2. Define Pain
Theories of Pain
Pain Gate Control theory
CONTENTS
3. 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 ?
4. 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)
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
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
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
10. 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
11. 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
27. Pain Gate control Theory
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
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
37.
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
39.
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
46. Pain Evaluation
Need to determine underlying cause if possible
Pain is subjective
Difficult to describe and characterize objectively
47. 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
48. OPQRST Format
Origin/Onset of pain
Position /pattern of pain
Quality of pain
Quantity of pain
Radiating pain
Signs &Symptoms
Treatment
ASSESSMENT OF PAIN
49. 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
50. Quantity of pain: intensity of pain
Radiation: characteristics of pain radiation
Signs and symptoms: Functional,
psychological
Treatment: Previous treatment
Current treatment effectiveness
51. Verbal rating scale
Wong/baker faces
Pain diagrams / Body diagrams
Visual analogue scale
McGill pain questionnaire
Tools used to measure pain
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
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}
60. 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