Chapter 4

Pain and Pain Relief

What is Pain?
An unpleasant sensory &
emotional experience associated
with actual or potential tissue
damage.
Why is dealing with pain
so tough?
 Modalities are directed to relieve pain
 Knowledge of pain improves the ability
to evaluate the injured athlete,
empathize with & understand the
response to injury & pain.
 Understand that all pain experiences
are not related to acute inflammatory
responses & that chronic and
persistent pain are significant
challenges.
 We are called to provide scientific
basis & outcomes data for treatments.
Pain is Multidimensional
Intensity dimension
Motivational:
 Affective dimension – feelings and
emotions
Mediators of the response
to injury and pain
 Past experience
 Family experience
 Culture
 Expectations
 Context in which injury occurs or
pain is experienced
symptom vs. pain as a
disease entity
Acute Pain: protection from injury
or a signal that something is
wrong
Acute Pain is of sudden onset and
results in muscle spasm &
guarding. This corresponds to
the events of the acute
inflammatory response (usually
resolves in <6 wks)
Persistent Pain
Lingering or recurrent pain
Symptom of a treatable condition
Several causative factors
1. Rest-reinjury cycle
2. Inaccurate or incomplete diagnosis
& eval
3. Myofascial pain
Stress, posture, length-tension imbalance,
trauma, somatization
Chronic Pain
Pain lasting beyond usefulness
No identifiable or treatable cause
Disease entity unto itself
1. RSD
2. Rheumatic diseases
3. Intractable back pain
4. Intractable phantom limb pain
Chronic vs. Persistent Pain
Chronic Persistent Pain
 Defy intervention  Generally
 What affect does tolerable once all
it have on the contributing
quality of life? factors are
identified and
addressed.
Individual’s response to
persistent/chronic pain
Anger and frustration with their
situation and the inability of the
health care system to help them
Erosion of family and social life and
support
Loss of identity and self esteem
Decreased quality of life
Pain & Patient Evaluation
What can injured physically active
people tell us about their pain
experience that can aid in the
evaluation?
Here is a formula to try!
P = Provocation: sudden onset or
insidious
Q = Quality: aching/burning/sharp/dull
R = Region: where? Radiating-dermatome
referred pain
S = Severity: pain scale
0 = no pain; 10 = cut my arm off
T = Timing: when did it begin, is there a
particular time of day it is worse,
present when you wake up, increase
with activity?
Physiology of Sensation –
Sensory Receptors
1. Mechanoreceptors-touch &
pressure
Superficial Deep
Meissner’s Golgi Tendon
corpuscles Organs
Pacinian corpuscles Muscle spindles
Found in the hair changes in muscle
follicles – easily length and tension
stimulated
Ruffini corpuscles
skin pressure
Sensory Receptors cont.
2. 3. Nociceptors
Thermoreceptor Free nerve endings
s
Response to Stimulated by:
temperature *mechanical stress
change: *thermal stress
Issues with *chemical stress
COLD *acute inflam.
WARM response
HOT
Neural Transmission
1st order afferent neurons (Primary)
transmit impulses from sensory
receptors to higher order centers.
-Amount of myelination determines rate
of conductivity
-Type AI,II,III deal with proprioception,
kinesthesia, & pain due to deep-tissue
damage
-Type A-beta are found in the skin
-Type A-delta: temperature, pressure,
noxious mech.
-Type C – unmyelinated:slow conduction
Ascending Spinal
Pathways
2nd Order Afferents
Sensory transmission to the brain
Pathways of the Ventral Spinal Cord
 Spinothalamic tract
 Spinoreticular tract
 Spinoencephalic tract
Nociceptive-specific second-order
afferents
3rd & 4th Order Afferents
3rd – connect input from reticular
formation to the thalamus
4th – transmission between centers
within the cerebral cortex
Interneurons – connection between
afferent and efferent neurons and
play a role in pain modulation
Transmitter Substances
 Neurotransmitters – acetylcholine
 Biogenic amine transmitters –
 Serotonin
 Norepinepherine
 Neuroactive peptides
1. Substance P- facilitate synaptic trans. in
nociceptive pathways
2. Enkephalins & Beta-endorphins (opioid
peptides) – inhibit transmission of pain
impulses
Key Concept!
Synaptic transmission will occur only if
the net effect of the transmitter
substances acting on the synapse is
facilitory. MOST transmitter substances
act to inhibit, rather than facilitate,
synaptic transmission. CONTEMPORARY
PAIN CONTROL THEORY hinges on the
notion that many therapeutic
interventions inhibit the transmission of
the pain message through activation of
inhibitory transmitter substances.
Higher Centers in the
Nociceptive System
Reticular formation of the medulla & pons
Sensory discrimination & motivation
(affective)
 Mesencephalon (PAG)
Sensory discrimination & motivation (afective)
 Thalamus
Somatosensory cortex
Limbic System – emotions, autonomic
responses, and endocrine responses to
injury and pain. Allows memory and
senses to regulate responses
Gate Control Theory of
Pain
A theory that proposes that pain
sensation could be altered by blocking
or gating impulses in the pain
pathways.
States that the large, myelinated
afferent fibers such as Type IA, IIA, and
A-beta can block transmission of
noxious stimuli at dorsal horn, thereby
prevent input reaching the brain.
Birth of TENS
 TENS
How does it work? – depolarize
afferent fibers, thereby allowing for
the blockage of the transmission.
A-beta fibers high input rate via
low-intensity stimulation, an
analgesic effect is produced.
Castel’s Model of Pain
Control
Level I: Endogenous opioids
 Release of enkephalin interneurons;
inhibition of substance P; prohibits
synaptic transmission; blocks pain at
1st synapse of nociceptive pathway;
therefore, similar to GATE Theory,
pain is modulated at the dorsal horn.
Level II Level III
Descending Influence Beta-Endorphin
Mediated
Analgesia through Analgesia through
brief intense stim. prolonged intense
stimulus
PAG raphe
Beta-endorphin (lg.
nucleus release peptide similar to
serotonin morphine) stimulates
depolar. raphe nucleus
enkephalin enkephalin
interneurons: interneuron
analgesia at
block substance P
segmental level
= PAIN
What about Cold & US?
COLD:
 slows nerve conduction in 1st order
afferents of nociceptive pathways
 This theory based on a DECREASED
neural input the dorsal horn (not an
inc. seen previous models)
US:
 Slows nerve conduction also
What else do we know?
Other methods to block out pain:
 Relaxation techniques
 Imagery
 Placebo effect
 Belief in the modality “ just give me
some ultra sound, it always makes
me feel better!”
Thank you