PHYSIOLOGY OF PAIN SENSATION

PHYSIOLOGY OF PAIN SENSATION

1. DR NILESH KATE
MBBS,MD
ASSOCIATE PROF
ESIC MEDICAL COLLEGE, GULBARGA.
DEPT. OF PHYSIOLOGY
PHYSIOLOGY
OF PAIN
SENSATION.

2. OBJECTIVES
Definition of pain
Types of pain
Varieties of pain
Pain pathway
 Pain inhibiting pathway
 Central analgesia
Referred pain
Applied physiology

3. Definition
The sensation of pain is defined as the The sensation of pain is defined as the
physical adjunct of an imperative physical adjunct of an imperative
protective reflex.protective reflex.
pain is an, unpleasant sensory and
emotional experience associated with actual
or potential tissue damage - The The
International Association for the Study of International Association for the Study of
Pain (IASP)Pain (IASP)

4. Types of pain
Fast pain is due to activity of
myelinated A d fibres and it is
appreciated as sharp bright
and localized sensation.
Slow pain is due to activity of
unmyelinated C fibres and it is
appreciated as dull aching
and more diffuse. Slow pain
follows fast pain.
PeripheralPeripheral
NerveNerve
C-FiberC-Fiber
A-delta FiberA-delta Fiber

5. Fast pain & Slow pain
Fast pain: is also described as
sharp pain, pricking pain,
Acute pain, electric pain. it is
elicited by mechanical and
thermal type of stimuli.
Slow pain is also called as,
slow burning pain, aching
pain, throbbing pain,
nauseous pain, chronic pain.
slow pain can be elicited by
mechanical, thermal and
chemical stimuli.

6. Types of Pain
Fast painFast pain Slow painSlow pain
Felt within about 0.1 second
after a painful stimulus.
Begins after 1 second or more
and then increases slowly
over many sec. or min.
“Bright," sharp, localized
sensation
Dull, intense, diffuse, and
unpleasant feeling
sharp pain, pricking pain, acute
pain, and electric pain
slow burning pain, aching pain,
throbbing pain, nauseous pain,
and chronic pain
Felt mainly in skin. Not felt in
most deeper tissues of the
body
It can occur both in the skin
and in almost any deep tissue
or organ

7. Types of Pain
Fast painFast pain Slow painSlow pain
Pin prick, cutting or Pin prick, cutting or
burning of skinburning of skin
Associated with tissue Associated with tissue
destruction.destruction.
Caused by mechanical or Caused by mechanical or
thermal stimuli.thermal stimuli.
Caused mainly by Caused mainly by
chemical stimulichemical stimuli
Transmitted by Aδ fibersTransmitted by Aδ fibers
(velocity 6-30 m/sec)(velocity 6-30 m/sec)
NT- GlutamateNT- Glutamate
Transmitted by C fibersTransmitted by C fibers
(velocity 0.5-2 m/sec)(velocity 0.5-2 m/sec)
NT- Substance PNT- Substance P
Neo-spinothalamic tractNeo-spinothalamic tractPaleo-spinothalamic tractPaleo-spinothalamic tract

9. TYPES OF PAIN
source of origin -- three 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

10. 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 @ 1
st
& later may be localized (i.e.
appendicitis)
Psychogenic Pain – individual feels pain but
cause is emotional rather than physical

11. VARIETIES OF PAIN
ACUTE PAIN
CHRONIC PAIN
CUTANEOUS PAIN
DEEP SOMATIC PAIN
VISCERAL PAIN
REFERRED PAIN
NEUROPATHIC PAIN
PHANTOM PAIN

12. CAUSES OF VISCERAL PAIN
Ischaemia: The substances released during
ischaemic reactions like bradykinin and
proteolytic enzymes stimulate the pain receptors
of viscera.
Chemical stimuli: The chemical substances like
acidic gastric juice leaks from ruptured ulcers into
peritoneal cavity and produce pain.
Spasm of hollow organs: spastic contraction of
muscles in gastrointestinal tract and other hollow
organs of viscera cause pain by stimulating the free
nerve endings.
Overdistension of hollow organs also cause pain.

13. Pains of Special Interest
Intermittent claudication: - recurrent pain in the calf
muscle during exertion, which stops on rest.
This is due to ischaemia of muscle which produces P-
factor – pain producing chemical agent which is
responsible for causation of pain. During rest the pain
stops because P factor is washed away by blood.
Eg:Thrombo Angitis Obliterans. (Buerger’s disease)
Inflammatory pain: - due to
increased tension causing pressure
on nerve terminals as well as due to
release of a chemical pain producing factor.

14. PAINS OF SPECIAL INTEREST
Coronary occlusion: In addition to P factor, there
is release of 5HT and plasma pain producing
polypeptide.
Nerve pain: partial compression of nerve or a
nerve root leads to irritability of the nerve or the
nerves concerned and gives rise to the formation
of areas of Hyperalgesia and pareaesthesia
Ischaemic Muscular pain: Due to release of P
factor during active work, on accumulation
cause pain. The P factor may be potassium or
kinin. Repeated muscular contraction compress
blood vessel.

15. REFERED PAIN
Definition:
The pain sensation produced in some part of
the body is felt in other structures away
from the place of development. This is
called refered pain.
The deep pain and some visceral pain are
referred to other areas. But superficial
pain is not referred.

16. REFERED PAIN
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.

17. Referred Pain

18. Referred Pain
Pain in organs is
poorly localized
May be displaced if
Multiple 1° sensory
neurons converge on
single ascending
tract

19. Mechanism of Referred Pain
When the visceral pain fibers are stimulated
pain signals from the viscera are conducted
through some of the neurons that conduct
pain signals from the skin and the person
has the feeling that,
the sensation
originate in the
skin itself.

20. Dermatomal Rule
Referred pain is always felt over a
structure that developed from the
same embryological segment or
dermatome from which the organ
which is the source of pain
developed. This phenomenon of
referred pain is called Dermatomal
rule.

21. 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.

22. 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.

23. 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.
 This causes impulses to travel up the somatic
spinothalamic pathway and causes the sensation
of pain in the skin.

24. How pain is transmitted to brain

25. Process of painphysiology
TRANSDUCTION
TRANSMISSION
PERCEPTION
MODULATION

26. 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).

27. 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.

28. 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.

29. Modulation
Inhibitory neurotransmitters like
endogenous opioids work to hinder
the pain transmission.
This inhibition of the pain impulse is
known as modulation

30. Receptors for Pain
The receptors in the skin and other tissues are
free nerve endings of small myelinated A d
and non myelinated C fibres.
They are widespread in the superficial
layers of skin as well as in certain internal
tissues such as the periosteum, arterial walls,
joint surfaces, falx and tentorium of cranial
vault.

31. Pain receptors (Nociceptors)
Free nerve endings
More in
Superficial layers of skin
Periosteum
Arterial walls
Joint surfaces
Falx, tentorium
Sparse in other deep
tissues.
Non-adapting in nature.

32. Effects of pain
Sympathetic responses
Pallor
Increased blood pressure
Increased pulse
Increased respiration
Skeletal muscle tension
Diaphoresis

33. Effects of pain
Parasympathetic responses
Decreased blood pressure
 Decreased pulse
Nausea & vomiting
Weakness
Pallor
Loss of consciousness

34. Sensory PathwaySensory Pathway
Stimulus Stimulus
Sensory receptor (= transducer)Sensory receptor (= transducer)
Afferent sensory neuronsAfferent sensory neurons
CNSCNS
Integration, perceptionIntegration, perception

35. 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)

36. 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

37. •Thalamus – ventrobasal complex
•Reticular formation
Spinothalamic tract
Spinal cord
(lamina I – lamina marginalis)
Peripheral fibers
Aδ fibers
Pain receptor
(Free nerve endings)
•Somatosensory cortex
•Other basal areas of brain

38. Pain pathwayPain pathway

39. •Reticular nuclei,Tectal area &
periaqueduvtal grey region
•Thalamus
Spinothalamic tract
Spinal cord
(lamina II & III – substantia gelatinosa)
Peripheral fibers
C fibers
Pain receptor
(Free nerve endings)
•Thalamus (IL & VL nuclei)
•Hypothalamus
•Other basal areas of brain

40. 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.
Substance P is the
neurotransmitter involved in
pain sensation. It is secreted by
the ending of pain nerve fibres
in dorsal grey horn.

41. 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
Endogenous opioid peptides - endorphins &
enkephalins causes analgesia.

42. PHYSIOLOGY OF PAIN PERCEPTION
InjuryInjury
Descending Descending
PathwayPathway
PeripheralPeripheral
NerveNerve
Dorsal Dorsal
RootRoot
GanglionGanglion
C-FiberC-Fiber
A-beta FiberA-beta Fiber
A-delta FiberA-delta Fiber
AscendingAscending
PathwaysPathways
Dorsal Dorsal
HornHorn
BrainBrain
Spinal CordSpinal Cord
42

43. Physiological Basis of Medical
measures to relieve pain
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.
Pain control system in spinal cord: This is in
dorsal grey horn. The dorsal grey horn is
considered as the gateway for pain impulses to
reach the brain (via) spinothalamic tract.

44. GATE CONTROL
THEORY
Melzack & Wall, 1965
Substantia Gelatinosa (SG) in dorsal horn of
spinal cord acts as a ‘gate’ – only allows one
type of impulses to connect with the SON
If A-beta neurons are stimulated – SG is
activated which closes the gate to A-delta &
C neurons
If A-delta & C neurons are stimulated – SG is
blocked which closes the gate to A-beta
neurons

45. 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 1
st
inhibit
pain impulses (acupuncture/pressure, cold, heat,
chem. skin irritation).
Brain
Pain
Heat, Cold,
Mechanical
Gate (T
cells/ SG)

46. Gate control theory
When pain sensation is produced-- other afferents
particularly the touch fibres reaching the
posterior column of spinal cord are also activated.

These dorsal column fibres send collaterals to the
cells of substantia gelatinosa in the dorsal grey
horn.
 Thus impulses ascending via dorsal column fibres
pass through the collaterals and reach substantia
gelatinosa.
 Here these impulses inhibit the release of
substance P by the pain nerve endings. So that the
pain sensation is suppressed.
 Thus the gating of pain in dorsal grey horn
level is similar to presynaptic inhibition.

47. •Periaqueductal grey
•Periventricular nuclei
Raphe magnus nucleus
Nucleus reticularis paragigantocellularis
Spinal cord
(pain inhibiting complex in dorsal horn)
Hypothalamus
(periventricular nucleus & MFB)
Pain suppression (Analgesia)
system of brain & spinal cord
NeurotransmittersNeurotransmitters
SerotoninSerotonin
Opiates (enkephalins)Opiates (enkephalins)

49. Pain control system in Brain
Acupuncture is also used to relieve pain. This
is based upon the pain inhibitory mechanism
of encephalins and endorphins released by
this procedure.
Pain control

NSAIDs (inhibit COX)NSAIDs (inhibit COX)

Opiates (inhibit NT release)Opiates (inhibit NT release)

50. Inhibition of pain transmission by tactile
sensory signals
Rubbing the skin near painful areas and
applying liniments often relieves pain.
 This is due to the stimulation of Aβ sensory
fibres from peripheral tactile receptors
depress transmission of pain signals.
 This results from a type of local lateral
inhibition.

51. Surgical procedure that relieve pain
Different surgical procedures are done in the
course of pain pathway to relieve pain. They
are
-Sympathectomy
-Cordotomy
-Thalamotomy
-Prefrontal lobotomy

52. Applied
Terminology
Algesia = pain
Analgesia = dec./loss of sensitivity to painful stimuli
Hyperalgesia = inc. sensitivity to painful stimuli
Allodynia = sensation of pain in response to an
innocuous stimulus
Brown-Sequard syndrome (hemisection of
the spinal cord.
Syringomyelia (loss of pain & temp. with
sparing of touch & vibration.

54. Applied
Tic douloureux- electric shock like pain in
sensory distribution of V or IX CN.
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

55. Applied
Treatment for pain
Remove the cause
NSAID (Non-Steroidal Anti-
Inflammatory drugs)
Opioid analgesics

56. APPLIED PHYSIOLOGY
Abnormal prolonged pain: Injuries and disease
process cause damage to peripheral nerves
cause severe debilitating and persistent
abnormalities of pain sensation.
Hyperpathia : Threshold for stimulation is
increased causing burning pain.
Phantom limb: Pain in absent limb.
Causalgia: spontaneous burning pain long after
trivial injuries.
Hyperalgesia is a condition in which pain is
produced by minor stimuli which normally do
not cause pain eg: Touch
If a normal innocuous tactile or thermal stimulus
evokes pain, the condition is called Allodynia.

57. RECAP
Definition of pain
Types of pain
Varieties of pain
Pain pathway, pain
inhibiting pathway , central analgesia
Referred pain
Applied physiology

58. Thank
You