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A. Neeharika
Ist year PG
1
› Introduction
› Definition
› Classification & types of Pain
› Theories of Pain
› Pain Pathways
– Neural Anatomy
– Neural Pathways
› Pain Assessment tools
› Applied Anatomy
2
› Pain is an unpleasant sensory action
› From perception of pain as ‘stimulus-response relationship’ , the
concept of pain has evolved to be a consequence of complex
interactions between sensory, emotional, and behavioral factors
› Derived from Greek – ‘Poin’ and Latin – ‘Poena’
3
› The concept of pain as a multidimensional experience has been described
in ancient texts, dating as far back as the Syriac Empire (circa 200 BC).
› In The Book of Medicines (Budge 2002), it is suggested that pain is the
product of bile and phlegm mingled with cold and heat.
› These simple combinations occur in the brain, and according to Syriac
medicine, pain is a product of the brain (a concept that has passed the test
of time and that we still hold true today).
4
› The International Association for the Study of Pain defines pain
as
“an unpleasant sensory and emotional experience
associated with actual or potential tissue damage, or described in
terms of such damage.” .
5
Though unpleasant, pain serves important adaptive purposes.
› Identifies and localizes noxious stimuli
› Protective – withdrawal reflex response- limits injury
› Experience of pain – avoids potentially harmful injuries
› Immobility due to pain – assists in healing
Cambridge University Press
978-0-521-87491-5 - Acute Pain Management 6
› Based on duration:
Acute
Convalescent
Chronic
Acute pain follows traumatic tissue injuries, is generally limited in
duration, and is associated with temporal reductions in intensity.
Chronic pain may be defined as discomfort persisting 3–6 months
beyond the expected period of healing.
7
Cambridge University Press; 978-0-521-87491-5 - Acute Pain Management8
› Based on Pathophysiologic mechanisms:
Physiologic
Nociceptive / Inflammatory
Neuropathic
Physiologic pain defines rapidly perceived nontraumatic discomfort of
very short duration.
Nociceptive pain is defined as noxious perception resulting from cellular
damage following surgical, traumatic, or disease-related injuries.
Inflammation and inflammatory mediators play a major role.
9
› Somatic nociceptive pain is well localized and generally follows
a dermatomal pattern. It is usually described as sharp, crushing,
or tearing in character.
› Visceral nociceptive pain defines discomfort associated with
peritoneal irritation as well as dilation of smooth muscle
surrounding viscus or tubular passages. Non dermatomal.
10
Neuropathic pain is defined by the International Association for the
Study of Pain as “pain initiated or caused by a pathologic lesion
or dysfunction” in peripheral nerves and CNS.
Disease states associated with classic neuropathic sysmptoms
include infection (eg, herpes zoster), metabolic derangements
(eg, diabetic neuropathy), toxicity (eg, chemotherapy), and
Wallerian degeneration secondary to trauma or nerve
compression.
11
› Neuropathic pain is usually constant and described as burning,
electrical, lancinating, and shooting.
Cambridge University Press; 978-0-521-87491-5 - Acute Pain Management
12
› By convention, symptoms related to peripheral lesions are termed
neuropathic, whereas symptoms related to spinal cord injuries are
termed myelopathic
13
› Based on clinical context:
Postsurgical
Malignancy related
Neuropathic
Degenerative
14
› Psychogenic pain was defined by the IASP as “Pain specifically
attributable to the thought process, emotional state, or personality of
the patient in the absence of an organic or delusional cause or
tension mechanism.”
› Such a system hardly seems an improvement, as one is still forced to
choose between psychological and physical factors.
15
› Nociceptor: A high-threshold sensory receptor of the peripheral
somatosensory nervous system that is capable of transducing and
encoding noxious stimuli.
› Hyperalgesia: Increased pain from a stimulus that normally provokes
pain
› Allodynia: Pain due to a stimulus that does not normally provoke pain
International Association for the Study of Pain: http://www.iasppain.
org/Content/NavigationMenu/GeneralResourceLinks/PainDefinitions/defa
ult.htm
16
› Sensitization: Increased responsiveness of nociceptive neurons to their
normal input, and/or recruitment of a response to normally
subthreshold inputs.
› Hyperpathia: Increased or exaggerated pain intensity with minor
stimulation
› Dysesthesia: Unpleasant sensation at rest or movement
› Paresthesia: Unpleasant often shock-like or electrical sensation
precipitated by touch or pressure (CRPS-II causalgia)
International Association for the Study of Pain: http://www.iasppain.
org/Content/NavigationMenu/GeneralResourceLinks/PainDefinitions/defa
ult.htm
17
› The propagation of pain is initiated with the activation of physiological
receptors, called nociceptors
› Present on skin, mucosa, membranes, deep fascias, connective tissues of
visceral organs, ligaments and articular capsules, periosteum, muscles,
tendons, and arterial vessels
18
› The receptors correspond to free nerve endings and represent the
more distal part of a first-order afferent neuron consisting of
small-diameter fibers, with little or unmyelinated, of the A-Delta
or C type, respectively.
19
Nociception is by
› Transduction: It is defined as responses of peripheral nociceptors
to traumatic or potentially damaging chemical, thermal, or
mechanical stimulation.
› Conduction: It refers to the propagation of action potentials from
peripheral nociceptive endings viamyelinated andunmyelinated
nerve fibers.
› Transmission: Transmission refers to the transfer of noxious
impulses from primary nociceptors to cells in the spinal cord
dorsal horn.
20
Cambridge University Press; 978-0-521-87491-5 - Acute Pain Management
21
22
› The portions of the nervous system responsible for the sensation
and perception of pain may be divided into three areas:
1. Afferent pathways
2. CNS
3. Efferent pathways
23
The afferent portion is composed of:
a) Nociceptors (pain receptors)
b) Afferent nerve fibres
c) Spinal cord network
Afferent pathways terminate in the dorsal horn of the spinal cord
(1st afferent neuron).
2nd afferent neuron creates spinal part of afferent system.
24
The portion of CNS involved in the interpretation of the pain signals are the
› Limbic system
› Reticular formation
› Thalamus
› Hypothalamus
› Cortex
Cortex
Thalamus
Cerebellum
Periqueductal
Gray matter
Limbic structures
hypothalamus
Reticular formation
Spinal tract nucleus of V
25
The efferent pathways, composed of the fibers connecting the
reticular formation, midbrain, and substantia gelatinosa, are
responsible for modulating pain sensation
26
› The propagation of pain is initiated with the activation of
physiological receptors called nociceptors.
› The receptors correspond to the free nerve endings i.e., A-Delta,
A-Beta or C type fibers.
27
› Many types of pain arise as a result of infection or damage to tissue.
› Both events initiate an inflammatory response that is intimately linked
with pain.
› The passage of nociceptive impulses generated in the peripheral nerve
fibers depends on
› The release of various neurotransmitters. These neurotransmitters act
either peripherally of centrally.
28
Various Pain mediators include:
› Plasma kinins: e.g. bradykinin
› Serotonin
› Histamine
› Prostaglandins
› Leukotrienes
› Cytokines
› Neuropeptides
29
› These pain mediators/ pain producing substances acts as
stimulators for nociceptors / the free nerve endings.
› These pain mediators are released by activation of Phospholipase
A2, which is activated by trauma or infection.
30
31
32
› The four most influential theories of pain perception include the
› Specificity (or Labeled Line) Theory
› Intensity Theory
› Pattern Theory
› Gate Control Theory
33
› One of the earliest ideas, termed the Specificity theory, was proposed
by Descartes.
› The theory suggested that specific pain fibers carry specific coding
that discriminates between different forms of noxious and nonnoxious
sensation.
› The fundamental tenet of the Specificity Theory is that each modality
has a specific receptor and associated sensory fiber (primary afferent)
that is sensitive to one specific stimulus (Dubner et al. 1978)
34
Moayedi M, Davis KD.
Theories of pain: from
specificity to gate control.
J Neurophysiol 109: 5–
12, 2013.
35
› The intensity theory, proposed by Sydenham, suggested that the
intensity of the peripheral stimulus determines which sensation is
perceived.
› The theory defines pain, not as a unique sensory experience but
rather, as an emotion that occurs when a stimulus is stronger than
usual
36
37
› Goldscheider suggested a neurophysiological model to describe
this summation effect: repeated subthreshold stimulation or
suprathreshold hyperintensive stimulation could cause pain.
› But the theory lost support with Sherrington’s evolutionary
framework regarding existence of sensory receptors that are
specialized to respond to noxious stimuli, for which he coined the
term “nociceptor”.
38
› J. P. Nafe postulated this “quantitative theory of feeling” in 1929.
› This theory ignored findings of specialized nerve endings and many of the
observations supporting the specificity and/or intensive theories of pain.
› The theory stated that any somaesthetic sensation occurred by a specific
and particular pattern of neural firing and that the spatial and temporal
profile of firing of the peripheral nerves encoded the stimulus type and
intensity
39
40
› In 1965, Ronald Melzack and Charles Patrick (Pat) Wall (Melzack and
Wall 1965) proposed a theory that would revolutionize pain research
› Melzack and Wall accepted that there are nociceptors (pain fibers) and
touch fibers and proposed that that these fibers synapse in two different
regions within the dorsal horn of the spinal cord: cells in the substantia
gelatinosa and the “transmission” cells.
41
› The model proposed that signals produced in primary
afferents from stimulation of the skin were transmitted to three
regions within the spinal cord:
1) the substantia gelatinosa,
2) the dorsal column, and
3) a group of cells that they called ‘transmission cells’.
42
› They proposed that the gate in the spinal cord is the substantia
gelatinosa in the dorsal horn, which modulates the transmission
of sensory information from the primary afferent neurons to
transmission cells in the spinal cord.
› This gating mechanism is controlled by the activity in the large
and small fibers.
43
44
› Large-fiber activity inhibits (or closes) the gate, whereas small-fiber
activity facilitates (or opens) the gate.
› When nociceptive information reaches a threshold that exceeds the
inhibition elicited, it “opens the gate” and activates pathways that
lead to the experience of pain and its related behaviors.
› Therefore, the Gate Control Theory of Pain provided a neural basis
45
46
47
Anesthesia Dolorosa: It is defined as perception of pain in an area that
is anesthetic. A complication of post-treatment of TN.
Deafferentation pain: Deafferentation pain is due to partial
or complete interruption of peripheral or central afferent neural
activity.
› Examples are postherpetic neuralgia, central pain (pain after CNS
injury), and phantom limb pain (pain felt in the region of an
amputated body part).
48
› Congenital analgesia - nociceptive stimuli are not processed
and/or integrated at a level of brain.
› Patient does not feel any pain
49
› Referred pain is pain that is present in an area removed or
distant from its point of origin. The area of referred pain is
supplied by the nerves from the same spinal segment as the
actual site of pain.
› Phantom limb pain - is pain that an individual feels in amputated
limb
50
Hemiagnosia :
› It is a loss of ability to identify the source of pain on one side (the
affected side) of the body. Application of painful stimuli to the
affected side thus produces anxiety, moaning, agitation and
distress but no attempt to withdrawal from or push aside the
offending stimulus.
› Hemiagnosia is associated with stroke that produces paralysis
and hypersensitivity to painful stimuli in the affected side
51
Visual Analogue Scale:
52
Verbal Scale:
53
McGill Pain
Questionnare:
› Sambulingam: Concise Textbook of Physiology
› Monheims: Textbook of Local Anaesthesia
› Moayedi M, Davis KD. Theories of pain: from specificity to gate
control. J Neurophysiol 109: 5–12, 2013.
› Cambridge University Press; 978-0-521-87491-5 - Acute Pain
Management
› International Association for the Study of Pain:
http://www.iasppain.
org/Content/NavigationMenu/GeneralResourceLinks/PainDefinit
ions/default.htm
54
55

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Pain physiology_ neeha

  • 2. › Introduction › Definition › Classification & types of Pain › Theories of Pain › Pain Pathways – Neural Anatomy – Neural Pathways › Pain Assessment tools › Applied Anatomy 2
  • 3. › Pain is an unpleasant sensory action › From perception of pain as ‘stimulus-response relationship’ , the concept of pain has evolved to be a consequence of complex interactions between sensory, emotional, and behavioral factors › Derived from Greek – ‘Poin’ and Latin – ‘Poena’ 3
  • 4. › The concept of pain as a multidimensional experience has been described in ancient texts, dating as far back as the Syriac Empire (circa 200 BC). › In The Book of Medicines (Budge 2002), it is suggested that pain is the product of bile and phlegm mingled with cold and heat. › These simple combinations occur in the brain, and according to Syriac medicine, pain is a product of the brain (a concept that has passed the test of time and that we still hold true today). 4
  • 5. › The International Association for the Study of Pain defines pain as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.” . 5
  • 6. Though unpleasant, pain serves important adaptive purposes. › Identifies and localizes noxious stimuli › Protective – withdrawal reflex response- limits injury › Experience of pain – avoids potentially harmful injuries › Immobility due to pain – assists in healing Cambridge University Press 978-0-521-87491-5 - Acute Pain Management 6
  • 7. › Based on duration: Acute Convalescent Chronic Acute pain follows traumatic tissue injuries, is generally limited in duration, and is associated with temporal reductions in intensity. Chronic pain may be defined as discomfort persisting 3–6 months beyond the expected period of healing. 7
  • 8. Cambridge University Press; 978-0-521-87491-5 - Acute Pain Management8
  • 9. › Based on Pathophysiologic mechanisms: Physiologic Nociceptive / Inflammatory Neuropathic Physiologic pain defines rapidly perceived nontraumatic discomfort of very short duration. Nociceptive pain is defined as noxious perception resulting from cellular damage following surgical, traumatic, or disease-related injuries. Inflammation and inflammatory mediators play a major role. 9
  • 10. › Somatic nociceptive pain is well localized and generally follows a dermatomal pattern. It is usually described as sharp, crushing, or tearing in character. › Visceral nociceptive pain defines discomfort associated with peritoneal irritation as well as dilation of smooth muscle surrounding viscus or tubular passages. Non dermatomal. 10
  • 11. Neuropathic pain is defined by the International Association for the Study of Pain as “pain initiated or caused by a pathologic lesion or dysfunction” in peripheral nerves and CNS. Disease states associated with classic neuropathic sysmptoms include infection (eg, herpes zoster), metabolic derangements (eg, diabetic neuropathy), toxicity (eg, chemotherapy), and Wallerian degeneration secondary to trauma or nerve compression. 11
  • 12. › Neuropathic pain is usually constant and described as burning, electrical, lancinating, and shooting. Cambridge University Press; 978-0-521-87491-5 - Acute Pain Management 12
  • 13. › By convention, symptoms related to peripheral lesions are termed neuropathic, whereas symptoms related to spinal cord injuries are termed myelopathic 13
  • 14. › Based on clinical context: Postsurgical Malignancy related Neuropathic Degenerative 14
  • 15. › Psychogenic pain was defined by the IASP as “Pain specifically attributable to the thought process, emotional state, or personality of the patient in the absence of an organic or delusional cause or tension mechanism.” › Such a system hardly seems an improvement, as one is still forced to choose between psychological and physical factors. 15
  • 16. › Nociceptor: A high-threshold sensory receptor of the peripheral somatosensory nervous system that is capable of transducing and encoding noxious stimuli. › Hyperalgesia: Increased pain from a stimulus that normally provokes pain › Allodynia: Pain due to a stimulus that does not normally provoke pain International Association for the Study of Pain: http://www.iasppain. org/Content/NavigationMenu/GeneralResourceLinks/PainDefinitions/defa ult.htm 16
  • 17. › Sensitization: Increased responsiveness of nociceptive neurons to their normal input, and/or recruitment of a response to normally subthreshold inputs. › Hyperpathia: Increased or exaggerated pain intensity with minor stimulation › Dysesthesia: Unpleasant sensation at rest or movement › Paresthesia: Unpleasant often shock-like or electrical sensation precipitated by touch or pressure (CRPS-II causalgia) International Association for the Study of Pain: http://www.iasppain. org/Content/NavigationMenu/GeneralResourceLinks/PainDefinitions/defa ult.htm 17
  • 18. › The propagation of pain is initiated with the activation of physiological receptors, called nociceptors › Present on skin, mucosa, membranes, deep fascias, connective tissues of visceral organs, ligaments and articular capsules, periosteum, muscles, tendons, and arterial vessels 18
  • 19. › The receptors correspond to free nerve endings and represent the more distal part of a first-order afferent neuron consisting of small-diameter fibers, with little or unmyelinated, of the A-Delta or C type, respectively. 19
  • 20. Nociception is by › Transduction: It is defined as responses of peripheral nociceptors to traumatic or potentially damaging chemical, thermal, or mechanical stimulation. › Conduction: It refers to the propagation of action potentials from peripheral nociceptive endings viamyelinated andunmyelinated nerve fibers. › Transmission: Transmission refers to the transfer of noxious impulses from primary nociceptors to cells in the spinal cord dorsal horn. 20
  • 21. Cambridge University Press; 978-0-521-87491-5 - Acute Pain Management 21
  • 22. 22
  • 23. › The portions of the nervous system responsible for the sensation and perception of pain may be divided into three areas: 1. Afferent pathways 2. CNS 3. Efferent pathways 23
  • 24. The afferent portion is composed of: a) Nociceptors (pain receptors) b) Afferent nerve fibres c) Spinal cord network Afferent pathways terminate in the dorsal horn of the spinal cord (1st afferent neuron). 2nd afferent neuron creates spinal part of afferent system. 24
  • 25. The portion of CNS involved in the interpretation of the pain signals are the › Limbic system › Reticular formation › Thalamus › Hypothalamus › Cortex Cortex Thalamus Cerebellum Periqueductal Gray matter Limbic structures hypothalamus Reticular formation Spinal tract nucleus of V 25
  • 26. The efferent pathways, composed of the fibers connecting the reticular formation, midbrain, and substantia gelatinosa, are responsible for modulating pain sensation 26
  • 27. › The propagation of pain is initiated with the activation of physiological receptors called nociceptors. › The receptors correspond to the free nerve endings i.e., A-Delta, A-Beta or C type fibers. 27
  • 28. › Many types of pain arise as a result of infection or damage to tissue. › Both events initiate an inflammatory response that is intimately linked with pain. › The passage of nociceptive impulses generated in the peripheral nerve fibers depends on › The release of various neurotransmitters. These neurotransmitters act either peripherally of centrally. 28
  • 29. Various Pain mediators include: › Plasma kinins: e.g. bradykinin › Serotonin › Histamine › Prostaglandins › Leukotrienes › Cytokines › Neuropeptides 29
  • 30. › These pain mediators/ pain producing substances acts as stimulators for nociceptors / the free nerve endings. › These pain mediators are released by activation of Phospholipase A2, which is activated by trauma or infection. 30
  • 31. 31
  • 32. 32
  • 33. › The four most influential theories of pain perception include the › Specificity (or Labeled Line) Theory › Intensity Theory › Pattern Theory › Gate Control Theory 33
  • 34. › One of the earliest ideas, termed the Specificity theory, was proposed by Descartes. › The theory suggested that specific pain fibers carry specific coding that discriminates between different forms of noxious and nonnoxious sensation. › The fundamental tenet of the Specificity Theory is that each modality has a specific receptor and associated sensory fiber (primary afferent) that is sensitive to one specific stimulus (Dubner et al. 1978) 34
  • 35. Moayedi M, Davis KD. Theories of pain: from specificity to gate control. J Neurophysiol 109: 5– 12, 2013. 35
  • 36. › The intensity theory, proposed by Sydenham, suggested that the intensity of the peripheral stimulus determines which sensation is perceived. › The theory defines pain, not as a unique sensory experience but rather, as an emotion that occurs when a stimulus is stronger than usual 36
  • 37. 37
  • 38. › Goldscheider suggested a neurophysiological model to describe this summation effect: repeated subthreshold stimulation or suprathreshold hyperintensive stimulation could cause pain. › But the theory lost support with Sherrington’s evolutionary framework regarding existence of sensory receptors that are specialized to respond to noxious stimuli, for which he coined the term “nociceptor”. 38
  • 39. › J. P. Nafe postulated this “quantitative theory of feeling” in 1929. › This theory ignored findings of specialized nerve endings and many of the observations supporting the specificity and/or intensive theories of pain. › The theory stated that any somaesthetic sensation occurred by a specific and particular pattern of neural firing and that the spatial and temporal profile of firing of the peripheral nerves encoded the stimulus type and intensity 39
  • 40. 40
  • 41. › In 1965, Ronald Melzack and Charles Patrick (Pat) Wall (Melzack and Wall 1965) proposed a theory that would revolutionize pain research › Melzack and Wall accepted that there are nociceptors (pain fibers) and touch fibers and proposed that that these fibers synapse in two different regions within the dorsal horn of the spinal cord: cells in the substantia gelatinosa and the “transmission” cells. 41
  • 42. › The model proposed that signals produced in primary afferents from stimulation of the skin were transmitted to three regions within the spinal cord: 1) the substantia gelatinosa, 2) the dorsal column, and 3) a group of cells that they called ‘transmission cells’. 42
  • 43. › They proposed that the gate in the spinal cord is the substantia gelatinosa in the dorsal horn, which modulates the transmission of sensory information from the primary afferent neurons to transmission cells in the spinal cord. › This gating mechanism is controlled by the activity in the large and small fibers. 43
  • 44. 44
  • 45. › Large-fiber activity inhibits (or closes) the gate, whereas small-fiber activity facilitates (or opens) the gate. › When nociceptive information reaches a threshold that exceeds the inhibition elicited, it “opens the gate” and activates pathways that lead to the experience of pain and its related behaviors. › Therefore, the Gate Control Theory of Pain provided a neural basis 45
  • 46. 46
  • 47. 47 Anesthesia Dolorosa: It is defined as perception of pain in an area that is anesthetic. A complication of post-treatment of TN. Deafferentation pain: Deafferentation pain is due to partial or complete interruption of peripheral or central afferent neural activity. › Examples are postherpetic neuralgia, central pain (pain after CNS injury), and phantom limb pain (pain felt in the region of an amputated body part).
  • 48. 48 › Congenital analgesia - nociceptive stimuli are not processed and/or integrated at a level of brain. › Patient does not feel any pain
  • 49. 49 › Referred pain is pain that is present in an area removed or distant from its point of origin. The area of referred pain is supplied by the nerves from the same spinal segment as the actual site of pain. › Phantom limb pain - is pain that an individual feels in amputated limb
  • 50. 50 Hemiagnosia : › It is a loss of ability to identify the source of pain on one side (the affected side) of the body. Application of painful stimuli to the affected side thus produces anxiety, moaning, agitation and distress but no attempt to withdrawal from or push aside the offending stimulus. › Hemiagnosia is associated with stroke that produces paralysis and hypersensitivity to painful stimuli in the affected side
  • 54. › Sambulingam: Concise Textbook of Physiology › Monheims: Textbook of Local Anaesthesia › Moayedi M, Davis KD. Theories of pain: from specificity to gate control. J Neurophysiol 109: 5–12, 2013. › Cambridge University Press; 978-0-521-87491-5 - Acute Pain Management › International Association for the Study of Pain: http://www.iasppain. org/Content/NavigationMenu/GeneralResourceLinks/PainDefinit ions/default.htm 54
  • 55. 55

Editor's Notes

  1. A detailed understanding of sensory perception and the experience of pain is fundamental to the practice of anesthesia.
  2. The words “pain” and “suffering” have often been used synonymously, but the experience of suffering has been differentiated from pain.
  3. or function understandable and necessary reaction that has an obvious protective function even in the absence of conscious perception.
  4. Physiologic pain alerts the individual to the presence of a potentially injurious environmental stimulus, such as a hot object, and initiates withdrawal reflexes that prevent or minimize tissue injury.
  5. detection of noxious or damaging stimuli Conduction: Passage of resulting sensory input from peripheral terminals to the spinal cord
  6. Two enzyme systems