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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. - PowerPoint PPT Presentation
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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
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 person’s entire life in major ways
There are many forms of pain
• Mild pain:
Does not interfere noticeably with everyday life
• Moderate pain:
May cause some annoyance and may be perceived as unpleasant
• Severe pain:
Affects a person’s entire life in major ways
Different forms of pain
• Acute pain
• Chronic pain
• Somatic pain
• Neuropathic pain
• Central neuropathic pain
Pain has many different forms, but the same name
Tinnitus has many different forms but the same name
There are different types of pain
• Somatic and visceral pain (Stimulation of 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
It is important to have different names for for different
disorders • We cannot think about matters that do not
have names
• The same words is used to describe very different forms of tinnitus and pain
• Using the same names for fundamentally different disorders is a disadvantage in studying and treating such disorders
Severe pain affects a person’s entire life in major ways
• Prevent or disturb sleep• Interfere with or prevents intellectual work • May cause suicide May involve limbic structures causing affective
reactionsOften accompanied by abnormal sensations from
touch
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 (Swedish study, 1996)
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 (Swedish study, 1996)
Pain
“The only tolerable pain is someone else’s pain”René Leriche, French surgeon, 1879–1955
There are different types of pain
• Somatic and visceral pain (Stimulation of 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
Pain
Non-nocicieptorpain
Stimulation ofnociceptors
Muscle pain
Somaticpain
Viscerapain
Fast painslow pain
Referredpain
Lesions tonerves or
cns
Centralneuropathic
pain
Inflamatory Neuropathicpain
• Central neuropathic pain:– Pain sensation caused by abnormal neural activity
in the CNS• Hyperacusis:
– Sounds are perceived louder than normal• Allodynia:
– Sensation of pain from normally innocuous stimulation (such as light touch)
• Hyperpathia:– Exaggerated and prolonged reactions to painful
stimuli
Somatic and visceral pain (Stimulation of nociceptors)
• Burning (temperature)• Injury• Inflammation• Chemicals• Compression of spinal nerve roots (nervi nervorum)
Muscle pain
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
K
K
K
J J J J
Tension type headaches with trigger zones in the temporalis muscle (), in suboccipital, sternocleidomastoid and upper trapezius muscles (), from where pain attacks can be elicited
Neuropathic pain
• Pain of the nervous system
• Neuralgias
• Anesthesia dolorosa
• Root pain
• Stroke pain
Neuropathic pain
• All pain of neural origin
The term is mostly used by neurologists for pain caused by disorders of peripheral nerves and cranial nerves
Normal Neuropathic
Central neuropathic pain
• Plastic changes in the function of the CNS(WDR neurons, thalamus)
Acute pain may promote development of central neuropathic
pain
• Central neuropathic pain is a neurologic disorder
Acute pain sensation may not be a sign of pathology
Pain sensation can be elicited by:
• Stimulation of nociceptors
• Overstimulation of other receptors
Acute pain has two phases: A fast (sharp) and a slow
(burning) sensation
• The slow and delayed pain is mediated by unmyelinated fibers (C-fibers).
• The fast phase is mediated by myelinated fibers (A).
Time
Time
Time
First pain Second pain
X
X
C fiber
DRG
DRG
DRG
DRG
DRG
DRG
Ad fiber
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
Different types of nerve fibers carry different kinds of pain
Temperature
There are four different temperature receptors:
Cool and warmth (sensory receptors)
Cold and heat (nociceptors)
Temperature
1. Cool and warmth receptors mediate sensation of temperature
2. Cold and heat receptors are nociceptors that mediate sensation of pain.
3. Cool and warmth receptors are innervated by small myelinated (A fibers, diameter 1-5 m, conduction velocity 5-30 m/sec).
4. Cold and heat receptor are innervated by unmyelinated fibers (C-fibers, diameter 0.2-2 m; conduction velocity 0.5-1 m/sec).
DRG
Receptors
Wide dynamic range neuron
THE ANTERIOR LATERAL SYSTEM MEDIATES PAIN
SENSATIONS
The spinothalamic tract is the best known of the anteriorlateral tracts
Brainstemreticular
formation
Ventralthalamus
PAG
DRG
cortex
Association cortex
Spinothalamictract
Dorsalthalamus
Midline
DorsalhornReceptor
SI
Spinothalamic tract
Spinalnerves
Anterolateralfuniculus
Trigeminalnerve
Reticularformation
Nonspecific (dorsal)thalamic nucleiCortex
Brain stem
Spinalcord
Brainstemreticular
formation
Ventralthalamus
PAG
DRG
cortex
Association cortex
Spinothalamictract
Dorsalthalamus
Midline
DorsalhornReceptor
SI
Trigeminalganglion
Thalamus
Cerebralcortex
Motornuclei
RFBrainstem
Midbrain
Spinalcord
III
SI
SII
VPL
VPI
Brainstem
Anteriror portionof STT
MIDLINEAscending projections of the anterior portion of the STT from neurons in lamina IV-V of the spinal horn.
VPI: Ventral posterior inferior (nuclei of thalamus); VPL: Ventral posterior lateral (nuclei of thalamus); SI: Primary somatosensory cortex; SII: secondary somatosensory cortex
III
3a (SI)
DorsalAnteriorinsula
VPIVMpo
Brainstem
Thalamus
Area 24c
PAG
Lateralportionof STT
MIDLINE
Projections of the lateral portion of the STT from cells in lamina I of the dorsal horn
SI (contralat.)
VPIVMpo
SII (contralat.) SII(ipsilateral)
Lateralportionof STT
DRG
III
MIDLINE
Projection of unmyelinated C fibers.
Notice: Projection to SII is bilateral but only the SI receives input from C fibers
Reticularformationof melulla
Dorsalhorn
DRG
Receptor
Reticularformationof pons
cortex
AssociationcortexMidline
Dorsalthalamus
SI
Spinoreticular tract
Dorsalhorn
DRG
Receptor
Periaqueductal grayPAG
Hypothalamus-amygdala
limbic system
Midline
Spinomesencephalic tract
Reticularformation
Ventralthalamus
cortex
Limbic system
Prefrontalcortex
SMP
Association cortex
AROUSAL
Anteriorlateral tract
Mediallemniscus
Dorsalthalamus
SII
"WHERE"
"WHAT"SI
Pathways involved in mediating the sensation of nociceptor pain
Hypothalamus
Amygdala
Locus coeruleus
Nucleus cuneiformis
Pontomedularreticular
formation
DRG
Fromnociceptors
Dorsalhorn
RVM
PAG
Ascendingpain pathways
Frontal lobe
Input to the periaquaductal gray (PAG) and pathways that modulate transmission of pain signals by the PAG through the rostral ventromedial medulla(RVM) pathway.
Dorsolateral pontomesencephalic tegmentum pathway (DLTP).
DLPT
DRG
Fromnociceptors
Dorsalhorn
PAG
Ascending(crossed)
pain pathways
NA serotoninpathway
DRG
Nociceptorfiber
Lamina Iinterneuron
Lamina IIinterneuron
Presynapticinhibition
Post synapticinhibition
From raphenucleus
To thalamus
Descending pathways from raphe nucleus (NA-serotonin pathway)
NA-serotoninpathway
Forebrain
Thalamus
Forebrain
Spinalpain neuron
NST
Innervation by the vagus nerve of organs in the lower abdomen involving the nucleusof the solitary tract (NST)
DLF: Dorsolateral funiculusVLF: Ventrolateral funiculusRVM: Rostroventral medulla
Visceral pain is different from somatic pain
• Inconsistent sensations
• Sometimes referred pain to body surface
• Often inescapable
Spinal cord
T11-L4
S3-S4
Viceralafferents
Uterus
Efferent
Nociceptors
Viceralafferents
DRGDRG
Viceralafferents
Painfibers
Viceralreceptors
Bladder
Visceral afferent innervation in the lower body and motor (efferent) innervation.
PAG
RVM5HT
non 5HT
DLPTNE
non NE
Dorsalhorn Primary
afferents
Thalamus
+ _
Two-way connections between PAG, DLPT and RVM and their connections to the dorsal horn
DRG
Fromnociceptor
Off-neuron(Morphineexcites)
On-neuron(Morphine inhibits)
Thalamus
Nocieptivedorsal
horn neuron
The dual input to dorsal horn cells from RVM
Hypothalamus
Dorsomedialthalamus
PAG
STT
Amygdala
Associationcotices
Reticularformation
Cingulategyrus
Spinothalamic tract activate dorsomedial thalamus
Corticalreceptivefield
Cerebral cortex
Cortex
Spinal cord
DRG
Receptive fields
Hypothesis about expansion of receptive field and creation of trigger points by unmasking of dormant synapses
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
Itch
• The basis of itching is poorly understood but it has similarities with pain.
CENTRAL NEUROPATHIC PAIN MAY INVOLVE THE
SYMPATHETIC NERVOUS SYSTEM
• REFLEX SYMPATHETIC DYSTROPHY, RSD
Role of sympathetic nervous system
in neuropathic pain
1. Sympathetic system is activated by stimulation of pain fibers
2. Sympathetic fibers secrete nor-epinephrine near mechanoreceptors
3. Sensitivity of mechanoreceptors increases4. Activation of sympathetic system increases5. Result: A viscous circle that causes RSD
Increased activity
Activation of thesympathetic
nervous system
Nociceptorsensitization
Liberation of noradrenalin
Trauma cause 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
Chronic excitation ofvisceral and deepsomatic afferents
Abnormalregualation of bloodflow and sweating
SwellingTrophic changes
Trauma with/withoutperipheral
nerve lesion
Pain
MOVEMENTDISORDERS
ABNORMALACTIVITY IN
MOTONEURONSTO SKELETAL
MUSCLE
ABNORMALSYMPATHETIC
ACTIVITY(VASO-SUDOMOTOR
ORTHERABNORMALITIES?
ABNORMAL STATE OFAFFERENT NEURONS
Sympatheticblock
Central lesion
DISTORTEDINFORMATION
PROCESSING INSPINAL CORD
Contemporary hypotheses of neural mechanisms involved in generating CRPS I and II following trauma
CRPS: Complex regional pain syndrome
Neuropathic pain
• Pain of the nervous system
• Neuralgias
• Anesthesia dolorosa
• Root pain
• Stroke pain
Central neuropathic pain
• Plastic changes in the function of the CNS(WDR neurons, thalamus)
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 be caused by:
• Chronic inflammation
• Sensitization of skin receptors
• Changes in the connectivity of the CNS (through neural plasticity)
Acute pain may promote development of central neuropathic
pain
• Central neuropathic pain is a neurologic disorder
Wide dynamic range neurons
Central neuropathic pain may develop from peripheral nerve
injuries
• The pain is referred to the peripheral location
• Treatment of that location will not help
• The patient and the surgeon are both frustrated
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 often accompanied by altered perception of touch and pain
stimuli
• 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 involve changes in function
• Normally innocuous stimulation becomes painful (allodynia)
• Stimuli that normally cause mild pain cause an exaggerated reaction (hyperpathia)
Allodynia: Pain from normally innocuous stimulation (of the skin)
Hyperalgesia: Extreme sensitiveness to painful stimuli.
Hyperpathia: Exaggerated subjective response to painful stimuli, with a continuing sensation of pain after the stimulation has ceased.
Neuropathic painNormal
From: Møller and Pinkerton, 1997
Pain
Tingling
Temporal integration
A B
Temporal integration during development of carpal tunnel syndrome
From: Møller and Pinkerton, 1997
Site A Site B Site C
2
4
6
8
10
12
14
1 cm
Before burn
After burn
CA
B
D
Mechanicalhyperalgesia
Flare
BA
Hyperalgesia from experimentally induced burns
Hypothesis for referred pain and sensitization of different nociceptors
Sensitization
• Peripherally:– Receptors
• Centrally– Increased synaptic efficacy– Expression of new neurotransmitters– Neuromodulators – Morphological re-organization
From: Møller: 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
40
30
20
10
00 10 20
ControlNMDA antagonist
Stimulus number
"Wind-up" is NMDA mediated. Response with and without an NMDA antagonist.
Severe neuropathic pain affects a person’s entire life in
major ways
• Prevent or disturb sleep• Interfere with or prevent• Intellectual work Involve limbic structures causing affective
reactions
How do we explain these symptoms and signs physiologically and
anatomically?
Where is the neural activity that give a sensation of pain
generated?
The anatomical location of the abnormality that cause pain may be different from that to which the pain
is referred
• Referred pain
• Central neuropathic pain
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
• PROJECT TO PRIMARY CORTICES WITH SPATIAL INFORMATION (“WHERE”)
• PROJECT OBJECTIVE INFORMATION (“WHAT”) TO MANY DIFFERENT PARTS OF THE CNS.
• NON-CLASSICAL PATHWAYS ALSO CONTRIBUTES TO AROUSAL
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: Møller: Sensory Systems, 2003
Reversal of neural plasticity
• “TENS” (transderm electric nerve stimulation) 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
Severe neuropathic pain affects a person’s entire life in
major ways
• Prevent or disturb sleep• Interfere with or prevent• Intellectual work Involve limbic structures causing affective
reactions
How can pain information reach the amygdala?
• Through the thalamus
• Through routes that are enhanced by expression of neural plasticity (re-routing of information)
From: Møller: Sensory Systems, 2003
Connections from a sensory system to the amygdala “the high route”
Connections from a sensory system to the amygdala “the low route”
From: Møller: Sensory Systems, 2003
The amygdala is involved in fear and other mood disorders
From: Møller: Sensory Systems, 2003
Connections from the amygdala
INESCAPABLE PAIN INVOLVES OTHER PARTS
OF THE CNS THAN ESCAPABLE PAIN
Activate different columns in the PAG coordinating either active of
passive coping