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Neuroplasticity and Sensitization
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Neuroplasticity and Sensitization Charles S. Greene JADA 2009;140(6):676-678 10.14219/jada.archive.2009.0253 The following resources related to this article are available online at jada.ada.org (this information is current as of July 3, 2014): Updated information and services including high-resolution figures, can be found in the online version of this article at: http://jada.ada.org/content/140/6/676
This article cites 6 articles, 3 of which can be accessed free: http://jada.ada.org/content/140/6/676/#BIBL Information about obtaining reprints of this article or about permission to reproduce this article in whole or in part can be found at: http://www.ada.org/990.aspx
Copyright © 2014 American Dental Association. All rights reserved. Reproduction or republication strictly prohibited without prior written permission of the American Dental Association.
Downloaded from jada.ada.org on July 3, 2014
CLINICAL PRACTICE
PA I N U P D AT E
Neuroplasticity and sensitization Charles S. Greene, DDS
Editor’s note: This new feature, which will appear quarterly, reviews pain phenomena as they pertain to dentistry.
CLINICAL PROBLEM
patient visits a new dental office with a complaint of pain in the maxillary left quadrant. The patient’s medical history reveals that tooth no. 13 had received a restoration, which was followed by some pain. The next steps performed by the patient’s previous dentist included removing the restoration and placing a temporary zinc oxide eugenol restoration, preparing for the crown, seating the crown, performing root canal treatment, performing an apicoectomy and extracting the tooth. The patient reports that some degree of pain persisted intermittently throughout these procedures and became worse over time. The pain now is severe and has continued for six months after extraction and socket healing. What is the most likely explanation for this series of events?
A
EXPLANATION
This fairly common phenomenon is an example of “neuroplasticity,” a term that describes how the nervous system changes in response to painful 676
JADA, Vol. 140
http://jada.ada.org
stimuli. To understand this process, dentists need to know that the simple Cartesian model of a painful stimulus leading to a proportional response has been replaced by a much more complex model of nervous system behavior. This pain update describes the new model, with an emphasis on how it can affect dental practice. Cartesian model. The Cartesian model (named after the 17th century French philosopher René Descartes) is based on the notion of a hardwired nervous system, in which pain signals are carried along a series of fixed connections. The brain in this model is seen as the central switchboard where pain stimuli are received and processed, and then appropriate responses (“fight or flight”) are initiated. A simple proportionality is presumed to be occurring between the strength of the stimulus and the degree of pain perceived. However, in 1965 Melzack and Wall1 proposed that modulations of these stimuli could occur under various circumstances. For example, as Beecher2 observed during World War II, a soldier wounded in battle might feel no pain until the chaotic stimulation of the battle subsided. In 1967, Casey and Melzack3 expanded this concept
June 2009
Copyright © 2009 American Dental Association. All rights reserved. Reprinted by permission.
Downloaded from jada.ada.org on July 3, 2014
C L I N I C A L P R A C T I C E PAIN UPDATE
when they proposed that motivational, cognitive areas also are involved. and behavioral factors could modulate a pain To some degree, all of these phenomena take stimulus (ascending) and response (descending), place every time a pain stimulus occurs, but the and that this modulation ultimately would deterprocess usually reverses itself fairly quickly. The mine how these pain events unfolded. Conseproblem of chronic pain arises when the sensiquently, each pain experience in any person, or tized central nervous system components fail to across populations, would be different depending return to their normal state, so that primary nocion these modulating variables. ceptive input is no longer required to initiate Neuroplasticity. The next major development pain. Understanding this process enables us to in the field of pain physiology was the discovery of appreciate how patients can report having proneuroplasticity in the late 20th century. Accordlonged pain long after the initial pathology or ing to this concept, every event of thinking, trauma has resolved. learning and acting can significantly change both CLINICAL IMPLICATIONS the brain’s physical structure (anatomy) and its functional organization (physiology). Although The main implication for dentists on a day-to-day this phenomenon has an obvious positive side, basis is linked to our use of local anesthetics for including all forms of learning and adaptive nearly every operative procedure. It turns out responses to injury or other personal experiences, that this routine blocking of peripheral pain it also can have a dark side. stimuli prevents the transmission of pain stimuli In the area of pain, this dark side to second-order neurons, so no sencan be manifested as expanded pain sitization can occur. General anesThe problem of (that is, the area of the body feeling thetics, however, do not confer this chronic pain arises pain is much more extensive than protection, even though patients that which was actually injured) or “feel no pain” during surgery, when the sensitized as chronic pain (that is, the original because the A delta fibers and C central nervous injury or disease has resolved, but fibers stimulated at the surgical system components the pain remains and may even site still carry impulses to the fail to return to their increase). Both of these are examdorsal horn or trigeminal spinal normal state. ples of a negative manifestation of tract nucleus, and these excite the neuroplasticity, which explains second-order neurons. The good news, then, is that we many previously misunderstood probably prevent a lot of prolonged pain phephenomena but also poses a significant managenomena as we perform dental procedures; howment challenge for pain therapists. Therefore, ever, the bad news is that some patients still will every dentist and physician need to understand develop persistent pain. Most of these problems how neuroplasticity works because it will affect occur in people who have had pain for a long time how they react to their patients’ pain complaints. before seeking treatment, so their nervous sysThe mechanisms underlying the neuroplastems already are sensitized. Recognizing this posticity of pain-conducting sensory nerves may sibility can help dentists resist the temptation to seem complicated, but let me try to simplify them. reoperate on painful surgical sites, as so often Every peripheral pain stimulus (for example, happens after seemingly failed endodontic protooth pain) must go through a junction with a cedures or dental extractions. second-order neuron on its way to the higher cenThere is no way to predict who will develop ters, where it is interpreted and reacted to by persistent or chronic pain, but the results of a excitatory or inhibitory processes. We now know recent study4 suggest that powerful genetic comthat the excitatory process that “turns nerves on” ponents are involved in this susceptibility. Curis based on a series of chemicals that are released rent research is focused on understanding these at every synapse. Therefore, when the secondphenomena more thoroughly, as well as on develorder neuron is stimulated by the impulses from a oping better treatments for patients with chronic toothache, the possibility exists that this neuron pain. Several pharmaceutical approaches to will become sensitized to further inputs from the reducing central sensitization already exist, and periphery. If this happens, the patient may permore are forthcoming. In addition, by following a ceive even nonpainful stimuli as additional pain, biopsychosocial model of pain management, cliniand he or she may begin to feel as if neighboring JADA, Vol. 140
http://jada.ada.org
Copyright © 2009 American Dental Association. All rights reserved. Reprinted by permission.
June 2009
677
Downloaded from jada.ada.org on July 3, 2014
C L I N I C A L P R A C T I C E PAIN UPDATE
cians will be able to deal with both the somatic and the behavioral components of these difficult pain problems. CONCLUSION
Dentists need to appreciate how the phenomena of neuroplasticity and sensitization might affect their patients, especially if symptoms and responses suggest a diagnosis of chronic pain. Awareness of these issues is essential to avoid making improper diagnoses and administering ineffective treatments. In general, such patients will require referrals to appropriate medical practitioners for management of these complex conditions. Fortunately, chronic pain clinics are found in most communities today, and they can be a valuable resource for dentists who wish to obtain a medical consultation. ■ Dr. Greene is a clinical professor, Department of Orthodontics (M/C 841), College of Dentistry, University of Illinois at Chicago. He also is
678
JADA, Vol. 140
http://jada.ada.org
the editor of JADA’s Pain Update section. Address reprint requests to Dr. Greene at 1041 Ridge Road, Apt. 304, Wilmette, Ill. 60091, e-mail “[email protected]”. Disclosure. Dr. Greene did not report any disclosures. Pain Update is published in collaboration with the Neuroscience Group of the International Association for Dental Research. 1. Melzack R, Wall PD. Pain mechanisms: a new theory. Science 1965;150(699):971-979. 2. Beecher HK. Relationship of significance of wound to pain experienced. JAMA 1956;161(17):1609-1613. 3. Casey KL, Melzack R. Neural mechanisms of pain: a conceptual model. In: Way EL, ed. New Concepts in Pain. Philadelphia: FL Davis; 1967:13-31. 4. Diatchenko L, Nackley AG, Slade GD, Fillingim RB, Maixner W. Idiopathic pain disorders: pathways of vulnerability. Pain 2006;123(3): 226-230. Suggested Readings Sessle BJ. Acute and chronic craniofacial pain: brainstem mechanisms of nociceptive transmission and neuroplasticity, and their clinical correlates. Crit Rev Oral Biol Med 2000;11(1):57-91. Woolf CJ, Chong MS. Preemptive analgesia: treating postoperative pain by preventing the establishment of central sensitization. Anesth Analg 1993;77(2):362-379. Woolf CJ, Salter MW. Neuronal plasticity: increasing the gain in pain. Science 2000;288(5472):1765-1769.
June 2009
Copyright © 2009 American Dental Association. All rights reserved. Reprinted by permission.
Neuroplasticity and Sensitization Charles S. Greene JADA 2009;140(6):676-678 10.14219/jada.archive.2009.0253 The following resources related to this article are available online at jada.ada.org (this information is current as of July 3, 2014): Updated information and services including high-resolution figures, can be found in the online version of this article at: http://jada.ada.org/content/140/6/676
This article cites 6 articles, 3 of which can be accessed free: http://jada.ada.org/content/140/6/676/#BIBL Information about obtaining reprints of this article or about permission to reproduce this article in whole or in part can be found at: http://www.ada.org/990.aspx
Copyright © 2014 American Dental Association. All rights reserved. Reproduction or republication strictly prohibited without prior written permission of the American Dental Association.
Downloaded from jada.ada.org on July 3, 2014
CLINICAL PRACTICE
PA I N U P D AT E
Neuroplasticity and sensitization Charles S. Greene, DDS
Editor’s note: This new feature, which will appear quarterly, reviews pain phenomena as they pertain to dentistry.
CLINICAL PROBLEM
patient visits a new dental office with a complaint of pain in the maxillary left quadrant. The patient’s medical history reveals that tooth no. 13 had received a restoration, which was followed by some pain. The next steps performed by the patient’s previous dentist included removing the restoration and placing a temporary zinc oxide eugenol restoration, preparing for the crown, seating the crown, performing root canal treatment, performing an apicoectomy and extracting the tooth. The patient reports that some degree of pain persisted intermittently throughout these procedures and became worse over time. The pain now is severe and has continued for six months after extraction and socket healing. What is the most likely explanation for this series of events?
A
EXPLANATION
This fairly common phenomenon is an example of “neuroplasticity,” a term that describes how the nervous system changes in response to painful 676
JADA, Vol. 140
http://jada.ada.org
stimuli. To understand this process, dentists need to know that the simple Cartesian model of a painful stimulus leading to a proportional response has been replaced by a much more complex model of nervous system behavior. This pain update describes the new model, with an emphasis on how it can affect dental practice. Cartesian model. The Cartesian model (named after the 17th century French philosopher René Descartes) is based on the notion of a hardwired nervous system, in which pain signals are carried along a series of fixed connections. The brain in this model is seen as the central switchboard where pain stimuli are received and processed, and then appropriate responses (“fight or flight”) are initiated. A simple proportionality is presumed to be occurring between the strength of the stimulus and the degree of pain perceived. However, in 1965 Melzack and Wall1 proposed that modulations of these stimuli could occur under various circumstances. For example, as Beecher2 observed during World War II, a soldier wounded in battle might feel no pain until the chaotic stimulation of the battle subsided. In 1967, Casey and Melzack3 expanded this concept
June 2009
Copyright © 2009 American Dental Association. All rights reserved. Reprinted by permission.
Downloaded from jada.ada.org on July 3, 2014
C L I N I C A L P R A C T I C E PAIN UPDATE
when they proposed that motivational, cognitive areas also are involved. and behavioral factors could modulate a pain To some degree, all of these phenomena take stimulus (ascending) and response (descending), place every time a pain stimulus occurs, but the and that this modulation ultimately would deterprocess usually reverses itself fairly quickly. The mine how these pain events unfolded. Conseproblem of chronic pain arises when the sensiquently, each pain experience in any person, or tized central nervous system components fail to across populations, would be different depending return to their normal state, so that primary nocion these modulating variables. ceptive input is no longer required to initiate Neuroplasticity. The next major development pain. Understanding this process enables us to in the field of pain physiology was the discovery of appreciate how patients can report having proneuroplasticity in the late 20th century. Accordlonged pain long after the initial pathology or ing to this concept, every event of thinking, trauma has resolved. learning and acting can significantly change both CLINICAL IMPLICATIONS the brain’s physical structure (anatomy) and its functional organization (physiology). Although The main implication for dentists on a day-to-day this phenomenon has an obvious positive side, basis is linked to our use of local anesthetics for including all forms of learning and adaptive nearly every operative procedure. It turns out responses to injury or other personal experiences, that this routine blocking of peripheral pain it also can have a dark side. stimuli prevents the transmission of pain stimuli In the area of pain, this dark side to second-order neurons, so no sencan be manifested as expanded pain sitization can occur. General anesThe problem of (that is, the area of the body feeling thetics, however, do not confer this chronic pain arises pain is much more extensive than protection, even though patients that which was actually injured) or “feel no pain” during surgery, when the sensitized as chronic pain (that is, the original because the A delta fibers and C central nervous injury or disease has resolved, but fibers stimulated at the surgical system components the pain remains and may even site still carry impulses to the fail to return to their increase). Both of these are examdorsal horn or trigeminal spinal normal state. ples of a negative manifestation of tract nucleus, and these excite the neuroplasticity, which explains second-order neurons. The good news, then, is that we many previously misunderstood probably prevent a lot of prolonged pain phephenomena but also poses a significant managenomena as we perform dental procedures; howment challenge for pain therapists. Therefore, ever, the bad news is that some patients still will every dentist and physician need to understand develop persistent pain. Most of these problems how neuroplasticity works because it will affect occur in people who have had pain for a long time how they react to their patients’ pain complaints. before seeking treatment, so their nervous sysThe mechanisms underlying the neuroplastems already are sensitized. Recognizing this posticity of pain-conducting sensory nerves may sibility can help dentists resist the temptation to seem complicated, but let me try to simplify them. reoperate on painful surgical sites, as so often Every peripheral pain stimulus (for example, happens after seemingly failed endodontic protooth pain) must go through a junction with a cedures or dental extractions. second-order neuron on its way to the higher cenThere is no way to predict who will develop ters, where it is interpreted and reacted to by persistent or chronic pain, but the results of a excitatory or inhibitory processes. We now know recent study4 suggest that powerful genetic comthat the excitatory process that “turns nerves on” ponents are involved in this susceptibility. Curis based on a series of chemicals that are released rent research is focused on understanding these at every synapse. Therefore, when the secondphenomena more thoroughly, as well as on develorder neuron is stimulated by the impulses from a oping better treatments for patients with chronic toothache, the possibility exists that this neuron pain. Several pharmaceutical approaches to will become sensitized to further inputs from the reducing central sensitization already exist, and periphery. If this happens, the patient may permore are forthcoming. In addition, by following a ceive even nonpainful stimuli as additional pain, biopsychosocial model of pain management, cliniand he or she may begin to feel as if neighboring JADA, Vol. 140
http://jada.ada.org
Copyright © 2009 American Dental Association. All rights reserved. Reprinted by permission.
June 2009
677
Downloaded from jada.ada.org on July 3, 2014
C L I N I C A L P R A C T I C E PAIN UPDATE
cians will be able to deal with both the somatic and the behavioral components of these difficult pain problems. CONCLUSION
Dentists need to appreciate how the phenomena of neuroplasticity and sensitization might affect their patients, especially if symptoms and responses suggest a diagnosis of chronic pain. Awareness of these issues is essential to avoid making improper diagnoses and administering ineffective treatments. In general, such patients will require referrals to appropriate medical practitioners for management of these complex conditions. Fortunately, chronic pain clinics are found in most communities today, and they can be a valuable resource for dentists who wish to obtain a medical consultation. ■ Dr. Greene is a clinical professor, Department of Orthodontics (M/C 841), College of Dentistry, University of Illinois at Chicago. He also is
678
JADA, Vol. 140
http://jada.ada.org
the editor of JADA’s Pain Update section. Address reprint requests to Dr. Greene at 1041 Ridge Road, Apt. 304, Wilmette, Ill. 60091, e-mail “[email protected]”. Disclosure. Dr. Greene did not report any disclosures. Pain Update is published in collaboration with the Neuroscience Group of the International Association for Dental Research. 1. Melzack R, Wall PD. Pain mechanisms: a new theory. Science 1965;150(699):971-979. 2. Beecher HK. Relationship of significance of wound to pain experienced. JAMA 1956;161(17):1609-1613. 3. Casey KL, Melzack R. Neural mechanisms of pain: a conceptual model. In: Way EL, ed. New Concepts in Pain. Philadelphia: FL Davis; 1967:13-31. 4. Diatchenko L, Nackley AG, Slade GD, Fillingim RB, Maixner W. Idiopathic pain disorders: pathways of vulnerability. Pain 2006;123(3): 226-230. Suggested Readings Sessle BJ. Acute and chronic craniofacial pain: brainstem mechanisms of nociceptive transmission and neuroplasticity, and their clinical correlates. Crit Rev Oral Biol Med 2000;11(1):57-91. Woolf CJ, Chong MS. Preemptive analgesia: treating postoperative pain by preventing the establishment of central sensitization. Anesth Analg 1993;77(2):362-379. Woolf CJ, Salter MW. Neuronal plasticity: increasing the gain in pain. Science 2000;288(5472):1765-1769.
June 2009
Copyright © 2009 American Dental Association. All rights reserved. Reprinted by permission.