Download pain impulses

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describe the multidimensional nature of pain,
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explain the role of pain in preserving health and well-being,
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discuss how the pain response can assist in evaluating an
injured person,
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describe how pain is sensed and how the “pain message” is
transmitted to the central nervous system, and
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discuss contemporary theories on modulating the pain message
in the central nervous system.
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“An unpleasant sensory & emotional experience associated with
actual or potential tissue damage, or described in terms of such
damage” –
The International Association for the Study of Pain
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Subjective sensation
Pain Perceptions – based on expectations, past experience, anxiety,
suggestions
◦ Affective – one’s emotional factors that can affect pain experience
◦ Behavioral – how one expresses or controls pain
◦ Cognitive – one’s beliefs (attitudes) about pain
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Physiological response produced by activation of specific types of
nerve fibers
Experienced because of nociceptors being sensitive to extreme
mechanical, thermal, & chemical energy.
Composed of a variety of discomforts
One of the body’s defense mechanism (warns the brain that tissues
may be in jeopardy)
Acute vs. Chronic –
◦ The total person must be considered. It may be worse at night when the
person is alone. They are more aware of the pain because of no external
diversions.
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Cutaneous Pain – sharp, bright, burning;
can have a fast or slow onset
Deep Somatic Pain – stems from tendons,
muscles, joints, periosteum, & b. 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
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Fast vs. Slow Pain –
◦ Fast – localized; carried through A-delta axons in
skin
◦ Slow – aching, throbbing, burning; carried by C
fibers
◦ Nociceptive neuron transmits pain info to spinal
cord via unmyelinated C fibers & myelinated Adelta fibers.
 The smaller C fibers carry impulses @ rate of 0.5 to 2.0 m/sec.
 The larger A-delta fibers carry impulses @ rate of 5 to 30 m/sec.
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Acute vs. Chronic
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Types of Nerves
Neurotransmitters
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Afferent (Ascending) – transmit impulses
from the periphery to the brain
◦ First Order neuron
◦ Second Order neuron
◦ Third Order neuron
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Efferent (Descending) – transmit impulses
from the brain to the periphery
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Stimulated by sensory receptors
End in the dorsal horn of the spinal cord
Types
◦ A-alpha – non-pain impulses
◦ A-beta – non-pain impulses
 Large, myelinated
 Low threshold mechanoreceptor; respond to light touch &
low-intensity mechanical info
◦ A-delta – pain impulses due to mechanical pressure
 Large diameter, thinly myelinated
 Short duration, sharp, fast, bright, localized sensation
(prickling, stinging, burning)
◦ C – pain impulses due to chemicals or mechanical
 Small diameter, unmyelinated
 Delayed onset, diffuse nagging sensation (aching, throbbing)
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Receive impulses from the FON in the dorsal
horn
◦ Lamina II, Substantia Gelatinosa (SG) - determines the
input sent to T cells from peripheral nerve
 T Cells (transmission cells): transmission cell that connects
sensory n. to CNS; neurons that organize stimulus input &
transmit stimulus to the brain
◦ Travel along the spinothalmic tract
◦ Pass through Reticular Formation
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Types
◦ Wide range specific
 Receive impulses from A-beta, A-delta, & C
◦ Nociceptive specific
 Receive impulses from A-delta & C
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Ends in thalamus
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Begins in thalamus
Ends in specific brain centers (cerebral cortex)
◦ Perceive location, quality, intensity
◦ Allows to feel pain, integrate past experiences &
emotions and determine reaction to stimulus
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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
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Stimulation of the PGA in the midbrain & NRM in
the pons & medulla causes analgesia.
Endogenous opioid peptides - endorphins &
enkephalins
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Chemical substances that allow nerve impulses to move
from one neuron to another
Found in synapses
◦ Substance P - thought to be responsible for the transmission
of pain-producing impulses
◦ Acetylcholine – responsible for transmitting motor nerve
impulses
◦ Enkephalins – reduces pain perception by bonding to pain
receptor sites
◦ Norepinephrine – causes vasoconstriction
◦ 2 types of chemical neurotransmitters that mediate pain
 Endorphins - morphine-like neurohormone; thought to  pain threshold by
binding to receptor sites
 Serotonin - substance that causes local vasodilation &  permeability of
capillaries
 Both are generated by noxious stimuli, which activate the inhibition
of pain transmission
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Can be either excitatory or inhibitory
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Nociceptive - normal
nerves transmit info to
CNS about trauma to
tissues
Neuropathic - disease/
degeneration of NS
Nociceptors = specialized terminal
peripheral branches of sensory nerve
fibers that are sensitive to noxious
stimuli
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Sensitive to repeated or prolonged stimulation
Mechanosensitive – excited by stress & tissue
damage
Chemosensitive – excited by the release of
chemical mediators
◦ Bradykinin, Histamine, Prostaglandins, Arachadonic Acid
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Primary Hyperalgesia – due to injury
Secondary Hyperalgesia – due to spreading of
chemical mediators
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A delta fibers - sharp,
immediate pain
C fibers - small, unmyelinated,
transmit prolonged, burning
pain
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Ad (small
myelinated) fibres
◦ 2-5 mm diameter
◦ conduct at 12-30
m/sec
◦ cause sharp,
localised sensation
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C (unmyelinated)
fibres
◦ 0.4-1.2 mm diameter
◦ conduct at 0.5-2
m/sec
◦ cause dull, diffuse
feeling
• Activated by
– low pH, heat (via TRPV1 etc)
– local chemical mediators (eg bradykinin,
histamine, prostaglandins)
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Occurs in about 0.1 seconds
Subjective description; sharp, acute, electric or prinking
Ad fibers synapse on cells in lamina I (lamina marginalis) in
the dorsal horns
Secondary neurons cross and travel through the anterolateral
pathway to ventral complex of the thalamus
Tertiary neurons go to the primary sensory cortex
LAMINA
MARGINALIS
VENTROBASAL
NUCLEUS
I
II
III
IV
VI
V
VII
SUBSTANTIA
GELITANOSA
IX
VIII
ANTEROLATERAL
PATHWAY
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Occurs after a second or more
Often associated with tissue destruction
Subjectively described as burning, aching, throbbing,
nauseous or chronic
C fibers synapse in the synapse substatnia gelitanosa
Final projection is the frontal cortex
LAMINA
MARGINALIS
VENTROBASAL
NUCLEUS
I
II
III
IV
VI
V
VII
SUBSTANTIA
GELITANOSA
IX
ANTEROLATERAL
PATHWAY
VIII
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Fast pain is generally mechanical or thermal
Slow pain can be all three
Chemical pain receptors; bradykinin, serotonin, histamine,
potassium ions, acids, acetylcholine and proteolytic enzymes.
Prostaglandins enhance pain perception
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Respond best to one but some to all
◦ Thermal
◦ Mechanical
◦ Chemical
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NTs: glutamate and Substance P
Capsaicin causes release of Sub P from nociceptor
axons
Large amounts of capsaicin cause analgesia due to
depletion of sub P from synapses
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Aspirin suppresses
synthesis of
prostaglandins
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Nociceptive fibres synapse in the dorsal
horn
Projection neurones cross the midline and
travel in the antero-lateral spinothalamic
tract
◦ some to the thalamus & cortex
 fine localization of sharp pain
◦ some to the reticular formation
 diffuse, chronic pain
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DRGN enters dorsal horn at each spinal cord level
Ascend/descend in Lissaur’s tract
Synapse in Substantia Gelatinosa
Decussate in ventral spinal cord
Ascend ventrally in spinal cord as the
Spinothalamic Tract
Synapse in thalamus (Ventral Posterior and
intralaminar Nuclei)
Thalamic axons travel to S1 somatosensory cortex
and synapse in layer 4.
Cortex
Thalamus
Reticular
formation
Gracile/cuneate
nucleus
Aa/b
Ad/C
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Gate control theory (by Melzack & Wall, 1965)
◦ activity in Aa/b fibres inhibits transmission from nociceptive fibres
to spinothalamic neurones
◦ Substantia Gelatinosa (SG) in dorsal horn of spinal cord acts as a
‘gate’
Brain
Gate (T
cells/ SG)
Pain
Heat, Cold,
Mechanical
Cortex
Thalamus
Reticular
formation
Gracile/cuneate
nucleus
Aa/b
Ad/C
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Descending controls
◦ stimulation of periaqueductal grey and nucleus raphe
magnus inhibit nociceptive transmission
◦ Stimulation of A-delta & C fibers causes release of B-endorphins
from the PAG
◦ Mechanism of action – similar to enkephalins to block ascending
nerve impulses
Cortex
Thalamus
Reticular
formation
PAG
Gracile/cuneate
nucleus
Aa/b
Ad/c
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Increased sensitivity to pain after tissue injury
Damaged tissue also releases molecules sa bradykinin
that gate other channels/bind receptors
Secretion of substances, substance P, bradykinin,
prostaglandin that cause inflammation
Can cause long lasting intracellular changes that
increased sensitivity of nociceptive ion channels
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Occurs away from pain site
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Types of referred pain:
◦ Myofascial Pain – trigger points, small hyperirritable
areas within a m. in which n. impulses bombard CNS &
are expressed at referred pain
 Active – hyperirritable; causes obvious complaint
 Latent – dormant; produces no pain except loss of ROM
◦ Sclerotomic & Dermatomic Pain – deep pain; may
originate from sclerotomic, myotomic, or dermatomic n.
irritation/injury
 Sclerotome: area of bone/fascia that is supplied by a single
n. root
 Myotome: m. supplied by a single n. root
 Dermatome: area of skin supplied by a single n. root
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Due to mixing of nociceptive axons from viscera with
those from skin at the level of spinal cord.
Perception of visceral information as coming from skin
areas
Angina: low oxygen in heart is
perceived as chest and arm pain
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Gate Control Theory
Central Biasing Theory
Endogenous Opiates Theory
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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
Transmission Cell (T-cell) – distal end of 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 - 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
Gate (T
cells/ SG)
Pain
Heat, Cold,
Mechanical
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Descending neurons are activated by: stimulation
of A-delta & C neurons, cognitive processes,
anxiety, depression, previous experiences,
expectations
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Cause release of enkephalins (PAG) and serotonin
(NRM)
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Enkephalin interneuron in area of the SG blocks Adelta & C neurons
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Least understood of all the theories
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Stimulation of A-delta & C fibers causes release
of B-endorphins from the PAG & NRM
Or
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ACTH/B-lipotropin is released from the anterior
pituitary in response to pain – broken down into
B-endorphins and corticosteroids
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Mechanism of action – similar to enkephalins to
block ascending nerve impulses
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Examples: TENS (low freq. & long pulse
duration)
◦ Peripheral pain modulation
 Targets desensitization of peripheral nociceptors
 Cryotherapy lessens the effects of chemical mediators and
slows conduction velocity of sensory input
◦ Spinal level pain modulation
 Gate control theory is proposed mechanism
 Can be evoked using “counterstimulation” techniques
◦ Noxious pain modulation
 Elicits pain in affected region to achieve desired analgesic
affect
 Possibly evokes descending pain modulation
◦ Nerve block pain modulation
 Application of medium-frequency currents creates an
action potential failure—Wedenski’s inhibition
Wedenski’s inhibition ; damping of muscle response resulting from application of a
series of rapidly repeated stimuli to the motor nerve where less frequent stimulation
produces muscle response
 Used briefly for superficial areas
◦ Suprapinal and descending pain modulation
 Involves reticular formation—PAG, Raphe nucleus, and enkephalin
 Serotonin released by stimulation of Raphe nucleus activates
inhibitory interneurons that block pain transmission
 Hypothalamus and pituitary also stimulated by pain impulses and
release precursors to analgesic and anti-inflammatory agents
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◦ Motor stimulation—electroacupuncture
 Goal is to enhance endorphin production through pulsed, rhythmic,
low-frequency stimulation
 Low-frequency stimulation of trigger and acupuncture points also
valuable
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Reduce pain!
Control acute pain!
Protect the patient from further injury while
encouraging progressive exercise
Higher brain center
Inhibition of pain
transmission
Therapist
TENS
Massage
Manipulation
Thermal
Traction
Compression, etc
Large diameter
afferents
Cutaneous
receptors
jt. Receptors,
muscle receptor
◦ Pain can be characterized as acute, persistent, or
chronic. These types of pain differ in purpose and
treatment.
◦ The physical therapist should understand the
contemporary pain theories that form the basis
for the analgesic response to therapeutic
modalities.
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Compare and contrast the fast pain and slow
pain.
In your own words, describe the gate control
theory of pain control.