This document discusses the relationship between acute and chronic pain. It begins by looking at epidemiological data on chronic pain, finding it affects approximately 30-50% of people. Chronic pain is often neuropathic in nature and can develop after surgery or dental procedures. The document then examines chronic post-surgical pain (CPSP) in detail, outlining its 4-point clinical definition. Risk factors for developing CPSP include the severity of acute postoperative pain, with higher pain levels correlating with greater risk. The most consistent predictor is the level of pain experienced during the acute phase.
Evaluating the Relationship Between Acute and Chronic Pain
1. An Evaluation of the
Relationship Between
Acute and Chronic Pain
Can Acute Pain Become a Chronic
Problem?
Jennifer L. Gibbs MAS, DDS, PhD
New York University Department of Endodontics
12. Pain History
“The tooth
hurt for about
3 months
before the root
canal”
13. Pain History
“The tooth
hurt for about
3 months
before the root
canal”
“The
pain was so
bad after the
treatment I had
to go back and
get vicodin ”
14. Pain History
“The tooth “The root
hurt for about canal was one of
3 months the most painful
before the root experiences of
canal” my life”
“The
pain was so
bad after the
treatment I had
to go back and
get vicodin ”
15. Pain History
“The tooth “The root
hurt for about canal was one of
3 months the most painful
before the root experiences of
canal” my life”
“The
pain was so
bad after the
treatment I had
to go back and “The pain
get vicodin ” never really
went away”
16. Pain History
“The tooth “The root
hurt for about canal was one of
3 months the most painful
before the root experiences of
canal” my life”
“The
pain was so
bad after the
Pre-Op Pain
treatment I had
to go back and “The pain
get vicodin ” never really
went away”
17. Pain History
“The tooth “The root
hurt for about canal was one of
3 months the most painful
before the root experiences of
canal” my life”
“The
pain was so
bad after the
Pre-Op Pain
treatment I had
to go back and “The pain
get vicodin ” never really
went away”
Post-Op Pain
18. Pain History
“The tooth “The root
hurt for about canal was one of
3 months the most painful
before the root experiences of
canal” my life”
“The
pain was so
bad after the
Pre-Op Pain Intra-Op Pain
treatment I had
to go back and “The pain
get vicodin ” never really
went away”
Post-Op Pain
19. Pain History
“The tooth “The root
hurt for about canal was one of
3 months the most painful
before the root experiences of
canal” my life”
“The
pain was so
bad after the
Pre-Op Pain Intra-Op Pain
treatment I had
to go back and “The pain
get vicodin ” never really
went away”
Post-Op Pain
Chronic Pain?
37. Epidemiology/
Risk Factors
of Chronic
Pain
Neuropathic Pain: Pain
arising as a direct
consequence of a lesion
or disease affecting the
somatosensory system.
Image from:georgiapainphysicians.com
50. Epidemiology/
Risk Factors
of Chronic
4- Point Definition
Pain
of CPSP
Macrae and Davies, IASP Press 1999
51. Epidemiology/
Risk Factors
of Chronic
4- Point Definition
Pain
of CPSP
Pain Developed
After a Surgical
Procedure
Macrae and Davies, IASP Press 1999
52. Epidemiology/
Risk Factors
of Chronic
4- Point Definition
Pain
of CPSP
Pain Developed Pain of at Least
After a Surgical 2 Month
Procedure Duration
Macrae and Davies, IASP Press 1999
53. Epidemiology/
Risk Factors
of Chronic
4- Point Definition
Pain
of CPSP
Pain Developed Pain of at Least
After a Surgical 2 Month
Procedure Duration
Exclude the
Possibility that
Pain is
Continuing From
a Pre-Existing
Problem
Macrae and Davies, IASP Press 1999
54. Epidemiology/
Risk Factors
of Chronic
4- Point Definition
Pain
of CPSP
Pain Developed Pain of at Least
After a Surgical 2 Month
Procedure Duration
Exclude the
Other Causes Possibility that
for the Pain Pain is
Have Been Continuing From
Excluded a Pre-Existing
Problem
Macrae and Davies, IASP Press 1999
55. Epidemiology/
Risk Factors
of Chronic
4- Point Definition
Pain
of CPSP
Pain Developed Pain of at Least
After a Surgical 2 Month
Procedure Duration
Exclude the
Other Causes Possibility that
for the Pain Pain is
Have Been Continuing From
Excluded a Pre-Existing
Problem
Macrae and Davies, IASP Press 1999
56. Epidemiology/
Risk Factors
of Chronic
4- Point Definition
Pain
of CPSP
Pain Developed Pain of at Least
After a Surgical 2 Month
Procedure Duration
Exclude the
Other Causes Possibility that
for the Pain Pain is
Have Been Continuing From
Excluded a Pre-Existing
Problem
Macrae and Davies, IASP Press 1999
57. Epidemiology/
Risk Factors
of Chronic
4- Point Definition
Pain
of CPSP
Pain Developed
After a Surgical
Procedure
p Pain of at Least
2 Month
Duration
Exclude the
Other Causes Possibility that
for the Pain Pain is
Have Been Continuing From
Excluded a Pre-Existing
Problem
Macrae and Davies, IASP Press 1999
58. Epidemiology/
Risk Factors
of Chronic
4- Point Definition
Pain
of CPSP
Pain Developed
After a Surgical
Procedure
p Pain of at Least
2 Month
Duration
p
Exclude the
Other Causes Possibility that
for the Pain Pain is
Have Been Continuing From
Excluded a Pre-Existing
Problem
Macrae and Davies, IASP Press 1999
59. Epidemiology/
Risk Factors
of Chronic
4- Point Definition
Pain
of CPSP
Pain Developed
After a Surgical
Procedure
p Pain of at Least
2 Month
Duration
p
Exclude the
Other Causes
?p
Possibility that
for the Pain Pain is
Have Been Continuing From
Excluded a Pre-Existing
Problem
Macrae and Davies, IASP Press 1999
60. Epidemiology/
Risk Factors
of Chronic
4- Point Definition
Pain
of CPSP
Pain Developed
After a Surgical
Procedure
p Pain of at Least
2 Month
Duration
p
Exclude the
Other Causes
?p ?p
Possibility that
for the Pain Pain is
Have Been Continuing From
Excluded a Pre-Existing
Problem
Macrae and Davies, IASP Press 1999
66. Epidemiology/
Risk Factors
of Chronic
Pain
Ballantyne, et al., IASP Clinical Update, January 2011
67. Epidemiology/
Risk Factors
of Chronic
Pain
Ballantyne, et al., IASP Clinical Update, January 2011
68. Epidemiology/
Risk Factors
of Chronic
Pain
Individual
Predisposition
for CPSP
Bruce, J. et al., Pain 2003
69. Epidemiology/
Risk Factors
of Chronic
Pain
Individual
Predisposition
for CPSP
Bruce, J. et al., Pain 2003
70. Epidemiology/
Risk Factors
of Chronic
Pain
Individual
Predisposition
for CPSP
12%
Bruce, J. et al., Pain 2003
71. Epidemiology/
Risk Factors
of Chronic
Pain
Individual
Predisposition
for CPSP
12%
Bruce, J. et al., Pain 2003
72. Epidemiology/
Risk Factors
of Chronic
Pain
Individual
Predisposition
for CPSP
12%
9%
Bruce, J. et al., Pain 2003
73. Epidemiology/
Risk Factors
of Chronic
Pain
Individual
Predisposition
for CPSP
12%
p=0.12 x 0.09 =0.01 or 1%
9%
Bruce, J. et al., Pain 2003
74. Epidemiology/
Risk Factors
of Chronic
Pain
Individual
Predisposition
for CPSP
12%
p=0.12 x 0.09 =0.01 or 1%
Incidence of Chronic
Pain at Both Sites=
9%
18%
Bruce, J. et al., Pain 2003
75. Epidemiology/
Risk Factors
of Chronic
Pain
What are some of the
risk factors for CPSP?
Patient Surgery
Specific Specific
87. Epidemiology/
Risk Factors
of Chronic
Pain
What are some of the
risk factors for CPSP?
Patient Surgery
Specific Specific
88. Epidemiology/
Risk Factors
of Chronic
Surgery
Pain Specific
Longer complicated
surgeries associated
with higher incidence
of chronic pain
89. Epidemiology/
Risk Factors
of Chronic
Surgery
Pain Specific
MASTECTOMY +
RECONSTRUCTION 49%*
MASTECTOMY 31%
BREAST REDUCTION 22%
Wallace MS et al., Pain 1996
90. Epidemiology/
Risk Factors
of Chronic
Surgery
Pain Specific
SURGICAL ENDO 23.8%*
NON-SURGICAL ENDO 10.7%
Polycarpou N. et al., IEJ 2005
91. Epidemiology/
Risk Factors
of Chronic
Surgery
Pain Specific
Minimize Chances of
Nerve Injury By Surgical
Strategy
93. Epidemiology/
Risk Factors
of Chronic
Pain
1. The Trigeminal System
2. Use of LA in dental procedures
3. Biologically programmed
denervation
But Could Teeth Be Different?
Bennet G., J Oraf Pain 2004
94. Epidemiology/
Risk Factors
of Chronic
Pain
1. The Trigeminal System
2. Use of LA in dental procedures
Text
3. Biologically programmed
denervation
But Could Teeth Be Different?
Bennet G., J Oraf Pain 2004
95. Epidemiology/
Risk Factors
of Chronic
Pain
1. The Trigeminal System
2. Use of LA in dental procedures
3. Biologically programmed
denervation
But Could Teeth Be Different?
Bennet G., J Oraf Pain 2004
96. Epidemiology/
Risk Factors
of Chronic
Pain
Does CPSP Occur In
Endodontics?
Polycarpou N. et al., IEJ 2005
97. Epidemiology/
Risk Factors
of Chronic
Pain
Does CPSP Occur In
Endodontics?
Polycarpou N. et al., IEJ 2005
98. Epidemiology/
Risk Factors
of Chronic
Pain
Risk Factor OR 95% CI
Pre-op Pain 7.8 (1.7, 35.6)
Chronic Pain 4.5 (1.5, 13.5)
Inter Appt Pain 3.9 (1.4, 10.7)
Gender 4.5 (1.2, 16.4)
Surgery 4.0 (1.0, 14.6)
102. Epidemiology/
Risk Factors
of Chronic
Pain Conclusions
Chronic Post Surgical Pain (CPSP) can occur
after dental surgeries including RCT.
Management of Pain, Pre-Op, Intra-Op, and
Post-Op to Minimize Risk
Minimize Invasive Procedures to Minimize
Risk
103. Epidemiology/
Risk Factors
of Chronic
Pain In The Future
Inform Our Patients About the Risk Factors for
Chronic Pain After All Dental Procedures (RCT,
EXT, IMPLANT)
Estimate an Individuals Risk for Developing
CPSP
Using Atypical Analgesics (e.g. Gabapentin) in
High Risk Cases
Emphasis on preserving vital pulp when
possible???
104. Epidemiology/ Mechanisms of
Risk Factors of Acute and
Chronic Pain Chronic Pain
Imaging the
Brain in
Chronic Pain
111. Mechanisms
of Acute and
Chronic Pain
Ectopic Activity
Contributes to spontaneous pain
Occurs in damaged and adjacent undamaged neurons
Nerve!
Injury!
113. Mechanisms
of Acute and
Chronic Pain
Deafferentation
Somatotopic
Reorganization
More Spontaneously
Active Neurons
Increased Receptive
Field Size Hu et al., J Phys, 1986
114. Mechanisms
of Acute and Control
Chronic Pain
Induction of
Glial
Activity 7D Post Pulp Exp
Increased GFAP
Expression After
Pulp Exposure.
Stephenson & Byers Exp Neurol 1995
115. Mechanisms
of Acute and
Chronic Pain Conclusions
Multiple Mechanisms Contribute to
Development of Chronic Pain
In Animal Models Similar Mechanisms of
Pulpal Deafferentation and Other Types of
Nerve Injury
Biologically Pulpal Degeneration or Removal
Has the Potential to Cause Chronic Pain
116. Epidemiology/ Mechanisms of
Risk Factors of Acute and
Chronic Pain Chronic Pain
Imaging the
Brain in
Chronic Pain
Our arena as endodontists and generalists is usually acute pain. Toothache or odontalgia is one of the most common types of moderate-severe pain experienced by both adults and children. We know that acute tooth pain is causes a fairly dramatic disruption in activities of daily living, affecting work attendance, mood, ability to eat, and generally is causes stress and anxiety for the person experiencing it. -Explain word cloud-Acute pain management certainly has challenges- pulpal anesthesia can be incredibly difficult, and patient management can be challenging for the person experiencing an acute pulpitis. Although we would still benefit from evidence based research in management of acute odontogenic pain, for the most part, we can get someone out of pain. \n
Where we get lost as clinicians is what does it mean when the pain doesn’t go away. We want to get our patients out of pain. But is it possible that sometimes no matter what we do, some patients aren’t going to get better. \n
Where we get lost as clinicians is what does it mean when the pain doesn’t go away. We want to get our patients out of pain. But is it possible that sometimes no matter what we do, some patients aren’t going to get better. \n
Pain is subjective. It’s influenced by your current emotional state and your past experiences with injury. It means something different to every person. \nImportant to note in the definition that there’s a sensory component and an emotional component. You don’t actually have to experience tissue injury to experience pain. Examples: empathetic pain, phantom limb pain. \n
But we need a starting point- so let’s begin with this statement. The burden on chronic pain is so profound that there is a big push to identify preventive factors that could prevent patients from developing chronic pain.\n
Because it’s hard to determine when the healing phase has ended a more common clinical definition involved a fixed time of persistent pain after it’s onset. \n
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Usually between 3 months or 6 months. Chronic back pain it’s 6 months. For herpes zoster/PHN it’s 3 months. For chronic post-surgical pain in medicine it’s usually 2 months after surgery. Since, to my knowledge we don’t have a strong evidence base for this in endodontics, it seems\n
She had a deep filling done that was symptomatic and got worse and worse until the root canal was performed. The more patients I see, the more familiar this story becomes. The question that comes to my mind is whether this patients’ cumulative pain experience contributed to her chronic pain. We’re going to discuss in clinical entity from the medical literature called “chronic post-surgical pain”. \n
She had a deep filling done that was symptomatic and got worse and worse until the root canal was performed. The more patients I see, the more familiar this story becomes. The question that comes to my mind is whether this patients’ cumulative pain experience contributed to her chronic pain. We’re going to discuss in clinical entity from the medical literature called “chronic post-surgical pain”. \n
She had a deep filling done that was symptomatic and got worse and worse until the root canal was performed. The more patients I see, the more familiar this story becomes. The question that comes to my mind is whether this patients’ cumulative pain experience contributed to her chronic pain. We’re going to discuss in clinical entity from the medical literature called “chronic post-surgical pain”. \n
She had a deep filling done that was symptomatic and got worse and worse until the root canal was performed. The more patients I see, the more familiar this story becomes. The question that comes to my mind is whether this patients’ cumulative pain experience contributed to her chronic pain. We’re going to discuss in clinical entity from the medical literature called “chronic post-surgical pain”. \n
She had a deep filling done that was symptomatic and got worse and worse until the root canal was performed. The more patients I see, the more familiar this story becomes. The question that comes to my mind is whether this patients’ cumulative pain experience contributed to her chronic pain. We’re going to discuss in clinical entity from the medical literature called “chronic post-surgical pain”. \n
She had a deep filling done that was symptomatic and got worse and worse until the root canal was performed. The more patients I see, the more familiar this story becomes. The question that comes to my mind is whether this patients’ cumulative pain experience contributed to her chronic pain. We’re going to discuss in clinical entity from the medical literature called “chronic post-surgical pain”. \n
She had a deep filling done that was symptomatic and got worse and worse until the root canal was performed. The more patients I see, the more familiar this story becomes. The question that comes to my mind is whether this patients’ cumulative pain experience contributed to her chronic pain. We’re going to discuss in clinical entity from the medical literature called “chronic post-surgical pain”. \n
She had a deep filling done that was symptomatic and got worse and worse until the root canal was performed. The more patients I see, the more familiar this story becomes. The question that comes to my mind is whether this patients’ cumulative pain experience contributed to her chronic pain. We’re going to discuss in clinical entity from the medical literature called “chronic post-surgical pain”. \n
By some definitions this was already a chronic pain patient before she even got the initial root canal treatment. Now, she certainly is a chronic pain patient. \n\nThis case raises so many questions- it sounds like it was odontogenic pain to start with... Was it her cumulative experience of pain that led her to have this persistent pain problem now. If so would aggressively treating her acute pain have prevented her current chronic pain?\n\nDoes she have TMD and would intervention to control TMD pain aid her “tooth” pain?\n\nIs she genetically susceptible to chronic pain? I think the take home message today is that “It’s complicated”. And the more we learn about pain the more complicated it gets. I’m going to raise a lot of questions that I don’t necessarily have answers to, but I will present our current evidence and theories of chronic pain that I hope will shed some light on these important questions. \n\nI think this is a case of chronic post-treatment pain. \n
Who gets it, what are the risk factors. Because chronic pain is so pervasive, I’m going to focus on the model of \n
Who gets it, what are the risk factors. Because chronic pain is so pervasive, I’m going to focus on the model of \n
Who gets it, what are the risk factors. Because chronic pain is so pervasive, I’m going to focus on the model of \n
Who gets it, what are the risk factors. Because chronic pain is so pervasive, I’m going to focus on the model of \n
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Some other characteristics of neuropathic pain include the observation that nerve damage is necessary but not sufficient to generate this type of pain. That is not everyone who has nerve damage will develop neuropathic pain and in fact the number that will is actually quite small. So we can take the case of painful diabetic neuropathy. Of all diabetic patients approximately 50% will develop neuropathy meaning altered sensory thresholds, usually manifesting as decreased sensitivity to mechanical or thermal sensitivity, relative to age matched healthy controls. Now neuropathy does not necessarily mean pain. Of those that exhibit neuropathy only 20-30% report pain meaning the patient now reports pain that can be spontaneous, dysesthesias, and thermal or mechanical allodynia or hyperalgesia. Most chronic post surgical pain is neuropathic \n\n
Trauma is another important source for neuropathic pain. Car accidents can cause damage to peripheral or central neurons. It’s important to remember that surgery is a type of trauma. Despite best efforts surgery can result in chronic post-surgical pain. The general consensus at this point is that this type of pain is neuropathic, resulting from some type of nerve injury. We’ll explore this topic more thoroughly in the talk\n
Trauma is another important source for neuropathic pain. Car accidents can cause damage to peripheral or central neurons. It’s important to remember that surgery is a type of trauma. Despite best efforts surgery can result in chronic post-surgical pain. The general consensus at this point is that this type of pain is neuropathic, resulting from some type of nerve injury. We’ll explore this topic more thoroughly in the talk\n
Trauma is another important source for neuropathic pain. Car accidents can cause damage to peripheral or central neurons. It’s important to remember that surgery is a type of trauma. Despite best efforts surgery can result in chronic post-surgical pain. The general consensus at this point is that this type of pain is neuropathic, resulting from some type of nerve injury. We’ll explore this topic more thoroughly in the talk\n
Population based surveys of the prevalence of neuropathic pain symptoms. Torrence= great britain. Bouhassira= france. \n
Population based surveys of the prevalence of neuropathic pain symptoms. Torrence= great britain. Bouhassira= france. \n
Population based surveys of the prevalence of neuropathic pain symptoms. Torrence= great britain. Bouhassira= france. \n
Population based surveys of the prevalence of neuropathic pain symptoms. Torrence= great britain. Bouhassira= france. \n
Population based surveys of the prevalence of neuropathic pain symptoms. Torrence= great britain. Bouhassira= france. \n
Population based surveys of the prevalence of neuropathic pain symptoms. Torrence= great britain. Bouhassira= france. \n
Again with the definitions....When it comes to actually defining things, things get complicated. \n
Some of these items are more difficult to define than others. \n
Some of these items are more difficult to define than others. \n
Some of these items are more difficult to define than others. \n
Some of these items are more difficult to define than others. \n
Let’s think about our case and whether using the criteria, if it could be classified as CPSP\n
Let’s think about our case and whether using the criteria, if it could be classified as CPSP.\nFirst 2, are clear. “other causes for pain”- confirm no other odontogenic causes. Confirm that root canal treatment is successful. We could consider doing a retreatment to be sure? Confirm that TMD is not contributing to pain. \n“pre-existing condition” - tricky. Seems unlikely that TMD would have caused the symptoms originally leading to the root canal. Story sounds consistent with irreversible pulpitis. We don’t have all the information now, but it’s possible this is a CPSP. \n
Let’s think about our case and whether using the criteria, if it could be classified as CPSP.\nFirst 2, are clear. “other causes for pain”- confirm no other odontogenic causes. Confirm that root canal treatment is successful. We could consider doing a retreatment to be sure? Confirm that TMD is not contributing to pain. \n“pre-existing condition” - tricky. Seems unlikely that TMD would have caused the symptoms originally leading to the root canal. Story sounds consistent with irreversible pulpitis. We don’t have all the information now, but it’s possible this is a CPSP. \n
Let’s think about our case and whether using the criteria, if it could be classified as CPSP.\nFirst 2, are clear. “other causes for pain”- confirm no other odontogenic causes. Confirm that root canal treatment is successful. We could consider doing a retreatment to be sure? Confirm that TMD is not contributing to pain. \n“pre-existing condition” - tricky. Seems unlikely that TMD would have caused the symptoms originally leading to the root canal. Story sounds consistent with irreversible pulpitis. We don’t have all the information now, but it’s possible this is a CPSP. \n
Let’s think about our case and whether using the criteria, if it could be classified as CPSP.\nFirst 2, are clear. “other causes for pain”- confirm no other odontogenic causes. Confirm that root canal treatment is successful. We could consider doing a retreatment to be sure? Confirm that TMD is not contributing to pain. \n“pre-existing condition” - tricky. Seems unlikely that TMD would have caused the symptoms originally leading to the root canal. Story sounds consistent with irreversible pulpitis. We don’t have all the information now, but it’s possible this is a CPSP. \n
A quick word on nomenclature. There are other terms to describe the phenomena I’m describing today. Phantom Tooth Pain was first described in the late 70s. The main distinction I’m making today is to use a terminology that’s rapidly gaining traction in the medical field, and to see if this might help us to better see through the murk. Atypical odontalgia is still difficult to define clinically. \n
It is thought that nerve damage is necessary, but not sufficient to cause CPSP. Most surgical procedures involve some damage to major or minor nerve branches. There is the potential however, that chronic inflammatory process could contribute. \n
\n
When you look at the amount of severe, disabling chronic pain, it’s much less, but still significant. \n
They are starting to be universal recognition that dental \n
The surgeries at both site are capable of producing chronic pain. Marshal Devor was looking at this data and made some interesting observations. If the probability was purely related to the injury at the site then the chance of having chronic pain at both sites should be less than either one. \n
The surgeries at both site are capable of producing chronic pain. Marshal Devor was looking at this data and made some interesting observations. If the probability was purely related to the injury at the site then the chance of having chronic pain at both sites should be less than either one. \n
The surgeries at both site are capable of producing chronic pain. Marshal Devor was looking at this data and made some interesting observations. If the probability was purely related to the injury at the site then the chance of having chronic pain at both sites should be less than either one. \n
The surgeries at both site are capable of producing chronic pain. Marshal Devor was looking at this data and made some interesting observations. If the probability was purely related to the injury at the site then the chance of having chronic pain at both sites should be less than either one. \n
The surgeries at both site are capable of producing chronic pain. Marshal Devor was looking at this data and made some interesting observations. If the probability was purely related to the injury at the site then the chance of having chronic pain at both sites should be less than either one. \n
The surgeries at both site are capable of producing chronic pain. Marshal Devor was looking at this data and made some interesting observations. If the probability was purely related to the injury at the site then the chance of having chronic pain at both sites should be less than either one. \n
\n
What we’re talking about is pre-operative pain and post-operative pain. The presence of preoperative pain, or its intensity or duration, is a risk factor for the development of severe early acute postoperative pain, as well as long term post-surgical pain, and ultimately the development of chronic pain. It’s likely that the mechanisms we’ll talk about in a bit, that occur in acute pain, if left unchecked cause changes to the nervous system that put the patient at risk for chronic pain. \n
I think we’re very familiar with this concept in endodontics. We have a lot of studies showing how pre-operative pain predicts post-operative pain. Here’s one example that stands out for the large number of cases involved. \n1191 cases, looking at post-operative pain at 7days after completion of RCT.\nWhat’s missing in our literature is what happens to these patients after 7 days. \n
Like many chronic pain conditions females are generally at a greater risk of developing CPSP\n
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Numerous studies have shown the relationship between pre-op anxiety levels and post-operative or chronic post-surgical pain.\n\nCatastrophizing: a tendency to exaggerated pessimism about outcome. \n\nFear of pain. \n
Catecholamine-o-methyl-transferase in an enzyme that’s involved in the regulation of catecholamine and enkephalin levels. There are several natural variations in the gene, called SNPs that occur frequently in the population. Researchers in North Carolina looked at whether experimental pain, and the development of TMD was related to the expression of these common mutations \n
Catecholamine-o-methyl-transferase in an enzyme that’s involved in the regulation of catecholamine and enkephalin levels. There are several natural variations in the gene, called SNPs that occur frequently in the population. Researchers in North Carolina looked at whether experimental pain, and the development of TMD was related to the expression of these common mutations \n
Catecholamine-o-methyl-transferase in an enzyme that’s involved in the regulation of catecholamine and enkephalin levels. There are several natural variations in the gene, called SNPs that occur frequently in the population. Researchers in North Carolina looked at whether experimental pain, and the development of TMD was related to the expression of these common mutations \n
The studies I just described are just one example of a gene shown to be involved in pain experience. There are many others including the gene that encodes the serotonin transporter, IL-1B and others. Important to point out that these studies don’t show whether the gene is affecting pain itself or associated with a pathological state that has pain as a comorbidity. Also there is not yet any specific association with any of these genes and CPSP.\n
\n
Minimally invasive procedures that spare nerve injury as much as possible are recommended. \n
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Small sample size, but suggestive of the fact that less invasive procedures are less likely to cause chronic pain. Perhaps a more realistic example is RCT on #30 and #31 is less likely to cause chronic pain than EXT and placement of 2 implants. Highly speculative of course. \n\n
Surgeries that avoid major nerve damage are less likely to have CPSP. I think we have a good understanding of this in endodontics. We’re more worried about surgeries that impinge on mental nerve or IAN nerve. However any trauma, surgical or otherwise to soft tissue, bone, etc. can damage nerve endings and lead to chronic pain. This line of research has led to recommendations for preventive strategies that we’ll discuss at the end.\n\n
\n
Maybe somehow the nerves in the trigeminal system are different and less susceptible to the mechanisms which occur after nerve injury – we actually know there are potentially important differences between the TG and the spinal system- example sprouting of sympathetic fibers into the DRG after nerve injury but not into the TG. On the other hand we know there’s plenty of neuropathic pain in the head and neck so this really isn’t that great of an argument.\n\n
The eruption and exfoliation of primary teeth represents one of the few examples of a biologically programmed denervation that occurs. Maybe there’s some evolutionary protective mechanisms to against the neuroplastic changes contributing to chronic pain in pulpal neurons. \n\n
We’re really good at local anesthesia. Unlike most of our medical colleagues, we perform almost all of our procedures under local anesthesia. Preventing the barrage of peripheral signal into the central nervous system may reduce the incidence of chronic pain. Evidence of this from the work of Sharon Gordon in 3rd molar ext studies. That same argument could be used to speculate on how chronic pain could develop in a typical toothache case. Lots of pre-op pain, barriers to receiving care, difficult local anesthsia when they do come in for treatment, sever post-op pain due to inadequate post-op analgesics. \n\n
Attempted to recall 400 sequential patients who had undergone surgical or non-surgical rct. Only recalled about half of them so there could be some bias in the study based on the patients they were able to recall; i.e. those with more pain were more likely to come in. Patients were brought in for a clinical and radiographic exam and evaluated for any persistent disease. Pre-op pain was recorded prospectively which makes this a stronger study. Another limitation of this study and pretty much any study that looks at endodontic outcomes is that we’re limited in our ability to detect disease. Just because there is no detectable disease does that mean there really isn’t any? Maybe with better diagnostics this number could go down. However that fact remains that although the number might go down it likely will not go down to 0. So even if it were 2%, 3%, 1% we would still have a serious problem on our hands given the MILLIONS of procedures performed annually. \n\n
It’s good to think back to our “chicken or egg” problem when thinking about this data. Did some of these patients have something else going on that looked like odontogenic pain, which then did not resolve with endodontics. \n\n
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Can we prevent the progression to CPSP?\nExample of successful intervention to prevent post-op pain. Important point that this was multimodal analgesia. \nRemember where gabapentin is working, centrally. There’s a lot of examples of unsuccessful trials, many with NSAIDS and Local anesthetics. Is the gabapentin key? Unsure. \n
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Sprouting of CGRP fibers evident after drilling into cervical dentin. Hardware changes.\n
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Neuroplasticity occurs on a larger scale with nerve injury. We’re going to talk more about neuroplasticity in the last part of the talk where we talk about brain imaging studies. \n
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Let’s go back to the current definition of pain: “ An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.” Peripheral Nociception- the act of a painful stimulus activating peripheral neurons (example of giving an injection) pain. However, the actual experience of pain is influenced by a number of factors. The same stimulus can be interpreted differently based on a number of factors- a relaxed person versus an anxious person, a distracted person versus someone anticipating the painful response. Also, there are instances when you don’t need the peripheral input at all to experience pain. Consider phantom limb syndrome. In that case the peripheral input is completely absent but the experience of pain is quite real. Therefor discussion of the brain is essential to our understanding of chronic pain. \n\n\n\n
Non invasive imaging of the human brain has allowed for numerous opportunities to explore brain function both in health and disease. There are several ways to image the brain including MEG, PET, EEG but the most common is functional MRI, an example of which is being shown in the image above. fMRI measures brain activity by measuring small changes in blood flow. In addition to functional activity you can also measure structural changes in the brain\n
Examples of brain imaging studies have made it into mainstream media. For example this study of London Taxi Drivers. \nIn order to qualify as a licensed London taxi driver, a trainee must learn the complex and irregular layout of London's ∼25,000 streets (Figure 1) within a 6-mile radius of Charing Cross train station, along with the locations of thousands of places of interest. This spatial learning is known as acquiring “the Knowledge” and typically takes between 3 and 4 years, leading to a stringent set of examinations, called “appearances,” which must be passed in order to obtain an operating license from the Public Carriage Office (PCO, the official London taxi-licensing body). This comprehensive training and qualification procedure is unique among taxi drivers anywhere in the world.\n\nIn this study Woollett and Maguire imaged brains of persons entering the training program and were able to compare those who successfully completed the training, those who didn’t , and a control group. What they see is a specific increase the grey matter volume in the posterior hippocampal grey area. \n\nFor the first time we’re able to quantitatively measure changes in the brain that correlate with changes in how the brain is functioning. You could imaging that imaging dental students brains before and after learning the waxing during the first years you might see some changes in brain structure involved in fine motor skills. \n\n
Examples of brain imaging studies have made it into mainstream media. For example this study of London Taxi Drivers. \nIn order to qualify as a licensed London taxi driver, a trainee must learn the complex and irregular layout of London's ∼25,000 streets (Figure 1) within a 6-mile radius of Charing Cross train station, along with the locations of thousands of places of interest. This spatial learning is known as acquiring “the Knowledge” and typically takes between 3 and 4 years, leading to a stringent set of examinations, called “appearances,” which must be passed in order to obtain an operating license from the Public Carriage Office (PCO, the official London taxi-licensing body). This comprehensive training and qualification procedure is unique among taxi drivers anywhere in the world.\n\nIn this study Woollett and Maguire imaged brains of persons entering the training program and were able to compare those who successfully completed the training, those who didn’t , and a control group. What they see is a specific increase the grey matter volume in the posterior hippocampal grey area. \n\nFor the first time we’re able to quantitatively measure changes in the brain that correlate with changes in how the brain is functioning. You could imaging that imaging dental students brains before and after learning the waxing during the first years you might see some changes in brain structure involved in fine motor skills. \n\n
There are numerous examples that have made it to mainstream media describing how the \n
There are numerous examples that have made it to mainstream media describing how the \n
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What came out of this line of research is called “The Pain Matrix”.The pain matrix is a network of connected structures distributed throughout the brain. Includes structures involved in sensory discrimination as well as structures involved in affect, cognition and evaluation. These areas of the brain consistently light up when a painful stimulus is applied in an experimental setting. However, there is a lot of individual variability in this matrix. Also important to note that there isn’t one pain center in the brain. So ablating or taking out one of these structures or even all of them wouldn’t necessarily eliminate pain. In other words these structures might not be necessary for the experience of pain.\n
The areas that are pain matrix are the most frequent to show activity in pain studies, but this is only relevant to acute simulated pain in healthy volunteers. What happens in chronic pain is more complex. Different etiology, different anatomical structures involved, different time courses. \n
Vania Apkarian’s group took a different experimental approach. They reasoned that the most burdensome and clinically relevant aspect of pain for the chronic pain patient is the experience of spontaneous pain. So they put patients in the scanner and they would record their spontaneous pain while their brain was imaged, without any external stimulation. This allowed them measure what parts of their brain were active when they were in pain as well as correlate brain activity with spontaneous pain intensity. What they found was that the brain areas activated by acute pain stimuli were only marginally associated with the experience of spontaneous pain in chronic pain patients, and seemed to be activated upon initiation of a bout of spontaneous pain. A distinct area of the brain was active during sustained periods of intense spontaneous pain called located within the medial prefrontal cortex. This brain areas is involved in emotion, cognition, and motivation. Based on other work that associated brain activities with this region, the researchers hypothesize that this activity reflects a negative emotional state in reference to the self. Perhaps suffering. \n
In another series of studies by Vania Apkarian, again using patients with Chronic Back Pain, they evaluated gross changes in brain morphology in pain patients versus age matched healthy controls. What they found was surprising. First, they found that total volume of grey matter was reduced in the pain patients compared to the healthy controls. They had to take into account age because as we age our grey matter volume decreases by about 0.5% per year. They found that having chronic back pain caused an brain matter atrophy equivalent to 10-20 years of aging.They also looked at specific regions of grey matter loss and found the greatest loss in the DLPFC as well as the thalamus. Both of these regions are activated with acute pain.They also found the loses in the DLPFC were more significant in patients with neuropathic back pain rather than non-neuropathic back pain. It was interesting that the DLPFC seemed to be more significantly related to chronic pain since this area is involved in working memory and executive function. So complex decision making- this area is involved in deciding which responses should be executed. Pain in some way seemed to be overloading the decision making system and possibly atrophying the system.\n
In another series of studies by Vania Apkarian, again using patients with Chronic Back Pain, they evaluated gross changes in brain morphology in pain patients versus age matched healthy controls. What they found was surprising. First, they found that total volume of grey matter was reduced in the pain patients compared to the healthy controls. They had to take into account age because as we age our grey matter volume decreases by about 0.5% per year. They found that having chronic back pain caused an brain matter atrophy equivalent to 10-20 years of aging.They also looked at specific regions of grey matter loss and found the greatest loss in the DLPFC as well as the thalamus. Both of these regions are activated with acute pain.They also found the loses in the DLPFC were more significant in patients with neuropathic back pain rather than non-neuropathic back pain. It was interesting that the DLPFC seemed to be more significantly related to chronic pain since this area is involved in working memory and executive function. So complex decision making- this area is involved in deciding which responses should be executed. Pain in some way seemed to be overloading the decision making system and possibly atrophying the system.\n
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Again, the same group studied how chronic pain patients performed on a specific task that involved emotional decision making. Patients performed a test called the “Iowa Gambling Task” where they drew cards from four decks of cards. Two of the decks were “good” decks (c and d) and two of the decks were “bad” decks (a and b) in the long run. Then they measure how long it takes the subject to figure out which decks pay off for them in the long run. It’s also interesting to note that healthy persons given acute pain stimuli are not affected in performing this task. This effect seems to be specific to chronic pain\n
Again, the same group studied how chronic pain patients performed on a specific task that involved emotional decision making. Patients performed a test called the “Iowa Gambling Task” where they drew cards from four decks of cards. Two of the decks were “good” decks (c and d) and two of the decks were “bad” decks (a and b) in the long run. Then they measure how long it takes the subject to figure out which decks pay off for them in the long run. It’s also interesting to note that healthy persons given acute pain stimuli are not affected in performing this task. This effect seems to be specific to chronic pain\n
This study looked at patients with chronic osteoarthritis pain in one hip. Like many other studies they found a loss in grey matter volume in particular areas of the brain. Hip replacement actually improves pain to a profound extent in most of these patients so they were able to scan these patients before and after hip replacement and determine whether pain relief reverses the loss of grey matter. The first bar is before hip replacement, the second is 6-8 weeks after, and the last is 16-18 weeks after surgery. The third scan showed a significant increase in grey matter volume relative to the first and second scans. Suggests that the changes observed in chronic pain patients are reversible.\n
The activation in the pre-frontal cortex that was related to pain in CBP patients was much less so in other pain states. \n
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One mature atlantic salmon participated in the study. The salmon was not alive at the time of the study. The salmon was shown a series of photographs depicting human individuals in social situations with a specified emotional valence\nIn fMRI, the problem is particularly severe. An MRI scan divides the brain up into cubic units called voxels. There are over 40,000 in a typical scan. Most fMRI analysis treats every voxel independently, and tests to see if each voxel is "activated" by a certain stimulus or task. So that's at least 40,000 separate comparisons going on - potentially many more, depending upon the details of the experiment. The conclusion of this “study” is that correction for multiple comparisons is essential for brain imaging studies. \n\n
Cost is about $500-$600 for a research scan. As a consequence large studies are often cost prohibitive. \n
The Human Connectome Project (HCP) is a project to construct a map of the complete structural and functional neural connections in vivo within and across individuals. The HCP represents the first large-scale attempt to collect and share data of a scope and detail sufficient to begin the process of addressing deeply fundamental questions about human connectional anatomy and variation. Uses Diffusion Tensor Imaging Technique that is still a type of neuroimaging, but not a lot of functional data techniques. Scientist at MIT are attemption to map every connection in the human brain. There are about 100 billion neurons in the brain and each neuons makes about 7000 synpatic connections with other neurons so this is an incredible challenge. As important and a bigger project than the human genome project. \n
Much of the brain imaging data we have so far is not so different from phrenology. Phrenology was a “scientific” area of study popular in the first half of the 19th century where it was thought measuring the skull would reveal certain truths about the functioning of the brain. By not accounting for the complex interactions and communication between individual neurons and brain regions and how they communicate, we’re running the risk of \n
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So different mechanisms. \n
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So where does this leave us? We spoke about some of the risk factors for chronic pain, we dug into what we know about CPSP and how it may or may not be relevant to us in dentistry. And finally we spoke about what we’ve learned about how the brain changes when it’s in pain. \n
Like many diseases, preventive strategies are often more useful than trying to reverse the disease. \n
I think is some respects you might find this talk unsatisfying, because there is so much that we don’t know. There’s not much practical advice to give at this point, but it’s more a glimpse into what I hope we’ll be able to understand in the future. \n
Avoid damaging nerves- non-neurotoxic material for obturating lower molars?\nGet patients out of pain : I’m preaching to the choir with this one in this venue. That’s what we do and we do it very well. However, what I worry about is all the patients we don’t see. \nIntra-op pain good anesthesia techniques, pre-medicate with ibuprofen, adjunctive approach like nitrous when needed\nPost-op pain: Ken Hargreaves presentation would cover much of this. Really need more research. What kind of analgesics? Does someone with vital or partially vital pulp need different analgesics than someone with an abscess. \n
Avoid damaging nerves- non-neurotoxic material for obturating lower molars?\nGet patients out of pain : I’m preaching to the choir with this one in this venue. That’s what we do and we do it very well. However, what I worry about is all the patients we don’t see. \nIntra-op pain good anesthesia techniques, pre-medicate with ibuprofen, adjunctive approach like nitrous when needed\nPost-op pain: Ken Hargreaves presentation would cover much of this. Really need more research. What kind of analgesics? Does someone with vital or partially vital pulp need different analgesics than someone with an abscess. \n
Avoid damaging nerves- non-neurotoxic material for obturating lower molars?\nGet patients out of pain : I’m preaching to the choir with this one in this venue. That’s what we do and we do it very well. However, what I worry about is all the patients we don’t see. \nIntra-op pain good anesthesia techniques, pre-medicate with ibuprofen, adjunctive approach like nitrous when needed\nPost-op pain: Ken Hargreaves presentation would cover much of this. Really need more research. What kind of analgesics? Does someone with vital or partially vital pulp need different analgesics than someone with an abscess. \n
Avoid damaging nerves- non-neurotoxic material for obturating lower molars?\nGet patients out of pain : I’m preaching to the choir with this one in this venue. That’s what we do and we do it very well. However, what I worry about is all the patients we don’t see. \nIntra-op pain good anesthesia techniques, pre-medicate with ibuprofen, adjunctive approach like nitrous when needed\nPost-op pain: Ken Hargreaves presentation would cover much of this. Really need more research. What kind of analgesics? Does someone with vital or partially vital pulp need different analgesics than someone with an abscess. \n