The document provides an extensive overview of pain, its definitions, classifications, and mechanisms. It details various types of pain such as acute, chronic, neuropathic, and their respective characteristics, while also discussing pain management strategies including pharmacological and non-pharmacological approaches. Additionally, it covers the pathophysiology of pain, assessment methods, and the role of the nervous system in pain perception.

1. PAIN PATHWAYS
&
PAIN MANAGEMENT

2. DEFINITION
The word pain is derived from the Latin word Peone and the Greek word
Poine meaning penalty or punishment
 Pain is defined by The International Association for the Study of Pain
as an unpleasant sensory and emotional experience associated with
actual or potential tissue damage, or described in terms of such damage.
(or)
 Pain is an unpleasant subjective experience that is the net effect of a
complex interaction of the ascending and descending nervous systems
involving biochemical, physiologic, psychological and neocortical
processes

3. HISTORY
 ARISTOTLE considered pain a feeling and classified it as a
passion of the soul, where the heart was the source or
processing centre of pain
 DESCRATES, GALEN, VESALIUS postulated that pain was a
sensation in which brain played an important role
 In 19th century, MUELLER, VAN FREY, GOLDSCHEIDER
hypothesized the concepts of neuroreceptors, nociceptors, and
sensory input

4. EPIDEMIOLOGY
 According to The American Pain Foundation, more than 50
million people in the US suffer from chronic pain.
 An additional 25%, 20 million experience acute pain from injury
or surgery
 The annual incidence of moderate – intensity back pain is 10% -
15 % in the adult population with a point prevalence of 15% -
30%
 The National Institute for Occupational Safety and health
estimated that the cost of low back pain alone was between 50
billions – 100 billions per year

5. CLASSIFICATION OF PAIN
Based on source/ location/ referral & duration
ACUTE PAIN /
TRAUMATIC PAIN
CHRONIC PAIN
VISCERAL
/SPLANCNIC
PAIN
SOMATIC PAIN MALIGNANT PAIN
OR
CANCER PAIN
NON – MALIGNANT
PAIN
OR
BENIGN PAIN
SUPERFICIAL PAIN
OR
CUTANEOUS PAIN
DEEP SOMATIC
PAIN
MUSCULOSKELETAL
PAIN
NEUROPATHIC PAIN

6. ACUTE PAIN
 Acute has a sudden onset, usually subsides quickly and is
characterized by sharp, localized sensations with an identifiable
cause
 Lasts > 30 days and occurs after muscle strains and tissue injury
such as trauma or surgery and is described as a linear process
 A poorly treated pain can cause psychological stress and
compromise the immune system due to the release of
endogenous corticosteroids

7.  Acute pain is usually characterized by increased autonomic
nervous system activity resulting in
 Psychological symptoms such as anxiety
 Tachypnoea
 Tachycardia with hypertension
 Pallor
 Diaphoresis
 Pupil dilation

8.  Visceral pain is a type of nociceptive pain that comes from the
internal organs
 Unlike somatic pain it is harder to pinpoint
 Pain is described as general aching or squeezing pain
 It is caused by the activation of pain receptors in the chest,
abdomen, or pelvic areas
 In cancer patients pain is caused by tumour infiltration,
constipation, radiation & chemotherapy
VISCERAL PAIN

9. SUPERFICIAL PAIN
 It is also known as cutaneous
pain
 It arises from superficial
structures such as skin &
subcutaneous tissues
 It is a sharp, bright pain with
a burning quality and may be
abrupt or slow in onset
DEEP SOMATIC
PAIN
 It originates in deep body
structures such as periosteum,
muscles, tendons, joints &
blood vessels
 Strong pressure, ischemia,
tissue damage act as stimuli
for brain damage
 Radiation of pain from original
site of injury occur

10. CHRONIC PAIN
 Chronic pain is arbitrarily defined as pain lasting longer than 3
to 6 months
 It begins when pain persists after the initial injury has healed
 It is persistent or episodic pain of duration or intensity that
adversely affects the function and well being of the patient
 It may be nociceptive, inflammatory, neuropathic or functional
in origin
 It varies from unrelenting extremely severe pain to pain of
escalating or non – escalating nature.

11. CHRONIC PAIN CYCLE

12. MAIN EFFECTS OF
CHRONIC PAIN
 Effect on physical function
 Psychological changes
 Social consequences
 Societal consequences
CONTRIBUTING
BIOLOGICAL FACTORS
 Peripheral mechanisms
 Peripheral central mechanisms
 Central mechanisms

13. PERIPHERAL
MECHANISMS
•Result from peripheral
stimulation of nociceptors
• They contribute to pain
associated with
• Chronic
musculoskeletal
• Visceral
• Vascular disorders
CENTRAL MECHANISMS
• Associated with disease or
injury of the CNS
• Characterised by burning,
aching, hyperalgesia,
dysesthesia. It is
associated with
• Thalamic lesions
• Spinal cord injury
• Surgical interruption of
pain pathways
• Multiple sclerosis
PERIPHERAL – CENTRAL
MECHANISMS
• These mechanisms involve
abnormal function of the
peripheral and central
portions of the
somatosensory system
• Associated with abnormal
functions of the peripheral
and peripheral portions of
SSNS, & loss of descending
inhibitory pathways

14. CHRONIC
MALIGNANT PAIN
 It occurs in 60-90 % of
patients with cancer
 Pain can be related to the
tumour or cancer therapy or
may be idiosyncratic
 Pain may also be found at the
metastasized regions and
treatment interventions may
activate peripheral nociceptors
 Pain can be somatic/visceral
CHRONIC
NONCANCER PAIN
 It is also referred to as
chronic non – malignant
pain
 Pain may last for many years
and is considered progressive
in nature
 May be nociceptive,
neuropathic or mixed in
nature

15. NEUROPTHIC PAIN
 Neuropathic pain is a result of an injury or malfunction of the
nervous system
 It is described as
 Aching
 Throbbing
 Burning
 Shooting
 Stinging
 Tenderness/ sensitivity of skin

17. MECHANISM OF NEUROPATHIC
PAIN
Nerve damage/ persistent stimulation
Rewiring of pain circuits both anatomically &
biochemically
Spontaneous nerve
stimulation
Autonomic neuronal
stimulation
Increased discharge of
dorsal horn neurons
NEUROPATHIC PAIN
Results in
causing
Finally leading to

18. MUSCULOSKELETAL PAIN
 This a type of chronic non cancer pain occurring due to
musculoskeletal disorders such as
 Rheumatoid arthritis
 Osteoarthritis
 Fibromyalgia
 Peripheral neuropathies

19. BASED ON TRANSMISSION
FAST PAIN
 Felt about 0.1 sec after a pain
stimulus is applied
 It is described as sharp pain,
pricking pain, acute & electric
pain
 Fast sharp pain is not felt in
most deeper tissues of the
body
SLOW PAIN
 Usually begins after 1 sec or
more and may range from
seconds to minutes
 Described as slow, burning,
aching, throbbing, nauseous
pain and chronic pain
 Associated with tissue
destruction

20. OTHER TYPES OF PAIN
REFERRED PAIN
 Pain that is perceived at the site
different from its point of origin
but innervated by the same
spinal segment
 Usually applies to pain that
originates from the viscera
 Eg. The pain associated with MI
commonly is referred to the left
arm, neck & chest
BREAKTHROUGH PAIN
 Pain is intermittent, transitory
& an increase in pain occurs
at a greater intensity
 Usually lasts from minutes to
hours and can interfere with
functioning and QOL
 Eg. Neuropathic pain
Lower back pain

22. PAIN RECEPTORS
NOCICEPTORS or PAIN RECEPTORS are sensory receptors that
are activated by noxious insults to peripheral tissues
 The receptive endings of the peripheral pain fibres are free
nerve endings
 These receptive endings are widely distributed in the
 Skin
 Dental pulp
 Periosteum
 Meninges

25. SKIN RECEPTORS FOR
PAIN
HIGH THRESHOLD
MECHANORECEPTOR
S
( HTMS)
POLYMODAL
RECEPTORS
 These receptors detect
local deformation
Eg: Touch
 These receptors detect a
variety of stimuli causing
injury
Eg: Heat
Noxious stimulation
 These do not have a
specialized and simple
nerve endings in the
periphery

26. NERVE FIBRES INVOLVED IN PAIN
TRANSMISSION
A FIBRES C FIBRES
A – BETA
FIBRES
A – DELTA
FIBRES
 Large
 Myelinated
 Fast conducting
 Low stimulation
threshold
 Respond to light
touch
 Small
 Lightly Myelinated
 Slow conducting
 Respond to heat,
pressure, cooling &
chemicals
 sharp sensation of
pain
 Small & unmyelinated
 Very slow conducting
 Respond to all types of
noxious stimuli
 Transmit prolonged dull
pain
 Require high intensity
stimuli to trigger a
response

28. SUBSTANCES
EXITING NCs
HISTAMINE
POTASSIUM
ATP
NEURO
TRANSMITTER
S INVOLVED
IN PAIN
STIMULATION
OF
NOCICEPTORS
BRADYKININ
SENSITIZATIO
N OF
NOCICEPTORS
PGE2
PGI2
DISCHARGE OF
PAIN RELEASING
SUBSTANCES BY
NOCICEPTORS
SUBSTANCE – P
GLUTAMATE
ACTIVATION OF
NOCICEPTORS
BY INTERACTING
WITH OTHER
CHEMICAL
MEDIATORS
PGI2
LTs

29. PATHWAYS OF PAIN SENSATION
 The pathways of pain sensation are as follows
 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
glossopharyngeal nerves
 Pathway from pelvic region – conveyed by sacral
parasympathetic nerves

30. PATHWAY FROM SKIN & DEEPER
TISSUES
FIRST ORDER
NEURONS
• These are the cells in
the posterior nerve
root ganglia, receive
impulses from pain
receptors through
dendrites
• These impulses are
transmitted through
the axons to spinal
cord
• Impulses are
transmitted by Aδ
fibre or C fibres
SECOND ORDER
NEURONS
• The neurons of marginal
nucleus & substantia
gelatinosa form the II
order neurons
• Fibres from these
neurons ascend in the
form of the lateral
spinothalamic tract
• Fibres of fast pain arise
from neurons of the
marginal nucleus
• The fibres of slow pain
arise from neurons of
substantia gelatinosa
THIRD ORDER
NEURONS
• The neurons of pain
pathway are the
neurons in Thalamic
nucleus, reticular
formation, tectum,
gray matter around
the aqueduct of
sylvius
• Axons from these
neurons reach the
sensory area of
cerebral cortex or
hypothalamus

31. PAIN PATHWAYS
ASCENDING PAIN PATHWAY

32. DESCENDING INHIBITORY PAIN PATHWAY

33. ENDOGENOUS ANALGESIC MECHANISMS
 The endogenous analgesic mechanism comprises of endogenously
synthesized opioid peptides, which are MORPHINE like substances
 The opioid like substances are found at different points of the
brain which are breakdown products of 3 large protein molecules
 Pro – opiomelanocortin: β – endorphin
 Pro – encephalin: Met – encephalin & Leu – encephalin
 Prodynorphins: Dynorphins
 These are found in peripheral processes of 10 afferent neurons,
human synovia, many regions of CNS

35. MECHANISMS OF PAIN
 Pain sensation involves a series of complex interactions between
peripheral nerves & CNS
 Pain sensation is modulated by excitatory and inhibitory NTs
released in response to stimuli
 Sensation of pain is composed of 4 basic processes
 Transduction
 Transmission
 Modulation
 Perception

37. PAIN THEORIES
 Pain theories are proposed to offer the possible physiologic
mechanisms involved in pain. They are as follows
 Specificity theory
 Pattern theory
 Neuromatrix theory
 Gate control theory
SPECIFICITY THEORY: This theory states pain as separate modality
evoked by specific receptors that transmit information to pain
centres or regions in the forebrain where pain is experienced.

38. PATTERN THEORY
Pain receptors share endings or pathways with other sensory
modalities but different patterns of activity of the same neurons
can be used to signal painful and non – painful stimuli
Eg. Light touch applied to skin would produce the sensation of
touch and intense pain pressure would produce pain through high
frequency firing of the same receptor
NEUROMATRIX THEORY
 This theory was put forward by MELZACK
 This theory explains the role of brain in pain as well as the
multiple dimensions and determinants of pain

39.  Acc to this theory the brain contains a widely distributed neural
network called the body self Neuromatrix that contains
somatosensory, limbic, & Thalamocortical components
 The body self Neuromatrix involves multiple input sources such
as
 Somatosensory inputs
 Other impulses/ inputs affecting the interpretation of
the situation
 Various components of stress regulation systems
 Intrinsic neural inhibitory modulatory circuits

40. GATE CONTROL MECHANISM
 Proposed by MELZACK & WALL IN 1965
 According to this theory, the pain stimuli transmitted by afferent
pain fibres are blocked by GATE MECHANISM located at the
posterior gray horn of the spinal cord
 If the gate is open pain is felt, and if the gate is closed pain
is suppressed
 Impulses in A – δ & C – fibres can be blocked by modulated by A
– β activity that can selectively block impulses from being
transmitted to the transmission cells in the spinal cord and then
to CNS resulting in no pain

41. ROLE OF BRAIN IN GATE CONTROL
MECHANISMGates in spinal cord are open
Pain signals reach the thalamus through lateral spinothalamic tract
Signals are processed in thalamus
Signal are sent to sensory cortex & perception of pain occurs in
cortex
Signals are sent from cortex back to spinal cord and the gate is
closed by releasing pain relievers such as opioid peptides
Minimizing the severity & extent of pain

43. ASSESSMENT OF PAIN
METHOD OF PAIN ASSESSMENT
 Comprehensive history intake
 Medical history
 Physical history
 Family history
 Physical exam
 Questioning on characteristic of pain – onset, duration,
location, quality, severity & intensity
 Evaluation of psychological status

44. PAIN ASSESSMENT PNUEMONIC
 P – Palliative/ Provocative/ Precipitating
 Q – Quality
 R – Radiation/ Region
 S – Severity
 T – Temporal/ Time related
The impact of pain on the patients functional status, behaviour
and psychological status should also be assessed

45. PAIN ASSESSMENT TOOLS
 Pain may be accompanied by physiologic signs and symptoms
and there are no reliable objective markers of pain
 The severity of pain can be assessed by rating scales &
multidimensional scales.
RATING SCALES
Provide a simple way to
classify the intensity of pain
and should be selected based
on the patients ability to
communicate
MULTIDIMENSIONAL SCALES
Helpful in obtaining
information about the pain
and impact on QOL, but are
more often time consuming to
complete

46. RATING SCALES
SIMPLE DESCRIPTIVE PAIN INTENSITY SCALE
NO PAIN MILD
PAIN
MODERATE
PAIN
SEVERE
PAIN
VERY
SEVERE
PAIN
WORST
POSSIBLE
PAIN
NUMERIC SCALE

47. VISUAL ANALOG SCALE (VAS)
FACES SCALE

48. VERBAL RATING SCALE
PAIN THERMOMETER

49. MULTIDIMENSIONAL ASSESSMENT
SCALES
 The following are the types of MAS
 Initial pain assessment tools
 Brief pain inventory
 McGill pain questionnaire
 The neuropathic pain scale
 The Oswestry disability index

50. DIAGNOSIS OF CHRONIC PAIN

51. CLINICAL PRESENTATION OF PAIN
 General:
 Acute distress/ trauma pain
 No noticeable suffering (Chronic pain)
 Symptoms:
 Sharp, dull, burning, shock like, tingling, shooting radiating,
fluctuating in intensity and varying in location
 Non – specific: Anxiety
Depression
Fatigue
Insomnia
Anger and fear

52. SIGNS OF PAIN
ACUTE PAIN
 Hypertension
 Tachycardia
 Diaphoresis
 Mydriasis
 Pallor
CHRONIC PAIN
 There may be no obvious pain signs in
some acute cases and in most
chronic/ persistent pain
LABORATORY TESTS
 Pain is always subjective i.e. there are
no laboratory tests
 It is diagnosed based on patients
description and history

53. MANAGEMENT OF PAIN
GOALS OF THERAPY
 To decrease the subjective intensity
 To reduce the duration of the pain complaints
 To decrease the potential for conversion of acute pain to
chronic persistent pain syndromes
 To decrease the physiological, psychological, & socioeconomic
sequelae associated with under treatment of pain
 To minimize ADRs, & Dis intolerance to pain management
therapies
 Improving the patients QOL and the ability to perform activities
of daily living

54. APPROACHES TO PAIN CONTROL

55. NON – PHARMACOLOGICAL
MANAGEMENT
 The non – pharmacological management involves the following
approaches
 Physiotherapy
 Psychological techniques
 Stimulation therapies – Acupuncture &
Transcutaneous Electrical Nerve Stimulation (TENS)
 Palliative care – involves the alleviation of symptoms
but does not cure the disease

56. SURGICAL PROCEDURE FOR THE RELIEF OF
PAIN
CORDOTOMY: In the thoracic
region , the spinal cord opposite
to the side of pain is partially
cut to interrupt the anterolateral
pathway
THALAMOTOMY: Involves
causter ization of specific pain
areas in the intrathalamic nuclei
in the thalamus, which often
relieves suffering type of pain

57. SYMPATHECTOMY
Excision of the segment of the
sympathetic nerve or one or more
sympathetic ganglia
RHIZOTOMY
Surgical removal of spinal nerve
roots for the relief of pain or
spastic paralysis

58. FRONTAL LOBOTOMY
Surgical process involving division of one or more nerve tracts in
a lobe of the cerebrum usually frontal lobe

59. PHARMACOLOGICAL
MANAGEMENT

60. OPIOID/ NARCOTIC ANALGESICS
 OPIUM is a raw extract of the poppy plant Papaver
somniferum
 During 19th century, MORPHINE was isolated from opium and
its pharmacological effects were characterized
OPIOD RECEPTORS
TYPE CHARACTERIZATION
µ - MU Highly selective for opioids
δ – DELTA Mixed agonist – antagonist
response
K - KAPPA Opioid analgesics selective for
these receptors are not
identified

61. LOCATION OF OPIOID RECPTORS

62. OPIOID CLASSIFICATION

63. MECHANISM OF ACTION OF OIPOIDS

64. MAJOR PHARMACOLOGICAL EFFECTS OF
OPIOIDS
ORGAN SYSTEM EFFECTS
CENTRAL NERVOUS SYSTEM Analgesia
Dysphoria
Miosis
Physical dependence
Respiratory depression
Sedation
CARDIOVASCULAR SYSTEM Decreased myocardial O2 demand
Vasodilation
Hypotension
GASTROINTESTINAL SYSTEM Constipation
Nausea & Vomiting
GENTIOURINARY SYSTEM Increased bladder sphincter tone
Urinary retention

65. ORGAN SYSTEM EFFECTS
NEUROENDOCRINE EFFECTS Inhibition of release of leutinizing hormone
(LH)
Stimulation of release of ADH & Prolactin
IMMUNE SYSTEM EFFECTS Suppression of function of natural killer
cells (NK cells)
DERMAL EFFECTS Flushing
Pruritus
Urticaria

66. OPIOID ANALGESIC THERAPY IN
PAIN

69. MANAGEMENT OF OPIOID ADVERSE
EFFECTS
ADVERSE EFFECT MANAGEMENT
EXCESSIVE SEDATION  Reduce dose by 25% or increase the dosing interval
CONSTIPATION  CASANTHROL – DOCUSATE 1 capsule at bed time/ BD
 SENNA 1 – 2 tablets at bed time/ BD
 BISACODYL 5 – 10mg daily + DOCUSATE 100mg BD
NAUSEA & VOMITINGS  HYDROXYZINE 25 – 100mg (PO/IM) every 4 – 6 hrs as
needed
 DIPEHNHYDRAMINE 25 – 50mg (PO/IM) every 6 hours
as needed
 ONDANSETRON 4mg IV or 16mg PO, 4 – 8mg IV every
8 hours as needed
 PROCHLORPERAZINE 5 – 10mg (PO/IM) every 3 – 4
hrs, 25mg/ rectum BD

70. ADVERSE
EFFECT
MANAGEMENT
GASTROPARESIS  METOCLOPRAMIDE 10mg (PO/IV) every 6 – 8 hours
VERTIGO  MECLIZINE 12.5 – 25mg PO every 6 hours
URTICARIA/ ITCHING  HYROXYZINE 25 – 100mg (PO/IM) every 6 hours as
needed
 DIPHENHYDDRAMINE 25 – 50mg (PO/IM) every 6
hours as needed
RESPIRATORY DEPRESSION  MILD: Reduce dose by 25%
 MODERATE – SEVERE:
 NALOXONE 0.4 – 2mg IV every 2 – 3 minutes (up to
10mg)
 0.1 – 0.2mg IV every 2 – 3 minutes until desired
reversal
CNS IRRITABILITY  Discontinue OPIOID, treat with BENZODIAZEPINES

71. INERTACTING DRUGS EFFECT
OPIOIDS + CNS DEPRESSANTS
Eg: ALCOHOL
ANESTHETICS
ANTIDEPRESSANTS
ANTIHISTAMINES
BARBITURATES
BENZODIAZEPINES
PHENOTHIAZINES
Additive CNS depressant effects
MEPERIDINE + MAO – I Result in severe reactions such as
Excitation, sweating, rigidity, and
hypertension
DRUG INTERACTIONS

72. NON OPIOID ANALGESICS
 Nonsteroidal Anti-inflammatory Drugs (NSAIDS) are usually
considered as Non Opioid Analgesics
CHARACTERISTICS FEATURES:
 Relieve pain without interacting with opioid receptors
 Possess anti – inflammatory properties
 Have antiplatelet activities
 Do not cause sedation & sleep
 Are not addicting

74. MECHANISM OF ACTION OF NSAIDS

75. MECHANISM OF ACTION OF COX – 2
INHIBITORS

76. NON – OPIOID ANALGESIC THERAPY

78. ADVERSE EFFECTS OF NON NARCOTIC
ANALGESICS
ORGAN SYSTEM EFFECTS
GASTROINTESTINAL Nausea
Abdominal pain
Dyspepsia
Constipation
Vomiting
Haematochezia
Intestinal obduction
Intestinal perforation
Pancreatitis
Peritonitis
PUD
Diarrhoea
HEMATOLOGICAL Aplastic anaemia
Leukopenia
Neutropenia
Pancytopenia
Thrombocytopenia
MALIGNANCIES Lymphomas

79. ORGAN SYSTEM EFFECTS
RENAL EFFECTS Interstitial nephritis
Impaired renin secretion
Enhanced tubular water/ Na+ reabsorption
INFECTIONS Sepsis leading death
MALIGNANCIES & INFECTIONS ARE AS A RESULT OF TNF - INHIBITORS
INTERACTING DRUGS EFFECT
ASPIRIN – ORAL ANTICOAGULANTS Gastric mucosal bleeding, & increased risk of
bleeding
SALYCYLATES - METHOTREXATE Blockage of METHOTREXATE tubular secretion
by SALICYLATES resulting in pancytopenia or
hepatotoxicity due to increased
METHOTREXATE
NSAIDS – TNF BLOCKING AGENTS Neutropenia

80. WHO ANALGESIC PAIN LADDER

82. ALGORITHM FOR ACUTE PAIN MANAGEMENT

84. ALGORITHM FOR CHRONIC CANCER PAIN
MANAGEMENT

87. THANK U