Sensory System Pain Overview

Sensory System
Pain
Dr. Sydney Samai
Registrar,Department
of Internal Medicine
COMAHS, USL.

Overview
 Pain sensation is an unpleasant sensation
produced by damage of the tissue.
 It differs from other sensations because its
purpose is not the inform the higher centers
about the quality of pain.
 It is useful to remove the damaging stimulus
or seek medical advise.

Overview
 Pain occurs whenever any tissues are being
damaged, and it causes the individual to react to
remove the pain stimulus.
 Even such simple activities as sitting for a long
time on the ischia can cause tissue destruction
because of lack of blood flow to the skin where it
is compressed by the weight of the body.
 When the skin becomes painful as a result of the
ischemia, the person normally shifts weight
subconsciously.

Types of Pain
 Pain can be classified according to its site of
origin:
 (A). Cutaneous pain
 (B). Deep pain
 (C). Visceral pain

A. Cutaneous Pain
 Cutaneous Pain from the skin is transmitted
by somatic cutaneous nerves.
 It includes two types:(1)Fast Pain (2) Slow
pain.

Fast Pain
 Fast pain is also described by many alternative
names, such as sharp pain, pricking pain, acute
pain, and electric pain.
 This type of pain is felt when a needle is stuck
into the skin, when the skin is cut with a knife, or
when the skin is acutely burned. It is also felt
when the skin is subjected to electric shock.
 Fast-sharp pain is not felt in most deeper tissues
of the body.

Fast Pain
 Characteristics of Fast Pain:
 (1). Felt within 0.1 sec
 (2). It is of short duration
 (3). Elicited by mechanical or thermal receptors
 (4). Well localized

Fast Pain
 (5). Carried by A-delta fibers which can be
blocked by pressure and oxygen lack. They end
in cerebral cortex. It is carried by spinothalamic
tract(neospinothalamic).Some fibers go the the
reticular activating system(RAS).
 (6). Usually not felt in deep tissue but can occur.

Slow Pain
 Slow pain also goes by many names, such as
slow burning pain, aching pain, throbbing pain,
nauseous pain, and chronic pain.
 This type of pain is usually associated with
tissue destruction.
 It can lead to prolonged, unbearable suffering. It
can occur both in the skin and in almost any
deep tissue or organ.

Slow Pain
 Characters:
 (1).Felt after one second or more and
increases in intensity. It can become
annoying and can lead to prolonged,
unbearable suffering.
 (2).It is elicited by stimulating all types of pain
receptors.
 (3). Poorly localized.

Slow Pain
 (4). Carried by C fibers which can be blocked by
local anesthetics e.g. cocaine.They end in
(a).reticular formation (b). Tectal area of mid
brain . (c) the periaqueductal gray region
surrounding the aqueduct of Sylvius. From the
reticular formation to nonspecific nuclei of the
thalamus to the whole cortex.
 (5). It can occur in skin and any deep structure. It
is perceived at the level of the thalamus, and
carried by paleospinothalamic tract.

Comparison between Fast and
Slow pain.
Fast pain Slow Pain
Immediately felt at the onset of
lesion
Felt several moments after the
lesion
Describe as sharp or cutting Describe as burning or aching
Well localized to injured area and of
short duration.
Not well localized and of longer
duration.
Elicited by mechanical or thermal
receptors
Elicited by all types of receptors
Carried by fast group ‘A’ fibers Carried by slow type ‘C’ fibers
Usually not felt in deep tissues. Can be felt in skin or deep tissues.
Pathway to the brain completely
crosses to opposite side.
Some fibers ascend without
crossing in the same side.

Causes of cutaneous pain.
 Injury of the skin.
 Inflammation of the skin
 Irritation of the dorsal roots.
 Referred pain from deep and visceral
diseased tissues.

B. Deep Pain
 Is a slow less localized dull aching pain.
 Emanates from deep structures such as
muscles, tendons, ligaments, capsule of
joints and bone periosteum-this is the most
sensitive to painful stimuli.
 It is conducted by the C fibers of somatic
sensory nerves.

Causes of deep pain
 Trauma of deep structures.
 Ischemia of muscles: Results from the release
of pain producing factor which may be
bradykinin, histamine, lactic acid and potassium
ions.
 NB: Ischemic pain is caused by interruption of
blood flow to a tissue. Examples of ischemic
pain are angina pectoris due to ischemia of
cardiac muscle and intermittent claudication
due to ischemia of skeletal muscles.

Causes of deep pain.
 Muscle spasm or cramp: Produced pain by
stimulating mechanical pain receptors directly or
secondary to compression of blood vessels
causing accumulation of lactate, potassium and
kinin.
 Inflammation: Causes irritation of surrounding
tissues or due to referred spasm as occurs in
muscles.

C. Visceral Pain
 It is a slow type of pain that arises from the
viscera.
 Dull aching, or rhythmic cramps.
 Diffuse and poorly localized.
 Accompanied by exaggerated autonomic
changes like nausea, vomiting, change in HR
and BP. Also there is reflex spasm of skeletal
muscle over the affected organ.

C. Visceral Pain
 Usually referred to surface area.
 It is carried by the autonomic or somatic
sensory afferent of slow conducting nerve
fibers(‘C fibers’).

Causes of visceral pain
 Ischemia causes pain due to accumulation of
metabolites and endogenous pain producing
substances e.g. bradykinin.
 Distention of hollow viscera e.g. stomach,
intestines, gall bladder and urinary bladder.
 Spasm of viscera e.g. intestine, bile duct.
 Chemical irritation e.g. perforated peptic ulcer
and intestinal perforation due to contact of
proteolytic and hydrochloric acid with
peritoneum.

Causes of Viscera
 Mechanical traction on a mesentry by huge
fluids and by tumor.

Afferent sensory nerves of
visceral pain
 (1). Sympathetic: Carry pain sensation from
thoracic and abdominal viscera.
 (2).Parasympathetic: (a).Glossopharyngeal and
vagus nerves carry pain sensation from the
pharynx, trachea and upper part of the
esophagus. (b). Pelvic nerve, carry pain
sensation from the distal colon, rectum, neck of
the urinary bladder, prostate, urethra, cervix and
upper part of vagina.

Afferent sensory nerves of
visceral pain
 (3). The phrenic nerve (C3&4): Carry pain
sensation from the central part of the
diaphragm and pericardum. The thoracic and
lumber nerves carries pain sensations from
parietal pleura and pericardium.

Insensitive Viscera.
 Few visceral areas are almost completely
insensitive to pain of any type.
 These include the parenchyma of the liver and
the alveoli of the lungs. Yet the liver capsule is
extremely sensitive to both direct trauma and
stretch, and the bile ducts are also sensitive to
pain. In the lungs, even though the alveoli are
insensitive, both the bronchi and the parietal
pleura are very sensitive to pain.

Referred Pain
 Often a person feels pain in a part of the body
that is fairly remote from the tissue causing the
pain. This is called referred pain.
 For instance, pain in one of the visceral organs
often is referred to an area on the body surface.
Knowledge of the different types of referred pain
is important in clinical diagnosis because in
many visceral ailments the only clinical sign is
referred pain.

Mechanism of Referred Pain.
 Branches of visceral pain fibers are shown to
synapse in the spinal cord on the same second-
order neurons (1 and 2) that receive pain signals
from the skin.
 When the visceral pain fibers are stimulated,
pain signals from the viscera are conducted
through at least some of the same neurons that
conduct pain signals from the skin, and the
person has the feeling that the sensations
originate in the skin itself.

Examples of referred pain.
 Cardiac pain: Is felt in the retrosternal region,
root of the neck, outer part of the chest and
inner part of the left arm and also in the
epigastrium.
 Gastric pain: Is felt between the umbilicus and
Xiphoid process.
 Gall bladder and liver pain: Is felt at the mid-
epigastrium and at the tip of right scapula.

Examples of referred pain.
 Renal pain is felt as a back pain that radiates
to the inguinal region and testicles.
 Appendicitis pain: Is felt around the
umbilicus.

Cutaneous VS Visceral Pain
Cutaneous Pain Visceral Pain
Transmitted by cutaneous nerves Transmitted by autonomic nerves
Pricking-burning or stitching. Colicky or dull aching(agonizing
pain)
Not referred to other areas Referred to other areas
Stimuli are cutting, pricking or
burning.
Stimuli are spasm, ischemia, toxins
or over distention.
Reach somatic sensory area 1 Perceived by the thalamus or
sensory 2
Well localized Not well localized
Accompanied by sympathetic
reactions as HR &BP.
Accompanied by parasympathetic
reactions as. HR&BP.

Body reactions to pain.
 1. Somatic reactions: Pain may initiate:
 (a).Withdrawal reflexes- These reflexes are
initiated by cutaneous pain. These reflexes
remove the body and limbs away from the
noxious stimulus.
 (b).Skeletal muscle spasm-These reflexes are
initiated by deep or visceral pain.

 2. Autonomic reactions: These reactions
depends on the site and intensity of pain
sensations.
 (a). Mild cutaneous pain- usually evokes
sympathetic activity or pressor reactions eg.
increase in HR &BP.
 (b). Deep pain- Visceral pain and severe
cutaneous pain produce excessive
parasympathetic activity e.g. bradycardia and
hypotension.

 3. Psychological or emotional reaction:
 Anxiety, fear, depression and crying.
 These reactions vary from one person to another
and in the same person from time to time
according to circumstances.
 Anxiety can augment the sensation of pain.
 On the other hand, strong emotional excitement,
may inhibit the sensation of pain-stress induced
analgesia.

 4. Localization of pain:
 Pain sensation is accurately localized in the
skin.
 The localization is the function of the cerebral
cortex.
 The visceral and deep pain is usually
referred to other sites- referred pain.

 5. Hyperalgesia:
 In cutaneous pain, the body exert intrinsic
mechanisms that can exaggerate the pain
sensation.
 6. Analgesia or Pain control systems:
 It is an endogenous analgesic system consists of
special areas in brain and spinal cord where the
endogenous opiate peptides are increased and
acts on opiate receptors and reduce pain
sensations.

Pain threshold.
 It appears that the majority of individuals not
show significant differences in pain threshold
however, it is affected by the following factors:
 1. Emotional factors may increase or decrease
the pain threshold.
 2. Damage of the skin decrease pain threshold in
primary hyperalgesia.
 3. Analgesic drugs increase the pain threshold.

Pain threshold.
 5. Endogenous analgesic substances in brain
stem and spinal cord increase the pain threshold.
 6. Effects of other sensation: Gait control may
increase threshold. Counter-irritants applied to
the skin suppress pain.
 N.B: Pain starts to be felt when the skin
temperature reachs 45 degree celcius. This is
considered as average threshold of pain.

Pain Receptors and Their
Stimulation
 Pain Receptors Are Free Nerve Endings.
 The pain receptors in the skin and other
tissues are all free nerve endings.
 They are widespread in the superficial layers
of the skin as well as in certain internal
tissues, such as the periosteum, the arterial
walls, the joint surfaces, and the falx and
tentorium in the cranial vault.

stimulation
 Most other deep tissues are only sparsely
supplied with pain endings; nevertheless,
any widespread tissue damage can summate
to cause the slow-chronic-aching type of pain
in most of these areas.

Stimulation
 Pain can be elicited by multiple types of stimuli.
They are classified as mechanical, thermal, and
chemical pain stimuli.
 In general, fast pain is elicited by the mechanical
and thermal types of stimuli, whereas slow pain
can be elicited by all three types.
 Some of the chemicals that excite the chemical
type of pain are bradykinin, serotonin, histamine,
potassium ions, acids, acetylcholine, and
proteolytic enzymes.

Pain Receptors and their
Stimulation
 In addition, prostaglandins and substance P
enhance the sensitivity of pain endings but
do not directly excite them.
 The chemical substances are especially
important in stimulating the slow, suffering
type of pain that occurs after tissue injury.

Chemical mediators released in
response to tissue damage.

Non-adapting Nature of Pain
Receptors.
 In contrast to most other sensory receptors of the
body, pain receptors adapt very little and
sometimes not at all.
 In fact, under some conditions, excitation of pain
fibers becomes progressively greater, especially
so for slow-aching-nauseous pain, as the pain
stimulus continues.
 This increase in sensitivity of the pain receptors
is called hyperalgesia.

Rate of Tissue Damage as a
Stimulus for Pain.
 The average person begins to perceive pain
when the skin is heated above 45°C.
 This is also the temperature at which the
tissues begin to be damaged by heat;
indeed, the tissues are eventually destroyed
if the temperature remains above this level
indefinitely.

Rate of Tisssue Damage as a
Stimulus for Pain.

Rate of Tissue Damage as a
Stimulus for pain.
 Therefore, it is immediately apparent that pain
resulting from heat is closely correlated with the
rate at which damage to the tissues is occurring
and not with the total damage that has already
occurred.
 The intensity of pain is also closely correlated
with the rate of tissue damage from causes other
than heat, such as bacterial infection, tissue
ischemia, tissue contusion, and so forth

Special Importance of Chemical
Pain Stimuli During Tissue
Damage.
 Extracts from damaged tissue cause intense
pain when injected beneath the normal skin.
 Most of the chemicals listed earlier that excite
the chemical pain receptors can be found in
these extracts.
 One chemical that seems to be more painful than
others is bradykinin.
 Many researchers have suggested that
bradykinin might be the agent most responsible
for causing pain following tissue damage.

Special Importance of Chemical
Pain Stimuli During Tissue
Damage.
 Also, the intensity of the pain felt correlates
with the local increase in potassium ion
concentration or the increase in proteolytic
enzymes that directly attack the nerve
endings and excite pain by making the nerve
membranes more permeable to ions.

Dual Pathways for Transmission
of Pain Signals into the Central
Nervous System.
 Even though all pain receptors are free nerve
endings, these endings use two separate
pathways for transmitting pain signals into the
central nervous system.
 The two pathways mainly correspond to the two
types of pain—a fast-sharp pain pathway and a
slow-chronic pain pathway.

Peripheral Pain Fibers—“Fast”
and “Slow” Fibers.
 The fast- sharp pain signals are elicited by either
mechanical or thermal pain stimuli; they are
transmitted in the peripheral nerves to the spinal
cord by small type A-delta fibers at velocities
between 6 and 30 m/sec.
 Conversely, the slow-chronic type of pain is
elicited mostly by chemical types of pain stimuli
but sometimes by persisting mechanical or
thermal stimuli.

 This slow- chronic pain is transmitted to the
spinal cord by type C fibers at velocities between
0.5 and 2 m/sec.
 Because of this double system of pain
innervation, a sudden painful stimulus often
gives a “double” pain sensation:
 A fast-sharp pain that is transmitted to the brain
by the A-delta fiber pathway, followed a second
or so later by a slow pain that is transmitted by
the C fiber pathway.

 The sharp pain apprises the person rapidly of a
damaging influence and, therefore, plays an
important role in making the person react
immediately to remove himself or herself from
the stimulus.
 The slow pain tends to become greater over
time. This sensation eventually produces the
intolerable suffering of long- continued pain and
makes the person keep trying to relieve the
cause of the pain.

 On entering the spinal cord from the dorsal
spinal roots, the pain fibers terminate on relay
neurons in the dorsal horns.
 Here again, there are two systems for
processing the pain signals on their way to the
brain:
 through (1) the neospinothalamic tract and (2)
the paleospinothalamic tract.

Neospinothalamic Tract for Fast
Pain.
 The fast type A-delta pain fibers transmit mainly
mechanical and acute thermal pain.
 They terminate mainly in lamina I (lamina
marginalis) of the dorsal horns, and there excite
second-order neurons of the neospinothalamic
tract. These give rise to long fibers that cross
immediately to the opposite side of the cord
through the anterior commissure and then turn
upward, passing to the brain in the anterolateral
columns.

Pain.
 A few fibers of the neospinothalamic tract
terminate in the reticular areas of the brain stem,
but most pass all the way to the thalamus without
interruption, terminating in the ventrobasal
complex along with the dorsal column–medial
lemniscal tract for tactile sensations.
 A few fibers also terminate in the posterior
nuclear group of the thalamus.

Pain.
 From these thalamic areas, the signals are
transmitted to other basal areas of the brain as
well as to the somatosensory cortex.
 Glutamate, the Probable Neurotransmitter of
the Type A-delta Fast Pain Fibers.
 This is one of the most widely used excitatory
transmitters in the central nervous system
usually having a duration of action lasting for
only a few milliseconds.

Paleospinothalamic Pathway for
Transmitting Slow-Chronic Pain.
 The paleospinothalamic pathway is a much older
system and transmits pain mainly from the
peripheral slow-chronic type C pain fibers,
 Although it does transmit some signals from type
A-delta fibers as well.
 In this pathway, the peripheral fibers terminate in
the spinal cord almost entirely in laminae II and
III of the dorsal horns, which together are called
the substantia gelatinosa.

 Most of the signals then pass through one or
more additional short fiber neurons within the
dorsal horns themselves before entering mainly
lamina V, also in the dorsal horn.
 Here the last neurons in the series give rise to
long axons that mostly join the fibers from the
fast pain pathway, passing first through the
anterior commissure to the opposite side of the
cord, then upward to the brain in the
anterolateral pathway.

Pathways for transmission of pain
to the CNS

 Substance P, the Probable Slow-Chronic
Neurotransmitter of Type C Nerve
Endings.
 Glutamate is the neurotransmitter most
involved in transmitting fast pain into the
central nervous system, and substance P is
concerned with slow-chronic pain

Projection of the
Paleospinothalamic Pathway
(Slow- Chronic Pain Signals) into
the Brain Stem and Thalamus.
 The slow-chronic paleospinothalamic pathway
terminates widely in the brain stem, in the large
shaded area shown in the next Figure
 Only one tenth to one fourth of the fibers pass all
the way to the thalamus. Instead, most terminate
in one of three areas:
 (1) the reticular nuclei of the medulla, pons, and
mesencephalon; (2) the tectal area of the
mesencephalon deep to the superior and inferior
colliculi;

Projection of the
 (3) the periaqueductal gray region
surrounding the aqueduct of Sylvius.
 From the brain stem pain areas, multiple
short-fiber neurons relay the pain signals
upward into the intralaminar and ventrolateral
nuclei of the thalamus and into certain
portions of the hypothalamus and other basal
regions of the brain.

Projection of the

Reception of pain signals
 Fast pain is precepted in the thalamus and
cortex.
 Slow pain is precepted mainly in the thalamus.
 Functions of the cortex in pain perception:
 1. Localization of pain- sharp pain is well
localized.
 2. Discrimination of pain
 3. Modulation of pain by emotional and
behavioral factors.

Arousal reaction to pain signals.
 The intra-laminal nuclei of the thalamus and
reticular formation of the brain stem have a
strong arousal effect on the nervous effect
throughout the brain.
 This explains why a person with severe pain
is strongly aroused and pain prevents sleep.

Pain Control
 Pain can be controlled by one of three ways:
 1. Pain control systems:
 (a).Analgesia system. (b). Brain opiate
system. (c).Gate theory.
 2. Surgical
 3. Electrical

Pain Control Systems.
 1. Analgesia System:
 This pain analgesia system consists of three
major components in different brain areas in
addition to the pain inhibitory complex in the
dorsal horn of the spinal cord.
 The component of the analgesia system are:
 (a). The periaqueductal gray area
 (b). Raphe magnus nucleus
 (c). Nucleus reticularis.

The Periaqueductal gray area.
 Found in midbrain and upper pons, surrounding
the aqueduct of sylvius.
 It has opiate receptors and it also secretes
endogenous enkephalins.
 It is activated by higher areas of the brain such
as the hypothalamus and limbic cortex in
conditions of stress, emotion and pain.
 The neurons of the periaqueductal area are
stimulated by beta-endorphin.

Raphe magnus nucleus.
 Located in the lower part of the pons and upper
medulla
 These neurons are serotonergic and connected
with pain inhibitory complex located in the dorsal
horn of the spinal cord by the lateral
reticulospinal tract.
 Can also be stimulated by substantia nigra
through the release of dopamine.

Nucleus reticularis.
 Located in the medulla.
 It also sends descending pathway through the
lateral reticulospinal tract to end on neurons of
the pain inhibitory complex in the spinal dorsal
horn.

Pain inhibitory complex.
 Located in the dorsal horn of the spinal cord,
probably in laminae II and III (Substantia
gelatinosa of Rolandi).
 Serotonin is released in the dorsal horn cells by
supraspinal control which activates local
interneurons in the dorsal horn to secrete
enkephalin.
 Enkephalin binds with opiate receptors causing
pre and post synaptic inhibition of the spinal
neurons excited by the pain fibers.

Pain inhibitory complex.
 Pain suppression is also done by opiate at
higher levels especially in reticular formation
of brain stem and intralaminar nuclei of
thalamus.

Analgesia system of the brain and
spinal cord.

Chemical transmitters in analgesia
system.
 Many transmitter substances are secreted by the
analgesia system neurons, mostly enkephalin
and serotonin:
 Fibers arising from the periaqueduct, and
interneuron of posterior horn of spinal cord all
secrete enkephalin at their terminals.
 Fibers arising from raphe magnus nucleus
secrete serotonin at the spinal cord.

Brain’s Opiate System
 Opiates are drugs that are derived from the
juice of opium poppy.
 There are some compounds that are derived
from opium poppy but still have analgesic effect
by binding to opiate receptors.
 Are useful therapeutically as powerful
analgesics.
 They exert their analgesic effect by binding to
specific opiate receptors.

Brain’s Opiate System.
 Opioids are defined as direct acting compounds
whose effects are specifically antagonized by
naloxone.
 There are different endogenous opioid peptides
produced in the body.

Types of endogenous opioid
peptides.
 There are three main endogenous peptides:
 1.Enkephalins:
 Meta and Leu enkephalins derived from large
protein molecule pro-enkephalin.
 Enkephalins are present in different parts of
analgesia system, limbic system, thalamus and
adrenal medulla.
 They act as neurotransmitters at the above
locations.

peptides.
 2. Endorphins: Present mainly in hypothalamus
and pituitary.
 They act as:
 (a). Neurotransmitter: Stimulate arcuate nucleus
and some specific areas of hypothalamus which
project to thalamus and periaqueductal gray
matter of brain stem secrete endorphins.

peptides.
 (b).Neuro-hormone:
 In stress conditions beta-endorphins are
secreted from hypothalamus and pituitary to
general circulation causing analgesia.
 This explains stress analgesia in battles and
accidents.
 NB: The release of endogenous cannabinoids
may also contribute to stress-induced analgesia.
 NE released from the amygdala may also have a
role in stress-induced analgesia.

peptides.
 3.Dynorphin:
 Derived from prodynorphin.
 Secreted from many areas in the nervous
system.
 Are very potent analgesics.
 Responsible for addiction and tolerance to
opiates.

C. Gate theory
 The different synapses of pain pathway act as
gates through which pain impulse reach the
lateral spinothalamic tract in which pain
transmission can be inhibited.
 The gates are :
 (a) The spinal gates at the dorsal horn cell
laminae II and III( substantia gelatinosa of
Rolandi).
 (b). The reticular formation in the brain stem
 (c). The intralaminar nuclei of the thalamus

C. Gate theory
 The gate can be closed by:
 (a). Impulses from:
 (i). A-beta fibers(rubbing of skin inhibits pain).
 (ii).A-delta fibers(counter irritant and
aquipuncture inhibits pain).
 (iii). Corticofugal
 NB: All these fibers cause presynaptic inhibition
of pain fibers by activating interneurons which
secrete GABA or enkephalin.

C. Gate theory
 The gate can be closed by:
 (b). Opioids from:
 (i). Interneurons activated by fibers from
dorsal nucleus
 (ii). Circulating endorphins.

2. Surgical Treatment.
 In cases of uncontrollable severe pain some
operations can be done:
 (a). Anterolateral cordotomy: To cut the
spinothalamic tract. May be ineffective
because pain fibers may enter above it.
 (b). Gyrectomy in frontal lobe, to abolish the
unpleasant component of pain

3. Electric Stimulation.
 Electrodes placed in the
intralaminar(nonspecific) nuclei of the
thalamus, or in paraventricular, or
periaqueductal areas have been shown to
lead to a dramatic relief of pain.

Thanks for your attention.
Consistency is what
transforms average
to excellence.

Sensory System Pain Overview

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