This document discusses the physiology of pain, including: - Types of pain receptors and the pathways for fast and slow pain transmission. - Pain is transmitted via A-delta fibers for fast pain and C fibers for slow pain to the spinal cord. - From the spinal cord, pain travels via the spinothalamic tracts to the thalamus and brain for perception. Modulatory pathways can inhibit pain transmission.

2.  Definition of pain
 Types of pain
 Varieties of pain
 Pain pathway
 Pain inhibiting pathway
 Central analgesia
 Applied physiology

3.  An unpleasant sensory and emotional
experience associated with actual or
potential tissue damage, or described in
terms of such damage.
› (International association for the study of
pain 1979)

6. Damaged tissues release proteolytic enzymes, K+
&histamine .Proteolytic enzymes act on globulins in
the interstitial Fluid to release kinins.
e.g bradykinin, K+ and histamine stimulate pain
receptors
Pain is a protective sensation.

8. Pain receptors . Free nerve endings
Three types
1. Mechanical pain Receptors.: stimulated
by mechanical injurious stimuli.
2. Thermal pain Receptors. : discussed
before.
3. Chemical pain Receptors.: stimulated by
chemical stimuli.
Chemical stimuli include:
bradykinin (most important) serotonin,
histamine & K+.

9. Distribution of pain receptors
- More : Skin, periosteum, arteries, joint surfaces, &
tentorium cerebelli and cranial sinuses.
- Less : deep tissues.
- Absent : liver parenchyma, lung alveoli and
brain.
►Nerve fibres: A delta and C fibres.
►Adaptation: Slowly (static-tonic) or nonadaptive
receptors.

10. Types of pain
Pain is classified according to the:
(a) Site of pain
1. Cutaneous pain.
2. Deep pain.
3. Visceral pain.
(b) Quality of pain
1. Epicritic i.e sharp pricking pain.
2. Protopathic i.e dull aching pain.
3. Burning pain.

11.  Fast pain is due to activity of
myelinated A  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.
Peripheral
Nerve
C-Fiber
A-delta Fiber

12.  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.

13.  From the pain receptors, the pain
stimulus is transmitted through peripheral
nerves to the spinal cord and from there
to the brain. This happens through two
different types of nerves fibers:
 A-delta "fast pain” and
 C-fibers “slow pain” nerve fibers.

14. TYPE OF
NERVE
CONDUCTION
VELOCITY
( MTS/SEC )
MELINATED TYPE OF PAIN
A- DELTA 20 (fast) YES SHARP,
PRICKING,WELL
LOCALIZED
C 1 (slow) No DULL ACHE,
DIFFUSE

15. Fast pain Slow pain
Pin prick, cutting or
burning of skin
Associated with tissue
destruction.
Caused by mechanical or
thermal stimuli.
Caused mainly by
chemical stimuli
Transmitted by Aδ fibers
(velocity 6-30 m/sec)
NT- Glutamate
Transmitted by C fibers
(velocity 0.5-2 m/sec)
NT- Substance P
Neo-spinothalamic tract Paleo-spinothalamic tract

16. 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

17.  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

18.  ACUTE PAIN
 CHRONIC PAIN
 CUTANEOUS PAIN
 DEEP SOMATIC PAIN
 VISCERAL PAIN
 REFERRED PAIN
 NEUROPATHIC PAIN
 PHANTOM PAIN

19.  A pain stimulus, e.g. if you cut yourself,
consists of two sensations.
 first “fast pain” sensation-is experienced
as sharp.
 “slow pain”, more a dull and burning.
 Occurs after a short time
 lasts a few days or weeks,
 Chronic pain-if inappropriately
processed by the body, it can last
several months

20.  nerves are called A-delta fibers.
 relatively thick size nerve fibers allow the
pain stimulus to be transferred very fast
(at a speed of five to 30 meter/second),
hence the name
 This is all to make the body withdraw
immediately from the painful and
harmful stimulus, in order to avoid further
damage.

21.  starts immediately after the fast pain
 is transmitted by very thin nerve fibers,
called C-nerve fibers (their diameter is
between 0.2 to 1 thousandth of a
millimeter).
 pain impulse can only be transmitted
slowly to the brain, at a speed of less
than 2 meters per second.
 Body response -immobilization (guarding,
spasm or rigidity), so that healing can
take place.

22.  Fast (Immediate, acute
 sharp or pricking)
 Felts within 0.1 sec ond .
 Short-duration.
 Mechanical &Thermal R.
 A delta fibres.
 Ends in cerebral cortex.
 Well localized.
 Not felt in deep tissues
 Blocked by hypoxia & pressure
 Neospinothalamic tract
 Neurotransmitter:
 Glutamate .
 Slow (Chronic, burning,
aching throbbing nauseous)
After one second .
Prolonged;annoying,intolerable.
Elicited by All types of R.
C fibres
Ends in non specific thalamic
nuclei & Reticular formation.
Poorly localized .
Occurs in skin & deep tissues
Blocked by local anesthesia.
Paleospinthalamic tract
Neurotransmitter
Substance P.

23.  Fast
 A Delta Fibers
 Glutamate
 Neospinothalamic
 Mechanical, Thermal
 Good Localization
 Sharp, Pricking
 Terminate in VB
Complex of Thalamus
 Slow
 C Fibers
 Substance P
 Paleospinothalamic
 Polymodal/Chemical
 Poor Localization
 Dull, Burning, Aching
 Terminate; RF
› Tectal Area of Mesen.
› Periaqueductal Gray

24.  Spinothalamic - Major
› Neo- Fast (A Delta)
› Paleo- Slow (C Fibers)
 Spinoreticular
 Spinomesencephalic
 Spinocervical (Mostly Tactile)
 Dorsal Columns (Mostly Tactile)

26. • A-DELTA→ Noxious Stimulation → change in
Membrane Potential → Receptor Potential → A. P.
• C-FIBERS: Damaged Cell → Proteolytic Enzymes
Circulating Gamma Globulins
Bradykinin, Substance P
Stimulation of Nerve Ending

27. Fast pain is transmitted by A delta fibers
(5-15 m/sec.) from skin
(mainly), parietal pleura, peritoneum a
& Synovial membrane.

30. (1) Somatic (motor) reflexes:- Spinal reflexes.
Flexor withdrawal reflex.
(2) Autonomic reactions:-
Cutaneous pain: Pressor effects (increased heart rate & ABP).
DEEP & visceral pain: Depressor effects (decreased heart rate &
ABP).
(3) Emotional reactions:-
-Acute pain: Crying and anxiety.
(4) Hyperalgesia:- mainly due to skin lesion. (increased pain
sensibility).

31. Deep pain C. Fibres
Diffuse, Dull aching and Depressor effects.
Causes: - inflammation, ischaemia or muscle
spasm.
- Bone fractures; due to stimulation of periosteal
pain receptors.
Characters of deep pain
1. Dull aching or rhythmic cramps.
2. Diffuse (poorly localized).
Depressor autonomic changes: decreased heart
rate, decreased arterial blood pressure ,nausea &
vomiting.

32. • Arises from Periosteum & Ligaments
• Continuous Contraction of Muscles
• Poorly Localized
• Associated with Sweating & Changes in Blood
Pressure
• Often Nauseating
• Transmitted via Antero Lateral System

34. Ischaemic pain
Type of deep pain felt in muscles when their
blood supply is decreased.
The Patients complains of severe pain in the
muscles upon walking or running due to
accumulation of pain producing substances as
lactic acid.
Examples
1. Cardiac muscle: angina pectoris.
2. Skeletal muscle: intermittent claudication.

35. Visceral pain C Fibres
Most of viscera contain only pain receptors.
Pain from viscera is carried a long; C fibres.
Pain from peritoneum, pleura or pericardium:Adelta.
It differs from cutaneous pain
. Sharp cut in the viscera does not cause pain (why).
. Diffuse stimulation of pain nerve ending ® severe
pain.

36. Causes Of Visceral Pain
1. Ischaemia: increased acidic metabolites,
bradykinin & proteolytic enzymes.
2. Inflammation of peritoneal covering of viscera.
3. Irritation (chemical irritation by HCI in peptic
ulcer).
4. Overdistension of a hollow viscus e.g urinary
bladder.
5. Spasm of a hollow viscus e.g gut, gall bladder
or ureter.
Both 4 & 5: Obliteration of blood vesssels ®
Ischaemic pain.

37. Characters of visceral pain
1. Dull aching or rhythmic cramps.
2. Diffuse (poorly localized).
3. Depressor autonomic changes: decreased heart rate,
decreased arterial blood pressure ,nausea & vomiting.
4. Rigidity of the overlying muscles.
Limitation of the spread of infection.
Decrease the mobility of the diseased viscus for relief of
pain.
5. Referred to the surface area i.e referred pain.

38. • Arises from Visceral Organs
• Receptors
– Free Nerve Endings of A Delta & C Fibers
– Sparsely Distributed
• Stimulus: Spasm, Distension, Ischemia, Chemical
• Ischemia
– Release Acid Metabolites
– Tissue Degeneration Products Produce Bradykinin &
Proteolytic Enzymes
• Chemicals
– Release of Proteolytic Acid Gastric Juice

39.  Input to CNS via Autonomic Nerves
 Cell Bodies of Ist Order Neuron
› DRG & Homologous Cranial Nerve Ganglia of VII, IX ,
X & Trigeminal Nerve
 Afferent also Enters via Sympathetic Ganglia for
Reflex Control of Visceral Functions

40. • In CNS Fibers Follow Same Route as that of Other
Pain Fibers
– Poorly Localized, Unpleasant
– Associated with Autonomic Changes & Nausea
– Usually Referred to Superficial Parts of Body
• REFERRED PAIN
– Visceral Pain Usually Referred
– Deep Pain May Also be Referred

42. Referred pain
Definition
Pain originating from viscera but felt in
somatic structures which supplied by the
same spinal dorsal root ( the same
dermatome) of the diseased viscus.

43.  Examples
 1. Cardiac pain: is felt in left shoulder.
 2. Gall bladder pain: is felt in tip of right shoulder.
 3. Appendicular pain: is felt around the umbilicus.
 4. Gastric pain: is felt between the umbilicus &
xiphoid process.
 5. Renal pain: is felt in the back, inguinal region &
testicles.
 6. Teeth pain: referred to other teeth.

45. • Superficial Pain Never Referred
• Visceral Pain - Local & Referred
– May also Radiate to Distant Site
– Cardiac Pain
• Inner Aspect of Left Arm, Right Arm, even to Neck &
Abdomen
– Distension of Ureter
• Pain in Testicles
– Irritation of Parietal Plura & Peritoneum
• Pain Referred to Overlying Surface of Body
– Of Diaphragm
• Tip of Shoulder

46. Referred Pain

47.  Mechanism
› Dermatome Rule
 Parts Develop from Same Embryonic Segment or
Dermatome
 Diaphragm Migrate from Neck
 Heart & Arm have Same Segmental Origin
 Convergence
› Somatic and Visceral Pain Afferents Converge on Same
Second Order Neuron
› Brain Unable to Differentiate Site of Origin
 Hence Pain Felt at Somatic Sites

48. Mechanism of referred pain
a. Convergence – projection theory
Afferent pain fibers from the skin and viscous
converge on the same cells of SGR or
thalamus and will finally activate the same
cortical neurons.
Whatever the source of pain, the cortex will
project it to the skin being the commonest
source of pain.

50. b. Facilitation theory
Afferents of diseased viscera,
give facilitation to cutaneous
pain cells in Substantia
Gelatinosa of Rolandi (SGR),
Which leads to facilitation of
their stimulation.

52.  Facilitation Effect:
› ↑ Activity in Visceral Pain Afferents Collaterals Fibers →
EPSP in Spinal Neurons Receiving Somatic Inputs → ↑
Activity in Somatic Neurons → Continuous Pain

53. • Intensity of Pain is Proportional to Degree of Tissue
Damage
• Ischemic Pain → Lactic Acid → Nerve Ending
Stimulation
• Muscle Spasm Mechanoreceptor Stimulation
Ischemia
• Transmission of Pain
– A – Delta Fibers: 6 to 30 M/Sec
– C – Fibers: 0.5 to 2 M/Sec

55. TRANSDUCTION
TRANSMISSION
PERCEPTION
MODULATION

56. Pain stimuli is converted to
electrical energy. This is known as
Transduction. This stimulus sends
an impulse across a peripheral
nerve fiber (nociceptor).

57.  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.

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

59. C fibre
Final pain perception
depends on activity of
the
•Ascending pain
impulse transmitting
tracts
•Descending pain
modulatory
(inhibitory) tracts

61.  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

62. • Mixed Spinal Nerve
• Dorsal Root Ganglia Dorsal Root Dorsal
Horn
• A – Delta Fibers
– Terminate in Lamina I of Dorsal Horn Gray Matter (Fast
Pain)Give Local Collateral Branch for Spinal Reflexes
• Second Order Neuron
– Cross to Opposite Side
– Form Anterior Spino-Thalamic Tract (Neospinothalamic
Tract)
• Joins Medial Laminiscus → Few Collaterals to R.F.

63. • First synapse in spinal cord is substantia
gelatinosa
substantia
gelatinosa
Neurotransmitter at the first synapse of the
pain pathway is substance P
• Acute pain : glutamate
• Chronic pain: substance P
• Pain inhibitory neurotransmitters: enkephalin, GABA

64.  Ascending pathway
 Crosses the midline
 Ascends up as the lateral spinothalamic tract
Pain
lateral
spinothalamic
tract
C fibre
substantia
gelatinosa

65. • Second Order Neuron Thalamus
Post Central Gyrus
• Localization is Good
• Neurotransmitter is Glutamate
• Few Fibers Ascends in Dorsal Column

66. •Slow pain: C –Fibers Ist Order Neuron
Lamina II and III
Substantia Gelatinosa of Rolando
Interneuron Lamina V Second Order Neuron
Cross → Lateral Spinothalamic Tract
(Paliospinothalamic Tract → Brain Stem Joins → Medial
Leminiscus → Thalamus → Cortex

67.  Brain Stem: Collaterals Given to:
› Reticular Formation at All Levels of Brain Stem
› Hypothalamus
› Peri Ventricular Gray Matter
› Peri Aqueduct Gray Matter
› Most Fibers End in Intralaminar and Reticular Nuclei of
Thalamus
› Non Specific Thalamo Cortical Projections to All Part of
Cerebral Cortex
› To Somato Sensory Cortex SI and SII

68. • While Entering Spinal Cord
– Fibers Ascends or Descends Few Segments → Enters
Spinal Cord
• Through Many Inter-Neurons
– Information Relayed to Anterior Horn Cells of Same &
Opposite Side for Local & Segmental Reflexes of Spinal
Cord

69. •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

70. Pain pathway

72. •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

73. 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.

74. Appreciation of pain
- Fast pain; is appreciated in thalamus and cortex.
- Slow pain; is appreciated mainly in thalamus.
Functions of the cortex in pain appreciation
1. Localization of pain 2. Discrimination of type of pain.
3. Modulation of pain by emotional and behavioral
factors.

75. Arousal reaction to pain signals
The non specific thalamic nuclei (intra-
laminar nuclei) and reticular formation
have a strong arousal effect on the brain
which prevents sleep during pain.

76. Injury
Descending
Pathway
Peripheral
Nerve
Dorsal
Root
Ganglion
C-Fiber
A-beta Fiber
A-delta Fiber
Ascending
Pathways
Dorsal
Horn
Brain
Spinal Cord
76

77. lateral
spinothalamic
tract
thalamus
C fibre
thalamoc
ortical
tracts

78.  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.

79.  Peripheral
 Gating Theory
› Involves Inhibitory
Inter-Neuron in Cord
impacting Nociceptive
Projection Neurons
 Inhibited by C Fibers
 Stimulated by AAlpha &
Beta Fibers
 TENS
 Central
 Direct Electrical + to
brain → Analgesia
 Nociceptive control
Pathways Descend to
Cord
 Endogenous Opioids

80.  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

81. Gate control theory
When pain fibre is stimulated, gate will be opened & pain is
felt
pain
pain is felt
+
gate is
opened

82. Gate control theory
When pain and touch fibres are stimulated together, gate
will be closed & pain is not felt
pain is
not felt
touch
pain
+ -
gate is
closed

84. GATE CONTROL MECHANISM
S.G.Cells
T- Cells
Type II Fibers
A-DELTA &
C Fibers
(-)
(-)
(+)
(-)
(+)
Spino
Thalamic
Pathway
(-)

86.  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
Heat, Cold,
Mechanical
Gate (T
cells/ SG)

87.  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.

88.  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.

91. Presynaptic inhibition
substance P
enkephalin
pain impulse
blocking of
pain impulse

92.  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.

93. • DESCENDING PAIN INHIBITING SYSTEM:
• Fibers Arise from: Peri-Aqueductal Gray matter
Peri-Ventricular Gray Matter
Hypothalamus
Medial Forebrain Bundle
Neurons around IIIrd & IV ventricle
Nucleus Reticularis in Medulla
Spinal Cord Nucleus Raphe
Magnus
Encephalins

94. • Nucleus Raphe Magnus
• Dorsal Horn of Spinal Cord in Substantia Gelatinosa
• Pre-Synaptic and Direct Inhibition by Blocking Ca ++
Channels
• Blocking of Pain Signals
Serotonergic
Neurons

96. •Periaqueductal grey
•Periventricular nuclei
Raphe magnus nucleus
Nucleus reticularis paragigantocellularis
Spinal cord
(pain inhibiting complex in dorsal horn)
Hypothalamus
(periventricular nucleus & MFB)
Neurotransmitters
Serotonin
Opiates (enkephalins)

98. Pain Control Systems
(I) Analgesic system
a) The neurons of the periaqueductal gray area are
stimulated by B endorphin reaching them from
hypothalamus (neurons of periventricular area) or
pituitary (through blood).
b) Fibres of periaqueductal and interneurones of sp.cd.
Secrete (Enkephalin)
c) Fibres of raphe magnus nucleus secrete (Serotonin)
d) Inhibitory interneurones in spinal cord secrete
(Enkephalin).

102. • Natural Opioids-
Endorphins
•released from their
storage areas in the
brain when a pain
impulse reaches the
brain,
• bind to receptors in
the pain pathway to
block transmission and
perception of pain.

103.  opioid pain
inhibition
at multiple levels
› spinal cord
› brain-stem
› thalamus

105. (II) Brain Opiate System
Opiate receptors in the brain cause pre and
postsynaptic inhibition of the nociceptive pathway.
Sites of opiate receptors
1. Periaqueductal gray area
2. Periventricular aea.
3. Raphe magnus nucleus in medulla.
4. Substantia nigra.

106. Opioid peptides
(1) Enkephalins.
Act as neurotransmitters at the analgesic system.
(2) Endorphins
-In hypothalamus act as neurotransmitters.
-In pituitary act as hormone.
Release during stress leading to stress analgesia.
(3) Dynorphin
Very potent analgesic.
Types of opiate receptors
Delta, Mu, Kappa, Sigma & Epislon.

107.  Opium
› Alkaloid
› Morphine Derived from Opium → Analgesia
› Receptors are Opioid Receptors
 Found in Many Areas of Brain
 Limbic System Hypothalamus, Peri-Ventricular Areas, Pituitary &
Spinal Cord
 Endogenous Substances which Mimic Action of
Opium → Opioid Peptides
› Brain’s Own Morphine
› Act like Neurotransmitter on Opioid Receptors

108.  Opioid Peptides
› Beta Endorphins
 Derived from Pro-opiomelanocortin
› Met-and Leu-Encephalins
 Derived from-Proencephalins
› Dynorphin
› Derived from Prodynorphin
 Opioid Peptides Cause Pre-synaptic Inhibition
› At Spinal Cord to Block Pain
 Inhibit Release of Substance P

110. • Cause Post Synaptic Inhibition
– Produce IPSP
• In Limbic Areas & Hypothalamus
– Pain Modulation
• Act Peripherally at Site of Injury
• Opioid Mediated Endogenous Analgesia System →
Activated by Administration of Exogenous Morphine
• Descending Analgesia System
– Under Tonic Inhibitory Control of Mid Brain & Medulla
– Opiates Inhibit these Inhibitory Inter-Neurons

112.  Examples
› Stress Analgesia
› War Situation When Person Emotionally Charged
› Pain Relieved by
 Acupressure & Acupuncture and Electrical Vibrator
 Gate Control Mechanism
› Proposed by Malzek & Wall

113.  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)
› Opiates (inhibit NT release)

114.  Different surgical procedures are done in the
course of pain pathway to relieve pain. They
are
-Sympathectomy
-Cordotomy
-Thalamotomy
-Prefrontal lobotomy

115. 2)Thalamic gate:
The same "gating" mechanism for pain is found also
at the thalamus where
pain signals could be blocked by corticofugal
fibers or facilitated by
intralaminar thalamic nuclei. In this way,
the thalamus considered as a secondary gate far
pain transmission.

116. Stress analgesia; During stress, Pain is
blocked at two levels :
A) At the thalamus: (the second gate of pain transmission ).
Corticofugal fibers to the thalamus block by presynaptic inhibition the
transmission of pain signals in the thalamus before they reach the
cerebral cortex.
B) At the dorsal horn of the spinal cord: (the first gate of
pain transmission).
The hypothalamus, and other parts of the central analgesia system,
activate the spinal PIC which blocks the transmission of pain signals at
the dorsal horn.

117. • Pain & Other Crude Sensations
– Perceived Even in Absence of Cerebral Cortex
• Cortex is Concerned With
– Discriminative, Exact & Meaningful Interpretation of Pain
– Emotional Components of Pain
• Post Injury Pain
– Irritation of Nerve Endings
• Allodynia
– Minor Touch Causes Pain
• Neuropathic Pain
– Occur at Sites Even after Healing of Injury
– Often Resistant to Analgesics

118. TERM DESCRIPTION
ALLODYNIA PERCEPTION OF NON-NOXIOUS STIMULUS AS PAIN
ANALGESIA ABSENCE OF PAIN PERCEPTION
ANESTHESIA ABSENCE OF ALL SENSATIONS
ANESTHESIA
DOLOROSA
PAIN IN AN AREA THAT LACKS SENSATION
DYSESTHESIA UNPLEASANT SENSATION WITH OR WITHOUT STIMULUS
HYPOALGESIA DIMINISHED RESPONSE TO NOXIOUS STIMULUS
HYPERALGESIA INCREASED RESPONSE TO NOXIOUS STIMULUS
HYPERASTHESIA INCREASED RESPONSE TO MILD STIMULUS
HYPOASTHESIA REDUCED CUTANEOUS SENSATION
NEURALGIA PAIN IN THE DISTRIBUTION OF A NERVE
PARASTHESIA
ABNORMAL SENSATION PERCEIVED WITHOUT AN
APPARENT STIMULUS
RADICULOPATHY FUNCTIONAL ABNORMALITY OF NERVE ROOTS