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      Ketamine as an adjuvant in sympathetic blocks for management of central sensitization following peripheral nerve injury

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          Abstract

          Proliferation of NMDA receptors and role of glutamate in producing central sensitization and 'wind up' phenomena in CRPS [complex regional pain syndrome] forms a strong basis for the use of Ketamine to block the cellular mechanisms that initiate and maintain these changes. In this case series, we describe 3 patients of CRPS Type II with debilitating central sensitization, heat/mechano allodynia and cognitive symptoms that we termed 'vicarious pain'. Each of these patients had dramatic relief with addition of Ketamine as an adjuvant to the sympathetic blocks after conventional therapy failed.

          All 3 patients suffered gunshot wounds and developed characteristic features of CRPS Type II. Within 2–3 weeks they developed extraterritorial symptoms typical of central sensitization. The generalized mechanical allodynia and debilitating heat allodynia described to be rare in human subjects had life altering affect on their daily life. Case 2 and 3 also described an unusual cognitive phenomenon i.e. visual stimuli of friction would evoke severe pain in the affected limb that we have termed as 'vicarious pain'. They responded positively to sympathetic blocks but the sympatholysis did not bring relief to the heat and mechanical allodynia. Addition of Ketamine 0.5 mg/kg to the sympathetic blocks elicited resulted in marked relief in the allodynia.

          Ketamine has a special role in patients with debilitating heat allodynia and positive cognitive symptoms via its action on central pain pathway. As an adjuvant in sympatholytic blocks it has a targeted action without significant neuropsychiatric side effects.

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          Most cited references21

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          Spinal glia and proinflammatory cytokines mediate mirror-image neuropathic pain in rats.

          Mirror-image allodynia is a mysterious phenomenon that occurs in association with many clinical pain syndromes. Allodynia refers to pain in response to light touch/pressure stimuli, which normally are perceived as innocuous. Mirror-image allodynia arises from the healthy body region contralateral to the actual site of trauma/inflammation. Virtually nothing is known about the mechanisms underlying such pain. A recently developed animal model of inflammatory neuropathy reliably produces mirror-image allodynia, thus allowing this pain phenomenon to be analyzed. In this sciatic inflammatory neuropathy (SIN) model, decreased response threshold to tactile stimuli (mechanical allodynia) develops in rats after microinjection of immune activators around one healthy sciatic nerve at mid-thigh level. Low level immune activation produces unilateral allodynia ipsilateral to the site of sciatic inflammation; more intense immune activation produces bilateral (ipsilateral + mirror image) allodynia. The present studies demonstrate that both ipsilateral and mirror-image SIN-induced allodynias are (1) reversed by intrathecal (peri-spinal) delivery of fluorocitrate, a glial metabolic inhibitor; (2) prevented and reversed by intrathecal CNI-1493, an inhibitor of p38 mitogen-activated kinases implicated in proinflammatory cytokine production and signaling; and (3) prevented or reversed by intrathecal proinflammatory cytokine antagonists specific for interleukin-1, tumor necrosis factor, or interleukin-6. Reversal of ipsilateral and mirror-image allodynias was rapid and complete even when SIN was maintained constantly for 2 weeks before proinflammatory cytokine antagonist administration. These results provide the first evidence that ipsilateral and mirror-image inflammatory neuropathy pain are created both acutely and chronically through glial and proinflammatory cytokine actions.
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            Lack of analgesic effect of opioids on neuropathic and idiopathic forms of pain.

            The aim of the present study has been to assess the responsiveness of various types of chronic pain to opioids given i.v. and tested against placebo in a double-blind, randomized fashion. Pain classified as primary nociceptive was effectively alleviated (P greater than 0.001) while neuropathic deafferentation pain was not significantly influenced by morphine or equivalent doses of other opioids. Also 'idiopathic' pain, defined as chronic pain with no or little demonstrable pathology, failed to respond. The results were not related to whether the patients were regular users of narcotic analgesics or not. The outcome of our double-blind opioid test has proved useful to justify a continued, or discontinued, use of narcotic medication in individual patients. It may also support the indication and choice of invasive stimulation procedures (spinal cord or brain). The results of the study illustrate the misconception of chronic pain as an entity and highlight the importance of recognizing different neurobiological mechanisms and differences in responsiveness to analgesic drugs as well as to non-pharmacological modes of treatment. The opioid test has thus become a valuable tool in pain analysis and helpful as a guide for further treatment.
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              Mechanisms of neuropathic pain.

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                Author and article information

                Journal
                J Brachial Plex Peripher Nerve Inj
                Journal of Brachial Plexus and Peripheral Nerve Injury
                BioMed Central
                1749-7221
                2008
                25 October 2008
                : 3
                : 22
                Affiliations
                [1 ]Asst Professor, Dept of Anaesthesiology, All India Institute of Medical Sciences, New Delhi, India
                [2 ]Former Resident, Dept of Anaesthesiology, All India Institute of Medical Sciences, New Delhi, India
                [3 ]Ex-Professor Dept of Anaesthesiology, All India Institute of Medical Sciences, Currently, Director – Delhi Pain Management Centre, New Delhi, India
                Article
                1749-7221-3-22
                10.1186/1749-7221-3-22
                2584055
                18950516
                3c067d33-7611-44ae-a3ad-40ae2f9e6ad3
                Copyright © 2008 Sunder et al; licensee BioMed Central Ltd.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 1 July 2008
                : 25 October 2008
                Categories
                Case Study

                Neurology
                Neurology

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