Download CHRONIC PAIN

OMM3 #2
Wed, Aug 6, 2003 2-3pm
Chad McCormick
Dr. McGill
Page 1 of 7
I.
General
a. Definitions
i. PAIN: (IASP) Unpleasant sensory and emotional experience
associated with potential or actual tissue damage
ii. PAIN: a conscious experience which may be influenced by
alterations in somatosensory processing following injury as well as
psychosocial factors.
iii. SUFFERING: a state of severe distress associated with events that
threaten the intactness of the individual
b.
SCOPE OF THE PROBLEM
i. Nine in ten have pain at least once a month
ii. 15% have severe pain
iii. Majority of us will suffer disabling pain
iv. 2 million in US disabled with back pain
v. COST: 80 billion dollars a year
vi. 58% of chronic pain patients are depressed
vii. Most pain RX is by the patient or primary care physician
viii. 50% have an anxiety disorder
II.
Mechanisms of Pain
a.
PROCESS OF PAIN
i. TRANSDUCTION
1. Noxious Stimuli translated into impulses
2. Three types of fibers
a. A-beta
i. Large diameter non-nociceptive
ii. Touch, moving stimuli
b. A-delta
i. Small diameter, fast nociceptors
ii. Produce sharp pain
iii. Pain not reduced by morphine
c. C
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Wed, Aug 6, 2003 2-3pm
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i. Small diameter, unmyelinated
ii. Slow nociceptors (up to 1 minute)
iii. Non-specific
iv. no localized pain
v. pain relieved by morphine
3.
Up to 50% of A-Delta and C fibers are “silent”
4. Chemical mediators
a. Potassium
b. Serotonin
c. Bradykinin
d. Histamine
e. Prostaglandins
f. Leukotrienes
g. Substance P
ii. TRANSMISSION
1. Propagation throughout the nervous system (From dorsal
horn to cortex)
2. Encoding of a generator potential into an impulse train
3. Varies with afferent type and conditions
4. Involves nociceptor fibers (non-linear)
5. Neurotransmitters
a. Exitatory Amino Acids
i. AMPA, NMDA receptors
b. Monoamines Noradrenaline
i. Alpha1 receptors
c. Monoamines Dopamine
i. D- 1,5 receptors
d. Monoamines 5-Hydroxytryptamine
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i. 5HT2,7 receptors
iii. MODULATION
1. Nociceptive transmission modified through neural
influences
2. Descending pathways can alter or inhibit
3. Transmission Modified Through
a. Inhibitory Amino Acids
i. GABA-a and GABA-b receptors
b. Monoamines Noradrenaline
i. Alpha2 receptors
c. Monoamines Dopamine
i. D-2,3,4 receptors
d. Monoamines 5-Hydroxytryptamine
i. 5HT1
e. Monoamines Opioids
i. MU, DELTA, KAPPA, ORLI
iv. PERCEPTION
1. Interacts with unique psychology of individuals to create
the final experience of “pain”
2. Reticular system
3. Somatosensory cortex
4. Limbic system (emotions)
III.
Pathways
a.
Gating Mechanism (seen in the power points)
i. touch sensation overcomes pain sensation due to gate being turned
on and off
ii. diagrams in powerpoints have been excluded for space and time
conservation
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IV.
V.
THREE DIMENSIONS OF PAIN
a.
Sensory-discriminative
b.
Affective-motivational
c.
Evaluative
NEUROMATRIX MODEL
a.
Neuromatrix
i. Large widespread network of neurons between the thalamus and
cortex, and between the cortex and limbic system. The distribution
and synaptic links are determined genetically and later sculpted by
sensory inputs.
b.
c.
d.
VI.
VII.
Body-self neuromatrix (Neurosignature)
i. A characteristic pattern implanted by the patterns of repeated
cyclic processing and synthesis of nerve impulses throughout the
neuromatrix
Sentient neural hub
i. The area of the brain in which the stream of nerve impulses is
converted into a continuously changing stream of awareness and
may also activate muscle movement.
New Conceptual Nervous System Components
i. The body-self neuromatrix
ii. Cyclic processing and synthesis in which the neurosignature is
produced
iii. The sentient neural hub (SNH) which converts the flow of
neurosignatures into the flow of awareness.
iv. Activation of an action neuromatrix to provide the pattern of
movements to bring about the desired goal.
CONVERGENCE
a.
Both specialized and “network” components
b.
Lamina I Spino-thalamo-cortical pathway
c.
i. Specialized neural system
Lamina V Integrative, intensity-related
TAKEAWAY POINTS
a.
Pain is a highly complex phenomenon involving multiple structures and
psychophysiological processes with constant counterbalancing of
facilitative and inhibitory processes.
b.
VIII.
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Just one manifestation of the mind-body's hemeostasis system (AD
Craig, Specificity and Integration in Central Pain Pathways, 10th World
Congress on Pain, 2002)
How does Pain change from Acute to Subacute?
a.
SENSITIZATION
i. Peripheral
1. Inflammation mediators sensitize nociceptor endings
2. Will now respond to weak stimuli i.e. Touch, soreness and
aching of deep tissues
ii. Central
1. Abnormal amplification
2. Amplifies signals from low threshold A-beta fibers
3. Noxious stimuli can produce primary and secondary
hyperalgesia
b.
State: Normal Transmission
i. Stimulus
Low
High
ii. Afferent
A-Beta
A-Delta/C
iii. Sensation
c.
d.
Innocuous
Pain
iv. Syndrome
Physiological Sensibility
v. Change
Normal Transmission
State: Suppressed
i. Stimulus
High
ii. Afferent
A-Delta/C
iii. Sensation
Innocuous
iv. Syndrome
Hyposensibility
v. Change
Reduced Exitation
vi.
Increased Inhibition
State: Sensitized (transient)
i. Stimulus
Low
High
ii. Afferent
A-Beta
A-Delta/C
iii. Sensation
Allodynia
Hyperalgesia
iv. Syndrome
Hypersensible
Inflammatory
v.
vi. Change
Neuropathic
Increased
Reduced
vii.
e.
exitation
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inhibition
State: Reorganized+ (persistent)
i. Stimulus
Low
High
ii. Afferent
A-Beta
A-Delta/C
iii. Sensation
Allodynia
Hyperalgesia
iv. Syndrome
Peripheral
Central
v.
neuropathic
neuropathic
vi.
pain
pain
vii. Change
Structural Reoganization
Experience of subacute pain
i. Variable unpleasantness
ii. Movement activates sensitized receptors
iii. Feeling of weakness, somnolence, exhaustion
iv. Emotions: fear, anger, helpless, embarrassment, remorse
v. Expectation the storm will pass
Properly Used Drugs and Pre-emptive Analgesia May Help to Prevent subacute Pain
f.
IX.
How Does Subacute Pain Become Chronic Pain?
a.
Gradual process (6 months or less)
b.
Not directly tied to late neurophysiological changes
c.
Varies by condition, physical status, and age
d.
X.
XI.
i. i.e., low risk with appendectomy, but 50% of thoracotomy patients
Behavior a major contributor
i. Inactivity
ii. Abnormal posture and gait trigger added physical disorders
e.
Emotional changes
f.
Dependency on medications
g.
Preoccupation with pain
h.
Social support system
i.
Pain may become “centralized : changes in CNS anatomy and
physiology
Diagnostic Phase : Comprehensive evaluation essential
a.
History
b.
Physical Examination
c.
Psychological/Behavioral Evaluation
d.
Appropriate diagnostic tests
MEASUREMENT OF PAIN Required by JCAOH Guidelines
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a.
GOOD NEWS: SIMPLE IS BEST
i. Visual Analog Scale
VISUAL ANALOG PAIN SCALE
0___________________________100
Place a mark on the line representing your pain level
ii. Faces Scale (Not included)
XII.
TREATMENT
a.
Acute management
b.
Invasive procedures
c.
Analgesics
d.
The best treatment for chronic pain is prevention through good acute
pain management.