Download PAIN CONTROL THEORIES

PAIN & PAIN CONTROL
THEORIES
Managing Pain
What is Pain?
“An unpleasant sensory & emotional experience associated with actual or
potential tissue damage, or described in terms of such damage” –
The International Association for the Study of Pain
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
Experienced because of nociceptors being sensitive to extreme mechanical,
thermal, & chemical energy.
Composed of a variety of discomforts
One of the body’s defense mechanism (warns the brain that tissues may be in
jeopardy)
Acute vs. Chronic –
The total person must be considered. It may be worse at night when the person is
alone. They are more aware of the pain because of no external diversions.
Where Does Pain Come From?
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
Pain Sources
Fast vs. Slow Pain –
Fast – localized; carried through A-delta axons in skin
Slow – aching, throbbing, burning; carried by C fibers
Nociceptive neuron transmits pain info to spinal cord
via unmyelinated C fibers & myelinated A-delta fibers.
• The smaller C fibers carry impulses @ rate of 0.5 to 2.0 m/sec.
• The larger A-delta fibers carry impulses @ rate of 5 to 30 m/sec.
Acute vs. Chronic
What is Referred Pain?
Occurs away from pain site
Example: Kerr’s sign
Types of referred pain:
Myofascial Pain – trigger points, small hyperirritable areas within
a m. in which n. impulses bombard CNS & are expressed at
referred pain
• Active – hyperirritable; causes obvious complaint
• Latent – dormant; produces no pain except loss of ROM
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
Terminology
Noxious – harmful, injurious
Noxious stimuli – stimuli that activate
nociceptors (pressure, cold/heat
extremes, chemicals)
Nociceptor – nerve receptors that
transmits pain impulses
Pain Threshold – level of noxious
stimulus required to alert an individual
of a potential threat to tissue
Pain Tolerance – amount of pain a
person is willing or able to tolerate
Hyperesthesia – abnormal acuteness
of sensitivity to touch, pain, or other
sensory stimuli
Paresthesia – abnormal sensation,
such as burning, pricking, tingling
Inhibition – depression or arrest of a
function
Inhibitor – an agent that restrains/retards
physiologic, chemical, or enzymatic action
Analgesic – a neurologic or
pharmacologic state in which painful
stimuli are no longer painful
Accommodation phenomenon –
adaptation by the sensory receptors to
various stimuli over an extended period
of time (e.g. superficial hot & cold
agents). Less sensitive to stimuli.
Questions to Ask about Pain
Pattern: onset & duration
Area: location
Intensity: level
Nature: description
P-Q-R-S-T format
Provocation – How the injury occurred & what activities   the pain
Quality - characteristics of pain – Aching (impingement), Burning (n. irritation),
Sharp (acute injury), Radiating within dermatome (pressure on n.)?
Referral/Radiation –
Referred – site distant to damaged tissue that does not follow the course of a
peripheral n.
Radiating – follows peripheral n.; diffuse
Severity – How bad is it? Pain scale
Timing – When does it occur? p.m., a.m., before, during, after activity, all the time
Pain Assessment Scales
Visual & Numeric Analog Scales
None
Severe
0
10
Locate area of pain on a pictures
McGill pain questionnaire
Evaluate sensory, evaluative, &
affective components of pain
• 20 subcategories, 78 words
McGill Pain Questionnaire
78 words that
describe pain are
grouped into 20 sets
and divided into 4
categories
representing
dimensions of the
pain experience
Completion may
take 20 minutes
Administered
every 2-4 weeks
Goals In Managing Pain
To control acute pain and protect
patient from further injury while
encouraging progressive exercise in a
supervised environment.
Reducing pain is an essential part of
treatment
Goals In Managing Pain
Encourage body to heal through
exercise designed to progressively
increase functional capacity and to
return the patient to work, recreational
and other activities as swiftly and safely
as possible
Transmission of Pain
Types of Nerves
Neurotransmitters
Types of Nerves
Afferent (Ascending) – transmit impulses
from the periphery to the brain
First Order neuron
Second Order neuron
Third Order neuron
Efferent (Descending) – transmit impulses
from the brain to the periphery
First Order Neurons
Stimulated by sensory receptors
End in the dorsal horn of the spinal cord
Types
A-alpha – non-pain impulses
A-beta – non-pain impulses
• Large, myelinated
• Low threshold mechanoreceptor; respond to light touch & lowintensity mechanical info
A-delta – pain impulses due to mechanical pressure
• Large diameter, thinly myelinated
• Short duration, sharp, fast, bright, localized sensation (prickling,
stinging, burning)
C – pain impulses due to chemicals or mechanical
• Small diameter, unmyelinated
• Delayed onset, diffuse nagging sensation (aching, throbbing)
Neural Transmission
(First Order Neurons)
First order or
primary afferents
transmit impulses
from the sensory
receptor to the
dorsal horn of the
spinal cord
Afferent First Order Neurons
Second Order Neurons
Receive impulses from the FON in the dorsal horn
Lamina II, Substantia Gelatinosa (SG) - determines the input sent
to T cells from peripheral nerve
• T Cells (transmission cells): transmission cell that connects sensory n.
to CNS; neurons that organize stimulus input & transmit stimulus to
the brain
Travel along the spinothalmic tract
Pass through Reticular Formation
Types
Wide range specific
• Receive impulses from A-beta, A-delta, & C
Nociceptive specific
• Receive impulses from A-delta & C
Ends in thalamus
Neural Transmission
(Second Order Neurons)
Second order
afferent fibers carry
sensory messages
from the dorsal horn
to the brain
Second order
afferent fibers are
categorized as wide
dynamic range or
nociceptive specific
Neural Transmission
(Second Order Neurons)



Wide dynamic range
second order afferents
receive input from A, A
and C fibers.
Second order afferents
serve relatively large,
overlapping receptor
fields
Nociceptive specific
second order afferents
respond exclusively to
noxious stimulation
• Receive input only from A
and C fibers
Third Order Neurons
Begins in thalamus
Ends in specific brain centers (cerebral
cortex)
Perceive location, quality, intensity
Allows to feel pain, integrate past experiences
& emotions and determine reaction to stimulus
Neural Transmission
(Third Order Neurons)
• All of these neurons
synapse with third
order neurons
which carry
information to
various brain
centers where the
input in integrated,
interpreted and
acted upon
Descending Neurons
Descending Pain Modulation (Descending Pain Control
Mechanism)
Transmit impulses from the brain (corticospinal tract in the
cortex) to the spinal cord (lamina)
Periaquaductal Gray Area (PGA) – release enkephalins
Nucleus Raphe Magnus (NRM) – release serotonin
The release of these neurotransmitters inhibit ascending neurons
Stimulation of the PGA in the midbrain & NRM in the
pons & medulla causes analgesia.
Endogenous opioid peptides - endorphins & enkephalins
Neurotransmitters
Chemical substances that allow nerve impulses to move from one
neuron to another
Found in synapses
Substance P - thought to be responsible for the transmission of painproducing impulses
Acetylcholine – responsible for transmitting motor nerve impulses
Enkephalins – reduces pain perception by bonding to pain receptor sites
Norepinephrine – causes vasoconstriction
2 types of chemical neurotransmitters that mediate pain
• Endorphins - morphine-like neurohormone; thought to  pain threshold by binding to
receptor sites
• Serotonin - substance that causes local vasodilation &  permeability of capillaries
• Both are generated by noxious stimuli, which activate the inhibition of pain
transmission
Can be either excitatory or inhibitory
Sensory Receptors
Mechanoreceptors – touch, light or deep pressure
Meissner’s corpuscles (light touch), Pacinian
corpuscles (deep pressure), Merkel’s corpuscles (deep
pressure)
Thermoreceptors - heat, cold
Krause’s end bulbs ( temp & touch), Ruffini
corpuscles (in the skin) – touch, tension, heat; (in joint
capsules & ligaments – change of position)
Proprioceptors – change in length or tension
Muscle Spindles, Golgi Tendon Organs
Nociceptors – painful stimuli
mechanosensitive
chemosensitive
Sensory Receptors
Nerve Endings
“A nerve ending is the termination of a nerve fiber in a
peripheral structure.” (Prentice, p. 37)
Nerve endings may be sensory (receptor) or motor
(effector).
Nerve endings may be:
Respond to phasic activity - produce an impulse when the stimulus
is  or , but not during sustained stimulus; adapt to a constant
stimulus (Meissner’s corpuscles & Pacinian corpuscles)
Respond to tonic receptors produce impulses as long as the
stimulus is present. (muscle spindles, free n. endings, Krause’s end bulbs)
Superficial – Merkel’s corpuscles/disks, Meissner’s corpuscles
Deep – Pacinian corpuscles,
Nerve Endings
Merkel’s corpuscles/disks Sensitive to touch & vibration
Slow adapting
Superficial location
Most sensitive
Meissner’s corpuscles –
Sensitive to light touch &
vibrations
Rapid adapting
Superficial location
Pacinian corpuscles Sensitive to deep pressure &
vibrations
Rapid adapting
Deep subcutaneous tissue location
Krause’s end bulbs –
Thermoreceptor
Ruffini corpuscles/endings
Thermoreceptor
Sensitive to touch & tension
Slow adapting
Free nerve endings Afferent
Detects pain, touch, temperature,
mechanical stimuli
Nociceptors
Sensitive to repeated or prolonged stimulation
Mechanosensitive – excited by stress & tissue damage
Chemosensitive – excited by the release of chemical
mediators
Bradykinin, Histamine, Prostaglandins, Arachadonic Acid
Primary Hyperalgesia – due to injury
Secondary Hyperalgesia – due to spreading of chemical
mediators
Pain Control Theories
Gate Control Theory
Central Biasing Theory
Endogenous Opiates Theory
Gate Control Theory
Melzack & Wall, 1965
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
Second or neurons (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
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).
Brain
Gate (T
cells/ SG)
Pain
Heat, Cold,
Mechanical
Gate Control Theory


Sensory information
coming from A fibers
is transmitted to higher
centers in brain
“Pain message" carried
along A & C fibers is
not transmitted to
second-order neurons
and never reaches
sensory centers
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
Least understood of all the theories
Stimulation of A-delta & C fibers causes release of Bendorphins 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)
Mechanisms of Pain Control
The theories presented are only models
Pain control is the result of overlapping
mechanisms
Useful in conceptualizing the perception
of pain and pain relief
Pain Management
Therapeutic modalities can be used to



Stimulate large-diameter afferent fibers(
TENS, massage, analgesic balms)
Decrease pain fiber transmission velocity
(cold, ultrasound)
Stimulate small-diameter afferent fibers
and descending pain control mechanisms
(accupressure, deep massage, TENS)
Pain Management
Therapeutic modalities can be used to

Stimulate release of endogenous opioids
through prolonged small diameter fiber
stimulation with TENS
Goals in Managing Pain
Reduce pain!
Control acute pain!
Protect the patient from further injury while
encouraging progressive exercise
Other ways to control pain
Encourage central biasing – motivation,
relaxation, positive thinking
Minimize tissue damage
Maintain communication w/ the athlete
If possible, allow exercise
Medications