The Physiology and psychology of pain

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The Physiology and psychology of pain

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Title: The Physiology and psychology of pain

1
The Physiology and psychology of pain

Chapter 2

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 bodys 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 bodys
integrity is at risk.
The emotional response may be expressed by
screaming, crying, fainting, or just thinking
_at_, 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 stimulis 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 _at_
is this jerk doing to me.
The cultural components of pain are almost too
complex to define.
However, pain perception has been linked to
ethnicity and socioeconomic status.
Example
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.

8
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

12
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 nerves 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
NSAIDs play and important role in the tx of
acute pain in that they block the formation
cyclooxygenase and prevent the synthesis of
prostaglandins.
Therefore, NSAIDs are important as an early
mediator for the interruption of the pain and
inflammation cycle

15
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
A-delta 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
This initial reaction allows an indiviual to
realized that trauma has occurred and to
recognize the response as pain
Very quickly, the stinging or burning sensation
becomes an aching or throbbing sensation, which
indicates activation of which fiber
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

18
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 non-noxious
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 gamma-aminobutyric
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.
The mechanoreceptors play a limited role in the
modulation and transmission of pain
Lamina V- is a major synapse of A-delta and C
fibers in the dorsal horn.
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 bodys 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 cortexs 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.

28
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 cortexs 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
PAG receives input from the cortex, limbic
system, hypothalamus, and PSTT.
The hypothalamus sends ß-endorphins via neurons
to the PAG
Here they are routed to the nucleusmagnocellularie
s 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 bodys 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,
ß-endorphins 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.

32
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.

34
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, Aristotles belief prevailed until
the 19th century, when German scientist provided
irrefutable evidence that the brain is involved
with sensory and motor function

37
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 brains pain
center
The pathway includes the peripheral nerves, the
lateral STT in the spinal cord and the
hypothalamus (the brains 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.

42
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.

43
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

44
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 words 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.

46
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
A-beta fibers, which activate the SG to close the
spinal gate
Thus inhibiting transmission of the painful
stimulus

49
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.

50
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
low-intensity score by selecting the 1st word in
each category.

51
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

52
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.

53
Referred pain
54
Chronic Pain