PAIN
By
Mr. Chacko.P.George. MPT(Neuro)
Associate Professor
Department of PHYSIOTHERAPY
EMS College of Paramedical
Sciences,EMCHRC,Perinthalmanna
 Define Pain
 Theories of Pain
 Pain Gate Control theory
CONTENTS
Pain is defined as unpleasant sensory
and emotional experience that is
associated with actual or potential
tissue damage.
(International association for the study of
pain,Merskey et al, 1979)
 Pain is one of the most common reasons
a person seeks medical attention.
Can you Define Pain ?
 Pain is a protective mechanism, person try to
remove the tissue damage.
 loss of pain perception can cause and increase
tissue damage (eg:- bed sores)
 Subjective sensation
 Pain Perceptions – based on expectations,
past experience, anxiety, suggestions
 Affective – one‟s emotional factors that can
affect pain experience
 Behavioral – how one expresses or controls pain
 Cognitive – one‟s beliefs (attitudes) about pain
 Physiological response produced by
activation of specific types of nerve fibers
Neurophysiology of Pain
Types of pain
 Fast pain (Aδ)
 Or
Sharp pain
Prickling pain
Acute pain
Electric pain
 Slow pain (C fibers)
or
Burning pain
Aching pain
Chronic pain
 Cutaneous Pain – sharp, bright, burning; can have a
fast or slow onset
 Deep Somatic Pain – stems from tendons, muscles,
joints, periosteum, & b. vessels
 Visceral Pain – originates from internal organs;
diffused @ 1st & later may be localized (i.e.
appendicitis)
 Psychogenic Pain – individual feels pain but cause is
emotional rather than physical
Referred pain
 Occurs away from pain site
 Example:Angina pectoris
 Types of referred pain:
 Myofascial Pain – trigger points, small hyperirritable
areas within a muscle in which nerve impulses
bombard CNS & are expressed at referred pain
 Sclerotomic & Dermatomic Pain – deep pain; may
originate from sclerotomic, myotomic, or dermatomic
n. irritation/injury
Sclerotome: area of bone/fascia that
is supplied by a single n. root
Myotome: m. supplied by a single
n. root
Dermatome: area of skin supplied by
a single n. root
Properties of pain fibers
Fast pain
 Receptors -Free nerve endings
 Afferent -Aδ(group III) fibers
 Action potential-Relatively slow
 Conduction velocity-5-30m/s
 Subjective sensation-Sharp,pricking pain
 Onset of sensation & Localisation-
Short latency,easily identified
 Duration -Short lasting
 Subjective response -Reflex withdrawl,
less emotional involvement
 Myelinated
 Large diameter fibers
Slow pain
1) Free nerve endings
2) C (group IV) fibers
3) Very slow
4) 0.5-2m/s
5) Dull,burning & Throbbing
pain
6) Poorly localised,diffuse
7) Long lasting
8) Difficult to
endure,possible emotional
& automatic response
9) Non myelinated
10) Small diameter fibers
The pain pathways
 Joints
 Muscles
 Soft tissues
The pain pathways
Pain physiology
Noxious Stimulus
activate pain receptor
transmission by nerve
fiber (Aδ ,c)
CNS
(S.C, Spinothalamic
tract, brain stem,
thalamus, cortex)
Peripheral Aspects
 Flexor withdrawal reflex
 Crossed extensor reflex
Central Aspects
2020-04-30 purushotham 22
 Several stages
1) Peripheral
2) Spinal segmental
3) Supraspinal
4) Cortical
Neuromodultaion of PAIN
Theories of Pain
 Gate Control Theory
 Central Biasing Theory
 Endogenous Opiates Theory
Pain Control Theories
Pain Gate control Theory
Pain Gate control Theory
Ronald Melzack
(1929)
Patrick Wall
(1925-2001)
 Substantia Gelatinosa (SG) in dorsal horn of spinal
cord acts as a „gate‟ – only allows one type of
impulses to connect with the SON
 Transmission Cell (T-cell) – distal end of the SON
 If A-beta neurons are stimulated – SG is activated
which closes the gate to A-delta & C neurons.
 If A-delta & C neurons are stimulated – SG is
blocked which closes the gate to A-beta neurons.
Pain Gate control Theory
 Gate - located in the dorsal horn of the spinal
cord
 Smaller, slower n. carry pain impulses
 Larger, faster n. fibers carry other sensations
 Impulses from faster fibers arriving @ gate 1st
inhibit pain impulses (acupuncture/pressure, cold, heat,
chem. skin irritation).
Pain Gate control Theory
Pain Gate control Theory
Central Biasing Theory
 Descending neurons are activated by: stimulation
of A-delta & C neurons, cognitive processes,
anxiety, depression, previous experiences,
expectations
 Cause release of enkephalins (PAG) and serotonin
(NRM)
 Enkephalin interneuron in area of the SG blocks
A-delta & C neurons
Endogenous Opiates Theory
 Stimulation of A-delta & C fibers causes release of B-
endorphins from the PAG & NRM
Or
 ACTH/B-lipotropin is released from the anterior
pituitary in response to pain – broken down into B-
endorphins and corticosteroids
 Mechanism of action – similar to enkephalins to block
ascending nerve impulses
 Examples: TENS (low freq. & long pulse duration)
1. Intensive (Summation ) Theory
2. Specificity Theory
3. Strong‟s Theory
4. Pattern Theories
5. Central summation Theory
6. The Fourth Theory of pain
7. Sensory interaction Theory
8. Pain Gate control Theory
Theories of Pain
 Erb -1874
 According to this theory “every stimulus was
capable of producing pain if it reached sufficient
intensity”.
 Developed by Goldscheider -1894
 Both stimulus intensity and central summation as
critical determinants of pain. It was implied that
the summation occurred in the dorsal horn cells.
Intensive (Summation ) Theory
 Von Frey -1895
 This theory is based on the assumption that the free
nerve endings are pain receptors, and that the other 3
types of receptors are also specific to a sensory
experience.
 Pain perception was viewed as a function of the
amount of physical damage alone.
Specificity Theory
 Strong – 1895
 Pain was an experience based on the noxious stimulus
& the psychic reaction or displeasure provoked by the
sensation
Strong‟s Theory
 Nafe – 1934
 All cutaneous qualities are produced by spatial &
temporal patterns of nerve impulses rather than by
separate, modality-specific transmission routes.
Pattern Theories
 Livingston – 1943
 The intence stimulation resulting from nerve &
tissue damage activated fibers that projected to
internuncial neuron pools within the spinal cord.
 Abnormal reverberating circuits were created, with
self activating neurons.
 Prolonged abnormal activity bombarded cells in the
spinal cord, & information was projected to the
brain for pain perception.
Central summation Theory
 Hardy, Woff & Goodell- 1940
 Expanded on strong theory
 Stated that pain was composed of 2 components:the
perception of pain & the reaction one has to it.
 Physiopsychological process involving cognitive functions
of the individual & influenced by past
experinces,culture, & various psychological factors that
produce great variation in the “reaction pain
threshold”
The Fourth Theory of pain
 Noordenbos – 1959
 2 systems involving transmission of pain & other
sensory information with a fast & slow system.
 The slow system, composed of unmyelinated small
diameter fibers, was presumed to conduct somatic &
visceral afferents.
 The fast system, composed of large fibers, was said
to inhibit transmission of the small fibers.
Sensory interaction Theory
Evaluation of pain
Pain Evaluation
 Need to determine underlying cause if possible
 Pain is subjective
 Difficult to describe and characterize objectively
 In all types of pain accurate assessment is essential.
 However simply asking the patient “how much does it
hurt” is not enough.
 There is no direct relationship between physical
pathology and the intensity of pain.
 The patient‟s subjective experience may be difficult to
communicate.
Pain Assessment
OPQRST Format
Origin/Onset of pain
Position /pattern of pain
Quality of pain
Quantity of pain
Radiating pain
Signs &Symptoms
Treatment
ASSESSMENT OF PAIN
 Origin /Onset of pain: how did the pain started:
suddenly/gradually
 Mechanism of injury
 Position/pattern: constant or periodic
Localized/ radiating
Aggravating and relieving factors
Improving/worsening/remain same
 Quality of pain: mechanical-pressing stabbing
Chemical-burning
Neural-numbness/pins and needles
Vascular- throbbing
 Quantity of pain: intensity of pain
 Radiation: characteristics of pain radiation
 Signs and symptoms: Functional,
psychological
 Treatment: Previous treatment
Current treatment effectiveness
 Verbal rating scale
 Wong/baker faces
 Pain diagrams / Body diagrams
 Visual analogue scale
 McGill pain questionnaire
Tools used to measure pain
Pain diagrams / Body diagrams
Visual Analogue Scale
 The VAS is a simple robust pain
measurement tool
 It can be used to measure severity & or
Improvement
 It can be reliably used for children over
the age of five
 The VAS is usually designed as a 10cm line
with descriptors at each end.
Visual Analogue Scale
No Pain Worst pain
Possible Pain
The example shows a patient recording a 9.0
i.e. The patient has made a mark 9cms from the no pain end
of the scale.
NB The VAS can be compromised if descriptors or numbers
are added between the end points.
{The 10 cm line allows for easy measurement and recording}
i. Sheila Kitchen.Electrotherapy:Evidence-Based Practice
ii. Val Robertson, Alex Ward, ohn Low and Ann
Reed.Electrotherapy Explained-Principles & Practice.
iii. Basana Kumar Nanda.Electrotherapy Simplified.
Newdelhi:Jaypee brothers;2008.
iv. Susan B O‟Sullivan, and Thomas J Schmitz. Physical
Rehabilitation. Newdelhi:Jaypee brothers;2007.
References
Pain
Pain

Pain

  • 1.
    PAIN By Mr. Chacko.P.George. MPT(Neuro) AssociateProfessor Department of PHYSIOTHERAPY EMS College of Paramedical Sciences,EMCHRC,Perinthalmanna
  • 2.
     Define Pain Theories of Pain  Pain Gate Control theory CONTENTS
  • 3.
    Pain is definedas unpleasant sensory and emotional experience that is associated with actual or potential tissue damage. (International association for the study of pain,Merskey et al, 1979)  Pain is one of the most common reasons a person seeks medical attention. Can you Define Pain ?
  • 4.
     Pain isa protective mechanism, person try to remove the tissue damage.  loss of pain perception can cause and increase tissue damage (eg:- bed sores)
  • 5.
     Subjective sensation Pain Perceptions – based on expectations, past experience, anxiety, suggestions  Affective – one‟s emotional factors that can affect pain experience  Behavioral – how one expresses or controls pain  Cognitive – one‟s beliefs (attitudes) about pain  Physiological response produced by activation of specific types of nerve fibers
  • 6.
  • 7.
    Types of pain Fast pain (Aδ)  Or Sharp pain Prickling pain Acute pain Electric pain  Slow pain (C fibers) or Burning pain Aching pain Chronic pain
  • 8.
     Cutaneous Pain– sharp, bright, burning; can have a fast or slow onset  Deep Somatic Pain – stems from tendons, muscles, joints, periosteum, & b. vessels  Visceral Pain – originates from internal organs; diffused @ 1st & later may be localized (i.e. appendicitis)  Psychogenic Pain – individual feels pain but cause is emotional rather than physical
  • 9.
    Referred pain  Occursaway from pain site  Example:Angina pectoris  Types of referred pain:  Myofascial Pain – trigger points, small hyperirritable areas within a muscle in which nerve impulses bombard CNS & are expressed at referred pain  Sclerotomic & Dermatomic Pain – deep pain; may originate from sclerotomic, myotomic, or dermatomic n. irritation/injury
  • 10.
    Sclerotome: area ofbone/fascia that is supplied by a single n. root Myotome: m. supplied by a single n. root Dermatome: area of skin supplied by a single n. root
  • 11.
    Properties of painfibers Fast pain  Receptors -Free nerve endings  Afferent -Aδ(group III) fibers  Action potential-Relatively slow  Conduction velocity-5-30m/s  Subjective sensation-Sharp,pricking pain  Onset of sensation & Localisation- Short latency,easily identified  Duration -Short lasting  Subjective response -Reflex withdrawl, less emotional involvement  Myelinated  Large diameter fibers Slow pain 1) Free nerve endings 2) C (group IV) fibers 3) Very slow 4) 0.5-2m/s 5) Dull,burning & Throbbing pain 6) Poorly localised,diffuse 7) Long lasting 8) Difficult to endure,possible emotional & automatic response 9) Non myelinated 10) Small diameter fibers
  • 13.
    The pain pathways Joints  Muscles  Soft tissues
  • 14.
  • 18.
    Pain physiology Noxious Stimulus activatepain receptor transmission by nerve fiber (Aδ ,c) CNS (S.C, Spinothalamic tract, brain stem, thalamus, cortex)
  • 20.
  • 21.
     Flexor withdrawalreflex  Crossed extensor reflex Central Aspects
  • 22.
  • 23.
     Several stages 1)Peripheral 2) Spinal segmental 3) Supraspinal 4) Cortical Neuromodultaion of PAIN
  • 24.
  • 25.
     Gate ControlTheory  Central Biasing Theory  Endogenous Opiates Theory Pain Control Theories
  • 26.
  • 27.
    Pain Gate controlTheory Ronald Melzack (1929) Patrick Wall (1925-2001)
  • 28.
     Substantia Gelatinosa(SG) in dorsal horn of spinal cord acts as a „gate‟ – only allows one type of impulses to connect with the SON  Transmission Cell (T-cell) – distal end of the SON  If A-beta neurons are stimulated – SG is activated which closes the gate to A-delta & C neurons.  If A-delta & C neurons are stimulated – SG is blocked which closes the gate to A-beta neurons. Pain Gate control Theory
  • 29.
     Gate -located in the dorsal horn of the spinal cord  Smaller, slower n. carry pain impulses  Larger, faster n. fibers carry other sensations  Impulses from faster fibers arriving @ gate 1st inhibit pain impulses (acupuncture/pressure, cold, heat, chem. skin irritation). Pain Gate control Theory
  • 30.
  • 33.
    Central Biasing Theory Descending neurons are activated by: stimulation of A-delta & C neurons, cognitive processes, anxiety, depression, previous experiences, expectations  Cause release of enkephalins (PAG) and serotonin (NRM)  Enkephalin interneuron in area of the SG blocks A-delta & C neurons
  • 34.
    Endogenous Opiates Theory Stimulation of A-delta & C fibers causes release of B- endorphins from the PAG & NRM Or  ACTH/B-lipotropin is released from the anterior pituitary in response to pain – broken down into B- endorphins and corticosteroids  Mechanism of action – similar to enkephalins to block ascending nerve impulses  Examples: TENS (low freq. & long pulse duration)
  • 35.
    1. Intensive (Summation) Theory 2. Specificity Theory 3. Strong‟s Theory 4. Pattern Theories 5. Central summation Theory 6. The Fourth Theory of pain 7. Sensory interaction Theory 8. Pain Gate control Theory Theories of Pain
  • 36.
     Erb -1874 According to this theory “every stimulus was capable of producing pain if it reached sufficient intensity”.  Developed by Goldscheider -1894  Both stimulus intensity and central summation as critical determinants of pain. It was implied that the summation occurred in the dorsal horn cells. Intensive (Summation ) Theory
  • 38.
     Von Frey-1895  This theory is based on the assumption that the free nerve endings are pain receptors, and that the other 3 types of receptors are also specific to a sensory experience.  Pain perception was viewed as a function of the amount of physical damage alone. Specificity Theory
  • 40.
     Strong –1895  Pain was an experience based on the noxious stimulus & the psychic reaction or displeasure provoked by the sensation Strong‟s Theory
  • 41.
     Nafe –1934  All cutaneous qualities are produced by spatial & temporal patterns of nerve impulses rather than by separate, modality-specific transmission routes. Pattern Theories
  • 42.
     Livingston –1943  The intence stimulation resulting from nerve & tissue damage activated fibers that projected to internuncial neuron pools within the spinal cord.  Abnormal reverberating circuits were created, with self activating neurons.  Prolonged abnormal activity bombarded cells in the spinal cord, & information was projected to the brain for pain perception. Central summation Theory
  • 43.
     Hardy, Woff& Goodell- 1940  Expanded on strong theory  Stated that pain was composed of 2 components:the perception of pain & the reaction one has to it.  Physiopsychological process involving cognitive functions of the individual & influenced by past experinces,culture, & various psychological factors that produce great variation in the “reaction pain threshold” The Fourth Theory of pain
  • 44.
     Noordenbos –1959  2 systems involving transmission of pain & other sensory information with a fast & slow system.  The slow system, composed of unmyelinated small diameter fibers, was presumed to conduct somatic & visceral afferents.  The fast system, composed of large fibers, was said to inhibit transmission of the small fibers. Sensory interaction Theory
  • 45.
  • 46.
    Pain Evaluation  Needto determine underlying cause if possible  Pain is subjective  Difficult to describe and characterize objectively
  • 47.
     In alltypes of pain accurate assessment is essential.  However simply asking the patient “how much does it hurt” is not enough.  There is no direct relationship between physical pathology and the intensity of pain.  The patient‟s subjective experience may be difficult to communicate. Pain Assessment
  • 48.
    OPQRST Format Origin/Onset ofpain Position /pattern of pain Quality of pain Quantity of pain Radiating pain Signs &Symptoms Treatment ASSESSMENT OF PAIN
  • 49.
     Origin /Onsetof pain: how did the pain started: suddenly/gradually  Mechanism of injury  Position/pattern: constant or periodic Localized/ radiating Aggravating and relieving factors Improving/worsening/remain same  Quality of pain: mechanical-pressing stabbing Chemical-burning Neural-numbness/pins and needles Vascular- throbbing
  • 50.
     Quantity ofpain: intensity of pain  Radiation: characteristics of pain radiation  Signs and symptoms: Functional, psychological  Treatment: Previous treatment Current treatment effectiveness
  • 51.
     Verbal ratingscale  Wong/baker faces  Pain diagrams / Body diagrams  Visual analogue scale  McGill pain questionnaire Tools used to measure pain
  • 54.
    Pain diagrams /Body diagrams
  • 58.
    Visual Analogue Scale The VAS is a simple robust pain measurement tool  It can be used to measure severity & or Improvement  It can be reliably used for children over the age of five  The VAS is usually designed as a 10cm line with descriptors at each end.
  • 59.
    Visual Analogue Scale NoPain Worst pain Possible Pain The example shows a patient recording a 9.0 i.e. The patient has made a mark 9cms from the no pain end of the scale. NB The VAS can be compromised if descriptors or numbers are added between the end points. {The 10 cm line allows for easy measurement and recording}
  • 60.
    i. Sheila Kitchen.Electrotherapy:Evidence-BasedPractice ii. Val Robertson, Alex Ward, ohn Low and Ann Reed.Electrotherapy Explained-Principles & Practice. iii. Basana Kumar Nanda.Electrotherapy Simplified. Newdelhi:Jaypee brothers;2008. iv. Susan B O‟Sullivan, and Thomas J Schmitz. Physical Rehabilitation. Newdelhi:Jaypee brothers;2007. References