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Pain Modulation
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Objectives:
At the end of this lecture the student should be able to:

1. Define pain.
2. Classify pain.
3. Describe the characteristics of different body receptors.
4. Explain pain perception.
5. Describe neural transmission of painful stimuli.
6. Discuss different neurophysiologic mechanisms of pain control.
7. List pre-requisites for effective pain management.
8. Explain the mechanism of pain reduction using different electrotherapy modalities.

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 Pain Modulation

Definitions:
1. Pain is a subjective unpleasant sensory and emotional experience associated with actual or
potential tissue damage, with more than one dimension and abundance of descriptions of
its qualities and characteristics.
2. Potential tissue damage means that the pain receptors are vigorously stimulated by
external stimulus without any actual damage or cut to the skin or other tissues.
3. Pain is essential to warn us about tissue damage and produce a withdrawal response or
guarding muscle spasm to protect the injured part. It can be also a cause for disability and
loss of function.

Classification of pain:
Pain can be classified according to its duration into:

1. Acute pain:
a. It is usually associated with tissue damage.
b. It is characterized by well-defined pain onset, i.e., the patient can tell when it exactly
started.
c. It responds to analgesic drugs and treatment of the underlying cause.
d. It can be sub-classified according to its type into;
i. Fast pain:
✓ It is well localized pain.
✓ It is brief in its duration.
✓ Well matched to the stimulus e.g., the initial pain of pinprick, burn with hot
pot, etc.
✓ It is transmitted through Aδ fibers.

ii. Slow pain:

✓ Poorly localized pain.
✓ It is an aching, throbbing or burning pain.
✓ Less related to the stimulus.
✓ It is transmitted through C fibers.
✓ It is not relieved quickly, because free nerve endings do not accommodate at
all.

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2. Chronic pain:
a. Chronic pain (OR persistent pain) is defined as pain lasting for six months or more OR
the pain that persists after apparent tissue healing.
b. It has an ill-defined onset, i.e., the patient CAN'T identify when it exactly started.
c. It usually produces significant changes in personality, lifestyle and functional ability.

3. Referred pain: (Figure: 14.01)

a. Referred pain is a pain caused by visceral tissue damage or visceral pathology but felt
in a remote area of skin, i.e., deep visceral pain is most commonly referred to a
cutaneous area and/or the underlying muscles e.g.,
i. Cardiac pain is felt in the medial aspect of the left arm, forearm and hand, left
side of the neck and left lower jaw.
ii. Pain in the spleen is felt in the left shoulder.
iii. Pain in the gall bladder is felt in the right shoulder.

b. Referred pain can be explained as;

i. Afferent nociceptors from the skin and afferents from viscera synapse on the
same posterior horn cells in the spinal cord.
ii. Peripheral sensory nerve of the posterior horn cells is bifurcated (divided into
two branches), one branch supplying the skin and the other supplying the
viscera.

Fig. 14.01: Mechanisms of referred pain.

Pain perception and transmission:

1. Body receptors:
a. Several types of sensory receptors are present in the body, e.g., Meissner's corpuscles,
Pacinian corpuscles and nociceptors.
b. Stimulation of skin or tissue nociceptors will produce pain.
c. Stimulation of other types of receptors may decrease pain perception.

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 d. It is important to know different types of body receptors and the kind of stimuli that
activate them.
e. Body receptors include; (Figure: 14.02)
i. Meissner's corpuscles respond to light touch.
ii. Pacinian corpuscles respond to deep pressure.
iii. Merkel's discs respond to movements of hair follicles and to deep pressure but
more slowly than Pacinian corpuscles.
iv. Ruffini end organs OR corpuscles respond to touch, skin tension and change in
joint position (in joint capsules and ligaments).
v. Krause's end bulbs are cold thermo-receptors.
vi. Pain receptors, nociceptors OR free nerve endings are sensitive to painful
(noxious) stimuli e.g., extreme mechanical, thermal or chemical stimuli and/or
actual tissue damage e.g., cuts, burns, sprains, etc.

Fig. 14.02: Different types of sensory receptors.

2. Pain Transmission:
a. Nociceptive neurons; (Figure: 14.03)
i. They are specialized sensory neurons called nociceptors.
ii. They transmit pain signals to higher centers.
iii. Their dendrites represent the peripheral nerve with their tip located in the skin,
which are called free nerve endings.
iv. The cell body lies in the dorsal root ganglion near the spinal cord.
v. The axon represents the dorsal root.

Fig. 14.03: Nociceptive neurons.

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b. Many chemical mediators are involved in signal transmission between different
neurons through the pain pathway;
i. Prostaglandin and bradykinin are released from damaged cells. They act to
sensitize pain receptors (decreasing depolarization threshold).
ii. Substance P;
✓ Is released from the nociceptors to start the action potential in their
membranes.
✓ It acts as the neurotransmitter between the first- and second-order neurons
in the pain pathway at the dorsal horn of the spinal cord.

c. Pain pathway; (Figure: 14.04 and 14.05)

i. For pain signals to reach the brain, it must pass through several afferent neurons,
which are named according to their order, i.e., first, second and third order
neurons.
ii. With trauma, damaged cells release prostaglandin and bradykinin, which
sensitize pain receptors.
iii. When the nociceptor is stimulated, it releases substance P which initiates action
potential in the nociceptive fibers.
iv. This action potential is then transmitted toward the spinal cord through the first
order neurons of pain pathway (C and Aδ fibers).
v. The Aδ and C fibers have different characteristics and pathway as they conduct
impulses to the brain; (Figure: 14.04)
vi. Thalamus can identify presence of pain but CANNOT locate or define type of
pain.
vii. Third order neurons projects from the thalamus to; (Figure: 14.06)
✓ The sensory cortex in the postcentral gyrus of the cerebrum OR area (3,1 and
2), to help in pain localization.
✓ Sensory association areas or area 5 and area 7which help in;
• Pain perception;
o Identify type of pain (pricking, burning, aching, throbbing, etc.)
o Identify pain severity.
• Integration of the current painful experience with past experiences and
emotions that form our response to pain.

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Fig. 14.04: Pain pathway and perception. Fig. 14.05: Pathway of pain signals

Fig. 14.06: Sensory area and sensory association area.

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Mechanisms of pain control:
Three different theories have been proposed to explain pain modulation which involve
stimulation of Aβ, Aδ and C fibers; (Figure: 14.07)

1. Stimulation of the ascending Aβ afferents

which blocks pain impulses carried along C
afferent fibers. (Gate control theory)
2. Stimulation of the descending dorsolateral
tract of the spinal cord by Aδ and C fibers
results in blocking of the impulses carried
through the Aδ and C afferent fibers.
3. The stimulation of Aδ and C afferent fibers
causes the release of β-endorphin resulting in
a prolonged activation of the descending
dorsolateral tract.
4. Pain relief is not produced by only one of the
following mechanisms, but may be a
combination of more than one mechanism at
the same time.
Fig.14.07: Sensory transmission of afferent stimuli
through Aβ, Aδ and C fibers.

1. Gate control Theory: (Figure: 14.08)

a. It was first described by Willem Noordenbos in 1959, and refined by Melzack and
Wall and Castel in 1965.

b. Components of the gate control theory;

i. C fibers transmit painful or noxious sensations.
ii. Aβ fibers transmit tactile and position sensations.
iii. Transmission cells (T-cells) located in the dorsal horn of spinal cord.
iv. Inhibitory interneurons in the Substantia Gelatinosa of Rolandi (SGR).
v. Substantia Gelatinosa of Rolandi represents lamina II and III in the spinal cord.

c. The gate control theory proposes the followings;

i. Both Aβ and C fibers stimulate the transmission cells (T-cells) to pass the
impulses to the higher centers of the brain.
ii. The inhibitory interneurons in the SGR inhibit the T-cells, i.e.,
✓ When the SGR is inhibited, the T-cell becomes stimulated and the gate is
"open".
✓ When the SGR is stimulated, the T-cell becomes inhibited and the gate is
"closed".

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 iii. Impulses transmitted through C fibers inhibit the SGR which opens the gate and
permit the passage of pain to higher brain centers.
iv. Impulses transmitted through Aβ fibers stimulate the SGR which closes the gate
and prevent the passage of impulses transmitted through C fibers.

v. So, when Aβ fibers are stimulated pain impulses transmitted through C fibers
are not transmitted to the second order neurons and CANNOT pass to higher
sensory centers.
vi. The balance between the input from the C fibers and Aβ fibers determines how
much of the pain impulses are blocked.
vii. Aβ fibers may also stimulate enkephalins interneurons in the spinal cord to
release enkephalins which inhibit transmission through T-cells and "close the
gate".

d. Gate control theory can be stimulated through;

i. Tactile stimulations, e.g.,
✓ Rubbing a contusion.
✓ Applying moist heat.
✓ Massaging sore muscles.
✓ Moving the painful joint in slow rhythmic movement.

ii. Applying electrical stimulation: conventional TENS, burst TENS, Interferential

current, HVPGS.

Fig.14.08: Gate control theory.

2. Descending pain control theory: (Figure: 14.09)

a. It involves central control of pain at the higher centers of the central nervous system
(CNS) which "closes the gate" at the dorsal horn.
b. Components of the descending pain control theory;
i. Aδ fibers transmitting fast sharp pain sensation.
ii. Peri-Aquaductal Grey matter (PAG) in the midbrain.
iii. Raphe Magnus Nucleus (RMN) in the pons and medulla oblongata.
iv. Encephalin interneurons in the dorsal horn of spinal cord.
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 c. Descending pain control theory;
i. Ascending pain impulses through Aδ fibers stimulate the PAG in the midbrain.
ii. The PAG stimulates the RMN in the Pons and medulla.
iii. The RMN stimulates the enkephalin interneurons in the dorsal horn through the
descending tracts (dorsal or dorsolateral tracts).
iv. The enkephalin interneurons and other descending tracts release enkephalin and
norepinephrine to block transmission through T-cells.

d. This mechanism can be stimulated through brief intense stimulation, e.g.,

i. Acupressure or acupuncture.
ii. Low TENS, burst TENS and brief intense TENS.

3. Beta (β) -Endorphin and Dynorphin theory: (Figure: 14.10)

a. β-endorphin and dynorphin are endogenous opioids with potent analgesic effect.
b. Prolonged stimulation of Aδ and C fibers for 20-40 minutes will;
i. Stimulate the release of endogenous opioids from the hypothalamus and spinal
cord.
ii. Inhibit pain through stimulation of the PAG and RMN.

c. The reticular formation in the brainstem (stimulated by C fibers) will stimulate the
hypothalamus to release β-endorphin and dynorphin.

d. This mechanism of pain control can be stimulated through;

i. Acupressure or acupuncture.
ii. Low TENS, burst TENS and brief intense TENS.
iii. Diadynamic current.

Fig. 14.09: Descending pain control theory. Fig. 14.10: Endogenous opioids pain control theory.
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Pain Assessment
1. Pain is a subjective experience that cannot be quantified by the therapist.
2. Pain assessment is very important to choose the best treatment modality.
3. It depends on self-report describing;
a. Pain intensity.
b. Location.
c. Duration.
d. Aggravating and alleviating factors.

4. Pain assessment scales:

a. Category scale:
i. Category scales consist of verbal descriptions of pain intensity.
ii. The patient chooses the word that best describes his pain;
✓ Mild.
✓ Discomforting.
✓ Distressing.
✓ Horrible.
✓ Excruciating.
iii. Advantages: it is used for;
✓ Old patients.
✓ Poorly educated patients.
iv. Disadvantages;
✓ It is not a continuous scale.

b. Numeric Rating Scale (NRS):

i. It is the simplest and most frequently used approach in pain assessment.
ii. Patient expresses his pain intensity on a scale from "0" to "10", i.e., "0" represents
no pain and "10" represents the worst pain.
iii. The numbers can be converted to faces that represent pain intensity. (Figure:
14.11)
iv. Advantages;
✓ It does not need training.
✓ It gives continuous measurements.

c. Visual Analog Scale (VAS): (Figure: 14.11)

i. It is a simple and efficient method of pain assessment.
ii. It consists of a 10 cm line with the title "no pain" at one end and "the worst pain"
on the other end.
iii. The patient marks on the line to indicate pain intensity then the therapist
measures the distance between the zero point and the mark on the scale.
iv. Disadvantages:
✓ It requires relatively long time to measure the scale.

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 Fig. 18.11: Visual Analog Scale (VAS).

d. McGill Pain Questionnaire (MPQ):

i. The MPQ is a multidimensional scale.
ii. It consists of 20 sets of words that describe pain, each set has two to six words
that vary in intensity or quality of pain.
iii. It scales pain in three dimensions;
✓ Sets no. 1-10 describe sensory quality.
✓ Sets no. 11-15describe affective dimension.
✓ Set no. 16 describes intensity.
✓ Sets no. 17-20 are miscellaneous words.

5. Algometer: (Figure: 14.12)

a. Algometer is a hand-held equipment that measures pain and pressure sensitivity.
b. It is an objective method of quantifying and documenting pain that CANNOT be
obtained by other methods, e.g., pain threshold and pain tolerance.
i. Pain threshold: is the minimum pressure which causes pain in tender and trigger
points.
ii. Pain tolerance: is the maximum pressure that can be tolerated over tender points.

c. It provides objective information about;

i. Pain threshold.
ii. Pain tolerance.
iii. Location of tender and trigger points.
iv. Treatment progress.

d. Procedure:
i. The therapist puts the rubber-tipped
head of the algometer over the trigger
point and press firmly and slowly.
ii. He records the amount of pressure
required to start pain sensation (pain
threshold) or maximum pain tolerated by
the patient (pain tolerance).
iii. This is repeated every few sessions to
follow up with the patient progress.
Fig. 14.12: Algometer.
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Pain management:
N.B.: There is NO single best therapeutic modality for pain control.
N.B.: Selection of the best therapeutic modalities depends on the patient's condition.
N.B.: Part of pain management is to change the patient's response of pain.

1. Prerequisites for effective pain management:

Selection of the best therapeutic modality is based on:

a. Identifying the primary cause of pain:
i. Undiagnosed pain might hide a serious disorder.
ii. Treating pain without treating the main cause is useless.

b. Understanding neurophysiology of pain perception, transmission and management.

c. Developing a clear rationale for the modality used based on;
i. Patient's condition.
ii. Knowledge of modalities.

2. Mechanism of action of different therapeutic modalities in pain control:

a. Cold application: relieves pain through;
i. Vasoconstriction and decreasing the release of chemical irritants.
ii. Stimulation of Aβ fibers to close pain gate.
iii. Decreasing nerve conduction velocity.
iv. Increasing pain threshold.
v. Reducing muscle spasm through prolonged icing.
vi. The most common techniques of cold application;
✓ Cold packs or bags.
✓ Cold immersion.
✓ Ice massage.
✓ Ice baths.
✓ Spray-stretch technique.

b. Hot application: relieves pain through;

i. Increasing circulation and washing out chemical irritants.
ii. Stimulation of Aβ fibers to close pain transmission.
iii. Reducing edema.
iv. Reducing muscle spasm.
v. Heating modalities include;
✓ Hot packs.
✓ Paraffin wax.
✓ Infrared radiations.
✓ S.W.D. and M.W.D.

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 Cold Vs Hot application in pain control

Cold application Hot application

Acute cases Sub-acute and chronic cases
After exercise to treat minor injuries Before mobilization exercises
After deep friction massage to reduce In cases of chronic edema
inflammation.
In cases of joint stiffness

c. Ultrasound: relieves pain through;

i. Indirect effect through treating the cause of pain, e.g.,
✓ Adhesions and scars.
✓ Muscle spasm.
✓ Inflammation.
✓ Edema.

ii. Friction with skin which stimulates Aβ fibers to close pain gate.
iii. Increasing pain threshold through its thermal effect.
iv. Phonophoresis.

d. LASER: relieves pain through;

i. Enhancing healing and anti-inflammatory effect.
ii. Increasing pain threshold.
iii. Decreasing nerve conduction velocity.
iv. LASER is used for pain relief in many acute and chronic conditions e.g.,
Musculoskeletal disorders (rheumatoid arthritis, osteoarthritis), soft tissue
injuries, inflammatory conditions (bursitis) and neurogenic pain.

e. Electrical stimulation: relieves pain through;

i. Direct effect through;
✓ Gate control mechanism.
✓ Descending pain control theory.
✓ Release of endogenous opiates.

ii. Indirect effect by assisting in the healing process.

iii. Different electrical stimulating currents:
✓ TENS.
✓ Interferential therapy.
✓ High Voltage Pulsed Galvanic Stimulation (HVPGS).
✓ Diadynamic current.

References:
1. Cameron MH.: Physical Agent in Rehabilitation from Research to Practice, 2nd Ed.
Saunders, 1999; Pp: 41-71.
2. Prentice WE: Therapeutic Modalities for Physical Therapists, 2nd Ed. New York, The
McGraw-Hill Companies, 2002; Pp: 28-48.

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