Putting Pain in
Perspective:
Pain Matters
Mary Christenson, PT, PhD
DPT 781 O
Fall 2010
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American Pain Foundation
Virtual March on Washington Launches September 1, 2010
September Pain Awareness Month is rapidly approaching!
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A Story

Mailis-Gagnon A,
Israelson D. Beyond Pain:
Making the Mind-Body
Connection. University of
Michigan Press; 2005:98.

What do you want to
learn in this course?
http://www.cvshealthresources.com/Imageb
ank/Articles_images/chronic-pain.jpg
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Who/What Is Affected
by Persistent Pain?
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Individual
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ADLs
Self-esteem
Confidence, other?
Family
Friends
Work environment
Society
 How will this present in the clinic?
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Reflection
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Who treats persistent pain?
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Why is the study of pain important?
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What do you currently know about the
treatment of persistent pain?
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Pain Defined

“An unpleasant sensory and emotional
experience associated with actual or
potential tissue damage, or described in
terms of such damage.” 2
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Statistics
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One out of six Americans, minimally, live with
chronic pain (American Chronic Pain Association)
20% globally have pain longer than 3 months 3
~$100 billions/year costs of persistent pain
(AACPI - American Alliance of Cancer Pain
Initiatives )
$61.2 billion/year lost business income due to
employees pain – only included musculoskeletal
problems6
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Statistics (continued)
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~50 million Americans have persistent
pain (American Pain Foundation)
Headaches are the most common type of
pain (National Headache Foundation)
Elderly :
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Community-dwelling – up to 50% c/o pain
Institutionalized – 71-83% c/o of at least one
source of pain4
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Terminology
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Acute Pain
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Occurs with tissue damage or potential damage = a
symptom
Protects from tissue damage and or until healing has
occurred
Persistent Pain (Chronic Pain)
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Extends beyond normal tissue healing time, and/or
Causes challenges greater than expected from tissue
injury or medical findings, and/or
Occurs without known tissue damage
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Terminology
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Hyperalgesia
Hyperpathia
Allodynia
Neurogenic pain
Neuropathic pain
Nociceptor
Nociception
Nociceptive pain
Sensitization
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Peripheral
Central
http://static.disaboom.com/content/images/articles/thumbna
il/chronic-pain-with-nmd-is-und_thumbnail1.jpg
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http://www.painfoundation.org/
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Models of Pain
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Historical
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Specificity Theory
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Separate nerve endings for each type of sensation
(temperature, touch, pain)
Challenged: Phantom limb pain? Blockage of pain pathways?
Pattern Theory
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Pain recognized by “sense organs” in skin
Consists of signals in the CNS
Sensation is a learned event – no specific pathways for each
sensation
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Models (continued)
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Gate Control Theory (Melzack and Wall, 1965)
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Physiological and psychological components of pain
Nerve ending signals are modulated in the spinal cord
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Large (non-nociceptor) and small (nociceptor) diameter
afferent signals to the substantia gelatinosa (SG) and T cell
T cell initiates consequences of pain
SG cells are inhibitory to the T cell
Nociceptor signals inhibit the SG neurons, therefore allowing
pain signals to continue
Increased signals from large diameter fibers results in
increased firing of SG neurons, which ultimately decreases
firing of T-cells (Result?) (Clinical application?)
System under control of supraspinal sites that affect
outcomes
Challenges
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http://www.lupusuk.org.uk/images/latestnews/lwcpfig1.gif
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Gate Control Theory (continued)

This theory resulted in recognition that
“pain is a CNS phenomenon, that
treatments for pain must be aimed not
only at the peripheral nervous system but
also at modulating the CNS, and that pain
is multidimensional.” 2
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Models (continued)
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Biomedical Model
Biopsychosocial Model (conceptual model
by the American College of Physicians)
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Nociception
Pain
Pain Appraisal
Pain Behaviors
Social Roles for Pain and Illness
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Biopsychosocial Models of Pain
http://www.continuingedcourses.net/active/courses/images/course033-image002.jpg
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http://www.painxchange.com.au/images/BiopsychosocialPain.png
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Peripheral Primary Afferent
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Nociceptors fire in response to a noxious
stimulus
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Mechanical
Thermal
Chemical
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Peripheral Nerve Fiber Types
Letter System
Conduction
velocity, m/sec
General Function
Type of
fiber
Diameter,
micrometer
s
A-alpha
13-22
70-120
alpha-motoneurons, muscle spindle
primary endings, Golgi tendon organs,
touch
A-beta
8-13
40-70
touch, kinesthesia, muscle spindle
secondary endings
A-gamma
4-8
15-40
touch, pressure, gamma-motoneurons
A-delta
1-4
5-15
pain, crude touch, pressure,
temperature
B
1-3
3-14
preganglionic autonomic
C
0.1-1
0.2-2
pain, touch, pressure, temperature,
postganglionic autonomic
http://www.unmc.edu/physiology/Mann/mann12.html
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Peripheral Nerve Fiber Types
Roman Numeral System
Conduction
velocity,
m/sec
General Function
Type of
fiber
Diameter,
micromet
ers
Ia
12-20
70-120
muscle spindle primary endings
Ib
11-19
66-114
Golgi tendon organs
II
5-12
20-50
touch, kinesthesia, muscle spindle secondary
endings
III
1-5
4-20
pain, crude touch, pressure, temperature
IV
0.1-2
0.2-3
pain, touch, pressure, temperature
II = Aβ ; III = Aδ ; IV = C
http://www.unmc.edu/physiology/Mann/mann12.html
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Peripheral Receptors
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Ia: muscle spindle
Ib: Golgi tendon organ
II: Meissner corpuscle, Merkel’s cell,
Pacinian corpuscle, Ruffini ending, hair
follicle, Paciniform endings, muscle spindle
III: Free nerve endings (noxious stim)
IV: Free nerve endings (noxious stim)
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Free Nerve Ending
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Silent Nociceptors
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~1/3 of nociceptors in skin, joints or
viscera do not respond to stimulus until
inflammation = “silent nociceptors”
May be activated by mediators such as
prostaglandins that are released during
inflammation
Increases pain response
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Peripheral Sensitization
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Increased responsiveness to stimuli after
initial injury
Potential mechanisms:
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Lower threshold to stimulus
Increase in neuron activity
Increase in area of receptor fields
Increase in response to the same stimulus
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Neuronal Activators of Pain
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Neuropeptides
Opioids
Glutamate
Ion Channels
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Non-neuronal Activators of Pain
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Inflammatory processes cause the release of
factors that can result in activating afferent
nerves
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Serotonin released from platelets
Bradykinin released plasma
Prostaglandins released from arachidonic acid
cascade
Cytokines released by macrophages
Others: mast cells, neutrophils, T and B cells
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Structures of Pain
http://journals.prous.com/journals/dnp/20041703/html/dn170172/images/Block_f1.jpg
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Physiology of Pain
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Central Mechanisms
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Spinal Cord
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Laminae I-VI make up the dorsal horn
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Sensory afferents terminate (majority) on “2nd
neuron”
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Noxious information from skin: I, II, V (primarily)
Noxious information from muscles/joints: I (primarily)
Interneurons
 Afferents from skin, joints, muscles, viscera may
terminate on one neuron – referred pain?
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Dorsal Horn
http://www.wdv.com/Cancer/Pain/Images/Anatomy1.gif
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Central Sensitization
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Neurons in dorsal horn
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High-threshold – respond to noxious stim
Low-threshold – respond to innocuous stim
Wide-dynamic-range (WDR) – respond to both
Tissue injury: increased sensitivity of highthreshold and WDR neurons
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Expansion of receptive fields in central neurons
common – referred pain?
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Sensitization
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Continued input from sensitized
nociceptors can maintain sensitization of
dorsal horn neurons
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Need to reduce peripheral input?
Sensitization of dorsal horn neurons can
also be maintained in absence of
peripheral input
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Need to reduce central sensitization?
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Potential Influences: Hyperalgesia
(found in spinal cord)
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Can produce hyperalgesia
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Glial cells
Neurotransmitters – Spinal Cord
Glutamate
 Substance P
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Can reduce hyperalgesia
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Adenosine
GABA
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Pain Sensory Pathways:
Spinal Cord to Brain
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Spinothalamic Tract
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Transmits nociceptive pain up through the thalamus (VPL
nucleus and medial thalamic nuclei) to higher centers
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VPL to 1o and 2o somatosensory cortex: location, duration quality,
and intensity of pain
Medial thalamic to anterior cinglate, etc.: “unpleasantness” of pain
Spinomesencephalic and Spinoreticular Tracts
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Transmits to midbrain/brainstem respectively
Integrates information with areas involved in descending
inhibition, facilitation, and autonomic pain responses
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Thalamus and Cortex
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Thalamus
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Integrate information from peripheral noxious
stimulation
Cortex
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S1 and S2: increased blood flow noted to
these areas with painful stimuli
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Homunculus (more to come)
Anterior cingulate cortex
Many other centers (to be continued)
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Brainstem Centers
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Contains centers that contribute
facilitation and or inhibition signals
A balance between all brain/brainstem
signals determines pain perception
Other brain influences?
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PAIN IS AN OUTPUT
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Measures of Pain
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Measures of Pain
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Associations
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American Academy of Pain Management
American Pain Foundation
American Pain Society
American Chronic Pain Association
International Association for the Study of
Pain (IASP)
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References
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1 Mailis-Gagnon A, Israelson D. Beyond Pain: Making the
Mind-Body Connection. University of Michigan Press;
2005:98.
2 Sluka KA, ed. Mechanisms and Management of Pain for
the Physical Therapist. Seattle, WA: IASP Press; 2009.
3 Butler DB, Moseley L. Explain Pain. Adelaide, Australia:
Notgroup Publications; 2003.
4 Galieze L. Chronic Pain in Elderly People. Pain.
1997;70(1):3-14.
5 Marchand F, Perretti M, McMahon SB. Role of the
immune system in chronic pain. Nature
Reviews/Neuroscience. 2005;6:521-532.
6 JAMA. 2003;290:2443-2454.
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