INTRODUCTION HISTORY EPIDEMIOLOGY DEFINITIONS OF PAIN BENEFITS OF PAIN NOCICEPTION PAIN RECEPTORS THEORIES OF PAIN CHARACTERISTICS OF PAIN PAIN PATHWAY MECHANISM OF PAIN PAIN ASSESSMENT APPLIED ASPECTS CONCLUSION REFERENCES

1. GOOD MORNING

2. Dr MANJUSHA P CHANDRAN
1STYEAR MDS STUDENT
DEPARTMENT OF PUBLIC HEALTH DENTISTRY

3.  INTRODUCTION
 HISTORY
 EPIDEMIOLOGY
 DEFINITIONS OF PAIN
 BENEFITS OF PAIN
 NOCICEPTION
 PAIN RECEPTORS
 THEORIES OF PAIN
 CHARACTERISTICS OF PAIN
 PAIN PATHWAY
 MECHANISM OF PAIN
 PAIN ASSESSMENT
 APPLIED ASPECTS
 CONCLUSION
 REFERENCES

4.  Pain is a distressing feeling often caused by intense or
damaging stimuli
 It motivates the individual to withdraw from
damaging situations, to protect a damaged
body part while it heals, and to avoid similar
experiences in the future
 It is a common reason for physician consultation and is a
major symptom in many medical conditions, and can
interfere with a person’s quality of life and general
functioning

5.  Earlier, pain was considered as a result of sin.
 1600’s:Opium
 1800’s:ether and chloroform
 1900’s:morphine and heroin

6.  Willow bark: Mesopotamia, China and Europe
 Turmeric: India and China
 Coca leaves

7.  Acupuncture :China (100 BC)
 1960’s:Formation of pain as a field of medicine
 1980’s: start of a 20 year campaign suggesting “low
incidence of addictive behavior” associated with opioids

8.  Trepanation:Hippocrates:Process of making a surgical hole
in the skull to drive the pain out as it was believed that the
pain was caused by demons that needed to be released

9.  Leeching :Egypt and Europe
 Soporific Sponge:Europe:sleep inducing properties
 Electric fish:Egypt:similar toTENS(Trans cutaneous
Electrical Nerve Stimulation)

10.  Prevalence of chronic pain among patients was found to be 19.23%
 Females reported pain much more commonly than males
 Young and middle aged reported chronic pain more than elderly
Deshpande AN. Prevalence of chronic pain based on primary health center data from a
city in central India. Indian J Pain 2018;32:81-5.

11.  Point prevalence of chronic pain in India was found to be 13 %
Dureja, G. P., Jain, P. N., Shetty, N., Mandal, S. P., Prabhoo, R., Joshi, M., …
Phansalkar,A. A. (2013). Prevalence of Chronic Pain, Impact on Daily Life, and
Treatment Practices in India. Pain Practice, 14(2), E51–E62. doi:10.1111/papr.12132
 Prevalence of dental pain was found to be 35%
Kumar,Y. S.,Acharya, S., & Pentapati, K. C. (2014). Prevalence of dental pain and
its relationship to caries experience in school children of Udupi district. European
Archives of Paediatric Dentistry, 15(6), 371–375. doi:10.1007/s40368-014-0124-1

12.  Whatever the experiencing person says it is, existing whenever she
or he says it does (McCaffery,1968)
 The psychical(pertaining to mind) adjunct of an imperative(urgent)
protective reflux (Sherrington)
 An unpleasant sensory and emotional experience associated with
actual or potential tissue damage, or described in terms of such
damage: International Association for the Study of Pain
(IASP in 1979)

13.  An unpleasant emotional experience usually initiated by
noxious stimulus and transmitted over a specialized neural
network to the central nervous system where it is
interpreted as such (Monheim)
 The subject’s conscious perception of modulated
nociceptive impulses that generate an unpleasant sensory
and emotional experiences associated with actual or
potential tissue damage or described in terms of such
damage (Bell)

14.  Gives warning signal about the existence of a problem or
threat
 Prevents further damage by causing reflex withdrawal of
the body from the source of injury
 It forces the person to rest or to minimize the activities thus
enabling the rapid healing of the injured part
 It urges the person to take required treatment to prevent
major damage

15.  Unconscious activity induced by a harmful stimulus applied
to sense receptors: IASP
 Nociception refers to the process by which information
about tissue damage is conveyed to the central nervous
system
 Involves 4 processes
1. Transduction
2. Transmission
3. Perception
4. Modulation

17.  Transduction : The conversion of the energy from a
noxious thermal, mechanical, or chemical stimulus into
electrical energy (nerve impulses) by sensory receptors
called nociceptors
 Clinical implications
 Some analgesics target the inflammatory process that
produces sensitization.
 Eg: NSAIDs inhibit cyclooxygenase (COX), thus decreasing
the synthesis of prostaglandins.
 Local anesthetics block or modulate channels, thus
inhibiting the generation of nerve impulses

18.  Transmission :the transmission of these neural signals from
the site of transduction (periphery) to the spinal cord and
brain
 Clinical implications
 Some analgesics inhibit nociception in the Dorsal Horn.
 Eg: Opioid analgesics bind to Opioid receptors on primary
afferent and DH neurons and mimic the inhibitory effects of
endogenous opioids.
 They also bind to Opioid receptors in the brain and activate
descending pathways that further inhibit DH nociceptive
transmission.

19.  Perception :The appreciation of signals arriving in higher
structures as pain
 Modulation: Descending inhibitory and facilitory input from
the brain that influences (modulates) nociceptive
transmission at the level of the spinal cord.

20.  Clinical implications
 Some analgesics enhance the effects of descending
inhibitory input.
 Eg: some antidepressants interfere with the reuptake of
serotonin and nor epinephrine at synapses, increasing their
relative interstitial concentration (availability) and the
activity of endogenous pain-modulating pathways.
 Thus, some, but not all, antidepressants are used to treat
some types of chronic pain.

21.  Receptors which mediate pain are called nociceptors
 They are located at the ends of small unmyelinated C fibers
or myelinated Aδ afferent neurons
 These receptors get stimulated by
 Thermal stimulation: temp above 45 ⁰C /cold(0⁰C)

22.  Mechanical stimulation
 Excessive pressure/tension on nerves eg: blow on the head,
pressure of child birth
 Compression of nerve by tumour,a prolapsed intervertebral
disc etc
 Chemical stimulation by irritant chemicals such as
histamine, kinins and prostaglandins released from damaged
tissues

23.  Cartesian DualisticTheory(Renee Descartes 1644)
 Protopathic & epicritic theory(Head & Rivers 1908)
 Intensity theory (Erb 1974)
 Gate control theory(Melzack &Wall 1965)
 Specificity theory(Von Frey 1895)
 The 4th theory of pain(Hardy, Wolff, Goodell 1940s)
 Strong’s theory(Strong 1895)

24.  Sensory interaction theory (Noordenbos 1959)
 Neuromatrix theory(Ronald Melzack 1990)
 Central summation theory (Livingstone 1943)
 Pattern theory(J.P. Nafe 1929)
 Biophychosocial model of pain(1977 by Engel)
 Loeser’s model of pain(1982)

25.  Pain could be a result of physical injury or psychological
injury.
 lacks explanation as to why no two chronic pain patients
have the same experience with pain even if they had similar
injuries

26.  Peripheral sensation is composed of 2 components
 Protopathic :Yields diffuse impression of pain including extreme of
temperature
 Epicritic :Touch, small changes in temperature

27.  Opposing concept:Trigeminal neuralgia

28.  States that when a stimulus gets sent to the brain, it must
first travel to 3 locations within the spinal cord.
1. Cells in the substantia gelatinosa in dorsal horn
2. Fibers in the dorsal column
3. Transmission cells in the dorsal horn
 The substantia gelatinosa serves to modulate the signals
that get through, acting similar to a “gate” for information
traveling to the brain.
 The sensation of pain that an individual feels is the result of
the complex interaction among these three components of
the spinal cord.

29.  Simply stated, when the “gate” closes, the brain does not
receive the information that is coming from the periphery to
the spinal cord.
 However, when the signal traveling to the spinal cord
reaches a certain level of intensity, the “gate” opens.
 Once the gate is open, the signal can travel to the brain
where it is processed, and the individual proceeds to feel
pain.

30.  Current research has also suggested that a negative state-
of-mind serves to amplify the intensity of the signals sent to
the brain as well.
 For example, somebody who is depressed has a “gate” that
is open more often
 Also, there are reports that certain unhealthy lifestyle
choices will also result in an “open gate”

32.  Four separate somatosensory modalities found throughout
the body which include cold, pain, heat, and touch
 Presence of distinct pathways for different sensations

33.  Proposed that pain has 2 components
 Perception of pain
 Reaction one has towards it

34.  suggested that pain consisted of the original sensation and
the psychic reaction provoked by the sensation
 Strong concluded that pain is a sensation:The first sensation
was the experience of heat and then came the sensation of
pain

35.  It describes two systems involving transmission of pain
 fast system: inhibit transmission of the small fibers.
 slow system: conduct somatic and visceral afferents

36.  Proposes that pain is a multidimensional experience
generated by a widely distributed neural network called
neuromatrix in the brain rather than directly by a sensory
input

37.  Prolonged intense stimulation can be considered as an
abnormal activity which leads to bombarding of cells in the
spinal cord
 The information is projected to the brain for pain perception

38.  Each sensation relays a specific pattern or sequence of signals
to the brain.
 The brain then takes this pattern and deciphers it & correlates
with the sensation felt

41.  Threshold and intensity:- If the intensity of the stimulus is below
the threshold (sub threshold), pain is not felt.
 Adaptation:- pain continues as long as the receptors continue to be
stimulated.
 Localization of pain:- Pain sensation is somewhat localized.
Superficial pain is comparatively better localized than deep pain.
 Emotional adjunct:- Pain sensations are commonly accompanied
by emotions.

42.  Influence of the rate of damage on the intensity of pain:- If
the rate of tissue damage or injury is high, intensity of pain is
also high & vice versa.
 Weber Fechner’s law:- Magnitude of sensation felt is
proportionate to the log of intensity of the stimulus, if
stimulus is increased 10 times sense perceived will be just
doubled

43.  Pain physiology (nociceptive, neuropathic, inflammatory)
 Time course (acute, chronic, break-through)
 Etiology (malignant, non-malignant)
 Anatomic location of the pain
 Intensity (mild-moderate-severe; 0-10 numeric pain rating scale)
 Type of tissue involved (skin, muscles, viscera, joints, tendons,
bones)
 Syndromes (cancer, fibromyalgia, migraine, others)
 Special considerations: Referred pain and Phantom pain

45.  Most common type of pain
 Physiologic response when nociceptors respond to noxious
or potentially harmful stimuli.
 The nervous system associated with nociceptive pain
functions properly.
 Protective role
 Transient duration
 May be acute or chronic
 May vary in intensity, quality & may be referred.
SOMATIC
VISCERAL
SUPERFICIAL
DEEP

47.  is caused by aberrant signal processing in the peripheral or
central nervous system.
 reflects nervous system injury or impairment.
 Common causes :Trauma, inflammation, metabolic diseases (eg:
diabetes), infections (eg: herpes zoster), tumors, toxins, and
primary neurological diseases.
 can be broadly categorized as peripheral or central in origin.

49.  Pain that arises from altered nociception despite no clear
evidence of actual or threatened tissue damage causing the
activation of peripheral nociceptors or evidence for disease
or lesion of the somatosensory system causing the pain(IASP
2017)
Trouvin, A.-P., & Perrot, S. (2019). New concepts of pain. Best Practice &
Research Clinical Rheumatology. doi:10.1016/j.berh.2019.04.007

50.  is a result of activation of the pain pathway by a variety of
mediators released due to tissue inflammation
 Cytokines,TNF, acids, lipids, mast cells, ATP, vasoactive
amines etc
 Examples include appendicitis, rheumatoid arthritis,
inflammatory bowel disease, and herpes zoster

51.  an overlap of nociceptive and neuropathic symptoms
 The patients experiencing mixed pain showed
 a greater clinical complexity
 had more comorbidities
 had more adverse psycho-social factors
 had a lower health-related quality of life
 responded less to treatments
 had a higher utilization of health care resource
Trouvin, A.-P., & Perrot, S. (2019). New concepts of pain. Best Practice &
Research Clinical Rheumatology. doi:10.1016/j.berh.2019.04.007

52.  Occurs within about 0.1 second when a pain stimulus is applied
 Relatively high levels of pathology usually accompany acute pain
and the pain resolves with healing of the underlying injury.
 Usually nociceptive, but may be neuropathic.

53.  Serves an important biological function, as it warns of the
potential for or extent of injury.
 A host of protective reflexes (e.g., withdrawal of a damaged
limb, muscle spasm, autonomic responses) often accompany
it.
 Alternate names :sharp pain, pricking pain, fast pain,
electric pain

54.  Subacute pain is a subset of acute pain
 It is pain that has been present for at least 6 weeks but less
than 3 months (vanTulder et al. 1997).
 refers to a medical problem that is not exactly acute or
chronic, but rather somewhere in between.

55.  Chronic pain was once defined as pain that extends 3 or 6
months beyond onset or beyond the expected period of
healing
 Chronic pain is now recognized as pain that extends beyond
the period of healing, with levels of identified pathology that
often are low and insufficient to explain the presence and/or
extent of the pain

56.  1. Chronic primary pain
 2. Chronic cancer pain
 3. Chronic postsurgical and posttraumatic pain
 4. Chronic neuropathic pain
 5. Chronic headache and Orofacial pain
 6. Chronic visceral pain
 7. Chronic musculoskeletal pain
Treede, R.-D., Rief,W., Barke, A., Aziz, Q., Bennett, M. I., Benoliel, R., …Wang, S.-J.
(2015). A classification of chronic pain for ICD-11. PAIN,
1. doi:10.1097/j.pain.0000000000000160

57.  Pain associated with potentially life-threatening conditions such
as cancer is often called “malignant pain” or “cancer pain”.
 It includes pain caused by the disease itself
eg: tumor invasion of tissue, compression or infiltration
of nerves or blood vessels etc
 and/or painful diagnostic procedures or treatments
( biopsy, postoperative pain etc).
 Its acute and chronic components and multiple etiologies make
it difficult to classify based on duration or pathology alone

58.  A subtype of chronic pain is CNCP, which refers to
persistent pain not associated with cancer.
 May last for many years
 Causes include acute injury that has proceeded to chronic
pain (e.g., whiplash) and various chronic conditions .
 In some cases, there is no discernable cause, and the pain is
considered the disease.
 CNCP can affect virtually any body system or region, and
pain severity ranges from mild to excruciating.

59.  A chronic pain syndrome is the combination of chronic
pain and the secondary complications that are making the
original pain worse.
 When you're in pain, you may start to repeat certain bad
behaviors even after the pain is gone or has lessened.
 CPS can affect people of all ages and both sexes, but it's
most common in women.
 People with major depression and other mental
health conditions are more likely to get CPS.

60.  Anxiety
 Depression
 Poor sleep
 Feeling very tired or wiped out
 Irritability
 Guilt
 Drug or alcohol abuse
 Marriage or family problems
 Job loss
 Suicidal thoughts

61.  A sudden increase in pain that may occur in patients who
already have chronic pain from cancer, arthritis or other
conditions.
 may occur with stress, illness, exercising or coughing, or when
the dose of pain medicine wears off
 episodes are sudden, and typically last for about 30 minutes
 can be managed by changing medication, avoiding triggers, and
trying alternative pain relief techniques.

62.  Stump pain is described as the pain in the residual portion of
the amputated limb whereas phantom sensations are the
non painful sensations experienced in the body part that no
longer exists
 Prevalence of PLP is more common among upper limb
amputees than lower limb amputees.
 more common among females than males

63.  Have been reported following amputation of different
body parts including the eyes, teeth, tongue, nose, breast,
bowel, bladder etc, but the most common occurrence is
following limb amputation
 may have its onset immediately or years after the
amputation.
 There are reports of two peak periods of onset, the first
within a month and the second a year after amputation

64.  PLP has been reported in people with congenital absence
of limbs
 Tingling, throbbing, piercing, and pins and needles
sensations were among the most commonly described types
of pain
 The rate of phantom pain or sensation was not reported to
be higher in people with bilateral limb amputation than
those with single limb amputation

65.  Proposed theoretical mechanisms
 Peripheral mechanism
 Stump and neuroma hyperactivity
 Central neural mechanisms
 Spinal cord sensitization and changes
 Cortical reorganization and cortical-motor sensory
dissociation
 Body schema, neuromatrix and neurosignature hypothesis
 Psychogenic mechanism
Subedi, B., & Grossberg, G.T. (2011). Phantom Limb Pain: Mechanisms andTreatment Approaches. Pain
Research andTreatment, 2011, 1–8. doi:10.1155/2011/864605

66.  Referred pain is the pain that is perceived at a site adjacent
to or away from the site of origin
 The deep and some visceral pain are referred to other areas
 Superficial pain is not referred
 MECHANISM:DERMATOMAL RULE
 According to which, pain is referred to a structure which is
developed from the same dermatome from which the pain
producing structure is developed

67.  A dermatome includes all the structures or parts of the body,
which are innervated by afferent nerve fibers of one dorsal
root.
 Significance :Knowledge of referred pain is important in the
early diagnosis and treatment of visceral problems

68. CONVERGENCE
PROJECTIONTHEORY
Pain fibers >common 2ndorder
neuron>brain
CONVERGENCE
FACILITATION THEORY
Pain fibers>different 2nd order
neurons>presence of synapse

70. SITE OF ORIGIN OF
PAIN
REFERREDTO
CARDIAC PAIN LEFT ARM AND
SHOULDER
APPENDIX UMBILICUS
GALL BLADDER RIGHT SHOULDER
OVARY UMBILICUS
TESTIS ABDOMEN
DUODENUM ANTERIOR
ABDOMINALWALL
ABOVE UMBILICUS
KIDNEY LOIN
DIAPHRAGM RIGHT SHOULDER
URETER TESTICLES

71.  Pain sensation to reach the cortex from the nociceptors it requires
three neuron sets
 1st order neuron
 2nd order neuron
 3rd order neuron

72.  Pathway from skin & deeper tissues
 Pathway from face – pain sensation is carried by trigeminal nerve
 Pathway from viscera – pain sensation from thoracic & abdominal
viscera are transmitted by sympathetic nerves & from oesophagus,
trachea & pharynx by vagus & Glossopharyngeal nerves
 Pathway from pelvic region – conveyed by sacral
parasympathetic nerves

73.  Even though all pain receptors are free nerve endings, these
endings use 2 separate pathways for transmitting pain
signals into the CNS.
 The 2 pathways mainly corresponds to:
(a) acute- sharp pain pathway
(b) slow chronic pain pathway
 On entering the spinal cord the signals take 2 pathways to
the brain:
1.Neospinothalamic tract ( for fast pain )
2.Paleospinothalamic tract (for slow pain)

76. Mediated by A- delta fibre
which transmits mainly
mechanical and thermal pain
↓ first order neuron
Spinal cord-terminate in
lamina I of dorsal horn
↓second order
neuron
Anterolateral Column
↓
Brain stem andThalamus
↓third order neuron
Cerebral Cortex

77. Transmits slow chronic pain mainly
transmitted from type C fibres
↓first order neuron
Spinal cord-terminates in lamina
II& III of dorsal horn
↓
Enter laminaV of dorsal horn
↓Second order neuron
Anterolateral column
↓
Brain stem and thalamus
↓Third order neuron
Cerebral cortex

78.  The slow chronic paleospinothalamic pathway terminates
widely in the brain stem.
 Only 1/10th of the fibers pass all the way to the thalamus.
 On their way to thalamus it gives collaterals to
 Reticular Activating System to alert the brain
 Tectum
 Peri Aqueductal Grey(PAG): to activate central pain
inhibiting mechanism
 Hypothalamus
 Limbic system:Amygdala and hypothalamus which are
responsible for the emotional responses caused by pain
sensation

79.  Gating of pain can also be affected by the descending
inhibitory pathway
 Different individuals will react differently to same type of
pain and same individual may react differently in different
situations
 This is due to difference in their central pain inhibiting
mechanism/Endogenous Analgesia System

80.  The important central structures are
 Peri Aqueductal Grey(PAG)
 Raphe Magnus Nucleus: lower pons &upper medulla
 Reticular Activating System
 IntralaminarThalamic Nuclei

82.  TRIGEMINAL PAIN PATHWAY

86.  Pain ,like pleasure, is an emotion and is affected by the
limbic system
 Indeed, painful stimuli may be interpreted as pleasurable
 There are still patients who will suck or wiggle a painful tooth
and seem to derive some pleasure from it

87.  Patient history
 Clinical examination
 Diagnostic studies

89. • Where is the pain?
• How does the pain feel?
• Aggravating & relieving factors
• Timing
• Severity
• Useful other data
• Perception on what caused the pain?
WHAT’S
UP
• Provoked
• Quality
• Region/Radiation
• Severity
• Timing
PQRST
• Onset
• Location
• Duration
• Characteristic
• Aggravating factor
• Radiation
• Treatment
OLD
CART

98.  A dolorimeter is an instrument used to measure pain threshold
and pain tolerance.
 Dolorimetry has been defined as "the measurement of pain
sensitivity or pain intensity".
 determine what level of heat or pressure or electric current or
amount of movement produces a sensation of pain
 The pressure is applied using a blunt object, or by locally
increasing the air pressure on some area of the body, and
sometimes by pressing a sharp instrument against the body.

100.  Facial expressions (grimacing)
 Less obvious: slight frown, rapid blinking, sad/frightened,
any distortion
 Vocalizations (crying, moaning, groaning)
 Less obvious: grunting, calling out, noisy breathing, asking
for help
 Body movements (guarding)
 Less obvious: rigid, tense posture, fidgeting, pacing,
rocking, limping, resistance to moving

101.  Analgesia :loss of pain sensation
 Paralgesia: abnormal pain sensation

102.  Pain is the most common reason for physician consultation in most
developed countries.
 It is a major symptom in many medical conditions, and can interfere
with a person's quality of life and general functioning.
 Psychological factors such as social support, hypnotic suggestion,
excitement, or distraction can significantly affect pain's intensity or
unpleasantness.
 In some debates regarding physician-assisted suicide or euthanasia,
pain has been used as an argument to permit people who are
terminally ill to end their lives.

103.  Ganong’s review of medical physiology:23rd edition
 Essentials of physiology for dental students:
K Sembulingam 2nd edition
 Textbook of Medical Physiology: Arthur C.Guyton, 7th edition
 AP Krishna:Textbook of Physiology
 Bell`s ‘Orofacial pain’, 5th edition, Jeffrey P. Okeson
 BD Chaurasia’s HumanAnatomy for dental students

104.  Physiology for dental students,D. B. Ferguson
 Pain: Current Understanding of Assessment, Management, and
Treatments
 Haefeli, M., & Elfering, A. (2005). Pain assessment. European
Spine Journal, 15(S1), S17–S24. doi:10.1007/s00586-005-1044-x
 Salaffi, F., Sarzi-Puttini, P., & Atzeni, F. (2015). How to measure
chronic pain: New concepts. Best Practice & Research Clinical
Rheumatology, 29(1), 164–186. doi:10.1016/j.berh.2015.04.023

105.  Han, D.-G. (2009). The other mechanism of muscular referred
pain:The “connective tissue” theory. Medical Hypotheses,
73(3), 292–295. doi:10.1016/j.mehy.2009.02.040
 Farasyn, A. (2007). Referred muscle pain is primarily peripheral
in origin:The “barrier-dam” theory. Medical Hypotheses, 68(1),
144–150. doi:10.1016/j.mehy.2006.05.063
 A short history of pain management:NCBI