UNIVERSITY OF
GUYANA
BMP 3201
PAIN
ASSIGNMENT 1
GROUP MEMBERS
Kamini Reddi
Jennifer Haynes
Satrupa Singh
ASSIGNMENT 1
PAIN
- Acute, Chronic and Referred Pain
-Mechanism Of Pain Reception
And Transmission
-Pain Modulation And ControlGate Control Theory &
Endogenous Opioid System
PAIN
Pain can be defined as an unpleasant feeling that is
a vital function of the nervous system because it
warns the body of the potential or actual injury.
Three types of Pain: (1) Acute
(2) Chronic
(3) Referred
TYPES OF PAIN:
ACUTE
This type of pain can be defined as the duration of
pain in less than 6 months which can be identified
as an underlying pathology
By limiting activity to prevent further damage and
promote tissue healing and recovery, acute pain
serves a protective function; however, it might also
affect an individual’s quality of life and impair the
ability to function well.
ACUTE PAIN CONT’D
Treatment resulting from musculoskeletal injury
includes: resolving the underlying disorder,
reduce inflammation and modify the
transmission of pain from the Periphery to the
CNS.
CHRONIC PAIN
Persists beyond the normal time for tissue
healing. Chronic pain is usually as a result of
activation of dysfunctional neurological or
pathological responses that cause the person to
continue to experience the sensation of pain even
when no damaging or threatening stimulus is
present. Acute pain is the start of chronic pain.
Chronic pain maybe the result of changes in
sympathetic nervous system and adrenal
activity , reduced production of endogenous
opioids or sensitization of primary afferents
(peripheral sensitization) and spinal cord
neurons.
CLASSIFICATIONS OF
CHRONIC PAIN
1) Nociceptive pain: caused by a stimulation of
pain receptors by noxious chemicals, mechanical
and thermal stimuli and ongoing tissue damage
Some conditions under this class are: arthritis,
ischemia, cancer chronic pancreatitis.
CLASSIFICATIONS OF
CHRONIC PAIN CONT’D
2) Neuropathic pain is the results of peripheral
or central nervous system dysfunction without
ongoing tissue damage.
Some conditions under this classification
include: diabetic neuropathy, postherpetic
neuralgia and phantom limb pain.
Mixed pain syndrome - are those with multiple or
unclear pathophysiology.
Example: recurrent headache and some vasculitis
syndrome
Psychological pain syndromes - are those in which
the psychological process plays a major role. This
type of pain may be seen in somata form disorder
and conversion reactions.
Chronic pain maybe the result of changes in
sympathetic nervous system and adrenal activity,
reduced production of endogenous opioids or
sensitization of primary afferents (peripheral
sensitization) and spinal cord neurons.
Decreased levels of enkephalins and increases
numbers and sensitivity of nociceptors have been
observed in individuals with chronic pain. Those
individuals have increased sensitivity to both
noxious (hyeralgesia) and innocuous (allodynia)
stimuli. This process is known as wind up or
central sensitization.
REFERRED PAIN
This is the experience of pain in one area when
the actual or tissue damage is in another area. The
pain maybe referred from one joint to another,
from a peripheral nerve to a distal area of
innervation, or from an internal organ to an area
of musculoskeletal tissue.
 E.g. Myocardial infarction or angina caused by
cardiac ischemia that is felt in the upper chest, left
shoulder, jaw and arm and pain originating from
the central portion of the diaphragm that is
frequently felt in the lateral tip of either shoulder.
REFERRED PAIN CONT’D
It is proposed that pain is referred in one of 3
ways:
(1) - from a nerve to its area of innervation
(2) - from one area to another derived from the same
dermatome
(3) - from one area to another derived from the same
embryonic segment
REFERRED PAIN CONT’D
The peripheral neural pathways of these
different areas conversed on the same or similar
areas of the spinal cord and synapse with the
same second order neurons to ascend the
spinal cord and reach the central cortex.
When pain that maybe of either viseral or
musculoskeleton orgin converges on the same
neuron in the spinal cord it is usually
interpreted to be of musculoskeletal origin.This
may be because musculoskeletal injury and pain
are so much more common that the brain
learns that activity arriving along that pathway is
associated with pain stimulus in particular
musculoskeleton.
MEC HANISMS OF PAIN
RECEPTION & TRANSMISSION
NOCICEPTORS
Specialised sensory receptors responsible for the
detection of noxious (unpleasant) stimuli,
transforming the stimuli into electrical signals, which
are then conducted to the central nervous system.
They are the free nerve endings of primary afferent
Aδ and C fibres.
Distributed throughout the body (skin, viscera,
muscles, joints, meninges) they can be stimulated by
mechanical, thermal or chemical stimuli.
NOCICEPTORS CONT’D
Inflammatory mediators (eg, bradykinin,
serotonin, prostaglandins, cytokines, and H+) are
released from damaged tissue and can stimulate
nociceptors directly.
The process of inflammatory mediators acting to
reduce the activation threshold of nociceptors so
that the stimulation required to cause activation is
less can be known as Primary Sensitisation.
PRIMARY AFFERENT FIBRES
In addition to the Aδ and C fibres that carry
noxious sensory information, there are primary
afferent Aβ fibres that carry non-noxious
stimuli.
Each of these fibre types possesses different
characteristics that allow the transmission of
particular types of sensory information
Aβ fibres are highly myelinated and of large
diameter, therefore allowing rapid signal
conduction. They have a low activation threshold
and usually respond to light touch and transmit
nonnoxious stimuli.
 Aδ fibres are lightly myelinated and smaller
diameter, and hence conduct more slowly than Aβ
fibres. They respond to mechanical and thermal
stimuli. They carry rapid, sharp pain and are
responsible for the initial reflex response to acute
pain.
C fibres are unmyelinated and are also the
smallest type of primary afferent fibre. Hence
they demonstrate the slowest conduction. C
fibres are polymodal, responding to chemical,
mechanical and thermal stimuli. C fibre
activation leads to slow, burning pain
PAIN MODULATION AND
GATE – CONTROL THEORY
PAIN MODULATION
Pain is modulated by two primary types of drugs
that work on the brain
analgesics
anesthetics.
The term analgesic refers to a drug that relieves
pain without loss of consciousness. The term
anesthesia refers to a drug that depresses the CNS.
It is characterized by the absence of all perception
of sensory modalities, including loss of
consciousness without loss of vital functions.
PAIN MODULATION CONT’D
In the CNS there is a circuit that can modulate
incoming pain information. The gate control
theory and the ascending/descending pain
transmission system are two suggestions of such
a circuit.
GATE CONTROL THEORY
The first pain modulatory mechanism called the
"Gate Control" theory was proposed by Melzack
and Wall in the mid-1960s. The concept of the
gate control theory is that non-painful input closes
the gates to painful input, which results in
prevention of the pain sensation from traveling to
the CNS (i.e., non-noxious input [stimulation]
suppresses pain).
GATE CONTROL THEORY
CONT’D
The theory suggests that collaterals of the large
sensory fibers carrying cutaneous sensory input
activate inhibitory interneurons, which inhibit
(modulate) pain transmission information carried
by the pain fibers. Non-noxious input suppresses
pain, or sensory input “closes the gate” to noxious
input.
GATE CONTROL THEORY
CONT’D
The gate theory predicts that at the spinal cord
level, non-noxious stimulation will produce
presynaptic inhibition on dorsal root nociceptor
fibers that synapse on nociceptors spinal neurons
(T), and this presynaptic inhibition will block
incoming noxious information from reaching the
CNS (i.e., will close the gate to incoming noxious
information).
GATE CONTROL THEORY
CONT’D
The gate theory was the rationale for the idea
behind the production and the use of
transcutaneous electrical nerve stimulation
(TENS) for pain relief. To be effective, the
TENS unit produces two different current
frequencies below the pain threshold that can be
tolerated by the patient. This procedure has
partial success in pain therapy.
PICTURE SHOWING THE
DIAGRAM OF GATE CONTROL
THEORY OF PAIN
STEPS OF PAIN MODULATION AND
GATE – CONTROL THEORY
Without any stimulation, both large and small
nerve fibers are quiet and the inhibitory
interneuron (I) blocks the signal in the projection
neuron (P) that connects to the brain. The "gate
is closed" and therefore NO PAIN.
With non-painful stimulation, large nerve fibers are
activated primarily. This activates the projection
neuron (P), BUT it ALSO activates the inhibitory
interneuron (I) which then BLOCKS the signal in the
projection neuron (P) that connects to the brain. The
"gate is closed" and therefore NO PAIN.
With pain stimulation, small nerve fibers become
active. They activate the projection neurons (P) and
BLOCK the inhibitory interneuron (I). Because
activity of the inhibitory interneuron is blocked, it
CANNOT block the output of the projection neuron
that connects with the brain. The "gate is open",
therefore, PAIN!!
THE ENDOGENOUS OPOID
SYSTEM
Pain perception is also modulated by endogenous
opiate- like peptides; called opiopeptins,
(previously known as endorphins).
Opiopeptins control pain by binding to specific
opiate receptors in the nervous system.
 An endogenous system of analgesia was first discovered
by three independent group of researchers who were
investigating the mechanism of morphine induced
analgesia.
 In 1975, two peptides, met-enkephalin (methionineenkaphalin) and leu-enkaphalin (leucine-enkaphalin),
which were isolated from the CNS of pig, were shown to
produce physiological effects similar to those of
morphine.
 These peptides also bind specifically to the opiate
receptor, and their action and binding are blocked by
naloxone, an opiate antagonist.
 Opiopeptins and opiate receptors have been found in many
peripheral nerve endings and in neurons in several regions of
the nervous system.
 Concentration of opiopeptins and opiate receptors have been
identified in various area of the brain, including the
periaqueductal grey matter (PAGM), and the raphe nucleus
of the brain stem, which are structures that induce analgesia
when electrical stimulated and various areas of the limbic
system.
 Opiopeptins are also found in high concentrations in the
superficial layer of the dorsal horn of the spinal cord (layers
I&II) and the enteric nervous system as well as in nerve
endings of C fibers.
Opioids and opiopeptins always have an inhibitory
action, causing presynaptic inhibition by
suppressing the inward flux of calcium and cause
postsynaptic inhibition by activating and outward
potassium current.
In addition opiopeptins indirectly inhibit pain
transmission by inhibiting the release of gammaamniobutyric acid (GABA) in the PAGM and the
raphe nucleus.
ES of the area with high levels of opiopeptins,
such as the PAGM, and the raphe nucleus,
strongly inhibits the transmission of pain messages
by some spinal dorsal horn neurons, thereby
causing analgesia
The endogenous opiate theory also provides an
explaination of the paradoxical pain relieving
effects of painful stimulation and acupuncture.
The brain stimulates the pituitary gland and
blocks the pain transmission by not allowing
depolarization to occur, A-delta or C fibers;
endogenous opiates; blocking noxious stimuli
A noxious stimulus (through A-delta and C
fibers) activates this descending pain control
mechanism.
KEY POINTS
 The pain experienced by patients is a result of the
interaction between sensory and emotional
experiences.
 Aδ fibres transmit rapid, sharp, localised pain.
 C fibres transmit slow, diffuse, dull pain.
KEY POINTS CONT’D
 Pain transmission can be modulated at a number
of levels, including the dorsal horn of the spinal
cord and via descending inhibitory pathways.
 The spinothalamic and spinoreticular tracts are
important ascending pain pathways
 Neuropathic pain can be spontaneous and is
often described as burning, shooting, or stabbing
CONCLUSION
Pain is both a sensory and emotional experience,
and patients past experiences, fears and anxieties can
play an important role.
Pain transmission is a result of complex peripheral
and central processes.
These processes can be modulated at different levels
and pain perception is a result of the balance
between facilitatory and inhibitory interactions.
CONCLUSION CONT’D
Current areas of interest in pain research include:
 investigating the effect of mood on pain
processing in the brain and
looking for novel drugs to block channels
involved in pain transmission.
REFERENCES
 An Introduction to Pain Pathways and Mechanisms. (n.d.).
Retrieved February 26, 2015, from https://www.ucl.ac.uk:
https://www.ucl.ac.uk/anaesthesia/StudentsandTrainees/PainPathw
aysIntroduction
 H.Cameron, M. (2009). Physical Agents in Rehabilitation .
 Introduction to Pain Pathways and Mechanism. (n.d.). Retrieved
February 27, 2015, from https://www.youtube.com:
https://www.youtube.com/watch?v=i5V_q7XqQN8