PHYSIOLOGY

OF PAIN
SENSATION.
OBJECTIVES
 Definitionof pain
 Types of pain
 Varieties of pain
 Pain pathway
 Pain inhibiting pathway
 Central analgesia
 Referred pain
 Applied physiology
 Definition
Pain is an unpleasant
sensory and emotional
experience associated
with actual or potential
tissue damage .
Stimuli: 3 Types

 Mechanical Fast pain

 Thermal Fast pain
 Chemical Slow pain
Receptors for Pain:
Nociceptors
Pain receptors (Nociceptors)
 Free nerve endings
 More in
 Superficial layers of skin
 Periosteum
 Arterial walls
 Joint surfaces

 Sparse in other deep

tissues.
 Non-adapting in
nature.
MAJOR TYPES
 1. Fast Pain

 2. Slow Pain
 Fast pain:
Sharp pain, pricking pain, Acute pain,
electric pain.

 Slow pain:
Burning pain, aching pain, throbbing pain,
nauseous pain, chronic pain.
 Types of Pain
 Fast pain is due to activity
of Myelinated A  fibres
(localized sensation)

 Slow pain is due to activity Peripheral

of Unmyelinated C fibres
Nerve

 Slow pain follows fast pain.

A-delta Fiber
C-Fiber
 Fast pain Slow pain
Felt within about 0.1 Begins after 1 second or
second after a painful more and then increases
stimulus. slowly over many sec. or min.
“Bright," sharp, localized Dull, intense, diffuse
sensation sensation
sharp pain, pricking pain, acute slow burning pain, aching pain,
pain, and electric pain throbbing pain, nauseous pain,
and chronic pain
Felt mainly in skin. Not felt It can occur both in the skin
in most deeper tissues of the and in almost any deep tissue
body or organ
 Types of Pain
Fast pain Slow pain
Pin prick, cutting Associated with
or burning of skin tissue destruction.
Caused by mechanical or Caused mainly by
thermal stimuli. chemical stimuli
Transmitted by Aδ fibers Transmitted by C fibers
(velocity 6-30 m/sec) (velocity 0.5-2 m/sec)
NT- Glutamate NT- Substance P
Neo-spinothalamic tract Paleo-spinothalamic tract
 OTHER TYPES OF PAIN

 Superficial Pain: pain arising from skin

and mucous membrane.
 Deep (somatic) Pain: pain originating
from somatic structures deep to the skin
are known as deep pain.
 Visceral Pain: pain arising from different
internal organs or viscera
Nociceptive (skin-
oriented)

Inflammatory (tissue &

joints-oriented)

Neuropathic (nervous-
system-oriented)
 Where Does Pain Come From?

 Cutaneous Pain – sharp, bright, burning; can

have a fast or slow onset
 Deep Somatic Pain – stems from tendons,
muscles, joints, periosteum, & bl. Vessels
 Visceral Pain – originates from internal organs;
diffused @ 1st & later may be localized (i.e.
appendicitis)
 Psychogenic Pain – individual feels pain but
cause is emotional rather than physical
VARIETIES OF PAIN

 ACUTE PAIN
 CHRONIC PAIN
 CUTANEOUS PAIN
 DEEP SOMATIC PAIN
 VISCERAL PAIN
 REFERRED PAIN
 NEUROPATHIC PAIN
 PHANTOM PAIN
Mediators Substances released from Damaged cells:
of Pain ATP
Bradykinin
Painful heat
Acids Substance P
Mechanical damage
Na+
Ca++

Free nerve ending

 Sensory Pathway
Stimulus

Sensory receptor (= transducer)

Afferent sensory neurons

CNS

Integration, perception
Somatic Senses
 Primary sensory
neurons from receptor to
spinal cord or medulla
 Secondary sensory
neurons always cross over
(in spinal cord or medulla)
 thalamus
 Tertiary sensory neurons
 somatosensory cortex
(post central gyrus)
 Dual Pathways for Pain
Transmission
 From Peripheral Receptors to Spinal cord:
 Aδ fibers (fast fibers) – for fast pain
 C fibers (slow fibers) – for slow pain

 From Spinal cord to Brain: via

Anterolateral (Spinothalamic) tract
 Neo-Spinothalamic tract – for fast pain
 Paleo-Spinothalamic tract – for slow pain
•Somatosensory Cortex
•Other basal areas of brain
•Thalamus – ventrobasal complex
• In the Brain Stem: Reticular formation
Neospinothalamic tract
(Lateral White Columns)
Spinal cord
(lamina I – lamina marginalis)
Peripheral fibers
Aδ fibers
Pain receptor
(Free nerve endings)
Pain pathway
SLOW PAIN
•Thalamus (IL & VL nuclei)
•Hypothalamus
•Other basal areas of brain
•1. Reticular nuclei, 2. Tectal area &
3. Periaqueductal grey region
•4. Thalamus

Paleospinothalamic tract
Spinal cord
(lamina II & III – substantia gelatinosa)
Peripheral fibers
C fibers
Pain receptor
(Free nerve endings)
Pain pathway
Friday, March 20, 2020
PHYSIOLOGY OF PAIN PERCEPTION

Injury Brain

Descending
Pathway

Dorsal
Peripheral Root
Nerve Ganglion

Ascending
Pathways
C-Fiber

A-beta Fiber Dorsal

A-delta Fiber Horn
Spinal Cord
 CENTER FOR PAIN SENSATION
The center for pain sensation is
in the Post Central Gyrus of
Parietal cortex.

Fibres reaching Hypothalamus

are concerned with arousal
mechanism due to pain
stimulus.
Function of Reticular Formation,
Thalamus & Cerebral Cortex in
appreciation of Pain

Cerebral cortex INTERPRETS

PAIN QUALITY

Lower Centers PERCEIVES the

pain
 Process of Pain Physiology

TRANSDUCTION
TRANSMISSION
PERCEPTION
MODULATION
 Modulation
 InhibitoryNeurotransmitters
like Endogenous Opioids work
to hinder the pain transmission.

 This inhibition
of the pain impulse is
known as modulation
 Transduction:

Pain stimuli is converted to

electrical energy. This electrical energy
is known as Transduction. This
stimulus sends an impulse across a
peripheral nerve fiber (nociceptor).
 Transmission

 A delta fibers (myelinated) send

sharp, localized and distinct
sensations.
 C fibers (unmyelinated) relay
impulses that are poorly localized,
burning and persistent pain.
 Pain stimuli travel- spinothalamic
tracts.
 Perception
 Person is aware of pain –
somatosensory cortex identifies the
location and intensity of pain
 Person unfolds a complex reaction-
physiological and behavioral
responses is perceived.
Effects of pain
Sympathetic responses
 Pallor
 Increased blood pressure
 Increased pulse
 Increased respiration
 Skeletal muscle tension
 Diaphoresis
Effects of pain
Parasympathetic responses
 Decreased blood pressure
 Decreased pulse
 Nausea & vomiting
 Weakness
 Pallor
 Loss of consciousness
 REFERRED PAIN
Definition:
The pain sensation produced in some part
of the body is felt in other structures
away from the place of development.

The deep pain and some visceral pain are

referred to other areas. But superficial
pain is not referred.
1) Heart pain is referred to
the inner aspect of left arm.
2) Diaphragmatic pain to the
tip of the shoulder
3) Ureteric pain to the testes
in male and the inner aspect
of the thigh in female.
4) Gall bladder pain referred
to epigastric region.
5) Pain from the maxillary
sinus referred to the nearby
tooth.
Friday, March 20, 2020
Dermatomal Rule
 Referred pain is always felt over a
structure that developed from the
same Embryological segment
or Dermatome from which the
pain producing structure is
developed
 Visceral or deep pain is referred to
the dermatome which has the same nerve
supply as the site of pain.
Mechanism of Referred Pain
Mechanism of Referred Pain
Visceral pain fibers are stimulated

pain signals from the viscera are

conducted through some of the
neurons that conduct pain signals
from the skin

the person has the feeling that, the

sensation originate in the skin itself.
Dermatomal Rule
 During Embryonic development, the
diaghragm migrates from the neck region
to its adult location between the chest and
abdomen and takes its nerve supply, the
phrenic nerve with it.
 Similarly the heart and the arm have the
same segmental origin.
 Testicles have migrated with its nerve
supply from the primitive urogenital ridge
from which kidney and ureter has
developed.
CONVERGENCE THEORY
 The number of peripheral pain afferent fibres
exceed the number of lateral spinothalamic
tract. So, Both the somatic and visceral
afferents converge upon the same
spinothalamic neurons at the spinal cord
level.
 Hence when visceral pain impulses travel in
the same pathway along which impulses from
the skin travels, the individual gets the
feeling that the pain originates in the skin
itself.
 FACILITATION THEORY
 Visceral and somatic
pain afferents connect
with separate but
adjoining
spinothalamic
neurons and there
may be some overlap
of the neurons,
visceral afferents have
collaterals connecting
to the spinopthalamic
neurons receiving
somatic pain afferents.

 DESCENDING NEURONS
 Descending Pain Modulation (Descending Pain
Control Mechanism)
 Transmit impulses from the brain
(Corticospinal tract in the cortex) to the
spinal cord (lamina)
 Periaquaductal Gray Area (PGA) –
release enkephalins
 Nucleus Raphe Magnus (NRM) – release
serotonin
 The release of these neurotransmitters inhibit
ascending neurons
How pain is transmitted to brain
Pain Suppression
( ANALGESIA) System
in the BRAIN & SPINAL
CORD
 ANALGESIA SYSTEM
 The CNS has its own control system which
inhibits the impulse of pain sensation. This is
also called Analagesia system.

 This control system is present in both

Brain and Spinal cord
 ANALGESIC PATHWAY

 It is considered as
DESCENDING PAIN PATHWAY
 Periventri
cular area

Periaqueduc
tal grey

Raphe Magnus
Nucleus

Pain
Inhibitory
Friday, March 20, 2020
Complex
 Pain control system in
BRAIN
1. The Periaqueductal Gray &
Periventricular ares ( Midbrain & Upper
Pons).
2(a) The Raphe Magnus Nucleus
( lower pons & Upper Medulla)
2 (b). Nucleus Reticularis Paragiganto-
cellularis ( lateral Medulla)
3. Pain inhibitory Complex (Spinal Cord)
I
 2 nd Order Neurons

Dorsolateral Columns in the Spinal

cord.
A Pain inhibitory Complex
located in the Dorsal horns of the
Spinal cord.
Pain Suppression (Analgesia)
system of Brain & Spinal cord
Frontal lobe of cerebral cortex &
Hypothalamus

•Periaqueductal grey Neurotransmitters

•Periventricular nuclei Serotonin
Opiates (enkephalins)

Raphe Magnus nucleus

Nucleus Reticularis Paragigantocellularis

Spinal cord
(Pain Inhibiting Complex in dorsal horn)
Endogenous Opioid peptides

Enkephalins & Serotonin

causes ANALGESIA.
( By causing both presynaptic &
postsynaptic inhibition of
incoming type C & A δ fibers)
Others Opiod peptides:

Endorphins and
Dynorphine.
Pain control system
in Spinal Cord
 Site: Dorsal Grey
Horn.
 The dorsal grey horn is
considered as the
GATEWAY for pain
impulses to reach the
brain (via) spinothalamic
tract.
GATE CONTROL
THEORY
1965
The pain stimuli transmitted by afferent pain
fibers are blocked by GATE mechanism
( Dorsal grey horn) .

 Substantia Gelatinosa (SG) in dorsal horn of

spinal cord acts as a ‘GATE’

 If the GATE is opened , pain is felt or

vice versa.
 GATE CONTROL THEORY
 Gate - located in the dorsal horn of the spinal cord
 Smaller, slower n. carry pain impulses
 Larger, faster n. fibers carry other sensations
 Impulses from faster fibers arriving @ gate 1st
inhibit pain impulses (acupuncture/pressure, cold,
heat, chem. skin irritation).
Brain

Pain
Gate (T
cells/ SG) Heat, Cold,
Mechanical
 Gate Control Theory
 Other afferents , the touch fibres reaching the
DORSAL COLUMN of spinal cord are also activated

 These TOUCH FIBRES send collaterals to the cells

of Substantia Gelatinosa & Marginal nucleus in the
dorsal grey horn.

 Here TOUCH IMPULSES impulses inhibit the

release of substance P & Glutamate by the pain
nerve endings.

 Thus the GATING MECHANISM of pain inhibition

in dorsal grey horn level is ativated.

 The pain sensation is suppressed

 Applied
 Tic douloureux- electric shock like pain in
sensory distribution of V or IX cranial nerves.
 Trigeminal neuralgia
 Glassopharyngeal neuralgia

 Headache –
 Dura
 Cerebral blood vessels
 CSF pressure
 Nasal & accessory nasal structures
 Eye disorders
 Muscle spasm of head & neck muscles
 Alcohol
 constipation
 Tic Douloureux
(Trigeminal Neuralgia or
Glossopharyngeal Neuralgia)

 Severe pain occasionally occurs in

some people over one side of the face
in the sensory distribution area of
the V or IX nerves; this phenomenon
is called Tic Douloureux
 HEADACHE
 Type of pain refered to the surface
of the head from deep head
structures.

Pain Stimuli:
 Inside or outside the cranium
Types of Intracranial
Headache
 Headache of
 Headache Caused by
.
Headache
Headache
Headache of Meningitis
Inflammation of
all meninges

Extreme pain
referred over
the entire head.
Headache Caused by Low
Cerebrospinal Fluid Pressure