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| EDITORIAL |
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| Year : 2016 | Volume
: 30
| Issue : 1 | Page : 1-2 |
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Neuroplasticity: Changing concept in understanding chronic pain
Subrata Ray1, Subrata Goswami2, Gautam Das3
1 Department of Anaesthesia and Pain, KPC Medical College and Hospitals, Kolkata, West Bengal, India
2 Department of Pain, ESI Institute of Pain Management, Kolkata, West Bengal, India
3 Daradia Pain Clinic, Kolkata, West Bengal, India
| Date of Web Publication | 7-Jan-2016 |
Correspondence Address:
Dr. Subrata Ray
Department of Anaesthesia and Pain, KPC Medical College and Hospitals, 1F, Raja S. C. Mullick Road, Kolkata - 700 032, West Bengal
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0970-5333.173430
How to cite this article:
Ray S, Goswami S, Das G. Neuroplasticity: Changing concept in understanding chronic pain. Indian J Pain 2016;30:1-2 |
The pathophysiology of chronic pain is poorly understood. Till the recent past any chronic pain syndrome was tried to be explained by neural hardwire damage, and the absence of which prompted to label loose diagnoses to the patient, such as malingering and somatoform disorder. In the nineteenth century and early part of twentieth century, it was believed by neuroscientist that the adult mammalian central nervous system (CNS), once developed in the intrauterine life and early childhood, was stable and no change occurs subsequently. This dogma in neurology was challenged by Liu and Chambers, who in mid-1950s first discovered the intraspinal axonal sprouting following hemipyramidotomy in monkeys (1958). This seminal discovery was the first example of structural changes in the CNS after damage. [1] Subsequent demonstration of axonal sprouting in brain as well as spinal cord did not attract much attention due to the lack of evidence that, these changes could have any correlation to organ dysfunction.
In the last two decades of twentieth century, there was renewed interest in the study of CNS changes in response to nerve lesions. The resurgence was due to series of pioneering works by Kaas, Merzenich, and a group of investigators. Their discoveries raised hope that structural changes in response to injury may have some therapeutic implication in patients with CNS injury. Merzenich first showed that the reduced sensory input created by a section of median nerve in owl and squirrel monkeys can induce changes in the cortical representation of the hand in areas 3b and 1 of the somatosensory cortex, up to an order of magnitude of 2 mm. [2] In extension to this work, it was found that even reverse phenomena, such as substantially increased afferent input created by behaviorally relevant body part movements, also induced changes in cortical representation areas. [3] Interestingly here also the order of magnitude of cortical changes was limited to 2 mm. At that point of time, it was argued to be due to anatomical limitation imposed by axonal length of neighboring thalamocortical projection neurons. Shortly, the seminal work of Pons reported massive cortical reorganization in adult macaques monkeys and the magnitude of cortical changes was greater than 10-14 mm, which is far beyond the axonal length of thalamocortical projection neurons. [4] They were looking for the mechanism of this massive reorganization and hoped that "answer to such question about mechanism and function could lead to harnessing the immense reorganizational capability of the adult nervous system for therapeutic purposes." [4]
Although a series of animal studies convincingly put evidence that CNS reorganization occurs in response to varieties of sensory input, its functional relevance could not be established in the absence of human study. In consistent with animal studies, the first evidence of cortical reorganization in human amputees, using magnetic source imaging, was reported by Yang et al. in 1994. [5] Another group also reported cortical reorganization in the human brain in the same year in Germany. [6] On the basis of substantial plasticity of the somatosensory cortex after amputation in adult monkeys, an investigation in human by Flor et al. found significant positive linear relationship between the amount of phantom limb pain and the amount of cortical reorganization in upper limb amputees using magnetic source imaging. [7]
In the past, it was widely believed that congenitally limb deficient people do not experience phantom limbs. Simmel was reluctant to give credence to phantom experiences in two subjects of her study in 1961. [8] Probably there was no conceptual framework to make sense of reports of phantom limb pain in aplasics, as they had supported the concept that the phantom is produced by the body schema described by Head and Holmes (1911-1912) as the product of acquired proprioceptive and somatic input. [9] The elegant work by Melzack has convincingly showed that congenitally limb deficient people experience phantom limb and phantom pain. [9] The hypothesis of neuromatrix proposed by Melzack described the idea of an innate structure for the neural basis of phantom, [9] and tried to explain the pathomechanism of many chronic pain syndromes as well.
Complex regional pain syndrome (CRPS) has unexpected similarities with phantom limb sensation and phantom limb pain. [10] By using magnetoencephalography (MEG), Maihofner et al. showed that the area of the cortex subserving the affected hand was reduced in size, and it was shifted in the direction of the representation of the lip. Like phantom limb pain, the amount of change in cortical reorganization was correlated with the intensity of pain and extent of hyperalgesia. [11] Interestingly, in the follow-up study, the cortical reorganization noted earlier was largely reversed and correlated with the reduction of CRPS pain. [10] There is an emerging view that the peripheral changes in CRPS should be considered a manifestation of changes in the cortex. [12]
Prior to the discovery of central sensitization, the prevailing view on pain pathway in the CNS was of largely passive neural relay, much like a telephone wire, from one site to another. [13] In addition to cortical reorganization, neural plasticity in the peripheral and spinal level includes activity-dependent synaptic plasticity, changes in microglia, astrocytes, gap junctions, and gene transcription. [13] There are several chronic pain syndromes, where the etiopathogenesis have been implicated to central sensitization and/or cortical reorganization, such as fibromyalgia, tension-type headache, migraine, temporomandibular joint disease, irritable bowel syndrome, CRPS, phantom limb pain, noncardiac chest pain, and many others. The discovery of central sensitization and cortical reorganization has changed the understanding of chronic pain with immense diagnostic and therapeutic implications.
| References | |  |
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| 8. | Simmel ML. The absence of phantoms for congenitally missing limbs. Am J Psychol 1961;74:467-70. |
| 9. | Melzack R, Israel R, Lacroix R, Schultz G. Phantom limbs in people with congenital limb deficiency or amputation in early childhood. Brain 1997;120:1603-20. |
| 10. | Maihofner C, Handwerker HO, Neundorfer B, Birklein F. Cortical reorganization during recovery from complex regional pain syndrome. Neurology 2004;63:693-701. |
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