This document provides an overview of a lecture on pain. It begins with the lecturer's name and credentials. The objectives of the lecture are then outlined, which include defining pain, differentiating between acute and chronic pain, and explaining pain management approaches. The document proceeds to discuss topics like nociceptors, the somatosensory pathway, endogenous pain mechanisms, and classifications of pain. Pathophysiological processes underlying pain are explored. Non-pharmacological pain management strategies like TENS, heat/cold therapy are also summarized.

1. Prepared by:
Hizbullah Khan
BScN, MScN

2. At the end of this lecture the students will be able to:
 Define pain
 Discuss different terminologies related to pain
 Differentiate between acute & chronic Pain
 Review the concept of somatosensory pathway.
 Describe the function of Nociceptors in response to
pain.
 Discuss endogenous analgesic mechanism
 Explain pain management (non-pharmacological
approach).

3.  The somatosensory system is designed to provide the
central nervous system (CNS) with information on touch,
temperature, body position, and pain related to deep and
superficial body structures.
 Sensory neurons can be divided into three types:
 General somatic afferent neurons have branches with
throughout the body that result in sensations such as pain,
touch, and temperature.
 Special somatic afferent neurons have receptors located
primarily in muscles, tendons, and joints. These receptors
sense position and movement of the body.
 General visceral afferent neurons have receptors on various
visceral structures that sense fullness and discomfort.

4.  Sensory systems can be theorized as a series of neurons
consisting of first-order, second-order, and third order
neurons.
 First-order neurons transmit sensory information from the
periphery to the CNS.
 Second-order neurons communicate with various reflex
networks and sensory pathways in the spinal cord and travel
directly to the thalamus.
 Third-order neurons relay/transmit information from the
thalamus to the cerebral cortex.
 Cortex is the outer layer that lies on top of cerebrum, it
has sensory, motor, and association areas.

5.  Dorsal root ganglia contain the cell bodies of primary sensory
neurons. A dorsal root ganglion (or spinal ganglion; also known
as a posterior root ganglion) is a cluster of neurons (a ganglion)
in a dorsal root of a spinal nerve. The cell bodies of sensory
neurons known as first-order neurons are located in the dorsal
root ganglia.

6.  An unpleasant sensory & emotional experience which is
associated with actual or potential tissue damage.
 Pain is a protective mechanism for the body because it is
a response to any kind of tissue injury.
 Pain is a common symptom that varies widely in intensity
and spares no age group. If it is severe, it can consume all
of a person’s attention.
 Pain is completely subjective.

7.  Noxious stimulus is “an actually or potentially tissue damaging
event”.
 Pain Threshold: Lowest intensity at which a person perceives a
stimulus to be painful. It is the point beyond which a stimulus
causes pain.
 Pain Tolerance: The maximum level of pain that the person is
able to tolerate.
 Nociceptor: Nerve ending that detects painful stimuli. It is a
sensory neuron that responds to damaging or potentially damaging
stimuli by sending signals to the brain via spinal cord.
 Pain Management: Strategies/techniques to deal with pain.
 Allodynia: Allodynia is pain resulting from a stimulus that does
not normally produce pain. E.g. light touch to sunburned skin
produces pain

8.  Afferent neurons are sensory neurons that carry nerve impulses
from sensory stimuli towards the central nervous system and brain.
 Efferent neurons are motor neurons that carry neural impulses
away from the central nervous system and towards muscles to
cause movement.

9.  Aδ Fibers: Large diameter (2-5 micro m) and myelinated nerve
fibers, have fast conduction velocities. Transmit impulses at a
rate of 6 to 30 m/second. Pain conducted by Aδ Fibers is called
Fast Pain.
 B fibers: Also myelinated, transmit information from cutaneous
and subcutaneous mechanoreceptors. Mechanoreceptors are a
type of somatosensory receptors stimulated by touch, pressure,
stretching, sound waves, and motion
 C Fibers: Unmyelinated and the smallest of all peripheral nerve
fibers (0.4-1.2 micro m in diameter). They transmit impulses at
the rate of 0.5 to 2.0 m/second. C fiber pain is called slow wave
pain because its onset is slow and for longer duration.

11. Acute Pain
 An abrupt onset of pain for
specific period of time. Acute pain
might be mild and last for just a
moment, or it might be severe and
last for weeks or months (less than
6 months).
 Responsive to specific treatment.
 Examples:
Surgery, invasive procedures,
Infection, Broken bones, Dental
problems, Burns or cuts, Labor and
childbirth etc.
Chronic Pain
 The pain that lasts for
prolonged period of time
(more than 6 months).
 Not amenable to specific
treatment.
 Examples:
Headache, Low back
pain, Cancer pain,
Arthritis pain,
Neurogenic pain (pain
resulting from damage to
nerves)

12.  Nociceptive Pain: Nociceptive pain is the most common type. It is
caused by potentially harmful stimuli being detected
by nociceptors around the body. It is of two types:
1. Somatic Pain: Pain originate in the skin, subcutaneous tissues,
muscles and bones.
• Somatic pain can be either superficial or deep. Superficial somatic
pain arises from nociceptive receptors in the skin and mucous
membranes, while deep somatic pain originates from structures
such as joints, bones, tendons, and muscles. Deep somatic pain may
be dull and aching, which is similar to visceral pain.
2. Visceral Pain: Pain that results from the activation of nociceptors
in the body organs

13.  Neuropathic pain: It is a sharp and persistent pain that arises
from peripheral nerve injury. Once the nerve is damaged, the
damaged nerve elicits sustained activation of nociceptors. E.g.
any direct injury to nerves.
 Psychogenic pain is also known as psychological pain or
psychalgia. There is often no physical/organic cause or any
tissue damage but the person feels pain in any organ. These are
categorized as persistent somatoform pain disorder or functional
pain syndrome
 Idiopathic Pain: It is also called pain of unknown
origin. There is no identifiable nerve or tissue damage that is
causing it.

14.  Referred Pain: Pain felt in a part of the body other than its
actual source. The pain is not localized to the site of its cause
(visceral organ) but instead is localized to a distant site. E.g.
Pain due to cholecystitis felt in epigastric region.
 Possible explanation is that the axons carry pain information
from the viscera enter into the spinal cord by the same route as
the cutaneous pain sensation axons.
 Phantom (Illusionary) Pain: Phantom pain sensations are
described as perceptions that an individual experiences
relating to a limb or an organ that is not physically present.
For example, an amputee will often apparently feel pain in a
part of his body that has been removed.
 There may be remaining cut ends of nerves which grow into
nodules called neuromas, or the pain may be due to overactive
spinal neurons.

16.  Globulin and protein kinases: Damaged tissue releases
globulin and protein kinases, which are believed to induce
severe pain
 Arachidonic acid: It is a chemical released during tissue
damage, metabolized into prostaglandin and cytokines which
make the nociceptors more sensitive
 Histamine: Tissue damage stimulates the mast cells to release
histamine to the surrounding area. Histamine excites the
nociceptors.
 Nerve growth factor (NGF): Inflammation or tissue damage
triggers the release of NGF. NGF then binds to receptors on
the surfaces of nociceptors leading to their activation which
elicit pain.


17.  Substance P (SP) and calcitonin gene-related peptide
(CGRP): These are released by injury. Inflammation of tissue
damage also results in SP and CGRP release, which excites
nociceptors.
 Potassium - K+: Most tissue damage results in an increase in
extracellular K+.
 Serotonin (5-HT), acetylcholine (ACh), low pH (acidic)
solution, and ATP: These substances are released with tissue
damage and excite nociceptors.
 Muscle spasm and lactic acid: When muscles are hyperactive
or when blood flow to a muscle is blocked, lactic acid
concentration increases and pain is induced. The greater the
rate of tissue metabolism, the more rapidly the pain appears.

18.  Tissue injury leads to release of inflammatory mediators with
subsequent nociceptor stimulation. The First order neurons (A-
delta and C fibers) when detect noxious stimuli, enters to the
dorsal horn of the spinal cord.
 Pain impulses are then transmitted to Second order neurons
located in the spinal cord. These neurons cross to the opposite
side of the cord (Decussation/cross over) and process
nociceptive information upwards.
 Second order neurons ascend via the spinothalamic tract to
reticular activating system and thalamus (relay station).
 The information in the thalamus is transmitted to the third
order neuron to the next level that is somatosensory cortex.
The localization and meaning/perception of pain occur at the
level of the somatosensory cortex.

23. Two Internal systems
1. Gate Control Theory
2. Descending Analgesic System

24.  Normal pathway of pain impulses transmission by the stimulation of
nociceptors through the first, second and third order neuron.
 Painful area is touched/rubbed/pressure/vibration/compression
applied. Touch receptors/mechanoreceptors/A beta fibers are
activated.
 Touch sensory neurons enter the spinal cord through the dorsal horn
and then pass upward through the Dorsal Column Medial Leminiscal
(DCML) pathway.
 Before going up, it gives small collaterals which activate the
inhibitory neuron (Interneuron), which releases Gamma
Aminobutyric acid (GABA).
 GABA inhibits action potential terminal of first order neuron and
here the gate is closed.
 Pain perception is decreased because less number of second order
neuron for pain are activated.

28. Descending Pathway (Efferent)
 This pathway begins in an area of the midbrain called the
periaqueductal gray (PAG) region (also called the
analgesia system).
 The PAG area receives input from widespread areas of the
CNS, including the cerebral cortex, hypothalamus, brain
stem reticular formation, and spinal cord.
 The neurons of the PAG have axons that descend into an
area in the medulla called the nucleus raphe magnus
(NRM) and here it synapses to the second neuron.
 The axons of these NRM neurons (called Serotonergic and
Noradrenergic neurons) enter to the dorsal horn of the
spinal cord (Substantia Gelatinosa), where they release its
content the Serotonin and Noradrenaline.

29.  These Serotonin and Noradrenaline has two important
functions:
1. Inhibit release of Substance P, thereby blocking 1st order
neuronal action potential to the 2nd order neuron.
2. It will stimulate a small neuron in Substantia Gelatinosa
(located in spinal cord) called Interneuron which is an
opioid neuron.
• Stimulation of interneuron releases an endogenous opioid
called Enkephalin.
• Enkephalin inhibits release of Substance P and
depolarization of 2nd order neuron which will stop
continuation of pain impulses to the Thalamus and so to
cortex.

31.  The rostral ventromedial
medulla (RVM) in the
brainstem is one major
endogenous modulatory
system and is involved in
the relay of sensory
information between the
spinal cord and brain.
 Periaqueductal gray is
stimulated by endorphins
and opiate analgesics to
reduce the perception of
pain by suppressing the
activity in the ascending
nociceptive pathways.

32. Transcutaneous electrical nerve stimulation acts by the
concept of Gate Control Theory.
 Selectively stimulate the A beta fibers [mechanoreceptive
fibers (touch, vibration e.t.c.)] by titrating the amplitude
of electrical current delivered across the surface of the
skin.
 This would prevent signals from nociceptive fibers from
reaching higher centers of the brain, thus reducing pain.

34.  Heat has long been used to relieve pain. Heat dilates
blood vessels and increases local blood flow. It also can
influence the transmission of pain impulses by reducing
the level of nociceptive stimulation.
 The heat sensation is carried to the posterior horn of the
spinal cord and may trigger the release of endogenous
opioids.
 Care must be taken not to use excessive heat as it may
itself becomes a noxious stimulus, which results in
actual or potential tissue damage and pain.

35.  The application of cold may produce a dramatic
reduction in pain.
 Cold exerts its effect on pain through circulatory and
neural mechanisms.
 The initial response to local application of cold is
sudden local vasoconstriction followed by vasodilation.
 Cold may reduce afferent activity reaching the
posterior horn of the spinal cord by modulating sensory
input.
 It also triggers the release of endogenous opioids from
the PAG area.

36. Thank
You