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UNDERSTANDING THE PAIN
4
Introduction
Definition : An unpleasant sensory and emotional experience
associated with actual or potential tissue damage.
Pain may not be directly proportional to amount of tissue injury.
Highly subjective, leading to under treatment
5
In cancer, the prevalence of pain in advanced
disease is 70-90%.
" In HIV disease, pain prevalence is about 50%.
" Other illnesses may have significant pain but no
clear data.
National Academy of Sciences in 2011
How pain occurs?
• Pain is unique to each individual.
• Arise from
• damage to
• any tissue that is innervated by nociceptors or can occur in the
absence of tissue damage
• Under vital signs.
The International Association for the Study of Pain (IASP)
Dimensions of pain
• the sensory discriminative,
• motivational affective,
• and the cognitive evaluative
by Melzack and Casey in 1968.
• The sensory discriminative refers to the sensation of pain
and includes the location, quality (e.g., burning, dull, sharp),
intensity, and duration.
• The motivational affective refers to the unpleasantness of
pain or how much the pain bothers the patient (e.g.,
nauseating, sickening).
• The cognitive evaluative puts pain in terms of past experiences and
probability of outcome and can as such modify both the sensory
discriminative and the motivational affective dimensions.
• Thus, it affects the outcome either positively or negatively based on
the patient’s beliefs in terms of past or prior experiences.
• So all three dimensions are to be linked for pain responses.
Some common terminologies to describe pain
Hyperalgesia.. Also includes threshold and suprathreshold
And
• Primary and secondary hyperalgesia.
Allodynia
• describe pain from a nonnociceptive stimulus. eg,
• brushing the skin after a sunburn
Referred pain
7
Classification
I. Acute
II.Chronic :
i. Non malignant
ii. Malignant
8
 Injury, trauma, spasm or disease to skin, muscle,
inflammation, somatic structures or viscera. (requires
clinical treatment) ?
 Perceived and communicated via peripheral mechanisms
(pathways)
 Well defined time of onset with clear pathology.
 Serves to protect from tissue damage.
Acute Pain
9
 Usually subsides quickly as pain producing stimuli
decreases
 Associated with anxiety-(decreases rapidly)
 Can be understood or rationalized as part of the healing
process.
Cont.
Chronic Pain
Pain can be considered chronic if
• outlasts normal tissue healing time,
• the impairment is greater than would be expected from the physical
findings or injury, and/or
• pain occurs in the absence of identifiable tissue damage. In addition,
many clinicians define chronic pain in terms of the number of months
after the initial injury, usually 3–6 months after injury.
• The use of a time frame to diagnose chronicity of pain is useful for
some conditions such as osteoarthritis.
• Chronic pain is difficult to treat and responds best to an
interdisciplinary approach.
CUTANEOUS PAIN VERSUS DEEP-TISSUE PAIN
Cutaneous - easy to locate
Sharp
does not usually refer
Deep-tissue pain from muscle, joint, or viscera -
difficult to locate,
Diffuse and refers to other structures distant from the site of injury.
e.g ; irritable bowel syndrome, osteoarthritis or myofascial pain.
• In human, painful intramuscular stimulation is rated as more
unpleasant than painful cutaneous stimulation. So, the pain is
• Long lasting
• &
• Referred pain is more frequent.
10
i. Non-malignant
 Pain persists beyond the precipitating injury
 Rarely accompanied by autonomic symptoms
 Sufferers often fail to demonstrate objective
evidence of underlying pathology.
 Characterized by location-visceral, myofacial, or
neurologic causes.
Chronic Pain
11
ii. Malignant
 Has characteristics of chronic pain as well as
symptoms of acute pain (breakthrough pain).
 Has a definable cause, e.g. tumor recurrence
 In treatment, narcotic habituation is generally
not a concern.
II. Chronic Pain
12
3 TYPES OF PAIN
13
 Types of Pain
 Somatic
 Visceral
 Bone
 Neuropathic
 Emotional/Spiritual
14
I- Somatic Pain
 Aching, often constant
 May be dull or sharp
 Often worse with movement
 Well localized
 Skin, Muscle, Joints, superficial or deep.
 Eg:
o Bone & soft tissue
o chest wall
15
II- Visceral Pain
 Constant or crampy
 Aching, burning
 Poorly localized
 Referred
 Organs of Thorax &Abdominal Cavity.
 Usually as a result of stretching, infiltration and
compression
 Eg:
o Liver capsule distension
o Bowel obstruction
16
 Both Somatic & Visceral pain
travel along the same
pathways. Pain stimuli arising
from the viscera is perceived
as somatic in origin.
 This can be confused by the
brain and is often described as
referred pain.
17
III- Bone Pain
 Poorly localized, aching, deep, burning.
 Common with malignancy of Breast, Lung, Prostate,
Bladder, Cervical, Renal, Colon, Stomach and Esophagus
 Can lead to pathological fractures.
 Vertebral Metastases can lead to cord compression.
18
IV- Neuropathic Pain
 Caused by disturbance of function or pathological changes
in a nerve.
 May arise from a lesion or trauma, infection,
compression or tumour invasion.
 Described as burning, shooting, tingling.
 Does not respond well to standard analgesics.
19
 Categories of Pain
 Classified by inferred pathophysiology:
I. Nociceptive pain (stimuli from somatic and
visceral structures)
II. Neuropathic pain (stimuli abnormally
processed by the nervous system)
20
I. Nociceptive:
 Caused by invasion &/or destruction &/or pressure on superficial
somatic structures like skin, deeper skeletal structures such as bone
& muscle and visceral structures and organs.
 Types: superficial somatic, deep somatic, & visceral.
21
II. Neuropathic:
 Caused by pressure on &/or destruction of peripheral,
autonomic or central nervous system structures.
 Radiation of pain along dermatomal or peripheral nerve
distributions.
 Often described as burning and/or deep aching &
associated with dysesthesia or lancinating pain.
22
Effects of
pain
 Sympathetic responses
o Pallor
o Increased blood pressure
o Increased pulse
o Increased respiration
o Skeletal muscle tension
o Diaphoresis
23
Effects of
pain
 Parasympathetic responses
o Decreased blood pressure
o Decreased pulse
o Nausea & vomiting
o Weakness
o Pallor
o Loss of consciousness
PAIN THEORIES
• Specificity Theory
• Pattern Theory
• Gate Control Theory of Pain
Specificity Theory
• The specificity theory suggests that there are separate nerve
endings for each variety of sensation arising from cutaneous
stimulation, that is, touch, cold, warmth, and pain. For pain,
the theory suggests that there are “pain receptors” that
when stimulated always produce the sensation of pain and
only pain.
Pattern Theory
• The pattern theory suggests that pain would result from a
patterned input from sense organs in the skin and CNS.
• States that there are no specialized receptors in the skin Rather
there are specialized sensory endings that respond to noxious
stimuli.
• spinothalamic tract (central pathways) transmit pain sensation.
Gate Control Theory
• Implies a non-painful stimulus can block the
transmission of a noxious stimulus.
• Is based on the premise that the gate, located in the
dorsal horn of the spinal cord, modulates the afferent
nerve impulses.
Gate Control Theory
• The gate control theory of pain as
initially described by Melzack
• Information from ascending A
afferents and (pain messages)
carried along A and C afferent
fibers enter the dorsal horn.
•
35
Gate Control Theory
• Impulses stimulate the substantia gelatinosa at
dorsal horn of the spinal cord inhibiting synaptic
transmission in A & C fiber afferent pathways.
• Large-diameter Aβ fibers are nonnociceptive (do
not transmit pain stimuli) and inhibit the effects of
firing by Aδ and C fibers.
• Myelinated "Aδ" fiber that carries messages
quickly with intense pain, and a small,
unmyelinated, slow "C" fiber that carries the
longer-term throbbing and chronic pain.
36
Gate Control Theory
Sensory information coming from A
fibers is transmitted to higher centers
in brain
“Pain message" carried along A & C
fibers is not transmitted to second-
order neurons and never reaches
sensory centers
37
Summary
Rubbing the area that hurts stimulates
receptors of innocuous stimuli like
touch, pressure and vibration.
These mechano-receptors send signals
along the Ab nerve fibers that (1)
stimulate spinal nerves (inhibitory
inter-neurons) that in turn inhibit
signaling in the 2nd order neurons
(projection neuron) and (2) directly
inhibit the 2nd order neuron to reduce
or stop pain signal from being sent to
the brain
TREATMENT MODELS OF PAIN
Using Biomedical Model, all pains have physiological cause
Treat physiological problems
Treat Acute pain is appropriate and necessary.
e.g;___________________.
However, for the treatment of chronic pain, the biomedical model is
inadequate.
Biopsychosocial Model views pain as (interaction
between BPS)
Useful for the treatment of chronic pain.
Described in variety of ways/components.
1. Nociception.
2. Pain
3. Suffering
4. Pain bahaviour
5. Replaced suffering (Pain appraisal)
• nociception is the first component and represents the detection of tissue
damage and activation of nociceptors and the nociceptive pathway in the
CNS.
• second component is pain and involves recognition of pain at the cortical
level. (important to).recognize that pain does not occur until the signal
reaches the cortex.
• next component suffering, often accompanies severe pain, but can occur
in its absence.
• Fourth component is pain behaviour, influenced by both verbal and
nonverbal behaviors.
• replaced suffering,
Eg: choose to continue working and socializing or may avoid all activity and
work.
PHYSICAL THERAPY PRACTICE IN GENERAL
PT’s
Team members
• The rehabilitation approach uses multiple potential techniques,
including education and selfmanagement, exercise and physical
activity, manual therapy, and electrophysical agents.
• May use biomedical approach and biopsychosocial to pain
management
• Howerver, biopsychosocial factor may precict poor outcome also such
as
• 1. Worse pain - higher pain intensity, longer pain duration, previous
pain episodes, and multiples sites of pain
PHYSICAL THERAPY PRACTICE IN GENERAL
2. higher psychological distress - fear, anxiety and depression.
3. lower social function - lower socioeconomic status, lower education.
4. general biological factors – Obesity and physical inactivity.
These factors are modifiable
And cannot use for acute – it may lead or transitioning to chronic.

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1. Understanding the pain basics.pptx

  • 2. 4 Introduction Definition : An unpleasant sensory and emotional experience associated with actual or potential tissue damage. Pain may not be directly proportional to amount of tissue injury. Highly subjective, leading to under treatment
  • 3. 5 In cancer, the prevalence of pain in advanced disease is 70-90%. " In HIV disease, pain prevalence is about 50%. " Other illnesses may have significant pain but no clear data. National Academy of Sciences in 2011
  • 4. How pain occurs? • Pain is unique to each individual. • Arise from • damage to • any tissue that is innervated by nociceptors or can occur in the absence of tissue damage • Under vital signs. The International Association for the Study of Pain (IASP)
  • 5. Dimensions of pain • the sensory discriminative, • motivational affective, • and the cognitive evaluative by Melzack and Casey in 1968.
  • 6. • The sensory discriminative refers to the sensation of pain and includes the location, quality (e.g., burning, dull, sharp), intensity, and duration. • The motivational affective refers to the unpleasantness of pain or how much the pain bothers the patient (e.g., nauseating, sickening).
  • 7. • The cognitive evaluative puts pain in terms of past experiences and probability of outcome and can as such modify both the sensory discriminative and the motivational affective dimensions. • Thus, it affects the outcome either positively or negatively based on the patient’s beliefs in terms of past or prior experiences. • So all three dimensions are to be linked for pain responses.
  • 8. Some common terminologies to describe pain Hyperalgesia.. Also includes threshold and suprathreshold And • Primary and secondary hyperalgesia. Allodynia • describe pain from a nonnociceptive stimulus. eg, • brushing the skin after a sunburn Referred pain
  • 9.
  • 10.
  • 11. 7 Classification I. Acute II.Chronic : i. Non malignant ii. Malignant
  • 12. 8  Injury, trauma, spasm or disease to skin, muscle, inflammation, somatic structures or viscera. (requires clinical treatment) ?  Perceived and communicated via peripheral mechanisms (pathways)  Well defined time of onset with clear pathology.  Serves to protect from tissue damage. Acute Pain
  • 13. 9  Usually subsides quickly as pain producing stimuli decreases  Associated with anxiety-(decreases rapidly)  Can be understood or rationalized as part of the healing process. Cont.
  • 14. Chronic Pain Pain can be considered chronic if • outlasts normal tissue healing time, • the impairment is greater than would be expected from the physical findings or injury, and/or • pain occurs in the absence of identifiable tissue damage. In addition, many clinicians define chronic pain in terms of the number of months after the initial injury, usually 3–6 months after injury.
  • 15. • The use of a time frame to diagnose chronicity of pain is useful for some conditions such as osteoarthritis. • Chronic pain is difficult to treat and responds best to an interdisciplinary approach. CUTANEOUS PAIN VERSUS DEEP-TISSUE PAIN Cutaneous - easy to locate Sharp does not usually refer
  • 16. Deep-tissue pain from muscle, joint, or viscera - difficult to locate, Diffuse and refers to other structures distant from the site of injury. e.g ; irritable bowel syndrome, osteoarthritis or myofascial pain. • In human, painful intramuscular stimulation is rated as more unpleasant than painful cutaneous stimulation. So, the pain is • Long lasting • & • Referred pain is more frequent.
  • 17. 10 i. Non-malignant  Pain persists beyond the precipitating injury  Rarely accompanied by autonomic symptoms  Sufferers often fail to demonstrate objective evidence of underlying pathology.  Characterized by location-visceral, myofacial, or neurologic causes. Chronic Pain
  • 18. 11 ii. Malignant  Has characteristics of chronic pain as well as symptoms of acute pain (breakthrough pain).  Has a definable cause, e.g. tumor recurrence  In treatment, narcotic habituation is generally not a concern. II. Chronic Pain
  • 20. 13  Types of Pain  Somatic  Visceral  Bone  Neuropathic  Emotional/Spiritual
  • 21. 14 I- Somatic Pain  Aching, often constant  May be dull or sharp  Often worse with movement  Well localized  Skin, Muscle, Joints, superficial or deep.  Eg: o Bone & soft tissue o chest wall
  • 22. 15 II- Visceral Pain  Constant or crampy  Aching, burning  Poorly localized  Referred  Organs of Thorax &Abdominal Cavity.  Usually as a result of stretching, infiltration and compression  Eg: o Liver capsule distension o Bowel obstruction
  • 23. 16  Both Somatic & Visceral pain travel along the same pathways. Pain stimuli arising from the viscera is perceived as somatic in origin.  This can be confused by the brain and is often described as referred pain.
  • 24. 17 III- Bone Pain  Poorly localized, aching, deep, burning.  Common with malignancy of Breast, Lung, Prostate, Bladder, Cervical, Renal, Colon, Stomach and Esophagus  Can lead to pathological fractures.  Vertebral Metastases can lead to cord compression.
  • 25. 18 IV- Neuropathic Pain  Caused by disturbance of function or pathological changes in a nerve.  May arise from a lesion or trauma, infection, compression or tumour invasion.  Described as burning, shooting, tingling.  Does not respond well to standard analgesics.
  • 26. 19  Categories of Pain  Classified by inferred pathophysiology: I. Nociceptive pain (stimuli from somatic and visceral structures) II. Neuropathic pain (stimuli abnormally processed by the nervous system)
  • 27. 20 I. Nociceptive:  Caused by invasion &/or destruction &/or pressure on superficial somatic structures like skin, deeper skeletal structures such as bone & muscle and visceral structures and organs.  Types: superficial somatic, deep somatic, & visceral.
  • 28. 21 II. Neuropathic:  Caused by pressure on &/or destruction of peripheral, autonomic or central nervous system structures.  Radiation of pain along dermatomal or peripheral nerve distributions.  Often described as burning and/or deep aching & associated with dysesthesia or lancinating pain.
  • 29. 22 Effects of pain  Sympathetic responses o Pallor o Increased blood pressure o Increased pulse o Increased respiration o Skeletal muscle tension o Diaphoresis
  • 30. 23 Effects of pain  Parasympathetic responses o Decreased blood pressure o Decreased pulse o Nausea & vomiting o Weakness o Pallor o Loss of consciousness
  • 31. PAIN THEORIES • Specificity Theory • Pattern Theory • Gate Control Theory of Pain
  • 32. Specificity Theory • The specificity theory suggests that there are separate nerve endings for each variety of sensation arising from cutaneous stimulation, that is, touch, cold, warmth, and pain. For pain, the theory suggests that there are “pain receptors” that when stimulated always produce the sensation of pain and only pain.
  • 33. Pattern Theory • The pattern theory suggests that pain would result from a patterned input from sense organs in the skin and CNS. • States that there are no specialized receptors in the skin Rather there are specialized sensory endings that respond to noxious stimuli. • spinothalamic tract (central pathways) transmit pain sensation.
  • 34. Gate Control Theory • Implies a non-painful stimulus can block the transmission of a noxious stimulus. • Is based on the premise that the gate, located in the dorsal horn of the spinal cord, modulates the afferent nerve impulses.
  • 35. Gate Control Theory • The gate control theory of pain as initially described by Melzack • Information from ascending A afferents and (pain messages) carried along A and C afferent fibers enter the dorsal horn. • 35
  • 36. Gate Control Theory • Impulses stimulate the substantia gelatinosa at dorsal horn of the spinal cord inhibiting synaptic transmission in A & C fiber afferent pathways. • Large-diameter Aβ fibers are nonnociceptive (do not transmit pain stimuli) and inhibit the effects of firing by Aδ and C fibers. • Myelinated "Aδ" fiber that carries messages quickly with intense pain, and a small, unmyelinated, slow "C" fiber that carries the longer-term throbbing and chronic pain. 36
  • 37. Gate Control Theory Sensory information coming from A fibers is transmitted to higher centers in brain “Pain message" carried along A & C fibers is not transmitted to second- order neurons and never reaches sensory centers 37
  • 38. Summary Rubbing the area that hurts stimulates receptors of innocuous stimuli like touch, pressure and vibration. These mechano-receptors send signals along the Ab nerve fibers that (1) stimulate spinal nerves (inhibitory inter-neurons) that in turn inhibit signaling in the 2nd order neurons (projection neuron) and (2) directly inhibit the 2nd order neuron to reduce or stop pain signal from being sent to the brain
  • 39. TREATMENT MODELS OF PAIN Using Biomedical Model, all pains have physiological cause Treat physiological problems Treat Acute pain is appropriate and necessary. e.g;___________________. However, for the treatment of chronic pain, the biomedical model is inadequate.
  • 40. Biopsychosocial Model views pain as (interaction between BPS) Useful for the treatment of chronic pain. Described in variety of ways/components. 1. Nociception. 2. Pain 3. Suffering 4. Pain bahaviour 5. Replaced suffering (Pain appraisal)
  • 41. • nociception is the first component and represents the detection of tissue damage and activation of nociceptors and the nociceptive pathway in the CNS. • second component is pain and involves recognition of pain at the cortical level. (important to).recognize that pain does not occur until the signal reaches the cortex. • next component suffering, often accompanies severe pain, but can occur in its absence. • Fourth component is pain behaviour, influenced by both verbal and nonverbal behaviors. • replaced suffering, Eg: choose to continue working and socializing or may avoid all activity and work.
  • 42. PHYSICAL THERAPY PRACTICE IN GENERAL PT’s Team members • The rehabilitation approach uses multiple potential techniques, including education and selfmanagement, exercise and physical activity, manual therapy, and electrophysical agents. • May use biomedical approach and biopsychosocial to pain management • Howerver, biopsychosocial factor may precict poor outcome also such as • 1. Worse pain - higher pain intensity, longer pain duration, previous pain episodes, and multiples sites of pain
  • 43. PHYSICAL THERAPY PRACTICE IN GENERAL 2. higher psychological distress - fear, anxiety and depression. 3. lower social function - lower socioeconomic status, lower education. 4. general biological factors – Obesity and physical inactivity. These factors are modifiable And cannot use for acute – it may lead or transitioning to chronic.

Editor's Notes

  1. For example, if a person experiences low back pain for the second time, he or she may be more likely to do well treatment during the first experience resolved pain quickly. On the other hand, if a person with low back pain has had multiple episodes of pain that were not adequately treated or resolved in prior occurrences, the pain may be more difficult to treat.
  2. Hyperalgesia is an increased sensitivity to a noxious stimulus and can occur both at the site of injury, primary hyperalgesia, and outside the site of injury, secondary hyperalgesia.