The document discusses the history, components, receptors, pathways, and management of pain. It provides definitions of pain and its various theories. It describes the transduction, transmission, modulation, and perception of pain. Non-pharmacological interventions like rest, modalities, and exercises are outlined. The pharmacological ladder includes non-opioid analgesics like NSAIDs that reduce inflammation. Opioids and other drug classes that help manage pain are also summarized.

1. PRESENTED BY :: Dr N
Kumar

2. – BY DR ALBERT
SCHWEITZER

3. History
 Latin word ‘poena’ – punishment from
God.
 Aristotle - first to distinguish 5 physical
senses and considered pain to be the
‘passion of the soul’
 Plato – contented pain and pleasure arose
from within the body.

4. Tumor -
Swelling
Calor - Heat
Dolor -
Pain
Rubor -
Redness
Functio
laesa -
loss of
function

5. An unpleasant sensory and emotional
experience associated with actual or potential
tissue damage or described in terms of such
damage.
- IASP
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

7. Components of pain
 Fast pain
 Slow pain
FIBRE
TYPE
FUNCTION CONDUCTION
VELOCITY
(minutes /
sec)
SPIKE
DURATION
(milisec)
Myelinated
Fibres
Aα Proprioception, somatic motor 30-120
0.4-0.5
Aβ Touch, pressure and motor
function
30-120
Aγ Motor to muscle spindles 15-35
Aδ Pain, temperature, touch 5-25
Myelinated
fibres
B Preganglionic autonomic fibres 3-15 1.2
Unmyelina
ted
Fibres
sC
(dorsal
root)
Pain, temperature, touch and
conducts impulses generated by
cutaneous receptors
0.7-1.3 2
d γ C Postganglionic sympathetic fibres 0.1-2.0 2

8. Sensory
receptor
s
Affere
nt
neuron
Ascendin
g tracts
Somatosenso
ry cortex
Efferent
neurons
Descending
tracts
SENSORY
COMPONENT MOTOR
COMPONENT

9. Development of Nociceptors
 Develop from neural crest stem cells.
 Neural crest cells are responsible mainly
for development of the peripheral
nervous system.
 Cells split off from the neural tube as it
closes, and nociceptors grow from the
dorsal part of this neural crest tissue.

10. Nociceptor
 Sensory input from various stimuli (either
external or internal) is received by specific
peripheral receptors, called as nociceptors.
 Nociception – responds as transducers and
transmit impulses.
 Perception of pain.
 Found in all areas of body.

11.  External nociceptors – skin, cornea and
mucosa.
 Internal nociceptors –
muscle, joint, bladder, gut and continuing
along the digestive tract.
 Cell bodies of these neurons are located in
either the dorsal root ganglia or
the trigeminal ganglia.

12. TRACT SITUATION FUNCTION
Anterior spinothalamic
tract
Anterior white funiculus Crude touch sensation
Lateral spinothalamic
tract Lateral white funiculus
Pain and temperature
sensation
Ventral spinocerebellar
tract
Subcutaneous
kinaesthetic sensation
Dorsal spinocerebellar
tract
Subcutaneous
kinaesthetic sensation
Spinotectal tract Concerned with
spinovisual reflex
Fasiculus dorsolateralis Pain and temperature
sensation
Spinoreticular tract Consciousness and
awareness
Spinoolivary tract Proprioception
Ascending pathways

13. FIRST ORDER
NEURONS
(Posterior nerve
root ganglia)
SECOND ORDER
NEURONS
(Substantia
gelatinosa)
THIRD ORDER
NEURONS
(Thalamic
nucleus, reticular
formation,
tectum, gray
matter)
SOMATOSEN
SORY
CORTEX
Sensory Neurons

15. Neospinothalamic fibres Paleospinothalamic fibres

16. Descending pathways
TRACT SITUATION FUNCTION
Pyramidal
Tracts
Anterior
corticospinal tract
Anterior white funiculus Voluntary movements
Lateral
corticospinal tract
Lateral white funiculus
Extrapyramidal
Tracts
Medial
Fasciculus
Anterior white funiculus Coordination of reflex-ocular
movements
and integration of
of eyes and
neck
Anterior
vestibulospinal
tract
Anterior white funiculus Maintains muscle tone and
posture
Position of head and body
during
acceleration
Lateral
vestibulospinal
tract
Lateral white funiculus
Reticulospinal
tract
Lateral white funiculus Controls voluntary and reflex
movements,
muscle tone, respiration and
blood vessels
Tectospinal tract Anterior white funiculus Movement of head in
response to visual

17. Neurophysiology of Pain
TRANSDUCTION
TRANSMISSIO
ON
MODULATION
N
PERCEPTION

18. Transduction
 Activation of nociceptor.
1. Intense thermal and mechanical stimuli,
noxious chemicals, noxious cold
2. Stimulation of inflammatory mediators
 Damaged tissue release bradykinin,
potassium, histamine, serotonin and
arachidonic acid.
 Arachidonic acid produce prostaglandins and

19. • Bradykinin + Leukotriene +
Prostaglandin
Plasma extravasation
Edema
• PG stimulate nociceptors directly.

20.  LK stimulates nociceptors indirectly by
PMNs
Release chemical mediators
Stimulates nociceptor
 BK causes sympathetic nerve terminal to
release PG thus stimulates nociceptor.

21.  Sympathetic nerve terminal release
another PG in response to its own
neurotransmitter (norepinephrine).
 Such ongoing inflammatory state causes
physiologic sensitization of nociceptors
thus generating a response even to a non-
painful stimuli and exaggerated response
to noxious stimuli.

22. Transmission
 Process by which peripheral nociceptive
information is relayed to CNS.
 First order neuron synapses with the
secondary order neuron from where
impulse is carried to higher structures of
brain.
 Repeated or intense C fibre activation
brings specific changes on N-methyl-D-
aspartate receptors resulting in central
sensitization, thus, response of secnd
order neurons increases as well as size of

23. Modulation
• It is the mechanism by which transmission
of impulse to the brain is reduced.
• Nociceptive transmission is influenced by :
a) Descending inhibitory systems that
originate supraspinally
b) Periaqueductal gray
c) Nucleus raphe magnus
d) Nucleus tractus solitarius
e) Locus ceruleus/subceruleus
f) Endogenous opioid peptides

24.  Endogenous opioid peptides are
naturally occurring pain-dampening
neurotransmitters and
neuromodulators employed in
suppression and modulation of pain
because they are present in large

25. Perception
 It is the subjective experience of pain.
It is the sum of complex activities in
CNS that may shape the character and
intensity of pain perceived and ascribe
meaning to pain.

26. Theories of pain
 Intensity Theory
 Specificity Theory
 Pattern Theory
 Gate Control Theory

27. Intensity theory
 Erb in 1874.
 Pain is a non-specific sensation and is
produced only during high intensity
stimulation.
 Not accepted – Trigeminal neuralgia,
patient can suffer excruciating pain even
when the stimulus is no greater than

28. Specificity theory
 Von Frey in 1895.
 Body has a separate sensory system for
perceiving pain, just as it does for hearing
and vision i.e. Meissner corpuscles - touch,
Ruffini end organs - warmth, Krause end
organs - cold, nociceptors – pain.
 Disapproved - it does not account for the

29. Pattern theory
 Goldschneider in 1920.
 There is no separate system for perceiving
pain and pain receptors are shared with other
senses, such as of touch.
 Peripheral sensory receptors, responding to
touch, warmth and other non-damaging as
well as to damaging stimuli, give rise to non-

30. Gate control theory
 Ronald Melzack and Patrick Wall in 1965.
 Variation in relative input of neural impulse
along large and small fibres.
 Small fibres - relay impulses to the cells of
substantia gelatinosa
 Large fibres relay impulses - marginal cells of
posterior gray horn because cells of substantia
gelatinosa terminate on small fibres just when

31.  Large fibres has the ability to modulate
synaptic transmission of small fibres within
the dorsal horn.
 Large fibres creates a hypothetical gate
that can open or close the system to pain
stimulation.

32. 3 factors for opening and closing of gate:
 Amount of activity in pain fibres.
 Amount of activity in peripheral fibres -
These fibers are called as Aβ fibres and
carry information about harmless stimuli or
mild irritation such as touching, rubbing, or
lightly scratching the skin. Activity in these
fibers tends to close the gate in the
presence of noxious stimuli and thus inhibits

33.  Impulses that descends from the brain –
Impulses sent by neurons located in
brainstem and cortex can open or close the
gate. The effects of some brain processes
opens or closes the gate for all inputs from
any areas of the body. But the impact of
other brain processes may be very specific,
applying to only some inputs from certain
parts of the body. This explains the fact that

36. Management of pain
Non-pharmalogical interventions
• Bed rest
• Distraction
• Therapeutic modalities
a. TENS
b. Superficial heat
c. Ultrasound
d. Cryotherapy
e. Acupuncture
• Exercise
• Hypnosis
Pharmacologic interventions
• Non-opioids analgesics
• Opioids analgesics

37. NON
PHARMACOLOGICAL
MANAGEMENT

38.  Bed rest – Bed rest may be beneficial to
allow for reduction of significant muscle
spasm brought on with upright activity.
 Distraction – It is nothing but just diversion
of one’s attention from pain to something
else as people has a ability to turn their
attention away from objects and events.

39.  TENS (Transcutaneous Electrical Nerve
Stimulation) – It is the local stimulation
of sore sites and strong neurologic sites in
the region of pain, followed by stretching
of the stiff muscle. Electrodes are placed
directly on the skin.
 Chronic pain conditions not in acute pain.

40.  Superficial heat – It is superficial heating
modality limited to a depth of 1-2 cm.
Deeper tissues are not heated because of
the thermal insulation of subcutaneous fat
and increased blood flow that dissipates
heat. It diminishes the pain and decreases
local muscle spasm. There is a new
emerging concept among it is Continuous
low level heat therapy that allows for

41.  Ultrasound – It is a deep heating modality
and is effective in heating structures where
superficial heat cannot reach.
 Not indicated in acute inflammatory
conditions where it may severe or
exacerbate the inflammatory response.

42.  Cryotherapy – It is the reduction of
intramuscular temperature to 3O - 7OC by
application of cold. It works by decreasing
nerve conduction velocity along pain fibres
with a reduction of muscle spindle activity
responsible for mediating local muscle
tone. It can be achieved by application of
ice

43.  Acupuncture – Most common form of strong
counterstimulation.
 Chronic pain.
 Local needling in sore sites and strong
neurologic sites in the region. 30 min of low
frequency electrical stimulation i.e. 2-3 Hz
is added by clipping the stimulator directly
to the inserted needle.

44.  Hypnosis – Application of techniques of
attention modification, paced
breathing and muscle relaxation. The
process of helping a patient to reach
hypnotic state is called induction.

45. PHARMACOLOGICAL
MANAGEMENT

46. WHO analgesic ladder, 1986
 Adjuvants include antidepressants,
antiepileptics, sodium channel blockers.

47. Nonselective COX inhibitors
 Salicylates: aspirin
 Propionic acid derivatives: ibuprofen
 Anthranilic acid derivatives: mephenamic acid
 Aryl-acetic acid derivatives: diclofenac
 Oxicam derivatives: piroxicam
 Pyrrolo-pyrrole derivative: ketorolac
 Indole derivative: indomethacin
 Pyrazolone derivatives: phenylbutazone
Preferential COX-2 inhibitors
 Nimesulide, meloxicam, nabumetone
Selective COX-2 inhibitors
 Celecoxib, valdecoxib
Analgesic-antipyretics with poor anti-inflammatory action
 Paraaminophenol derivative: paracetamol
 Pyrazolone derivatives: metamizol
 Benzoxazocine derivative: nefopam

48.  PG, prostacyclin and thromboxane A2 are produced from
arachidonic acid by enzyme cyclooxegenase which exists
in the constitutive(COX-1) and inducible(COX-1)
isoforms. Non opioid analgesics inhibits COX-1 COX-2
nonselectively or COX-2 selectively.
 Salicylates acts by obtunding peripheral pain receptors
and prevents PG mediated sensitization of nerve
endings. They raise the threshold to pain perception.
 Propionic acid derivatives inhibit PG synthesis, platelet
aggregation and prolongs bleeding time.
 Anthranilic acid derivatives inhibits COX and antagonise

49.  Aryl-acetic acid derivatives inhibits PG synthesis
and has short lasting antiplatelet action.
 Oxicam derivatives lowers PG concentration in
synovial fluid and inhibits platelet aggregation.
 Pyrrolo-pyrrole derivative and Indole derivative
inhibits PG synthesis.
 Selective COX-2 inhibitors inhibits only COX-2
without affecting COX-1 function. They do not
depress thromboxane A2 production by platelets
thus platelet aggregation remains undepressed

50. Opioids
 Natural opium alkaloids: morphine,
codeine
 Semisynthetic opiates:
diacetylmorphine, pholcodeine
 Synthetic opiods: pethidine, fentanyl,
tramadol

51.  Opioid analgesics exert their actions by
interacting with specific receptors present
on neurons in CNS and in peripheral tissues.
They inhibit the release of excitatory
transmitters from primary afferents
carrying impulses.
 Action at supraspinal sites in medulla,
midbrain, limbic and cortical areas alter

52.  Mu receptors are located widely
throughtout the CNS especially in the
limbic system and thalamus, striatum,
hypothalamus and midbrain.
 Kappa receptors are located primarily in
the spinal cord and cerebral cortex.
 Delta receptors are mainly present in
dorsal horn of spinal cord.

53. Antidepressants
1. Reversible inhibitors of MAO-A:
Moclobemide
2. Tricyclic antidepressants
a. NA + 5-HT reuptake inhibitors:
imipramine
b. Predominantly NA reuptake
inhibitors: desipramine
3. Selective serotonin reuptake
inhibitors: fluoxetine, sertraline

54.  It is known that descending pain
modulation pathways release serotonin (5-
hydroxytryptamine or 5-HT) and
norepinephrine (NE) to suppress pain
transmission.
 The depressed patient has a dysfunctional
5-HT or NE system implying a dysfunctional
pain modulation pathway.

55. Antiepileptics
 Barbiturate: phenobarbitone
 Deoxybarbiturate: primidone
 Hydantoin: phenytoin
 Iminostilbene: carbamazepine
 Succinimide: ethosuximide
 Aliphatic carboxylic acid: valproic acid
 Benzodiazepines: diazepam
 Phenyltriazine: lamotrigine
 Cyclic GABA analogue: gabapentin
 Newer drugs: vigabatrin

56.  They limit neuronal excitation and enhance
inhibition. Various sites of action include
CNS voltage-gated ion channels involved in
pain transmission (i.e. sodium and calcium
channels), the excitatory receptors for
glutamate including N-methyl-D-aspartate
receptors, and the inhibitory receptors for
GABA and glycine.

57. Clinical aspects
Tooth ache
 Pulpitis (acute / chronic)
 Periapical pathology
 Trauma
Management
NSAIDS followed by RCT / Extraction

58. Temporomandibular disorders – Limitation of
opening, episodes of joint locking, pain with
mandibular dysfunction, facial pain and
headache.
Management
 Physical therapy
 Pharmacotherapy - analgesics, nonsteroidal
anti-inflammatory drugs (NSAIDs), local
anesthetics, oral and injectable cortico

59.  NSAIDS - Commonly used NSAIDs include
ibuprofen and naproxen, celecoxib.
 Local anesthetics – They are primarily
used when a myofascial trigger point is
present. Myofascial trigger points are
usually detected in the mastication
muscles. The trigger point injection
technique involves locating the trigger

60.  TMJ injections - Intracapsular injection of
corticosteroids significantly reduces TMJ
pain. It is indicated for acute and painful
arthritic TMJ that has not responded to
other modalities of treatment.
Triamcinolone or dexamethasone, in
addition to 2% lidocaine without
epinephrine is used.

61.  Muscle relaxants – It can be prescribed
for acute muscle tension associated with
TMJ disorders. A commonly used and
effective muscle relaxant is
cyclobenzaprine, started at lower
dosages (5–10 mg) and taken 1–2 hours
before bedtime.
 Antidepressants - Tricyclic

62.  Occlusal appliance therapy – They are
processed acrylic devices that are used
for the purpose of equally distributing
jaw parafunctional forces, reducing the
forces placed on the masticatory
muscles, and protecting the occlusal
surfaces of the teeth from chronic
nocturnal bruxing.

63. • Surgical intervention - When non-surgical
therapy has been ineffective, surgical
recommendations, such as arthrocentesis
and arthroscopy, depend on the degree of
internal derangement.
1. Arthrocentesis is a conservative
treatment that involves an intra-articular
lavage with or without deposit of

64. 2. Arthroscopy is a closed surgical
procedure that is useful in hypomobility
due to joint derangement58 as well as
fibrosis.
3. Arthrotomy is an open surgical procedure
that modifies joint anatomy.
• Acupuncture – It involves the stimulation
of acupuncture points that are thought to

65. Trigeminal neuralgia – It is a chronic
paroxysmal neuropathic pain condition
that is described as a severe, lancinating,
and electric-like unilateral pain.
 There is usually a trigger zone in the
trigeminal distribution which, when
stimulated, can result in an excruciatingly
painful attack.

66.  The etiology is vascular compression that
may result in focal demyelination. The
superior cerebellar artery compression on
the trigeminal root is responsible for attacks
of TN pain.
Management
 Pharmacological intervention – Antiepileptic
medications are the drugs of choice for the
management of TN.

67.  Surgical intervention – If pain attacks recur
and medications are no longer effective,
neurosurgical options such as
microvascular decompression or gamma
knife radiosurgery may be considered.

68. Glossopharyngeal neuralgia – It is a rare
condition associated with pain in the area
supplied by the glossopharyngeal nerve
including nasopharynx, posterior part of
the tongue, throat, tonsil, larynx, and ear.
Management
 Pharmacological intervention –
Antiepileptic medications are the drugs of

69.  Surgical intervention – If medication
management fails, then microvascular
decompression, radiofrequency
thermocoagulation, gamma knife
radiosurgery, or rhizotomy.

70. Peripheral trigeminal neuropathic pain – It
can arise as a result of a traumatic nerve
injury resulting in chronic aching,
continuous burning like pain at the site of
the injury.
Management
 Topical medications can be used. Capsaicin
is a common locally acting pharmacologic
agent that can be utilized in cream or gel

71. the use of a stent that covers the affected
area (neurosensory stent).
Cream may also include
analgesics/sedatives such as ketamine,
NSAIDs such as diclofenac, anticonvulsant
drugs such as gabapentin and
carbamazepine, and tricyclic antidepressant

72. Centralized trigeminal neuropathic pain -
Prolonged stimulation of peripheral
nociceptors may eventually lead to central
neural changes. The pain in these cases is
described as continuous, aching, and
burning.
Management
 Centrally acting systemic medications are
used. Antiepileptic drugs, such as

73. Atypical odontalgia – It is a centralized
trigeminal neuropathy often localized in a
tooth or tooth area.
Management
 If the pain is localized to a peripheral origin,
a topical medication can be used and a
neurosensory stent can be fabricated.
Systemic approaches such as tricyclic
antidepressants, calcium channel blockers

74. References
 Human physiology 3rd edition
- by Prof A K Jain
 Concise medical physiology 5th edition
- by Sujit K Chaudhari
 Essentials of medical physiology 2nd edition
- by K Sembulingam
 Monheims local anesthesia and pain control
in dental practice 7th edition
- by C Richard Bennett

75.  Oral and Maxillofacial Surgery Clinics of
North America – Orofacial pain and
Dysfunction .
(Volume 2008, Number 2, May 2008)
 Non pharmacologic management of pain –
Journal of American Osteopathic Association
(Supplement 8, Volume 104, Number 11,
November 2004)
 Commentary article on “Is theWHO analgesic

76.  Journal of pain research – Orofacial
pain management : current
prospectives (Volume 7, Pages 99-115,
Year 2014)

77. Thank you