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Page 1: Pain sensations
Page 2: Pain sensations

Definition of pain

Types of pain

Varieties of pain

Pain pathway

Pain inhibiting pathway

Central analgesia

Applied physiology

Page 3: Pain sensations

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)

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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

receptorsPain is a protective sensation.

Page 7: Pain sensations
Page 8: Pain sensations

Pain receptors . Free nerve endings

Three types1. 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+.

Page 9: Pain sensations

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.

Page 10: Pain sensations

Types of painPain 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.

Page 11: Pain sensations

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.

PeripheralNerve

C-Fiber

A-delta Fiber

Page 12: Pain sensations

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.

Page 13: Pain sensations

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.

Page 14: Pain sensations

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

Page 15: Pain sensations

Fast pain Slow painPin 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

Page 16: Pain sensations

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

Page 17: Pain sensations

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

Page 18: Pain sensations

ACUTE PAIN

CHRONIC PAIN

CUTANEOUS PAIN

DEEP SOMATIC PAIN

VISCERAL PAIN

REFERRED PAIN

NEUROPATHIC PAIN

PHANTOM PAIN

Page 19: Pain sensations

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

Page 20: Pain sensations

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.

Page 21: Pain sensations

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.

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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.

Page 23: Pain sensations

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

Page 24: Pain sensations

Spinothalamic - Major

› Neo- Fast (A Delta)

› Paleo- Slow (C Fibers)

Spinoreticular

Spinomesencephalic

Spinocervical (Mostly Tactile)

Dorsal Columns (Mostly Tactile)

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• 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

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Fast pain is transmitted by A delta fibers

(5-15 m/sec.) from skin

(mainly), parietal pleura, peritoneum a & Synovial membrane.

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(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).

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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.

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• Arises from Periosteum & Ligaments

• Continuous Contraction of Muscles

• Poorly Localized

• Associated with Sweating & Changes in Blood

Pressure

• Often Nauseating

• Transmitted via Antero Lateral System

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Page 34: Pain sensations

Ischaemic painType 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.

Examples1. Cardiac muscle: angina pectoris.

2. Skeletal muscle: intermittent claudication.

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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.

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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.

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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.

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• 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

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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

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• 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

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Referred painDefinition

Pain originating from viscera but felt in

somatic structures which supplied by the

same spinal dorsal root ( the same dermatome) of the diseased viscus.

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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.

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• 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

Page 46: Pain sensations

Referred Pain

Page 47: Pain sensations

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

Page 48: Pain sensations

Mechanism of referred paina. 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.

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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.

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Facilitation Effect:

› ↑ Activity in Visceral Pain Afferents Collaterals Fibers →

EPSP in Spinal Neurons Receiving Somatic Inputs → ↑

Activity in Somatic Neurons → Continuous Pain

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• 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

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Page 55: Pain sensations

TRANSDUCTION

TRANSMISSION

PERCEPTION

MODULATION

Page 56: Pain sensations

Pain stimuli is converted to

electrical energy. This is known as

Transduction. This stimulus sends

an impulse across a peripheral

nerve fiber (nociceptor).

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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.

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Inhibitory neurotransmitters like

endogenous opioids work to hinder

the pain transmission.

This inhibition of the pain impulse is

known as modulation

Page 59: Pain sensations

C fibre

Final pain perception

depends on activity of

the

•Ascending pain

impulse transmitting

tracts

•Descending pain modulatory

(inhibitory) tracts

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Page 61: Pain sensations

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

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• 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 (NeospinothalamicTract)

• Joins Medial Laminiscus → Few Collaterals to R.F.

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• 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

Page 64: Pain sensations

Ascending pathway

Crosses the midline

Ascends up as the lateral spinothalamic tract

Pain

lateral

spinothalamic

tract

C fibre

substantia

gelatinosa

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• Second Order Neuron Thalamus

Post Central Gyrus

• Localization is Good

• Neurotransmitter is Glutamate

• Few Fibers Ascends in Dorsal Column

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•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

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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

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• 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

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•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

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Pain pathway

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•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

Page 73: Pain sensations

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.

Page 74: Pain sensations

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.

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Arousal reaction to pain signalsThe non specific thalamic nuclei (intra-

laminar nuclei) and reticular formation

have a strong arousal effect on the brain which prevents sleep during pain.

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Injury

Descending Pathway

PeripheralNerve

Dorsal RootGanglion

C-Fiber

A-beta Fiber

A-delta Fiber

AscendingPathways

Dorsal Horn

Brain

Spinal Cord

76

Page 77: Pain sensations

lateralspinothalamic tract

thalamus

C fibre

thalamocorticaltracts

Page 78: Pain sensations

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.

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Peripheral

Gating Theory

› Involves Inhibitory

Inter-Neuron in Cord

impacting Nociceptive

Projection Neurons

Inhibited by C Fibers

Stimulated by A Alpha &

Beta Fibers

TENS

Central

Direct Electrical + to

brain → Analgesia

Nociceptive control

Pathways Descend to

Cord

Endogenous Opioids

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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

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Gate control theory

When pain fibre is stimulated, gate will be opened & pain is

felt

pain

pain is felt

+gate is

opened

Page 82: Pain sensations

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

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GATE CONTROL MECHANISM

S.G.CellsT- Cells

Type II Fibers

A-DELTA &

C Fibers

(-)

(-)(+)

(-)(+)

Spino

Thalamic

Pathway

(-)

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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)

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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.

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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.

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Presynaptic inhibitionsubstance P

enkephalin

pain impulse

blocking of

pain impulse

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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.

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• 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

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• 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

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•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)

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Pain Control Systems(I) Analgesic systema) 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).

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• 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.

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opioid pain

inhibition

at multiple levels

› spinal cord

› brain-stem

› thalamus

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(II) Brain Opiate System

Opiate receptors in the brain cause pre and

postsynaptic inhibition of the nociceptive pathway.

Sites of opiate receptors1. Periaqueductal gray area

2. Periventricular aea.

3. Raphe magnus nucleus in medulla.

4. Substantia nigra.

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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) DynorphinVery potent analgesic.

Types of opiate receptorsDelta, Mu, Kappa, Sigma & Epislon.

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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

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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

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• 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

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Page 112: Pain sensations

Examples

› Stress Analgesia

› War Situation When Person Emotionally Charged

› Pain Relieved by

Acupressure & Acupuncture and Electrical Vibrator

Gate Control Mechanism

› Proposed by Malzek & Wall

Page 113: Pain sensations

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)

Page 114: Pain sensations

Different surgical procedures are done in the

course of pain pathway to relieve pain. They

are

-Sympathectomy

-Cordotomy

-Thalamotomy

-Prefrontal lobotomy

Page 115: Pain sensations

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.

Page 116: Pain sensations

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.

Page 117: Pain sensations

• 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

Page 118: Pain sensations

TERM DESCRIPTION

ALLODYNIA PERCEPTION OF NON-NOXIOUS STIMULUS AS PAIN

ANALGESIA ABSENCE OF PAIN PERCEPTION

ANESTHESIA ABSENCE OF ALL SENSATIONS

ANESTHESIA

DOLOROSAPAIN 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

PARASTHESIAABNORMAL SENSATION PERCEIVED WITHOUT AN

APPARENT STIMULUS

RADICULOPATHY FUNCTIONAL ABNORMALITY OF NERVE ROOTS