Download Pain Control System

‫بسم هللا الرحمن الرحيم‬
‫﴿و ما أوتيتم من العلم إال قليال﴾‬
‫صدق هللا العظيم‬
‫االسراء اية ‪58‬‬
By
Dr. Abdel Aziz M. Hussein
Assist Prof of Medical
Physiology
Objectives
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1. definition of pain
2. types of pain
3. Body reactions or responses to pain
4. perception of pain
5. neural pathways for pain
6. referred and radiating pain
7. modulation of pain perception
8. endogenous analgesia system
9. gate control theory
10. applications of this theory (acupuncture and
TENS)
Def :
•Pain is an unpleasant sensory and emotional experience
associated with actual or potential tissue damage according to;
International association for the study of pain (IASP).
Significance:
1. Pain is a warning signal for tissue damage. It is the prominent
symptom of tissue damage
2. Pain has a protective function. It initiates protective reflexes
that;
•Get rid of the painful stimulus.
•Minimize tissue injury or damage.
A) According to its mechanism or cause:
•Pain is classified into 3 main types;
1. Physiological
Pain
Also called
Nociceptive pain
Caused by stimulation
of pain receptors by
tissues damage e.g. in
inflammation
2. Pathological
Pain
Also called
neuropathic
pain
Caused by
damage of nerve
pathway
3. Psychogenic
Pain
In depression and
anxiety
Difficult to
differentiate whether
2ry to or actual
cause of pain
N.B.
Neuropathic pain:
according to site of injury is classified into;
a. Central → Central pain e.g. thalamic infarct
b. Peripheral → e.g. nerve compression, neuralgias.
c. Mixed → e.g. post herpetic neuralgia.
Character: neuropathic pain is characterized by burning, tingling,
numbness, squeezing, itching, constant +/- intermittent shooting,
and electric.
B) According to its duration:
•Both nociceptive and neuropathic pains are classified into 2
types;
a) Acute pain: less than 7 weeks
b) Chronic pain : more than 7 weeks
C) According to the quality or character :
•A pain it is classified into 5 types;
a) Pricking or Cutting Pain:
b) Burning Pain:
c) Aching Pain:
d) Throbbing Pain:
e) Colicky Pain:
1. Pricking
pain
• Sharp and localized pain.
• Of skin origin (mainly)
• e.g. in pricking or cutting the
skin by sharp object
2. Burning
pain
• Less well localized, has
unpleasant burning nature.
• Usually of skin origin
• Caused by wide spread irritation
of skin
3. Aching pain
4.Throbbing
pain
5.Colicky pain
• disagreeable pain of dull- aching
nature
• More diffuse and felt coming from
deeper tissues e.g. rheumatic
pains
• Fluctuation of its intensity with
arterial pulsations
• localized inflammation in deep
tissues e.g. abscess
• Comes in cramps, so it has a
colicky nature, e.g. intestinal
colic and ureteric colic
• Spasm of smooth ms in the walls
of hollow viscera
D) According to site of origin: 3 types;
Cutaneous
pain
• Pain comes from skin and
subcutaneous tissues
• Usually pricking or burning pain
Deep pain
• Pain comes from structures deep
to the skin e.g. skeletal muscle,
joints, and tendons
• Usually dull aching or throbbing
Visceral pain
• Pain comes from internal viscera
e.g. stomach
• Usually colicky or dull aching
1) Somatic reactions:
a) Withdrawal reflex :
• It occurs in cutaneous pain
• This is a protective reaction which get rid of injurious agent
b) Reflex spasm of nearby muscle:
• It occurs in deep pain
• It immobilize pained parts to decrease pain sensation
c) Reflex spasm of overlying muscle:
• It occurs in visceral pain
• It produce guarding rigidity of abdominal muscle (guarding
reaction)
2) Autonomic reactions:
•
•
Mild and moderate cutaneous pain → sympathetic
stimulation → ↑ heart rate and ABP (pressor reaction)
Sever cutaneous, deep, and visceral pain →
parasympathetic stimulation →↓ HR and ABP (depressor
reaction)
3) Emotional or psychogenic reactions:
• In the form anxiety, fear, crying, and depression
• These reactions vary:
a. From person to person on exposure to similar pain stimuli.
b. In the same person according to his emotional state:
-Worry about the cause of pain augment the feeling of pain.
-Strong emotional excitement & sever physical exertion may
block the feeling of pain.
-Thus, seriously wounded soldiers in a battlefield suffer little or
no pain till the battle is over.
4) Cutaneous hyperalgesia:
•It is 2 types;
PRIMARY
Site:
Duration
Characteristics:
Mechanism:
In the red area
SECONDARY
In healthy skin area around red
area
It develops within 30 to 60 It duration is much shorter than
minutes and lasts for several that of 1ry hyperalgesia
hours or days after injury.
When non-noxious stimuli When a noxious stimulus is
such as touch or mild applied, the pain felt is more
warming are applied they severe than usual.
cause pain.
It is due to lowered Convergence -Facilitation
threshold of pain receptors in theory:
the red area due to local -No lowering of the pain threshold
axon reflex
-The pain impulses from the area
of 1ry hyperalgesia facilitates
(↑ed excitability) those from the
area of 2ry hyperalgesia.
Area of injury
Area of redness
Healthy skin
Antidromic impulse
Secreting substance P
Area of injury
Area of redness
Healthy skin
Convergence facilitation
Pain sensation
Painful
stimulus
22
1)Types:
•They are morphologically similar but functionally they are specific
a) Morphological types: are specific free nerve endings
b) Functional types: classified according to their adequate stimulus into:1) Mechanical Pain Rs:
•
Respond to strong mechanical forces, such as cutting, or pricking
2) Thermosensitive pain Rs:
• Respond to excessive changes in temp. (above 45°C and below 10°C).
3) Chemical Pain Rs: respond to noxious chemical stimuli.
4) Polymodal Pain Rs:
• Respond to a combination of mechanical, thermal, and chemical noxious
stimuli
2)Distribution:
• Pain Rs are found in most tissue of the body.
a) Abundant in the skin and some internal tissue such as the
periosteum, arterial wall, joint surfaces, and the dura of the
tentorium cerebelli.
b) Few in deep tissues and all viscera. So, for pain to occur,
painful stimulus must by intense and widespread. The deep &
visceral pain is poorly localized.
c) Brain itself and the parenchymal tissues of the liver, kidneys,
and lungs have no pain receptors “pain insensitive structures”
N.B.: Serious diseases in these organs don’t produce pain till
they extend to a pain sensitive structure like arterial wall or
serous covering.
3) Mechanism of stimulation:
Chemical stimuli
Mechanical stimuli
Thermal stimuli
Strong acids or Alkalies
Cutting or pricking
temp. > 45 C and < 10 C
Tissue damage
1st class
K ions, Histamine,
Serotonin, and Bradykinin
Directly stimulate
Pain Receptors
Release of Pain
Producing
Compounds (PPS)
2nd class
PGE2, leukotriens and
Substance P
Sensitize the pain Rs
by lowering its
threshold to stimuli
Tissue
Damage
Direct
stimulators
Sensitizers
4) Adaptation:
• Pain Rs do not adapt to continuing noxious stimuli
• This serves a protective function to keep the individual trying
to remove the damaging stimulus or to get away from it.
Pathway: Neospinothalamic tract
A) 1st order neuron :
• A delta afferent fibers
• End in lamina I of dorsal horn of spinal cord
B) 2nd order neuron :
• Axons of neurons lamina I of dorsal horn of spinal cord cross
the opposite side in front of central canal and ascend as
neospinothalamic in spinal cord and as spinal leminiscus in
brain stem
• End in posteroventral nucleus of thalamus (PVNT)
Pathway:
C) 3rd order neuron :
• Axons of neurons of PVNT ascend in sensory radiations
• End in primary somatic sensory area (area 3,1,2)
Note:
• The chemical transmitter released at the central end of A
delta fibers that carry fast pain is glutamate
PVNT
Sensory Radiations
Spinal Leminiscus
Lamina I
A delta
Receptors
Free nerve endings
Lateral spinothalamic tract
Pathway: Paleospinothalamic tract
A) 1st order neuron :
• C afferent fibers
• End in lamina II and III (called substantia Gelatinosa of Rolandi
SGR) of dorsal horn of spinal cord
B) 2nd order neuron :
• Axons of neurons SGR of dorsal horn of spinal cord cross the
opposite side in front of central canal and ascend in spinal cord
and as;
1. Spinoreticular tract end in RF of MO and Pons
2. Spinotectal tract end in PAG areas of midbrain
3. Paleospinothalamic tract end in non specific thalamic nuclei
(intralaminar and midline)
Pathway:
C) 3rd order neuron :
• Axons of neurons from RF and NSTN of thalamus ascend in
sensory radiations
• Terminate diffusely in all areas of the cerebral cortex
Note:
• The chemical transmitter released at the central end of c
fibers that carry fast pain is substance P
All cortical areas
Non-specific nuclei
of thalamus
Periaqueductal gray
area (PAG) in
midbrain
Reticular formation
In MO and Pons
SGR
Laminae II, III
Receptors
Free nerve endings
Afferent
C fibers
Paleospinothalamic tracts
Comparisons Between Slow and Fast Pain
Source
Stimulus
Quality
Onset
Duration
Localization
Afferent
Tract
Centre
Chemical
trans.
Acute (Fast)
Chronic (Slow)
Skin only
Skin, deep tissues,
and viscera
All types
Mechanical and
thermal
Pricking
Within 0.1 sec after
stimulation
Short (one second)
Well –localized
A-delta
Neospinothalamic
tract
Cerebral cortex
Glutamate
Burning
One or more seconds
after stimulation
Long (few minutes)
Diffuse
C
Paleospinothalamic
tract
Thalamus
Substance P
Def:
•
•
Referred pain is pain felt away from the site of its origin
Radiating pain is pain appear to migrate away from the its
original site
• Referred pain is a part of radiating pain
N.B.
• Visceral pain usually referred, deep pain may be referred but
cutaneous pain never referred
Site of referral is determined by dermatomal rule:
•The pain from a viscera is referred to a somatic structure (skin
or deep structure) which were developed in the same embryonic
segment and supplied by the same dorsal root ganglia.
•Abnormal sites are due to migration of viscera.
Mechanism :
Convergence Projection Theory:
•
•
•
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Afferents pain fibers from skin area and diseased viscera
converge on the same 2nd order neuron and finally stimulate
the same cortical neuron
The cortex project (feel) pain as it is coming from the skin
because the sensory cortex is accustomed to receive pain
from the skin
Skin is the commonest site of pain
Convergence may occurs also at the level of thalamus or
sensory cortex
• There is endogenous analgesic system as proved by:
1. Stress analgesia e.g. soldiers wounded by the heat of the
battle may feel no pain until the battle is over.
2. The pain felt from an injured area is reduced when the skin
around the injured area is rubbed or stroked.
3. Morphine injected in minute doses in experimental animals
in the third ventricle of the brain produce marked analgesia.
• This Pain Control System can modulate pain sensation
(mainly inhibitory) by release of endogenous opiate like
(opioid) peptides such as encephalins, endorphins
• It cause both presynaptic and postsynaptic control of
nociception in the dorsal horn via enkephalin release which
inhibits release of substance P, transmitter at pain nerve
endings
1) Def,
• System which control pain transmission in CNS or
inhibit pain transmission i.e. endogenous analgesia
system
2) Sites:
1.Periventricular area of hypothalamus
2.Periaqueductal area (PAG) around aqueduct of sylivus in
midbrain and Pons
3. Nucleus raphe magnus (NRM) AND Nucleus reticularis
paragigantocellularis (NRPG) in lower Pons and upper medulla
4. Pain inhibitory complex (PIC): interneuron in dorsal horn of
spinal cord
3) Neurochemistry:
• This system act through the release of endogenous opioid
peptides which act on opiate receptors.
Opioid peptides:
• They include 3 groups; enkephalins, endorphins and dynorphins.
Opiate Receptors:
• 3 types of opiate receptors : delta (δ), kappa (κ), and muta (μ).
 Enkephalins bind with the delta (δ) receptors
 Endorphins bind with the muta (μ) receptors
 Dynorphins bind with the kappa (κ) receptors.
•These receptors can be blocked by naloxone, which is a
morphine antagonist
Activation of the Pain Control System
Clinical (Experimental)
Natural (physiological)
1- Electrical stimulation of
certain regions of pain control
system
Exposure to severe stress,
particularly when associated with
strong emotional excitement.
2- Local application of opiates
(such as morphine) at particular
regions in the nervous system.
Stress induced analgesia
(pharmacological analgesia)
Periventricular nucleus of hypothalamus
Endorphins
++
Periaqueductal gray area
Encephalin
++
Stress
Nucleus raphe magnus
Serotonin
++
Ascending
pathway
Encephalins
-Substance P
Posterior horn of spinal cord
1st order
neuron of pain
• The sites of synapses along the pain pathway are considered
as gates through which pain transmission can be;
 Facilitated (if the gate is open) or
 Blocked (if the gate is closed).
Sites:
 The main pain gates are:
1- Spinal gate: at the SGR.
2- Brain stem gate: at the nuclei of reticular formation.
3- Thalamic gate: At neurons of PVLNT & intalaminar thalamic
nuclei.
3
2
1
At spinal gate pain transmission is blocked by;
1. Descending inhibitory impulses through the pain control
system activating enkephalin-secreting interneuron
2. Stimulation of the large diameter nerve fibers (A delta
and A beta) terminating peripherally in mechanoreceptors,
such as tactile receptors or proprioceptors (A beta), and
pricking pain fibers (A delta).
•
•
This may explain why simple maneuvers such as rubbing the
skin (thus exciting tactile and pressure receptors), near a
painful area is often effective in relieving certain types of pain
→ A beta
Also block of pain by acupuncture (A delta fibers)
Interneuron
Rubbing of the skin
A beta fibers
Pain C fiber
Painful stimuli
Interneuron
Acupuncture
A delta fibers
Pain C fiber
Painful stimuli
• This theory provides basis for various methods of
pain relief
1. Massaging a painful area
2. Applying irritable substances to a painful area
(counter-irritation)
3. Transcutaneous Electrical Nerve Stimulation (TENS)
4. Acupuncture ?
•Acupuncture has been practiced in China for more than
4000 years as a method for pain relief.
Mechanism:
1- Needles in appropriate body regions are thought to excite
certain sensory neural pathways which
feed into
the
brain stem centers (such as the PAG) involved in the pain
control system, with release of endogenous opioid peptides.
2- Simultaneous suppression of pain transmission at the spinal
pain-gate by acupuncture
Def.,
•TENS is any stimulating device which delivers electrical
currents across the intact surface of the skin
Mechanism:
•TENS causes relieve of pain by activate large diameter
‘touch’ fibres (Aβ) without activating smaller diameter
nociceptive fibres (Aδ and C) this causes;
1- Excitation of certain sensory neural pathways which activate
PAG area involved in the pain control system, with release of
endogenous opioid peptides.
2- Simultaneous suppression of pain transmission at the spinal
pain-gate by acupuncture
TENS
Physical
conditions
Conditions that
open the Gate
Extent of injury
Extra activity
Conditions that closes
the Gate
medications
Counter stimulation, e.g.
massage, heat
Emotional
conditions
Depression, tension
Anxiety, worry
Relaxation
Positive emotion
Mental
conditions
Focusing on pain
Distraction
Involvement in life
activity
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