PAIN PATHWAYS

&
PAIN MANAGEMENT
 DEFINI
TION
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 S t u d y of Pain

as an unpleasant sensory and emotional experience associated with
actual or potential tissue damage, or described in terms of su c h 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
 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

 D ES C R A T ES , G AL E N, V E S ALIU S postulated that pain was

a

 sensation
In century,
1 9 th
in which brain played a n important role
MU E L L ER , VAN F R E Y,
GOLDSCHEIDER
hypothesized the concepts of neuroreceptors, nociceptors, and

sensory input
 CLASSIFICATION
OF PAIN
B as ed on source/ location/ referral & duration

AC U T E PAIN / C H RO N I C PAIN
TRAUMATIC PAIN

V IS C ER AL S OMATI C PAIN MALIGNANT PAIN NON – MALIGNANT

/ S PLANC NIC OR PAIN
PAIN C A N C E R PAIN OR
B EN IG N PAIN
SU PERFICIAL PAIN D E E P SOMAT I C
OR PAIN
C U TA N E O U S PAIN
M U S C U LO S K E LETAL NEU ROPATHIC PAIN
PAIN
 ACUTE
PAIN
 Acute ha s a sudden onset, usually subsides quickly and is
characterized by sharp, localized sensations with a n identifiable
cause

 Lasts > 30 days and occurs after muscle strains and tissue injury
s uc h as trauma or surgery and is described as a linear process

 A poorly treated pain cause psychological stress and

can compromise the system due to the release
of
immune endogenous
corticosteroids
 Acute pain is usually characterized by increased
autonomic
nervous system activity resulting in

 Psychological symptoms s uc h as anxiety

 Tachypnoea

 Tachycardia with hypertension

 Pallor

 Diaphoresis

 Pupil dilation
 VISCERAL
 Visceral pain PAIN
is a type of nociceptive pain that com es from
the internal organs

 Unlike somatic pain it is harder to pinpoint

 Pain is described as general aching or squeezing pain

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

 It is persistent or episodic pain of du ration or intensity

tha t 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.
CHRONIC PAIN
CYCLE
MAIN EFFECTS OF CONTRIBUTING
CHRONIC PAIN BIOLOGICAL FACTORS
 Effect on physical function  Peripheral mechanisms

 Psychological changes  Peripheral central mechanisms

 Social consequences  Central mechanisms

 Societal consequences
 PERIPHERAL CENTRAL MECHANISMS PERIPHERAL – CENTRAL
MECHANISMS MECHANISMS
• Associated with disease or
•Result from • These mechanisms involve
injury of the C N S
peripheral stimulation of abnormal function of the
• Characterised by burning,
•nociceptors
They c ontribute pain peripheral and central
aching, hyperalgesia,
to associated with portions of the
dysesthesia. It is
• Chronic somatosensory system
associated with
musculoskeletal • Associated with abnormal
• Thalamic lesions
• Visceral functions of the peripheral
• Spinal cord injury
and peripheral portions of
• Vascular
• Su rgical interruption
disorders S S N S , & loss of descending
of pain pathways
inhibitory pathways
• Multiple sclerosis
 C CHRONIC
MALIGNAN NONCANCER PAIN
T PAINin 60-90
 It occurs of  It is also
referred to as
% patients with cancer chronic non – malignant
pain
 Pain can be related
to the
tumour or cancer therapy  Pain may last for many years
or may be idiosyncratic and is considered progressive
in nature
 Pain may also be found at the
metastasized regions and  May be nociceptive, may
treatm ent interventions neuropathic or mixed in
activate peripheral nociceptors nature

 Pain can be somatic/visceral

 NEUROPTHI
 Neuropathic
C PAIN
pain is a result of an injury or m alfunction of
the nervous system

 It is described as

 Aching

 Throb
bing

 Burni
ng

 Shooti
ng

 Stingi
ng
 MECHANISM OF
NEUROPAT
Nerve damage/ HIC
persistent PAIN
stimulation
Results in

Rewiring of pain circuits both anatomically &

biochemically
causing

Spontaneous nerve Autonomic neuronal Increased discharge of

stimulation stimulation dorsal horn neurons

Finally leading to

NEUROPATHIC PAIN
 MUSCULOSKELE
TALnon
 This a type of chronic PAIN
cancer pain occurring due to
musculoskeletal disorders s u c h as

 Rheumatoid arthritis

 Osteoarthritis

 Fibromyalgia

 Peripheral neuropathies
 BASED ON
TRANSMISSION
FAST PAIN SLOW PAIN

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

 Pain that is perceived at the site  Pain is intermittent, transitory

different from its point of origin & a n increase in pain occurs
but innervated by the same at a greater intensity
spinal segment
 Usually lasts from minutes
 Usually applies to pain that
to hours and can interfere with
originates from the viscera
functioning and Q O L
 E g . The pain associated with MI
 Eg . Neuropathic pain
commonly is referred to the left
arm, neck & chest Lower back pain
 PAIN
RECEPTOR
S
N O C I C E P TO RS or PAIN R E C E P TO R S 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
 SKIN RECEPTORS FOR PAIN

HIGH THRESHOLD POLYMODAL RECEPTOR

MECHANORECEPTOR
S These receptors detects
( HTMS) variety of stimuli causing
 These receptors detect
injury
local deformation
Eg: Heat
Eg: Touch
Noxious stimulation
 These not have a
do and
specialized
nerve endings
simplein
the periphery
 INVOLVED IN
PAIN
A FIBRES TRANSMISSION
C FIBRES

 Small & unmyelinated

A – BETA A – DELTA
FIBRES FIBRES  Very slow conducting
 Small  Respond to all types of
 Large
 Lightly noxious stimuli
 Myelinated Myelinated  Transmit prolonged dull
 Fast conducting  Slow conducting
 Respond to heat, pain
 Low stimulation
pressure, cooling &  Require inten sity
threshold
chemicals high stimuli trigger a
 Respond to light
 sharp sensation to
touch
of pain response
 NEURO SUBSTANCE
TRANSMITTE S EXITING
R S NCs
INVOLVED IN HISTAMINE
PAIN POTASSIU M
ATP

STIMULATION S N OF
OF NOCICEPTORS
E
NOCICEPTORS N PG E 2
BRADYKININ S PGI 2
I
T
ACTIVATION OF DISCHARGE IOF
NOCICEPTORS PAIN RELEASING
Z
BY INTERACTING SUBSTANCESA
WITH OTHER BY
CHEMICAL T
NOCICEPTORS
MEDIATORS I
SUBSTANC EO–
PGI 2 P GLUTAMATE
LTs
 PATHWAYS OF PAIN
SENSATION
 The pathways of pain sensation are as follows

 Pathway from s k i n & deeper tissues

 Pathw ay from fa c e – pain is carried by

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

or
PATHWAYS
ASCENDING PAIN
PATHWAY
DESCENDING INHIBITORY
PAIN PATHWAY
 ENDOGENOUS ANALGESIC
 The MECHANISMS
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 1 0 afferent

neurons,
h u m a n synovia, many regions of C N S
 MECHANISMS
OF PAIN
 Pain sensation involves a series of complex interactions between
peripheral nerves & C N S

 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
 PAIN
 Pain theories
THEORIES
are proposed to offer the physiologic
possible 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.
 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 M E L Z AC K

 This theory explains the role of brain in pain as well as

the multiple dimensions and determinants of pain
 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 s uc h

as

 Somatosensory inputs

 Other impulses/ inputs affecting the interpretation of

the situation

 Various components of stress regulation systems

 Intrinsic neural inhibitory modulatory circuits

 GATE CONTROL
MECHANISM
 Proposed by M E L Z AC K & WALL IN 1965

 According to this theory, the pain stimuli transmitted by afferent

pain fibres are blocked by GAT E MEC H A N IS M 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 C N S resulting in no pain
ROLE OF BRAIN IN GATE CONTROL
MECHANISM
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 su ch as opioid peptides

Minimizing the severity & extent of pain

 ASSESSMENT
OF PAIN
METHOD OF PAIN ASSESSMENT

 Comprehensive history in ta ke

 Medical history

 Physical history

 Family history

 Physical exam

 Questioning on characteristic of pain – onset,

duration,
location, quality, severity & intensity

 Evaluation of psychological status

 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
 RATING
SCALES
SIMPLE DESCRIPTIVE PAIN INTENSITY SCALE

N O PAIN MILD M OD ERA TE VE RY WORST

S E VE RE
PAIN PAIN SEVERE POSSIBLE
PAIN
PAIN PAIN

NUMERIC SCALE
VISUAL ANALOG SCALE (VAS)

FACES SCALE
 VERBAL RATING SCALE

PAIN THERMOMETER
 MULTIDIMENSIONAL
ASSESSMENT
SCALES
 The following are the types of M AS

 Initial pain assessment tools

 Brief pain inventory

 McGill pain questionnaire

 The neuropathic pain scale

 The Oswestry disability index

DIAGNOSIS OF
CHRONIC PAIN
 PRESENTATION
 General:
OF
PAIN
 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

 SIGNS OF
ACUTE PAIN
PAIN
CHRONIC PAIN

 Hypertension  There may be no obvious pain signs in

some acute cases and in most
 Tachycardia
chronic/ persistent pain
 Diaphoresis

 Mydriasis
LABORATORY TESTS
 Pallor  Pain is always subjective i. e. there
are
no laboratory tests
 It is diagnosed based on
patients
description and history
 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 acu te pain to

of chronic persistent pain syndromes

 To decrease the physiological, psychological, &

socioeconomic sequelae associated with under treatment of
pain

 To minimize A D R s , & Dis intolerance to pain

management therapies

 Improving the patients Q O L and the ability to perform activities

of daily living
APPROACHES TO PAIN
CONTROL
 NON –
PHARMACOLOG
 The nonICAL
– pharmacological management involves the
following approaches

 Physiotherapy
 Psychological techniques

 Stimulation therapies – &

Acupuncture
Transcutaneous Electrical Nerve Stimulation (TENS)
 Palliative ca re – involves the alleviation of
sym ptoms but does not cure the disease
 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
 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
 FRONTAL LOBOTOMY

Surgical process involving division of one or more nerve tracts

in a lobe of the cerebrum usually frontal lobe
PHARMACOLOGICAL
MANAGEMENT
 OPIOID/ NARCOTIC
 O PIUM
ANALGESICS
is a raw extract of the poppy plant
Papa ver somniferum

 During 19 t h century, MORPHINE was isolated from opium and

its pharmacological effects were characterized

TYPE OPIOD CHARACTERIZATION

RECEPTORS
µ - MU Highly selective for opioids
δ – DELTA Mixed agonist – antagonist
response
K - KAPPA Opioid analgesics selective for
these receptors are not
identified
LOCATION OF OPIOID
RECPTORS
OPIOID
CLASSIFICATION
MECHANISM OF ACTION
OF OIPOIDS
PHARMACOLOGICALOPIOIDS
EFFECTS OF
ORGAN SYSTEM EFFECTS
CENTRAL N E RVO U S S Y S T E M Analgesia
D ysphoria
Miosis
Physical dependence
Respiratory depression
Sedatio
n
C A R D I OVAS C U L A R SY S T E M Decreased myocardial O 2 demand
Vasodilation
Hypotension
GASTROINTESTINAL S Y S T E M Constipation
Nausea & Vomiting

GENTIOURINARY S Y S T E M Increased bladder sphincter tone

Urinary retention
 ORGAN SYSTEM EFFECTS
N E U RO E N D O C R I N E E F F E C T S Inhibition of release of leutinizing hormone
(LH)
Stimulation of release of A DH & Prolactin

IMMUNE S YS T E M E F F E C T S Suppression of function of natural killer

cells (NK cells)

D ER MA L E F F E C T S Flu shing
Pruritus

U rticaria
OPIOID ANALGESIC
THERAPY IN
PAIN
 MANAGEMENT OF
OPIOID
ADVERSE EFFECT
ADVERSE
EFFECTS
MANAGEMENT
E X C E S S I V E SEDATION  Reduce dose by 25% or increase the dosing interval

CONSTIPATION  C A S A N T H R O L – D O C U S AT E 1 capsule at bed time/ B D

 S E N N A 1 – 2 tablets at bed time/ B D
 BI SACO DYL 5 – 10mg daily + D O C U S AT E 100mg B D

NAU SEA & VOMITINGS  H YD ROX YZ I NE 25 – 100mg (PO/IM) every 4 – 6 hrs as

needed
 DIPEHNHYDRAMINE 25 – 50mg (PO/IM) every 6 hours
as needed
 O N DA N S ET RO N 4mg IV or 16mg P O, 4 – 8mg IV every
8 hours as needed
 P RO C H LOR P E R AZ IN E 5 – 10mg (PO/IM) every 3 – 4
hrs, 25mg/ rectum B D
 ADVERS
MANAGEMENT
E
EFFECT
GAST RO PA R E S I S  M ETOCLOPRAMIDE 10mg (PO/IV) every 6 – 8 hours

V E R TIG O  M EC LI ZI NE 12.5 – 25mg PO every 6 hours

URTICARIA/ ITCHING  H YROX YZ I NE 25 – 100mg (PO/IM) every 6 hours as

needed
 DIPHE N H YDDR AMINE 25 – 50mg (PO /IM )
every 6 hours as needed

RESPIRATORY D E P R E S S I O N  MILD: Reduce dose by 25%

 M OD E RATE – S E V E R E :
NA LOXO NE 0.4 – 2mg IV every 2 – 3 minutes (up to
10mg)
 0.1 – 0.2mg IV every 2 – 3 minutes until desired
reversal

C N S IRRITABILITY  Discontinue OPIOID, treat with B E N ZO D I A Z E P I NE S

 INTERACTION
S
INERTACTING DRUGS EFFECT
OPIOIDS + C N S D E PR E SSANTS Additive C N S depressant effects
Eg: A L C O H O L
AN ESTHETICS
ANTID EPR E S S ANTS
ANTIHISTAMINES
BARBITURATES
B E N ZO D IAZEPINE S
PHENOTHIAZINES

ME P ERIDINE + MAO – I Result in severe reactions such

as Excitation, sweating, rigidity,
and hypertension
 NON OPIOID
 Nonsteroidal
ANALGESICS
Anti-inflammatory D rugs are usually
(NSAIDS) considered as Non Opioid Analgesics

C H A R AC T E R I ST I C S F EAT U R ES :

 Relieve pain without interacting with opioid receptors

 Possess anti – inflammatory properties

 Have antiplatelet activities

 Do not cause sedation & sleep

 Are not addicting

NON – OPIOID
ANALGESIC THERAPY
 ADVERSE EFFECTS OF
NON NARCOTIC
ORGAN SYSTEM ANALGESICS
EFFECTS
GASTROINTESTINAL Nausea
Abdominal pain
Dyspepsia
Constipation
Vomiting
Haematochezia
Intestinal obduction
Intestinal perforation
Pancreatitis
Peritonitis
PUD
Diarrhoea
HEMATOLOGI C AL Aplastic anaemia
Leukopenia
Neutropenia
Pancytopenia
Thrombocytopenia
MALIGNANCIES Lymphomas
ORGAN SYSTEM EFFECTS
RENAL E F F E C T S Interstitial nephritis
Impaired renin secretion
Enhanc ed tubular water/ Na + reabsorption
INFECTIONS Sepsis leading death
MALIGNANCIES & INFECTIONS A RE AS A RES U LT O F TNF - INHIBITORS

INTERACTING DRUGS EFFECT

ASPIRIN – ORAL ANTICOAGULANTS Gastric mucosal bleeding, & increased risk of
bleeding

SALYCY LATES - METHOTR EXATE Blockage of METHOT REXATE tubular secretion

by SALICYLATES resulting in pancytopenia or
hepatotoxicity due to increased
METHOT REXATE

N SA ID S – TNF B L O C K I N G AG E N T S Neutropenia
WHO ANALGESIC
PAIN LADDER
ALGORITHM FOR ACUTE PAIN
MANAGEMENT
ALGORITHM FOR CHRONIC CANCER
PAIN MANAGEMENT
THANK U