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Physiology & Psychology
of Pain
What is Pain??
Introductory Ideas
Sensation of the affected level of unpleasantness
Perception of actual or threatened damage
Perception based on expectations, past experience,
anxiety, suggestions, cognitive factors
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Acute
Chronic
Pain is Subjective
Simple Spinal Reflex Arc
First Order Neurons
Stimulated by sensory receptors
End in the dorsal horn of the spinal cord
Types
 A-alpha – non-pain impulses
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A-beta – non-pain impulses
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NCV – 36-72m/sec
A-delta – pain impulses due to mechanical pressure
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NCV - 70-120m/sec
Large diameter, myelinated, NCV – 4-30m/sec
Short duration, sharp, prickling, localized
C – pain impulses due to chemicals or mechanical
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Small diameter, unmyelinated, NCV - .5-2m/sec
Delayed onset, diffuse, aching, throbbing
Neurotransmitters
Chemical substances that allow nerve impulses
to move from one neuron to another
Found in synapses
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Norepinephrine
Substance P
Acetylcholine
Enkephalins
Endorphins
Serotonin
Can be either excitatory or inhibitory
Descending Neurons
Transmit impulses from the brain
(corticospinal tract in the cortex) to the spinal
cord (lamina)
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Periaquaductal gray area (PAG) – release
enkephalins
Nucleus Raphe Magnus (NRM) – release
serotonin
The release of these neurotransmitters inhibit
ascending neurons
Assessment of pain
Visual analogue scale

Picture
McGill pain questionnaire
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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 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.
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Groups 1-10= somatic in nature
Groups 11-15= affective
Group 16= evaluative
Group 17-20= miscellaneous words that are used in the scoring
process.
Pain Scales
Visual Analog Scale
None
Severe
0
10
Locate area of pain on a picture
McGill pain questionnaire

Evaluate sensory, evaluative, & affective components
of pain
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20 subcategories, 78 words
Scoring
Add up the total number of words chosen, up
to the maximum of 20 words (one for each
category)
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The level of intensity of pain is determined by the
value assigned to each word.
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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 from 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
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
Pain Control
Theories
Where have we been?
Where are we now?
Where have we been?
Specificity theory
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4 types of sensory receptors – heat, cold, touch, pain
A nerve responded to only one type
Nerve was continuous from the periphery to the brain
Pattern theory
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A single nerve responded to each type of sensation
by creating a code (i.E. Different telephone rings)
Gate control theory
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Melzack & wall, 1965 – the basis for theories today
Non-painful stimulus can block the transmission of a
painful stimulus
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
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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.
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However, pain perception has been linked to ethnicity
and socioeconomic status.
Example
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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 destruction
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 chemosensitive
receptors perpetuates the cycle
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
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Lowers the nerve’s threshold to noxious
stimuli and magnifying the pain response
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 to 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, an
athlete feels
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Sharp, well-localized, stinging or burning sensation
coming from which fibers??
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A-delta fibers
This initial reaction allows an individual to realise 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
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C-fibers
A third type of peripheral afferent nerve fiber
warrants mention. A-beta fibers, respond to light
touch and low intensity mechanical information.
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Rubbing and injured area
These interrupt nociception to the dorsal horn
The brains limbic system aids in integrating
higher brain function with motivational and
emotional reactions.
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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
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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.
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.
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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
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.
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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
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.
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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
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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.
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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.
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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 (spinothalamic tract) 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.
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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
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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.
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
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“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.
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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.
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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 gate,
located in the dorsal horn of the spinal
cord, modulates the afferent nerve
impulses.
The SG (substantia gelatinosa) acts as a modulating
gate or a control system between the peripheral nerve
fibers and central cells that permits only one type of
nerve 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
occurring 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, non-pain 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 non-painful stimulus is allowed to pass on to the T
cell.
Example:
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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
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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
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All Treatments ™ have some degree of
placebo effect
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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.
Two main categories of
pain
1. Acute - is a relatively brief sensation,
usually less than six months duration usually a response to a specific trauma
- forms the basis for danger warnings
and subsequent learning.
Two main categories of
pain
2. Chronic - lasts more than six months exists beyond the time for normal organic
healing The pain begins to impair other
functions Patients may begin to experience
learned helplessness and hopelessness this
leads to the classic signs of depression
(lethargy, sleep disturbance, weight loss) May
quit work and adopt a self imposed invalid
existence.
Chronic Pain
Characteristics of
Symptoms last longer than 6 months
 Few objective medical findings
 Medication abuse
 Difficulty sleeping
 Depression
 Manipulative behavior
 Somatic preoccupation
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Categories of Chronic
Pain
*Chronic recurrent pain -- benign condition
consisting of intense pain alternating with
pain-free periods. eg, migraine, tension
headaches, endometriosis.
* Chronic intractable-benign pain -- benign
condition where pain is persistent with no
pain free periods, although the pain may vary
in intensity eg low back pain.
Categories of Chronic
Pain
* Chronic progressive pain --malignant
condition where pain is continuous and
increases in intensity as the organic
condition (disease) worsens eg. Cancer
and rheumatoid arthritis.
Congenital Analgesia
A well-known case of congenital
insensitivity to pain is a girl referred to
as 'miss C' who was a student at McGill
university in Montreal in the 1950s. She
was normal in every way, except that
she could not feel pain. When she was
a child she had bitten off the tip of her
tongue and had suffered third-degree
burns by kneeling on a radiator.
Congenital Analgesia
When she was examined by a psychologist
(Charles Murray) in 1950 she did not feel any
pain when she was given strong electric
shocks or when exposed to very hot and very
cold water. When these stimuli were
presented to her she showed no change in
heart rate, blood pressure or respiration. She
did not remember ever having coughed or
sneezed, and did not show a blinking reflex.
She died at the age of 29 as a result of her
condition.
Congenital Analgesia
Although during a post-mortem there were no
obvious signs of what had caused the
analgesia in the first place, she had damaged
her knees, hips and spine. This damage was
due to the fact that she did not shift her
weight when standing or sitting, did not turn
over in bed and did not avoid what would
normally be considered to be uncomfortable
postures. This caused severe inflammation in
her joints.
Congenital Analgesia
Although there is some evidence that this
condition may be inherited, there are other
causes such as neurological damage.
However, some cases cannot be explained in
this way. Most people with this condition learn
to avoid causing themselves too much harm
but, as in the case of 'Miss C, may die as a
result of the problems caused by the
analgesia.
Episodic Analgesia
Serious injury (e.g. loss of limb) - little pain
felt.
6 characteristics (Melzack and Wall 1988).
1. The condition has no relationship to the
severity or the location of the injury.
2. No simple relationship to circumstances occurs in battle or at home.
3. Victim fully aware of injury but feels no pain
4. Analgesia is instantaneous
5. Analgesia lasts for a limited time
Episodic Analgesia
6 Analgesia is localised, pain can be felt
in other parts of the body (arm blown
off is not felt, but injection is!)
Episodic Analgesia
Carlen et al (1978) - Israeli soldiers Yom Kippur War. Loss of arm - 'bang',
'thump' or 'blow'.
Melzack, Wall and Ty (1982) - 37% of
accident victims reported the
experience of episodic analgesia.
Fibromyalgia: Pain
Without Injury
The occurrence of body-wide pain in the
absence of tissue damage, as in fibromyalgia,
interferes with all aspects of a person's life
and undermines their credibility. The problem
is that normal activities can be exhausting,
sleep is disturbed, the ability to concentrate is
impaired, gastrointestinal function is often
abnormal, persistent headaches are
common, and the unrelenting pain that no
one can see is often detrimental to their
personal and professional lives--as it creates
a "credibility gap."
Pain - Injury
Neuralgia - sharp pain along a nerve
pathway. Causalgia - burning pain Both
develop after wound or disease has ended.
Triggered by a simple stimulus e.g. breeze or
vibration. Physiological cause of headaches
not known. Melzack and Wall (1988) report
that migraine causes dilation of blood
vessels, not the other way around! Pain out of
proportion to the injury Some cancers
produce little pain until they are advanced.
(Serious illness, little pain). Kidney stones are
not serious, but produce excruciating pain.
Purpose of pain
1.
Prevents serious damage. If you touch
something hot, you are forced to withdraw
your hand before it gets seriously burnt.
2. Teaches one what to avoid
3. If pain is in joints, pain limits the activity, so
no permanent damage can occur.
but pain can become the problem, and cause
people to want to die.
Phantom limb pain
1.
2.
3.
4.
Melzack (1992) 7 features
Phantom limb feels real. Sometimes
amputees try to walk on their phantom limb.
Phantom arm hangs down at the side when
resting. Appears to swing in time with other
arm, when walking.
Sometimes gets stuck in awkward position.
If behind the patients back, then patient
feels obliged to sleep on stomach.
Artificial limb appears to fit like a glove. See
artificial limb as part of their body.
Phantom limb pain
5 Phantom limbs give impression of
pressure and pain
6 Even if phantom limb is experienced
as spatially detached from the body, it
is still felt to belong to the patient.
7 Paraplegic people experience
phantom limbs. They can even
experience continually cycling legs.
Phantom limb pain
Not just the cut nerve endings (neuromas)
sending messages to the brain,
because cuts made along the neural
pathways only produce a temporary
relief from pain.
Phantom limb pain
Melzack believes - brain contains a
neuromatrix of the body image neurosignature - like a hologram.
Phantom limb pain
Connections to this neuromatrix - sensory
systems, emotional and motivational
systems. It is the emotional and
motivational systems that cause the
phantom limb experience.
Phantom limb pain
Neuromatrix pre-wired - young
amputees experience phantom limb
pain.
People born without limbs also
experience phantom limb pain.
Gate Control Theory
Proposed by Melzack and Wall in the 1960's
Gate opened or closed
by 3 factors
1. Activity in the pain fibres - opens the
gate
2. Activity in other sensory nerves - closes
the gate
3. Messages from the brain concentrating on the pain or trying not
to think about it
Conditions that open or close the gate
Physical conditions
Emotional
Conditions
Mental conditions
Conditions that open the
gate
Conditions that close the
gate
Extent of the injury
Medication
Inappropriate activity level
Counterstimulation, eg
massage
Anxiety or worry
Positive emotions
Tension
Relaxation
Depression
Rest
Focusing on the pain
Intense concentration or
distraction
Boredom
Involvement and interest in
life activities
Three variables control this
gate
A-Delta fibres (sharp pain)
2. C fibres (dull pain)
3. A-Beta fibres that carry messages of
light touch
1.
Pain Gate Theory
Special neurons located in the grey
matter of the spinal cord make up the
gate This gate has the ability to block the
signals from the a-delta and c-delta fibres
preventing them from reaching the brain.
Pain Gate Theory
The special neurons in the spinal cord are
inhibitory ie they keep the gate closed.
These special neurons make a pain
blocking agent called enkephalin. This is
an opiate substance similar to heroin
which can block Substance P the
neurotransmitter from the C fibres and
the A-delta fibres and this keeps the gate
closed.
Pain Gate Theory
C-Fibres and A-Delta fibres obstruct
(inhibitory) the special gate neurons and
tend to open the gate. A-beta fibres are
irritable (excitatory) to the special gate
neurons and tend to keep the gate closed.
Pain Gate Theory
If impulses in the C and A-Delta Fibres
are stronger than the A-beta Fibres the
gate opens. A-delta fibres are always
stronger.
Pain Gate Theory
Specialised nerve impulses arise in the
brain itself and travel down the spinal
cord to influence the gate. This is called
the central control trigger and it can send
both obstructive and irritable messages
to the gate sensitising it to either C or Abeta fibres.