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WHAT WE KNOW ABOUT PAIN
Husni Tanra
Hasanuddin University Faculty of Medicine
Departement of Anesthesiology, IC and
Pain Management. Makassar
Presented in the IVth National meeting of ISAPM , Manado 16-17 October 2015.
Understanding the Pain
Pain was
faithfully
transmitted
from
periphery to
brain
Specificity theory
Descartes
(17th Century)
Modified by AHT
Rene Descartes
 One unit of pain stimulus produce one
unit of pain.
 Pain system was a straight forward
channel from the peripheral to the brain.
 Nervous System is just like
 “a church bell system”
 “a hard wire system”
 No Modulation
Cartesian model
Mechanistic concept
Progress in understanding pain
-1965-
VIth Worid Congres on Pain in Adelaid, Australia 1990
2. Gate Control Theory
Aβ fiber
C fiber
(Melzack & Wall, 1965)
First central transmission cell
Pain
Substantia gelatinosa
Gate Controle Theory Melzack & Wall
The beginning of Modulation
Placebo Effect (1966)
 Henry Knowles Beecher  Beecher
 Pioneering American
Anesthesiologist
 Medical Ethicist
 Investigator of
Placebo Effect
Modulation effect
Beecher
Prof. Hyodo
The Meaning of injury
1979 H. MERSKEY (psychiatric) proposed
pain definition, which was accepted by IASP
PAIN IS “AN UNPLEASANT SENSORY AND
EMOTIONAL EXPERIENCE ASSOCIATED WITH
ACTUAL OR POTENTIAL TISSUE DAMAGE, OR
DESCRIBED IN TERM OF SUCH DAMAGE”.
Why unpleasant?
Because pain is so important symptom that
human should not ignore it.
Cortex
Thalamus
Midbrain
Projection
To PGA
Brainstem
Reticular
formation
Spinothalamic
tract
Spinoreticular
tract
Dorsal horn
Of spinal cord
Cell body in
DRG
Noxious
stimulus
Nociceptors
C fiber
A fiber
Pain is unpleasant sensory and
emotional experience.
So, pain has two dimentions (physical
and psychological).
Normal Situation Limbic System
Sensitization Theory by C J. Woolf
in 1990
Allodynia
Hyperalgesia
Normal Situation
Innocuous
Sensation
Low intensity
Stimulation
High intensity
Stimulation
High threshold A 
and c fiber
nociceptors
Brief Pain
A
fiber
After Tissue Damage
Low threshold
mechanoreceptor A
Sensitized nociceptor
A and C fibers
Hyperexcitable of
DHN
Pain
Low intensity
stimulation
Allodynia Hyperalgesia
So, after the surgery there is a
change in NS
what we called:
“Neuro-Plasticity of the Nervous
System”
Neuroplasticty is defined as “ the capacity of neuron to
change their structure, function, or chemical profile” play
a key role in chronic pain disorders.
After the surgery, it occurs
plasticity of the
Nervous System
• HYPERALGESIA
• ALLODYNIA
Clinical Features of
Postoperative Pain
Primary
Hyperalgesia
Secondary
Hyperalgesia
Inflammed
area
Non-Inflammed
area
C. Woolf 1990
Among nociceptive pain, postoperative
pain is well understood.
• We know what causes it
• We know the mechanism
• We know how to treat it
• We know the best drugs for it
• We know mostly self limited
(Lema MJ, Department of Anesthesiology, Buffalo State University)
So, no more reason to feel pain after surgey
Nature of post operative pain
 Four out or five patients undergoing surgery
experiences postoperative pain
 86% of these patient rating
 Moderate
 Severe
 Extreme pain
 > 50% of patients report inadequate pain relief
 10% to 50% acute post operative pain may become
chronic, depending on the surgical procedure
Pain, ASHP advantage E-NEWSLETTER, March 2014
Our problem now days is not
Acute Pain
but
Chronic Pain
Phantom Limb Pain
 Feeling of pain in an absent
limb or locations where
sensory nerve roots have
been completely destroyed
 Pain without nociception
Post-Amputation
Pain
Phantom
Limb Pain
If postoperative pain is prototype of acute pain
Phantom limb pain is prototype of neuropathic
pain, or chronic pain.
The Paradigm Shift
 Peripheral  Central
 The brain as an active
organ
 Accounts for pain with no
physical pathology
 Reconceptualization of
“psychogenic pain”
Phantom Limb Pain is a „Pain
Memory‟!
 In 57% of subjects with phantom pain,
this resembled preamputation pain.
 “… somatosensory inputs of sufficient
intensity and duration can produce long-
lasting changes in central neural
structures”
Katz&Melzack, Pain 1990;43:319
Pain in Neuromatrix in the brain
(Melzack, 2001)Perception of a unified body
Continuous neural pattern
 Brain areas and structures that are involved in pain
processing
Pain Matrix
(Dillworth et al., 2012)
SomatoSensory
Cortices (SSC1&2)
Insular
Cortex (IC)
PreFrontal
Cortex (PFC)
Anterior
Cingulate
Cortex (ACC)
Thalamus
Hippocampus
Amygdala
Pain is Integrating of Sensory and
Emotional experiences
Thalamus
Pre Frontal cortex
(PFC)
Hippocampus
Insular cortex
(IC)
Primary / secondary
Somatosensor
Cortex (S1 & S2)
Anterior
Cingulated
Cortex (ACC)
Amygdala
Somatosensory
Cortices
Insular
Cortex
Prefrontal
Cortex
Anterior
Cingulate
Cortex
Thalamus
Signals from periphery and spinal cord
Hippocampus
Amygdala
Somatosensory
Cortices
Insular
Cortex
Prefrontal
Cortex
Anterior
Cingulate
Cortex
Thalamus
 Thalamus
Primary relay center for transmission to somato-
sensory and emotional signals
Hippocampus
Amygdala
Signals from periphery and spinal cord
 Anterior Cingulate Cortex (ACC)
 Affective/ emotional component
 (e.g. sense of suffering)
 Initiation and facilitation of coping behavior
Somatosensory
Cortices
Insular
Cortex
Prefrontal
Cortex
Anterior
Cingulate
Cortex
Thalamus
Hippocampus
Amygdala
Signals from periphery and spinal cord
 Prefrontal Cortex
 Cognitive aspects of pain
 Meaning of pain, what to do about the pain
Somatosensory
Cortices
Insular
Cortex
Prefrontal
Cortex
Anterior
Cingulate
Cortex
Thalamus
Hippocampus
Amygdala
Signals from periphery and spinal cord
 Somatosensory Cortices
 Primary (S1): Location of pain
 Secondary (S2): Severity and quality of pain
Somatosensory
Cortices
Insular
Cortex
Prefrontal
Cortex
Anterior
Cingulate
Cortex
Thalamus
Hippocampus
Amygdala
Signals from periphery and spinal cord
 Insular Cortex
 Survival instinct
 Active with the presence of threat
Lack of oxygen, pain, low blood sugar
Somatosensory
Cortices
Insular
Cortex
Prefrontal
Cortex
Anterior
Cingulate
Cortex
Thalamus
Hippocampus
Amygdala
Signals from periphery and spinal cord
 Hippocampus
 Aversive input pain memory
Somatosensory
Cortices
Insular
Cortex
Prefrontal
Cortex
Anterior
Cingulate
Cortex
Thalamus
Hippocampus
Amygdala
Signals from periphery and spinal cord
 Amygdala
 Excecution decision, what to do due to pain
Somatosensory
Cortices
Insular
Cortex
Prefrontal
Cortex
Anterior
Cingulate
Cortex
Thalamus
Hippocampus
Amygdala
Signals from periphery and spinal cord
Neuroanatomy of Pain
Main brain region
that activate
during a painful
experience,
highlighted as
bilaterally active but
with increased
activation on
contra lateral
hemispheres (orange)
Tracey & Mantyh 2007
Begitu pentingnya nyeri
dalam hidup kita, sehingga
seluruh Tubuh kita harus
dibertahu.
So, Where in the brain is the pain?
 The Philosopher, Bertrand Russell
was asked by his dentist, “where
does it hurt?”
“In my mind of course”, Russell
Replied
Pain is NOT experienced unless these brain
areas are active
NO BRAIN, NO PAIN
So,… we can conclude that
 There is no one pain area in the brain.
 But there are area that lay up or
correlate to pain location and intensity 
SENSORY DISCRIMINATIVE.
 Another different area that lay up or
active correlated to emotional power of
pain  LIMBIC SYSTEM AFFECTIVE
MOTIVATIONAL
So …”The bane of pain is
plainly in the brain.”
But where and to what extent.
It depends on :
1. Who was stimulated
2. The psychological state of the subject
when he/she was stimulated.
3. How much attention is paid to the
stimulus.
4. How much pain you expect to
experience.
 It depends on who was stimulated…
 It depends on…
the psychological state of the subject
when he/she was stimulated…
 It depends on…
how much attention is paid to the
stimulus…
It depends on…
how much pain you expect to
experience…
Take home message
 There is no pain area in the Brain but
there are area that correlate to .....
 Sensory- Discriminative:
oLocation, Modality, Intensity
Affective –Motivational
oHow unpleasant or upsetting is the pain?
oWhat will I do about the pain?
Pain has multidimensional
experience
1. sensory – discriminative
 Identifies the intensity, type and location of pain
2. Affective – motivational
 Assessing the injury the meaning of injury,
(Fear, anxiety or depression)
3. Emotional – behavioral component
 Attention, mood and behavioral due to pain.
Clinical Management of Pain
Multi-disciplinary Team Approach
16th Century
21st Century
Prior
experiences
From
symplicity
to
Complexity
Attention Mood
(Psychological
state)
Ecpectation
The
meaning
of pain
Pain
Experience
Noxious
stimulus
In other word
 Pain is how your brain
interpret the stimulus is
What we know about pain very new   prof husni

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What we know about pain very new prof husni

  • 1. WHAT WE KNOW ABOUT PAIN Husni Tanra Hasanuddin University Faculty of Medicine Departement of Anesthesiology, IC and Pain Management. Makassar Presented in the IVth National meeting of ISAPM , Manado 16-17 October 2015.
  • 3. Pain was faithfully transmitted from periphery to brain Specificity theory Descartes (17th Century) Modified by AHT
  • 4. Rene Descartes  One unit of pain stimulus produce one unit of pain.  Pain system was a straight forward channel from the peripheral to the brain.  Nervous System is just like  “a church bell system”  “a hard wire system”  No Modulation Cartesian model Mechanistic concept
  • 6. VIth Worid Congres on Pain in Adelaid, Australia 1990
  • 7. 2. Gate Control Theory Aβ fiber C fiber (Melzack & Wall, 1965) First central transmission cell Pain Substantia gelatinosa
  • 8.
  • 9. Gate Controle Theory Melzack & Wall The beginning of Modulation
  • 10. Placebo Effect (1966)  Henry Knowles Beecher  Beecher  Pioneering American Anesthesiologist  Medical Ethicist  Investigator of Placebo Effect Modulation effect
  • 11.
  • 13. 1979 H. MERSKEY (psychiatric) proposed pain definition, which was accepted by IASP PAIN IS “AN UNPLEASANT SENSORY AND EMOTIONAL EXPERIENCE ASSOCIATED WITH ACTUAL OR POTENTIAL TISSUE DAMAGE, OR DESCRIBED IN TERM OF SUCH DAMAGE”. Why unpleasant? Because pain is so important symptom that human should not ignore it.
  • 14. Cortex Thalamus Midbrain Projection To PGA Brainstem Reticular formation Spinothalamic tract Spinoreticular tract Dorsal horn Of spinal cord Cell body in DRG Noxious stimulus Nociceptors C fiber A fiber Pain is unpleasant sensory and emotional experience. So, pain has two dimentions (physical and psychological). Normal Situation Limbic System
  • 15. Sensitization Theory by C J. Woolf in 1990 Allodynia Hyperalgesia
  • 16. Normal Situation Innocuous Sensation Low intensity Stimulation High intensity Stimulation High threshold A  and c fiber nociceptors Brief Pain A fiber
  • 17. After Tissue Damage Low threshold mechanoreceptor A Sensitized nociceptor A and C fibers Hyperexcitable of DHN Pain Low intensity stimulation Allodynia Hyperalgesia
  • 18. So, after the surgery there is a change in NS what we called: “Neuro-Plasticity of the Nervous System” Neuroplasticty is defined as “ the capacity of neuron to change their structure, function, or chemical profile” play a key role in chronic pain disorders.
  • 19. After the surgery, it occurs plasticity of the Nervous System • HYPERALGESIA • ALLODYNIA Clinical Features of Postoperative Pain Primary Hyperalgesia Secondary Hyperalgesia Inflammed area Non-Inflammed area C. Woolf 1990
  • 20. Among nociceptive pain, postoperative pain is well understood. • We know what causes it • We know the mechanism • We know how to treat it • We know the best drugs for it • We know mostly self limited (Lema MJ, Department of Anesthesiology, Buffalo State University) So, no more reason to feel pain after surgey
  • 21. Nature of post operative pain  Four out or five patients undergoing surgery experiences postoperative pain  86% of these patient rating  Moderate  Severe  Extreme pain  > 50% of patients report inadequate pain relief  10% to 50% acute post operative pain may become chronic, depending on the surgical procedure Pain, ASHP advantage E-NEWSLETTER, March 2014
  • 22. Our problem now days is not Acute Pain but Chronic Pain
  • 23. Phantom Limb Pain  Feeling of pain in an absent limb or locations where sensory nerve roots have been completely destroyed  Pain without nociception Post-Amputation Pain Phantom Limb Pain If postoperative pain is prototype of acute pain Phantom limb pain is prototype of neuropathic pain, or chronic pain.
  • 24. The Paradigm Shift  Peripheral  Central  The brain as an active organ  Accounts for pain with no physical pathology  Reconceptualization of “psychogenic pain”
  • 25. Phantom Limb Pain is a „Pain Memory‟!  In 57% of subjects with phantom pain, this resembled preamputation pain.  “… somatosensory inputs of sufficient intensity and duration can produce long- lasting changes in central neural structures” Katz&Melzack, Pain 1990;43:319
  • 26. Pain in Neuromatrix in the brain (Melzack, 2001)Perception of a unified body Continuous neural pattern
  • 27.  Brain areas and structures that are involved in pain processing Pain Matrix (Dillworth et al., 2012) SomatoSensory Cortices (SSC1&2) Insular Cortex (IC) PreFrontal Cortex (PFC) Anterior Cingulate Cortex (ACC) Thalamus Hippocampus Amygdala
  • 28. Pain is Integrating of Sensory and Emotional experiences Thalamus Pre Frontal cortex (PFC) Hippocampus Insular cortex (IC) Primary / secondary Somatosensor Cortex (S1 & S2) Anterior Cingulated Cortex (ACC) Amygdala
  • 30. Somatosensory Cortices Insular Cortex Prefrontal Cortex Anterior Cingulate Cortex Thalamus  Thalamus Primary relay center for transmission to somato- sensory and emotional signals Hippocampus Amygdala Signals from periphery and spinal cord
  • 31.  Anterior Cingulate Cortex (ACC)  Affective/ emotional component  (e.g. sense of suffering)  Initiation and facilitation of coping behavior Somatosensory Cortices Insular Cortex Prefrontal Cortex Anterior Cingulate Cortex Thalamus Hippocampus Amygdala Signals from periphery and spinal cord
  • 32.  Prefrontal Cortex  Cognitive aspects of pain  Meaning of pain, what to do about the pain Somatosensory Cortices Insular Cortex Prefrontal Cortex Anterior Cingulate Cortex Thalamus Hippocampus Amygdala Signals from periphery and spinal cord
  • 33.  Somatosensory Cortices  Primary (S1): Location of pain  Secondary (S2): Severity and quality of pain Somatosensory Cortices Insular Cortex Prefrontal Cortex Anterior Cingulate Cortex Thalamus Hippocampus Amygdala Signals from periphery and spinal cord
  • 34.  Insular Cortex  Survival instinct  Active with the presence of threat Lack of oxygen, pain, low blood sugar Somatosensory Cortices Insular Cortex Prefrontal Cortex Anterior Cingulate Cortex Thalamus Hippocampus Amygdala Signals from periphery and spinal cord
  • 35.  Hippocampus  Aversive input pain memory Somatosensory Cortices Insular Cortex Prefrontal Cortex Anterior Cingulate Cortex Thalamus Hippocampus Amygdala Signals from periphery and spinal cord
  • 36.  Amygdala  Excecution decision, what to do due to pain Somatosensory Cortices Insular Cortex Prefrontal Cortex Anterior Cingulate Cortex Thalamus Hippocampus Amygdala Signals from periphery and spinal cord
  • 37. Neuroanatomy of Pain Main brain region that activate during a painful experience, highlighted as bilaterally active but with increased activation on contra lateral hemispheres (orange) Tracey & Mantyh 2007 Begitu pentingnya nyeri dalam hidup kita, sehingga seluruh Tubuh kita harus dibertahu.
  • 38. So, Where in the brain is the pain?  The Philosopher, Bertrand Russell was asked by his dentist, “where does it hurt?” “In my mind of course”, Russell Replied
  • 39. Pain is NOT experienced unless these brain areas are active
  • 40. NO BRAIN, NO PAIN
  • 41. So,… we can conclude that  There is no one pain area in the brain.  But there are area that lay up or correlate to pain location and intensity  SENSORY DISCRIMINATIVE.  Another different area that lay up or active correlated to emotional power of pain  LIMBIC SYSTEM AFFECTIVE MOTIVATIONAL
  • 42.
  • 43.
  • 44. So …”The bane of pain is plainly in the brain.” But where and to what extent.
  • 45. It depends on : 1. Who was stimulated 2. The psychological state of the subject when he/she was stimulated. 3. How much attention is paid to the stimulus. 4. How much pain you expect to experience.
  • 46.  It depends on who was stimulated…
  • 47.
  • 48.
  • 49.  It depends on… the psychological state of the subject when he/she was stimulated…
  • 50.
  • 51.  It depends on… how much attention is paid to the stimulus…
  • 52.
  • 53.
  • 54.
  • 55.
  • 56. It depends on… how much pain you expect to experience…
  • 57.
  • 58.
  • 59.
  • 60. Take home message  There is no pain area in the Brain but there are area that correlate to .....  Sensory- Discriminative: oLocation, Modality, Intensity Affective –Motivational oHow unpleasant or upsetting is the pain? oWhat will I do about the pain?
  • 61. Pain has multidimensional experience 1. sensory – discriminative  Identifies the intensity, type and location of pain 2. Affective – motivational  Assessing the injury the meaning of injury, (Fear, anxiety or depression) 3. Emotional – behavioral component  Attention, mood and behavioral due to pain.
  • 62. Clinical Management of Pain Multi-disciplinary Team Approach
  • 63. 16th Century 21st Century Prior experiences From symplicity to Complexity Attention Mood (Psychological state) Ecpectation The meaning of pain Pain Experience Noxious stimulus
  • 64. In other word  Pain is how your brain interpret the stimulus is