Transcript The Physiology and psychology of pain

The Physiology and
psychology of pain
Chapter 2
Pain

Of all the components of the injury response,
none is less consistent or less understood than
an individuals response to pain
 The sensation of pain is a diffuse entity inherent
to the nervous system and basic to all people
 It is a personal experience that all humans
endure
 Acute pain is the primary reason why people
seek medical attention and the major complaint
that they describe on initial evaluation.

Chronic pain may be more debilitating than the
trauma itself and, in many instances, is so
emotionally and physically debilitating that it is a
leading cause of suicide.
 Pain serves as one of the body’s defense
mechanisms by warning the brain that its tissues
may be in jeopardy, yet pain may be triggered
without any physical damage to tissues.
 The pain response itself is a complex
phenomenon involving sensory, behavioral
(motor), emotional, and cultural components.

Once the painful impulse has been initiated and
received by the brain, the interpretation of pain
itself is based on interrelated biological,
psychological, and social factors.
 What are the nerve fibers that stimulate pain?

Nociceptors.
Once these are stimulated, “pain” impulses are
sent to the brain as a warning that the body’s
integrity is at risk.
 The emotional response may be expressed by
screaming, crying, fainting, or just thinking
“#@%&, that hurts!”

 When
the pain is intense or unexpected,
an immediate reflex loop activates the
behavioral response by sending
instructions to motor nerves to remove the
body part from the stimulus.


Sticking your finger with a needle
Placing your hand on a hot stove
 These
stimuli’s activate specialized nerve
fibers to send signals through a peripheral
nerve network

Routing the impulses up the spinal cord to the
brain

When the afferent impulse reach the spinal cord,
a reflex loop is formed within the tract to activate
the muscles necessary to remove your hand or
finger from the stimulus.
 The remaining impulses of the reflex continue on
to the brain, where they are translated as pain,
and you respond by saying “ouch!” or other
choice words.
 If an individual has knowledge about a
potentially painful stimulus, such as receiving an
injection, cognitive mechanisms can inhibit the
reflex loop and block portions of the behavioral
response.
 As a the painful stimulus increases, so does the
conscious effort required to keep from trying to
escape from the stimulus.

The emotional component may still be in place
as you grimace, make a fist, or think “what the
@%^$ is this jerk doing to me.”
 The cultural components of pain are almost too
complex to define.


Example


However, pain perception has been linked to ethnicity
and socioeconomic status.
Italian patents are less inhibited in the expression of
pain than are the Irish or Anglo-Saxon patients
Ultimately, cultural components can be viewed
as any variable that relates to the environment in
which a person was raised and how that
environment deals with pain and responses to
pain.
Pain Process

Noxious input or nociceptive stimulus causes the
activation of pain fibers.
 The painful impulse is triggered by the initial
mechanical force of the injury (whether sudden
or gradual onset) and is continued by chemical
irritation resulting from the inflammatory process
 In subacute and chronic conditions, pain may be
continued by reflex muscle spasm in a positive
feedback loop or through the continued
presence of chemical irritation

The pain response is initiated by stimulation of
nociceptors


Nociceptors- specialized nerve endings that
respond to painful stimuli
Mechanical stress or damage to the tissues
excite mechanosensitive nociceptors
 Chemosensitive nociceptors are excited by
various chemical substances released during
the inflammatory response
 Chemical irritation of nerve endings may
produce a severe pain response without true
tissue distruction
 Unlike
other types of nerve receptors,
nociceptors display a sensitization to
repeated or prolonged stimulation
 During the inflammatory process, the
threshold required to initiate an action
potential is lowered, and the continued
stimulation of the chemosensitve receptors
perpetuates the cycle

To understand the complexity of pain,
comprehension of the various
neurophysiological pathways involved in
transmission, perception, and inhibition of pain is
critical.
 The nervous system

Forms a complex network of afferent and efferent
pathways.
• Transmitting and reacting to impulses that the brain
perceives as being painful

All noxious impulses are transmitted afferently to
the thalmus

This produces the “painful” stimulus which triggers the
physiological and psychological process described
earlier
Modulation of Pain
 Acute
pain response begins with a noxious
stimulus.

IE. A burn or cut externally or internally a
muscle strain or ligament sprain
 After
trauma chemicals are released in
and around the surrounding tissues.
 Immediately after the trauma, primary
hyperalgesia occurs

Lowers the nerve’s threshold to noxious
stimuli and magnifying the pain response

Within hours, secondary hyperalgesia occurs

↑ the size of the painful area as the chemicals diffuse
into the surrounding tissues
• Causes hypersensitivity

The initiation of the pain process always begins
with a chemical stimulus.


Review chemical precursors
During acute trauma



Cell walls become damaged
Causes dopamine and norepinephrine (NE) to be
released from precursors in the cell membrane
Causes the activation of phospholipas
• Allowing the cell membrane to release arachidonic acid
• When released in the presence of cyclooxygenase, it
converts to prostaglandin

Prostaglandins have many roles in inflammation,
but they also sensitize the nerve endings to
other chemicals

IE bradykinin
• Which in turn initiate nociception

Bradykinin, found in plasma and released during
coagulation that follows injury, are direct activators of
nociception.
• Powerful vasodilators, ↑ vascular permeability during the
inflammatory response

NSAID’s play and important role in the tx of
acute pain in that they block the formation
cyclooxygenase and prevent the synthesis of
prostaglandins.

Therefore, NSAID’s are important as an early
mediator for the interruption of the pain and
inflammation cycle
Pain fibers
 A-delta
fibers- a type of nerve that
transmits painful information that is often
interpreted by the brain as burning or
stinging pain
 C-fibers-
a type of nerve that transmits
painful information that is often interpreted
by the brain as throbbing or aching

After an injury, A-delta and C fibers carry
noxious stimuli from the periphery (using which
pathway?) to the dorsal horn of the spinal cord.
 The noxious stimuli activates 10-20% of the Adelta fibers and 50-80% of the C-fibers.
 Triggered by strong mechanical pressure or
intense heat, A-delta fibers produce a fast,
bright, localized pain sensation.
 C-fibers are triggered by thermal, mechanical,
and chemical stimuli and generate a more
diffuse, nagging sensation

After an injury, such as a sprained ankle, you
athlete feels

Sharp, well-localized, stinging or burning sensation
coming from which fibers??
• A-delta fibers


Very quickly, the stinging or burning sensation
becomes an aching or throbbing sensation,
which indicates activation of which fiber


This initial reaction allows an indiviual to realized that
trauma has occurred and to recognize the response
as pain
C-fibers
A third type of peripheral afferent nerve fiber
warrants mention. A-beta fibers, respond to light
touch and low intensity mechanical information.


Rubbing and injured area
These interrupt nociception to the dorsal horn
Ascending Pathways

First-order neurons- A-beta, A-delta, and C
nerve fibers.

Because they all originate in the periphery and
terminate in different areas of the dorsal horn

The gray matter of the spinal cord is divided into
10 layers of cell bodies called Laminae
 Before synapsing in the laminae the peripheral
afferent nerves course into the tract of Lissauer


Where A-delta and C fibers divide and send impulses
up and down one to two segments of the spinal
column.
Once in the dorsal horn of the spinal cord, the
small A-delta and C fibers synapse with neurons
and terminate in the various laminae
 Lamina
I contains several types of
neurons

The 2 of interest to us are
• Wide-dynamic-range (WDR) neurons
• Nociceptive-specific (NS) neurons


WDR- respond to both noxious and nonnoxious stimuli
NS- respond only to noxious stimuli
 These
neurons in lamina I are part of the
cells that make up the Long spinothalamic
tract (STT)
 The
Substantia Gelatinosa (SG), found
partially within lamina II, contain small
internuncial neurons


These neurons can excite (stalked cells) or
inhibit (islet cells) the transmission of noxious
stimuli
These neurons in the SG send axons to lamina
I and release enkephalin and gammaaminobutyric acid.
• Both which inhibit the transmission of noxious
stimuli

Enkephalin- a substance released by the body that
reduces the perception of pain by bonding to pain
receptors sites

Lamina III and IV- composed of WDR neuron
cells and low-threshold mechanoreceptors.


Lamina V- is a major synapse of A-delta and C
fibers in the dorsal horn.


The mechanoreceptors play a limited role in the
modulation and transmission of pain
It also has a large # of WDR cells that respond to a
spectrum of stimuli from light touch to mechanical
pressure and heat
WDR cells from laminae I & 5 make up the
majority of fiber in the STT.

Where first order neurons terminate and second order
neurons originate
• Second order- A nerve that has its body located in the spinal
cord. It connects second and third order neurons
• Third order- a nerve that has its body in the thalamus and
extending into the cerebral cortex
 1st
order neurons course from the periphery
to synapse in the dorsal root ganglion and
the laminae before crossing the spinal cord
to the STT

Once in the STT, noxious stimulus is then
transmitted to the brain via 2 different portions
of the STT
• The neospinothalamic (lateral) tract (NSTT)
• Paleospinothalamic (ventral) tract (PSTT)

This dual-tract system of afferent pain
pathways enables the body to have immediate
warning of the presence, location, and intensity
of an injury as well as the slow, aching
reminder that tissue damage has occurred.

NSTT receives input from A-delta fibers that synapse
with the nociceptive-specific neurons and the WDR
neurons in Laminae I & V.
 These neurons of the NSTT immediately cross the
ventral white column of the spinal cord to the
opposite antrolateral white column.
 Once in the ant horn, the fibers of the NSTT and a
portion of STT synapse with motor units or stimulate
preganglionic neurons of the sympathetic or
parasympathetic system and then communicate with
the thalamus.

This transmission is responsible for the motor and
autonomic response associated with tissue damage and
info pertinent to the site
• Intensity
• And duration of the painful stimulus

The NSTT has been described as the sensory
discriminative pathway of pain.
 The PSTT is located more medially, but still is in
the anterolateral portion of the white matter of
the spinal cord.

The PSTT receives input predominately from the C
fibers.
• These synapse with the nociceptive-specific neurons and the
WDR neurons in Laminae I & V

2nd order neurons of Laminae I & V cross over the
spinal cord and project to the reticular formation (RF)
• A diffuse network of cells and fibers located in the brain stem.
Influences alertness, waking, sleeping, and certain reflexes.

The RF is located in the central portion of the brain
stem, medulla oblongata, hypothalamus, thalamus,
limbic system, and periaqueductal gray (PAG).
 The
RF is responsible for evoking motor,
sensory, and autonomic responses to
noxious stimuli.

This allows the injured person to respond
rapidly to the stimuli.
 The
PSTT has multiple synapses with
other areas of the central brain
responsible for poorly localized, dull,
aching pain as well as for the behavioral,
emotional, and affective aspects of pain.

The brains limbic system aids in integrating
higher brain function with motivational and
emotional reactions.




Contains afferent nerves from the hypothalamus and
the brain stem.
Receives descending influence from the cortex.
This communication is responsible for the emotional
response to painful experiences.
When an injury occurs, the neural
communication between the limbic system,
thalamus, RF, and cortex produces reactions
such as fear, anxiety, or crying.
 In short , the limbic system is responsible for the
body’s affective qualities of reward, punishment,
aversive drives, and fear reactions to pain
 AKA: motivational-affective system.



The integration of the cortex is an important component
in both the ascending and descending aspects of pain
modulation.
Via axons, ascending pain stimuli are transmitted from
the thalamus to the central sulcus in the parietal lobe
(somatosensory cortex), where the pain is discriminated
and localized.
Because of the proliferation of nerve cells and the
cortex’s functions







Consciousness
Speech
Hearing
Memory
Thought
It is unlikely that the afferent synapses that occur during
noxious stimulation affect only one efferent neuron.
Thus, many areas of the cortex can be stimulated during
a painful experience.
Descending Pathways

The descending pain modulation mechanisms
could influence both the input and the mediation
of the noxious stimuli
 One of the descending mechanisms originates
in the cortex’s corticospinal tract.


The corticospinal tract descends from the cortex to
the medulla, where fibers cross over to the opposite
side of the medulla and to lower levels of the spinal
cord, where it terminates in laminae I-VII and
transends through the dorsolateral funiculus (large
fiber tract)
This tract could act to exert postsynaptic (descending)
control over the afferent transmission of thermal,
mechanical, and C fiber input at laminae I & II

A second structure exerting descending control
of noxious stimuli is the PAG


The hypothalamus sends ß-endorphins via
neurons to the PAG


PAG receives input from the cortex, limbic system,
hypothalamus, and PSTT.
Here they are routed to the nucleusmagnocellularies
of the rostral medulla that descends laterally to the
dorsal horn.
Another descending control system arises form
the nucleus raphae magnus in the upper
medulla

Descending axons from this region of the brain track
down to the lower medulla and the spinal cord, where
they release serotonin at their terminal end, producing
analgesia at laminae I, II, and V.

The notion of central control and descending
inhibition of pain is based on the body’s ability to
use and produce various forms of endogenous
opiates.


Each having a distinct function and a specific receptor
affinity.
The enkephalins are found throughout the
central nervous system, but particularly in the
dorsal horn.
 Thus, the aggregation of noxious stimuli may
cause both presynaptic and postsynaptic control
of nociception in the dorsal horn via enkephalin
release

Dynorphins are primarily located in laminae I &
5, making it feasible for them to inhibit pain.


Levels of dynorphin ↑ in laminae I & 5 during periods
of hyperstimulation.
However, their rapid degradation limits their role in
long-term pain reduction.
During periods of intense noxious input, ßendorphins are released and provide temporary
inhibition to noxious stimulation.
 This concept is based on their location in the
PAG and the idea that their release would block
interneuron interaction.

Review of the process of Pain
Transmission
 Much
decision making in the tx of pain can
be based on the understanding of the
physiological and chemical interaction that
occurs after trauma.
 In simple terms, pain transmission
appears to be fairly straightforward.

The acute pain response is initiated when
substances are released form injured tissues,
causing a noxious stimulus to be transmitted
via A-delta and C fiber to the dorsal horn

Once in the dorsal horn, the stimulus is
transmitted to the higher brain centers via the
STT, which bifurcates into 2 tracts.




The impulse is propagated via the NSTT to the
thalamus and then to the cortex, where discrimination
and location of the stimulus are assessed.
At the same time, noxious stimulation is projected
upward toward the RF, the PAG matter, the
hypothalamus, and the thalamus via the PSTT
Neurons in the thalamus send axon projections to the
limbic system and the cortex.
Once the noxious stimuli have reached the higher
centers of the brain, the descending control
mechanisms are activated, the incoming noxious
stimuli can be inhibited at various levels, and
endogenous opiates can be released.
Pain Theory: Historical
Perspectives
 Theories
regarding the cause, nature, and
purpose of pain have been debated since
the dawn of humankind.
 Most early theories were based on the
assumptions that pain was related to a
form of punishment.
 The word “pain” is derived from the Latin
word “poena” meaning fine, penalty, or
punishment.
 The
ancient Greek believed that pain was
associated with pleasure because the
relief of pain was both pleasurable and
emotional.
 Aristotle reassessed the theory of pain and
declared that the soul was the center of
the sensory processes and that the pain
system was located in the heart

The Romans, coming closer to contemporary
thought, viewed pain as something that
accompanied inflammation.
 In the 2nd century, Galen offered the Romans his
works on the concepts of the nervous system.


However, the views of Aristotle weathered the winds
of time.
In the 4th century, successors of Aristotle
discovered anatomic proof that the brain was
connected to nervous system

Despite this, Aristotle’s belief prevailed until the 19th
century, when German scientist provided irrefutable
evidence that the brain is involved with sensory and
motor function
Specificity Theory of Pain
Modulation
 Modern
concepts of pain theory continue
to advance from the ideas of Aristotle.

However, controversy still exists as to which
theories are correct.
 The
theories accepted at the turn of the
century were the specificity theory and the
pattern theory, two completely different
and seemingly contradictory views

The specificity theory suggests that there is a
direct pathway from peripheral pain receptors to
the brain.



The pain receptors are located in the skin and are
purported to carry pain impulses via a continuous
fiber directly to the brain’s pain center
The pathway includes the peripheral nerves, the
lateral STT in the spinal cord and the hypothalamus
(the brain’s pain center)
This theory was examined and refuted using clinical,
psychological, and physiological evidence by Melzack
and Wall in 1965.
• They discussed clinical evidence describing pain sensations
in severe burn patients, amputee patients, and patients with
degenerative nerve disease.

These syndromes do not occur in a fixed, direct
linear system
 Rather in the quality and quantity of the
perceived pain are directly related to a
psychological variable and sensory input.
 This theory had been previously addressed by
Pavlov, who inflicted dogs with a painful
stimulus, then immediately gave them food.
 The dogs eventually responded to the stimulus
as a signal for food and showed no responses to
the pain

The psychological aspect of pain perception was later
addressed by Beecher, who studied 215 soldiers
seriously wounded in the Battle of Anzio, finding that only
27% requested pain-relieving medication (Morphine).
 When the soldiers were asked if they were experiencing
pain, almost 60% indicated that they suffered no pain or
only slight pain, and only 24% rated the pain as bad.
 This was most surprising because 48% of the soldiers
had received penetrating abdominal wounds.
 Beecher also noted that none of the men were suffering
from shock or were insensitive to pain because inept
intravenous insertions resulted in complaints of acute
pain.




The conclusion was drawn that the pain experienced by
these men was blocked by emotional factors.
The physical injuries that these men had received was
an escape from the life-threatening environment of battle
to the safety of a hospital, or even release form the war.
This relationship suggests that it is possible for the
central nervous system to intervene between the
stimulus and the sensation in the presence of certain
psychological variables.
No physiological evidence has been found to suggest
that certain nerve cells are more important for pain
perception and response than others; therefore, the
specificity theory can be discounted.
Contemporary Pain Control
Theories

Although both the specificity and pattern theories
of pain transmission were eventually refuted,
they did provide some lasting principles that are
still present in contemporary pain modulation
theories


The strengths of these 2 theories, plus findings
obtained through additional research, were factored
together to for the basis of the current perspective
regarding pain transmission and pain modulation.
Still, there is much to be learned and studied
before the exact mechanisms of pain
transmission and perception are understood.
Next time



Gate control theory
Levels Theory of pain control
Assessment of pain








Visual analogue scale
McGill pain questionaire
Submaximal effort tourniquet test
Placebo effect
Referred pain
Chronic Pain
Pain management techniques
Chapter 3: Development and delivery of
treatment protocol
Pattern Theory of Pain
 States
that there are no specialized
receptors in the skin.
 Rather, a single “generic” nerve responds
differently to each type of sensation by
creating a uniquely coded impulse formed
by a spatiotemporal pattern involving the
frequency and pattern of nerve
transmission.

An analysis of the word’s elements



“Spatio”- the distance between the nerves impluses
“temporal”- the frequency of the transmission
An example of this type of coding can be found
with most institutional phone systems.

A call from inside a university has a different ring from
an outside call.

Although this theory was closer to being
neurological correct there were still
shortcomings
 Melzack and Wall refuted this theory as well,
based on the physical evidence of physiological
specialization of receptor-fiber units.

Plus this theory failed to account for the brains role in
pain perception.
Gate Control Theory

Implies a non-painful stimulus can block the
transmission of a noxious stimulus.
 Is based on the premise that the SG, located in
the dorsal horn of the spinal cord, modulates the
afferent nerve impulses.
 This then influences the first central transmission
(T) cells, which corresponds with the NSTT or
the PSTT and activate a central control
triggering the mechanisms responsible for the
response and perception of pain.






The SG acts as a modulating gate or a control system
between the peripheral nerve fibers and central cells that
permits only one type of never impulse (pain or no pain)
to pass through.
Serving in a capacity similar to that of a “switch operator”
in a railroad yard, the SG monitors the amount of activity
occuring on both incoming tracts in a convergent system
Opening and closing the gate to allow the appropriate
information to be passed along to the T cell.
Impulses traveling on the fast, nonpain fibers ↑ activity in
the SG.
Impulses on the slower pain fibers exert an inhibitory
influence.
When the SG is active, the gate is in its “closed” position
and a nonpainful stimulus is allowed to pass on to the T
cell.
 Example:

Bumping the head
• The initial trauma activates the A-delta and,
eventually, C fibers
• Rubbing the traumatized area stimulates the Abeta fibers, which activate the SG to close the
spinal gate
• Thus inhibiting transmission of the painful stimulus
Assessment of pain

Visual analogue scale


Picture
McGill pain questionnaire



Part I: is used to localize the pain and identify whether the
perceived source of the pain is superficial (external), internal, or
both.
Part II: incorporates the VAS that was described in the visual
analogue scale.
Part III: is the pain rating index, a collection of 76 words grouped
into 20 categories. Patients are to underline or circle the words in
each group that describes the sensation of pain being
experienced.
•
•
•
•
Groups 1-10= somatic in nature
Groups 11-15= affective
Group 16= evaluative
Group 17-20= miscellaneous words that are used on in the scoring
process.
Scoring

Add up the total number of words chosen, up to
the maximum of 20 words (one for each
category)

The level of intensity of pain is determined by the
value assigned to each word.
• 1st word = 1 point
• 2nd word = 2 point
• And so on

Pt could have a high score of 20, but have a lowintensity score by selecting the 1st word in each
category.
Submaximal Effort Tourniquet Test



In 1966, Smith et al described a method of matching a
patients pain using a SETT.
The SETT is performed by inflating a BP cuff to above
systolic pressure on the pt elevated arm.
Once the cuff is inflated, the pt is instructed to open and
close the hand or fist rhythmically.


A handgrip dynamometer and a metronome can be used for
standardization.
The pt should continue opening and closing the hand or
fist until the cramping sensation that he or she feels
“matches” the pain from the “original” pathology.
 The amount of time that elapses form onset to fruition of
matched pain is the recorded objective measure.
 The SETT can be repeated at every tx session to gauge
tx progress and is effective in matching all types of pain
Placebo Effect
 Placebo
stems from the Latin word for “I
shall please”


Used to describe pain reduction obtained from
a mechanism other than those related to the
physiological effects of the tx.
Linked to psychological mechanisms
 All

TM have some degree of placebo effect
Most studies involving TM involving the use of
a sham TM (ultrasound set at the intensity of
0) and an actual treatment have shown ↓
levels of pain in each group.
Referred pain
Chronic Pain
 Characteristics







of
Symptoms last longer than 6 months
Few objective medical findings
Medication abuse
Difficulty sleeping
Depression
Manipulative behavior
Somatic preoccupation
Pain Management Techniques
 Physical
measures
 Behavioral
and cognitive measures
On to Chapter 3
Development and Delivery of
Treatment Protocol