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Pain is subjective
Self-experience
Experience depends on circumstances
Pain can cause many different reactions: Activate autonomic system (heart rate, blood
pressure, sweating, etc.)
Muscle activity
Mood (fear, anxiety, depression) Prevent sleep
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Pain occurs with different
degrees of severity Mild pain:Does not interfere noticeably with everyday life
Moderate pain:May cause some annoyance and perceived as unpleasant
Severe chronic pain:Affects a persons entire life in major ways
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There are many forms of pain
Mild pain:
Does not interfere noticeably with everydaylife
Moderate pain:
May cause some annoyance and may be
perceived as unpleasant
Severe pain:
Affects a persons entire life in major ways
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Different forms of pain
Acute pain
Chronic pain
Somatic pain Neuropathic pain
Central neuropathic pain
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Pain has many different forms,but the same name
Tinnitus has many differentforms but the same name
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There are different types ofpain
Somatic and visceral pain (Stimulation ofnociceptors)
Pain ceases when stimulation ceases
Neuropathic pain
Pain is related to the nervous system
Central neuropathic pain
Plastic changes in the function of the CNS May be persistent
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It is important to have differentnames for for different
disorders
We cannot think about matters that do not
have names
The same words is used to describe verydifferent forms of tinnitus and pain
Using the same names for fundamentallydifferent disorders is a disadvantage instudying and treating such disorders
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Severe pain affects a persons
entire life in major ways
Prevent or disturb sleep
Interfere with or prevents intellectual work May cause suicide
May involve limbic structures causing affectivereactions
Often accompanied by abnormal sensations fromtouch
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How prevalent is severe
pain?
Some pain was reported by 86% of
individuals above the age of 65(Iowa study, 1994)
The prevalence of severe pain was 33% for
people at age 77 and above (Swedishstudy, 1996)
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How prevalent is severe
pain?
Some pain was reported by 86% of
individuals above the age of 65(Iowa study, 1994)
The prevalence of severe pain was 33% for
people at age 77 and above (Swedishstudy, 1996)
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Pain
The only tolerable pain is someone elses pain
Ren Leriche, French surgeon, 18791955
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There are different types of
pain
Somatic and visceral pain (Stimulationof nociceptors)
Pain ceases when stimulation ceases
Neuropathic pain
Pain is related to the nervous system
Central neuropathic pain
Plastic changes in the function of the CNS
May be persistent
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Pain
Non-nocicieptorpain
Stimulation ofnociceptors
Muscle pain
Somaticpain
Viscerapain
Fast pain
slow pain
Referred
pain
Lesions to
nerves orcns
Central
neuropathicpain
Inflamatory Neuropathicpain
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Central neuropathic pain:
Pain sensation caused by abnormal neural activityin the CNS
Hyperacusis:
Sounds are perceived louder than normal
Allodynia:
Sensation of pain from normally innocuousstimulation (such as light touch)
Hyperpathia:
Exaggerated and prolonged reactions to painfulstimuli
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Somatic and visceral pain
(Stimulation of nociceptors)
Burning (temperature) Injury
Inflammation
Chemicals
Compression of spinal nerve roots (nervi nervorum)
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Muscle pain
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MUSCLE TONE(general tone)
Contractileactivity
Viscoelastic tone(specific tone)
Electrogenicspasm
(pathological)
Contracture(no EMGactivity)
Electrogeniccontraction
(normal)
Viscoelasticstiffness
Elasticstiffness
Relationship between commonly used terms to characterize
muscle tension:
Tone, stiffness, contracture, and spasm
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Tension type headaches
with trigger zones in
the temporalis muscle (
),in suboccipital,
sternocleidomastoid
and upper trapezius
muscles (), from where
pain attacks can be elicited
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Neuropathic pain
Pain of the nervous system
Neuralgias
Anesthesia dolorosa
Root pain
Stroke pain
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Neuropathic pain
All pain of neural origin
The term is mostly used by neurologistsfor pain caused by disorders of peripheral
nerves and cranial nerves
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Normal Neuropathic
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Central neuropathic pain
Plastic changes in the function of the CNS
(WDR neurons, thalamus)
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Acute pain may promote
development of central neuropathic
pain
Central neuropathic pain is a neurologicdisorder
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Acute pain sensation may not
be a sign of pathology
Pain sensation can be elicited by: Stimulation of nociceptors
Overstimulation of other receptors
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Acute pain has two phases:
A fast (sharp) and a slow
(burning) sensation
The slow and delayed pain is mediatedby unmyelinated fibers (C-fibers).
The fast phase is mediated by
myelinated fibers (A).
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Time
Time
Time
First pain Second pain
X
X
C fiber
DRG
DRG
DRG
DRG
DRG
DRG
Ad fiber
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Fast and slow pain are different
Fast pain (stinging):
Well defined with regards to location Its strength is defined
Slow pain (aching):
Diffuse, poorly localized anatomically Difficult the estimate its strength
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Different types
of nerve fibers
carry differentkinds of pain
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Temperature
There are four different temperature
receptors:
Cool and warmth (sensory receptors)
Cold and heat (nociceptors)
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Temperature
1. Cool and warmth receptors mediate sensation oftemperature
2. Cold and heat receptors are nociceptors that mediatesensation of pain.
3. Cool and warmth receptors are innervated by smallmyelinated (A fibers, diameter 1-5 m, conductionvelocity 5-30 m/sec).
4. Cold and heat receptor are innervated by unmyelinatedfibers (C-fibers, diameter 0.2-2 m; conduction velocity
0.5-1 m/sec).
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DRG
Receptors
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Wid d i
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Wide dynamic
range neuron
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THE ANTERIOR LATERALSYSTEM MEDIATES PAIN
SENSATIONS
The spinothalamic tract is the best
known of the anteriorlateral tracts
A i iMidline
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Brainstemreticular
formation
Ventralthalamus
PAG
DRG
cortex
Association cort ex
Spinothalamictract
Dorsal
thalamus
DorsalhornReceptor
SI
Spinothalamic tract
Nonspecific (dorsal)C
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Spinal
nerves
Anterolateralfuniculus
Trigeminalnerve
Reticularformation
p ( )thalamic nucleiCortex
Brain stem
Spinalcord
Brainstemreticular
formation
Ventralthalamus
PAG
DRG
cortex
Association cortex
Spinothalamictract
Dorsalthalamus
Midline
DorsalhornReceptor
SI
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Trigeminalganglion
Thalamus
Cerebralcortex
Motornuclei
RFBrainstem
Midbrain
Spinalcord
SIMIDLINEAscending projections of
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I
II
SII
VPL
VPI
Brainstem
Anteriror portionof STT
MIDLINEAscending projections of
the anteriorportion
of the STT from neurons
in lamina IV-V of the
spinal horn.
VPI: Ventral posterior
inferior (nuclei of thalamus);
VPL: Ventral posteriorlateral (nuclei of thalamus);
SI: Primary
somatosensory cortex;
SII: secondary
somatosensory cortex
3 (SI)MIDLINE
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I
II
3a (SI)
Dorsal
Anterior
insulaVPI
VMpo
Brainstem
Thalamus
Area 24c
PAG
Lateral
portion
of STT
Projections of the
lateral portion of
the STT from cells
in lamina I of the
dorsal horn
MIDLINE
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SI (contralat.)
VPI
VMpo
SII (contralat.) SII
(ipsilateral)
Lateralportion
of STTDRG
I
II
Projection of
unmyelinated C fibers.
Notice: Projection
to SII is bilateral
but only the SI
receives input
from C fibers
AssociationMidli
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Reticularformationof melulla
Dorsalhorn
DRG
Receptor
Reticularformationof pons
cortex
AssociationcortexMidline
Dorsalthalamus
SI
Spinoreticular tract
Midline
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Dorsalhorn
DRG
Receptor
Periaqueductal grayPAG
Hypothalamus-amygdala
limbic system
Spinomesencephalic tract
Limbic system Association cortex
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Reticularformation
Ventral
thalamus
cortex
Prefrontal
cortex
SMP
AROUSAL
Anteriorlateral tract
Mediallemniscus
Dorsalthalamus
SII
"WHERE"
"WHAT"SI
Pathways involved
in mediating the
sensation ofnociceptor pain
Frontal lobe
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Hypothalamus
Amygdala
Locus coeruleus
Nucleus cuneiformis
Pontomedular
reticular
formation
DRG
Fromnociceptors
Dorsalhorn
RVM
PAG
Ascending
pain pathways
o ta obe
Input to the
periaquaductal gray
(PAG) and
pathways that modulate
transmission of painsignals by the PAG
through the rostral
ventromedial medulla
(RVM) pathway.
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Dorsolateralpontomesencephalic
tegmentum pathway (DLTP).DLPT
DRG
Fromnociceptors
Dorsalhorn
PAG
Ascending(crossed)
pain pathways
From rapheDescending pathways from raphe nucleus(NA t i th )
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NA serotoninpathway
DRG
Nociceptorfiber
Lamina Iinterneuron
Lamina II
interneuron
Presynapticinhibition
Post synapticinhibition
From raphenucleus
To thalamus
(NA-serotonin pathway)
Forebrain
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NA-serot oninpathway
Forebrain
Thalamus
Forebrain
Spinal
pain neuron
NST
Innervation by the
vagus nerve of organs
in the lower abdomen
involving the nucleus
of the solitary tract (NST)
DLF: Dorsolateral funiculus
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DLF: Dorsolateral funiculus
VLF: Ventrolateral funiculus
RVM: Rostroventral medulla
Vi l i i diff t f
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Visceral pain is different from
somatic pain
Inconsistent sensations
Sometimes referred pain to body surface
Often inescapable
Spinal cordVisceral afferent
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T11-L4
S3-S4
Viceralafferents
Uterus
Efferent
Nociceptors
Viceralafferents
DRG
DRG
Viceralafferents
Painfibers
Viceralreceptors
Bladder
Visceral afferent
innervation in the
lower body and
motor (efferent)innervation.
Thalamus
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PAG
RVM5HT
non 5HT
DLPTNE
non NE
Dorsalhorn
Primaryafferents
+ _
Two-way connections
between PAG, DLPT
and RVMand their connections
to the dorsal horn
The dual input to dorsal horn cells from RVM
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DRG
From
nociceptor
Off-neuron(Morphineexcites)
On-neuron
(Morphine inhibits)
Thalamus
Nocieptivedorsal
horn neuron
p
Spinothalamic tract activate dorsomedial thalamus
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Hypothalamus
Dorsomedialthalamus
PAG
STT
Amygdala
Associationcotices
Reticularformation
Cingulate
gyrus
Hypothesis about expansion of receptive field and creation oft i i t b ki f d t
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Corticalreceptivefield
Cerebral cortex
Cortex
Spinal cord
DRG
Receptive fields
trigger points by unmasking of dormant synapses
Mean EMG amplitudes recorded from a muscle
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0
10
20
30
40
50
N=8
7.53(0.36) 3.83
(0.94)
46.21(5.92)
6.08(1.08)
45.59(8.06)
4.84(0.52)
Trigger point
Adjacentnon-tendermuscle
N=29 N=25
Normalsubjects
Tensionheadachepatients
Fibromyalgiapatients
Mean EMG amplitudes recorded from a muscle
at a trigger point and at an adjacent
non-tender muscle
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Itch
The basis of itching is poorly understood
but it has similarities with pain.
CENTRAL NEUROPATHIC
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CENTRAL NEUROPATHIC
PAIN MAY INVOLVE THE
SYMPATHETIC NERVOUS
SYSTEM
REFLEX SYMPATHETIC
DYSTROPHY, RSD
Role of sympathetic nervous
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Role of sympathetic nervous
system
in neuropathic pain
1. Sympathetic system is activated by stimulation ofpain fibers
2. Sympathetic fibers secrete nor-epinephrine nearmechanoreceptors
3. Sensitivity of mechanoreceptors increases
4. Activation of sympathetic system increases5. Result: A viscous circle that causes RSD
Increased activity
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Increased activity
Activation of the
sympatheticnervous system
Nociceptorsensitization
Liberation of noradrenalin
Trauma causeactivation of pain
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activation of pain
fibers (C-fibers),
which sensitize WDR
neurons
Sensitized WDR
neurons cause
pressure to activate
pain circuits
(allodynia)
Mechanoreceptors are
activated by
epinephrine that is
secreted from
sympathetic nerves in
absence of mechanical
stimulation
Contemporary hypotheses of neural mechanisms involved
i ti CRPS I d II f ll i t
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Chronic excitation of
visceral and deep
somatic afferents
Abnormal
regualation of blood
flow and sweating
Swelling
Trophic changes
Trauma with/ without
peripheral
nerve lesion
Pain
MOVEMENT
DISORDERS
ABNORMAL
ACTIVITY INMOTONEURONS
TO SKELETAL
MUSCLE
ABNORMAL
SYMPATHETICACTIVITY
(VASO-SUDOMOTOR
ORTHER
ABNORMALITIES?
ABNORMAL STATE OF
AFFERENT NEURONSSympathetic
block
Central lesion
DISTORTED
INFORMATIONPROCESSING IN
SPINAL CORD
in generating CRPS I and II following trauma
CRPS: Complex regional pain syndrome
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Neuropathic pain
Pain of the nervous system
Neuralgias
Anesthesia dolorosa
Root pain
Stroke pain
Central neuropathic pain
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Central neuropathic pain
Plastic changes in the function of the CNS
(WDR neurons, thalamus)
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Central neuropathic pain
All pain of neural origin
The term is mostly used for pain
caused by disorders of peripheral nerves
and cranial nerves
Central neuropathic pain may
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Central neuropathic pain may
be caused by:
Chronic inflammation
Sensitization of skin receptors
Changes in the connectivity of the CNS
(through neural plasticity)
Acute pain may promote
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Acute pain may promote
development of central neuropathic
pain
Central neuropathic pain is a neurologicdisorder
Wide dynamic
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range neurons
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Central neuropathic pain may
develop from peripheral nerveinjuries
The pain is referred to the peripheral
location
Treatment of that location will not help
The patient and the surgeon are both
frustrated
C t l thi i
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Central neuropathic pain may
involve changes in function
Normally innocuous stimulation
becomes painful (allodynia)
Stimuli that normally cause mild pain
cause an exaggerated reaction
(hyperpathia)
Central neuropathic pain is
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Central neuropathic pain is
often accompanied by altered
perception of touch and painstimuli
Touch may cause pain (allodynia)
Increased sensitivity to pain
(hyperalgesia) Painful stimulation may cause
exaggerated reaction to pain and
prolonged pain (hyperpathia)
Central neuropathic pain may
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Central neuropathic pain may
involve changes in function
Normally innocuous stimulation
becomes painful (allodynia)
Stimuli that normally cause mild paincause an exaggerated reaction
(hyperpathia)
All d i P i f ll
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Allodynia: Pain from normally
innocuous stimulation (of the skin)
Hyperalgesia: Extreme sensitiveness
to painful stimuli.
Hyperpathia: Exaggerated subjective
response to painful stimuli, with acontinuing sensation of pain after the
stimulation has ceased.
Temporal integration
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Neuropathic painNormal
From: Mller and Pinkerton, 1997
Pain
Tingling
Temporal integration during development of
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A B
carpal tunnel syndrome
From: Mller and Pinkerton, 1997
Hyperalgesia from experimentally induced burns
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Site A Site B Site C
2
4
6
8
10
12
14
1 cm
Before burn
After burn
C
A
B
D
Mechanical
hyperalgesia
Flare
BA
Hypothesis for referred pain andsensitization of different nociceptors
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p
S iti ti
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Sensitization
Peripherally:
Receptors
Centrally
Increased synaptic efficacy
Expression of new neurotransmitters
Neuromodulators
Morphological re-organization
Oth h i t d
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From: Mller: Sensory Systems, 2002
Wind-up
Response to second stimulus is stronger than
the response to the first one
Change in temporal integration
Other phenomena associated
with chronic pain
"Wind-up" is NMDA mediated.Response with and without an NMDA antagonist.
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40
30
20
10
0
0 10 20
ControlNMDA antagonist
Stimulus number
p g
S thi i
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Severe neuropathic pain
affects a persons entire life inmajor ways
Prevent or disturb sleep
Interfere with or prevent
Intellectual work
Involve limbic structures causing affectivereactions
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How do we explain these
symptoms and signsphysiologically and
anatomically?Where is the neural activity that
give a sensation of pain
generated?
The anatomical location of the
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abnormality that cause pain may be
different from that to which the painis referred
Referred pain
Central neuropathic pain
The abnormal neural activity that
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The abnormal neural activity that
causes symptoms are not
generated at the location where
the symptoms are felt
Example:
Posttraumatic central neuropathic pain
Phantom pain
Central pain pathways for pain
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Central pain pathways for pain
PROJECT TO PRIMARY CORTICESWITH SPATIAL INFORMATION
(WHERE) PROJECT OBJECTIVE INFORMATION
(WHAT) TO MANY DIFFERENT PARTS
OF THE CNS. NON-CLASSICAL PATHWAYS ALSO
CONTRIBUTES TO AROUSAL
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SUMMARY OF PATHWAYS
INVOLVED IN MEDIATING
THE SENSATION OF PAIN
CENTRAL PAIN PATHWAYS
PROJECT TO PRIMARY
CORTICES WITH SPATIAL
INFORMATION (WHERE)
OBJECTIVE INFORMATION
(WHAT) TO MANY
DIFFERENT PARTS OF THE
CNS (FOR EXAMPLE THE
AMYGDALA)
NON-CLASSICAL
INFORMATION ALSO
CONTRIBUTES TO
AROUSAL
From: Mller: Sensory Systems, 2003
R l f l l ti it
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Reversal of neural plasticity
TENS (transderm electric nervestimulation) has been used for many years
in treatment of chronic pain
Recently, sound stimulation in various
forms have been introduced in treatment
of severe tinnitus
S thi i
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Severe neuropathic pain
affects a persons entire life inmajor ways
Prevent or disturb sleep
Interfere with or prevent
Intellectual work
Involve limbic structures causing affectivereactions
How can pain information reach
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p
the amygdala?
Through the thalamus
Through routes that are enhanced by
expression of neural plasticity (re-routingof information)
Connections from a sensory system to the amygdala
the high route
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From: Mller: Sensory Systems, 2003
the high route
Connections from a sensory system to the amygdala
the low route
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the low route
From: Mller: Sensory Systems, 2003
The amygdala is involved in fear
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yg
and other mood disorders
Connections from the amygdala
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From: Mller: Sensory Systems, 2003
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INESCAPABLEPAIN
INVOLVES OTHER PARTSOF THE CNS THAN
ESCAPABLE PAINActivate different columns in the
PAG coordinating either active of
passive coping