve ending
Pain Receptors:

15. Three types of stimuli excite pain receptors

16. Neurotransmitter for Aδand C Fibers :
Glutamate transmitter gives a faster pain
sensation, while the substance P transmitter gives
more lagging sensation.

17. MECHANISM OF PAIN CAUSATION :

18. MECHANISM OF PAIN CAUSATION :

19. Neural pathway of pain : Field
•Transduction
•Transmission
•Modulation
•Perception

20. DETAILS OF PAIN PATHWAY:
(BASICS OF PAIN TRNSMISSION)
pain sensation to reach the cortex from the nociceptors it
requires three neuron sets.

21. FIRST ORDER NEURONS :
SPINAL CORD
•Three classes of nociceptive afferent neurons provide the
input whereby the brain perceives pain.
1.Mechanothermalafferents are primarily A∂ fibers respond to
intense thermal and mechanical stimuli.
2.Poly modelafferent c fibers, conduct more slowly, respond to
mechanical, thermal and chemical stimuli.
3.High Thresholdmechanoreceptiveafferents are chiefly A ∂
Fiber normal respond to intense mechanical stimuli.

22. Classification of Nerve fibers
Gasser and Erlanger
Class of nerve
fiber
Diameter of
fiber (in mµ)µ
Velocity of
conduction
(m/sec)
Identity of nerve
Aα 22 –12 120 –70 Motornerve (somatic)
Proprioceptive(sensory)
A β 12 –6 70 –30 Afferent for touch
Aγ 6 –3 30 -15 Motor nerve to the intrafusal
muscle of spindle
Aδ 5 –2 30 –12 Afferent for thermal senes
B 2 10 –3 Preganglionicfibers of autonomic
system
C 1.5 -O.3 2 -0.5 Afferent for pain, post ganglionic
sympathetic

24. Three classes of nociceptive afferent neurons
provide the input whereby the brain perceives pain.
1.Mechanothermalafferents are primarily A∂
fibers respond to intense thermal and mechanical
stimuli.
2.Poly modelafferent c fibers, conduct more
slowly, respond to mechanical, thermal and
chemical stimuli.
3.High Thresholdmechanoreceptiveafferents are
chiefly A ∂ Fiber normal respond to intense
mechanical stimuli.

25. 2nd Order neurons :
2nd Order neurons (Transmission cells)
transferthe impulseontohighercenters.
Dorsal horn of spinal cord
Types :
1.LowThreshold mechanosensitive neuron (LTM)--light touch, pressure &
proprioception.
2.
Nociceptive Specific neurons (NS) --exclusively carry impulse related to noxious
stimulation.
3.Wide dynamic range neuron (WDR) --Neurons are able to respond to a
wide range of stimulus intensities from nonnoxious to noxious.

26. Central processing of pain :
•Convergence:
moreprimaryafferent
neuronsenterCNS
than2
nd
orderneurons,
and2
nd
orderneurons
aremoreinnumber
than3
rd
orderneurons.
1
st
orderneuron
synapse
2
nd
orderneuron
synapse
3
rd
orderneuron

28. Nonadaptingnature of pain receptors:

29. Dual pain pathways of pain in
the spinal cord and brain stem :
On entering the spinal cord, the pain signals take two
pathways to brain 1. Neospinothalamic.
2. Paleospinothalamic.

30. Neospinothalamic tract :
•The fast type Aδ pain
fibers --mechanical and
acute thermal pain.
•Terminate mainly Lamina I
(Lamina marginalis)
•Excites 2nd order neurons
of the Neospinothalamic
tract.
•fibers --cross --opposite
side of the cord through
ant.commisure --pass
upward to the brain stem
in the anterolateral
column.

31. Termination of Neospinothalamic tract in Brain stem
and Thalamus :
reticular areas.
thalamus ventral posteolateral
nucleus (VPL).
post. Nuclear gr of thalamus (PO)
THALAMUS
basal areas of the brain somatosensory cortex.
(Post central gyrus)

32. Capability of Nervous system to localize fast pain in
the body :

33. PALEOSPINOTHALAMIC TRACT :
•Transmits pain by C fibers --
terminate --laminae II & IIIof the
dorsal horns,
(SUBSTANTIA GELATINOSA
ROLANDI).
•Most of the signals pass by
additional short fiber neurons to
lamina V.
•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 .
commisureto opposite side of cord.
Then upwards to brain in
anterolateral pathway.

34. Termination of Paleospinothalamictract in CNS :

35. Localization of pain :

36. NEURONAL TRANSMISSION IN THE HEAD
AND NECK REGION :
PAIN PATHWAY OF
HEAD AND NECK
REGION
FROM THE
ANTERIOR ASPECT
FROM THE
POSTERIOR
ASPECT
FACE, MOUTH, TEETH AND EYES
Through cranial nerves.
(Gasserianganglion)
POSTERIOR ASPECT OF
HEAD AND NECK
Through spinal nerves.
(Dorsal root ganglion)

37. Pathways Of Pain To OrofacialRegion :
AREA SUPPLIED
Skin of face, fore head, scalp conjunctiva, oral
and nasal mucosa, anterior 2/3 of tongue,
masticatorymuscles, TMJ.
Skin of the hollow of the auricle of external ear
and small area of skin behind ear.
Mucosa of pharynx, palatine tonsils, posterior
1/3
rd
of tongue, skin of external ear.
Pharynx, larynx, skin at the back of the ear,
posterior wall of external auditory meatus.
Lateral, posterior and back of the head and neck.
NERVES
TRIGEMINAL N (V)
FACIAL N (VII)
GLOSSOPHARYNGEAL N (IX)
VAGUS N (X)
CERVICAL (2 & 3)

38. PATHWAYS OF PAIN FROM OROFACIAL REGION
TRIGEMINAL
PATHWAY
BRAIN STEM
THALAMUS
SPINOTHALAMIC
PATHWAY
SPINAL CORD
THALAMUS
CORTEX

39. The Trigeminal system –BELL
•Sensory input from
face and mouth
carried by 5
th
cranial
nerve.
•The cell bodies of
Trigeminal afferent
neurons located in the
large gasserian
ganglion.

40. Sensory afferent pass to
1.Mesencephalic nucleus – Proprioception.
2.Principal nucleus -Touch, Pressure.
3.Spinal nucleus - Pain, Temp.
Fibers from all 3 divisions
Ascending Br. Descending Br.
Touch, Pressure. Touch, Pressure, Pain, Temp.
Principal nucleusSpinal tract of Trigeminal N.
( C-2 or 4)

42. Trigeminal nuclei
The sensory trigeminal nerve nuclei
1.The mesencephalicnucleus
-proprioception
2.The chief sensory nucleus (or
"pontinenucleus" or "primary
nucleus") –touch
3.The spinal trigeminal nucleus
–pain & temperature.

43. Fibers nearest to lips terminate highest in nucleus caudalis
Applicable to all three divisions
Fibers mediating pain

44. Secondary pathways :
1.Fibers from principal nucleus -Cross the midline -
Along with Medial Lemniscus -Thalamus
(Ventroposteromedial Nucleus)
2.From Spinal nucleus—Homologous to
Neospinothalamic tract
3.From Spinal nucleus—Reticular formation

45. Pathwayfromdentalpulptocortex:-(mand.molar)
•Oncethenociceptorslocatedinthepulpactivated,
•theimpulseiscarriedintotheCNSbyprimaryafferentneuroninthe
mandibularbranchof5
th
nerve.
GASSERIAN ORTRIGEMINAL GANGLION.
nucleuscaudalis.
(Thenucleusoralismayalsoplayimp.,roleinnociceptionofintra-oral
structure).
.
Fast pain Slow pain
Thalamus Reticular formation
Sensory cortex

46. Dental pain of pulpal origin ;

47. Dental pains of PDL origin;

48. Theories of pain :

49. Intensity theory :
•True for nerves mediating the sensation of touch temperature.
Trigeminal neuralgia --?

50. Specificity theory :
JohnnesMuller, 1842
Direct line From receptor to Brain.

51. pressure warmth vibration pain
Touch

52. Protopathic& Epicritictheory
(Head & Rivers -1908) :

53. Pattern theory :
Goldscheider[1894]
•Proposesthat pain is generated by non specified
receptor.
•Pain sensation depends upon the spatio-temporal
pattern of nerve impulses reaching the brain.
•Pain,warmth,cold--codes of neural activity evoked
from the skin by changes in its environment
•Nerve impulse entering CNS –Diff. For diff. region
and will vary from fromperson to person due to
anatomical variation
•A stimulus evoke certain pattern that the brain
receives and recognizes.
•Receptors not specialized as in SPECIFICITY theory

54. CHEMICAL MESSENGERS
ENDORPHINS, ENKEPHALINS,
GABA.
Produced in the brain.
These act as pain Inhibiting
substancesand Increase the
patients pain threshold.
SUBSTANCE- P
Produced in the sensory
Nerve, spinal cord pathways
and some parts of brain
they acts as pain stimulant
and facilitate pain transmission
+
-
The balance between these two groups of chemical messengers determines
the pain out come.
CHEMICAL THEORY :

55. 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
LINDAHL BIOCHEMICAL THEORY :

56. Modulation of pain :
gate control theory.

57. Gate control theory :
•Noordenbos (1959) postulated, the fast fibers exert
an inhibiting influence on slowly conducting fibers.
Ronald melzack and patric Wall-1960.

58. 1.Information about the presence of injury is transmitted to the
central nervous system by small peripheral nerves.
2.Cells in the spinal cord or nucleus of the fifth cranial nerve, which
are excited by these injury signals, are also facilitated or inhibited
by other large peripheral nerves that also carry information
about innocuous events (for example, temperature or pressure).
3. Descending control systems originating in the brain modulate the
excitability of cells that transmit information about injury.
Gate control theory postulates

59. •Therefore, the brain receives messages about injury by way of
the gate control system, which is influenced by
(l) injury signals
(2) other types of afferent impulses, and
(3) descending control
Gate control theory postulates

60. –Large myelinated fibers-3 to 20 micron in dia
–Carry fast pain at rate of 100 meter / sec
–Unmyelinated small fibers-0.05 to 1 micron in
dia
–Conduct slow pain at 0.5 to 2 meter / sec

61. Sustantiagelatinosa

63. •The signal that triggers the action system responsible
for pain experience and response occurs when the output
of transmission cells reach or exceeds the critical levels.
•The brain is able to control over, sensory input by
means of its descending fibers, depending upon attention
, emotion, memories of past experience , anticipation
anxiety and suggestion, hypnosis etc.
•Soothing effect by rubbing over toothache.

65. •An important aspect of the gate control theory is the ability of
nervous System centerslocated within the brain to either
facilitate or inhibit neural transmission at first synaptic levels.
•Another system descends in directly from the periaqueductal
graymatter of the midbrain to the substantia gelatinosa .
Stimulation of this area produces profound analgesia in humans
and animals
•The descending system may be activated by pharmacological or
psychological factors.
•It has long been recognized that “mind set“ may alter an
inditidual’sability to tolerate pain.
Descending control

66. •As early as the first World War Beecher noted that battle
casualties tolerated their injuries more easily than civilians at
home suffering similar traumas.
•
More recently, medical and dental professionals have come to
realize that fear, anxiety, and apprehension only serve to
heighten an individual's painful experience.
•Conversely, elimination of these aspects either by
pharmacological or psychological methods greatly increases a
person’s ability to tolerate noxious stimuli most probably by
activating descending control mechanisms
Descending control

67. REFERRED PAIN :
Referred pain frequently occurs within a single nerve root, passing from one branch to another.
Eg. Mandibular molar presenting with a source of pain will commonly refer pain to a maxillary
molar. This is fairly common occurrence with dental pain.

68. 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. For example, if the pain fibers traveling in
the ulnar nerve are stimulated at the elbow, the pain is still
perceived to originate in the hand. This phenomenon is called
projected pain.

69. Phantom pain :
Thephantomlimbsometimesalsoexperiencespain,whichis
knownasphantompain.Thisphenomenonisbasicallybecausethe
brainhasbeeninterpretingsignalsconveyedbythosenervefibers
ascomingfromthelostlimb.
Followingtheamputationoflimb,thecutendsofseverednervesinnervatethe
skincoveringthestump.Stimuliexistingthenervefibersatthestumpare
interpretedasoriginatinginthelimbwhichdoesnotexistanymore.

70. Endogenous Pain Relief System :

71. Gate Control Theory Revisited :
Winnie a reg anesth1989

72. DIAGNOSIS OF PAIN:
1.Accurately identifying the location.
2.Establishing the correct pain category (genesis
and mechanisms of pain).
3.Choosing the particular pain disorder that
correctly accounts for the incidence and
behavior of the patient`s pain.

73. Features to include in an oro facial pain history;
–Location of pain
–Onset of pain
•Associated factors
•Progression
–Characteristics of pain
•Quality of pain
•Behavior of pain
–Temporal
–Frequency
–Duration
•Intensity
•Concomitant symptoms
•Flow of the pain

74. –Aggravating and alleviating factors
•Physical modalities
•Function and parafunctions
•Sleep disturbances
•Medications
•Emotional stress
–Past consultation & treatments
–Relationships to other complaints

75. TOOLS TO MEASURE DEGREE OF PAIN OR
DISCOMFORT :

76. Visual analog scale :

77. Age and measures of pain intensity. -
McGrath PJ et al (1990)
Age Self-report
measures
Behavior
Measures
Physiologic
measures
Birth-3 years Not availableOf primary
importance
Of secondary
importance
3-6 years Specialized,
developmentally
appropriate
scales available
Primary if self-
report not
available.
Of secondary
importance.
>6 years Of primary
importance
Of secondary
importance
Of secondary
importance.

78. MANAGEMENT OF PAIN:
Special emphasis of pain management
Management of pain should primarily encompass two essential elements
Pain perception control Pain reaction control
Raising the level of pain threshold
1.Removing the cause
2. Blocking the path way
of painful impulses
Ex: GA
LA
•Analgesics
-non narcotics
-narcotics
-NSAID`s
-muscle relaxants
-antideprassents etc.
1.Preventing pain reaction
by cortical depression.
2.Using psychosomatic methods.
Ex: Conscious sedation.
Behavior management

79. Other methods of Pain control :
•Counterirritation
•Cutaneousstimulation-heat,cold,massage
•Electricalstimulation
•Biofeedback
•Relaxation

80. Surgical interruption of pain pathway :

81. CONCLUSION :

82. REFERENCES :
1.
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