Anticonvulsant drugs for management of pain: a systematic review

McQuay, Henry J; Carroll, Dawn; Jadad, Alejandro R.; Wiffen, Philip J; Moore, Andrew

doi:10.1136/bmj.311.7012.1047

Cited by 655 publications

(272 citation statements)

References 34 publications

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“…Neuropathic pain, regardless of whether it arises from traumatic or inflammatory insults, is essentially uncontrolled by currently available drug therapies. Indeed, it is common for these pharmacological treatments to provide no pain relief for 60 -80% of patients and only partial relief for the rest (McQuay et al, 1995(McQuay et al, , 1996Sindrup and Jensen, 1999). The present data suggest that these therapies may fail because they target neurons rather than glia.…”

Section: Discussionmentioning

confidence: 68%

Spinal Glia and Proinflammatory Cytokines Mediate Mirror-Image Neuropathic Pain in Rats

et al. 2003

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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 ϩ mirror image) allodynia. The present studies demonstrate that both ipsilateral and mirrorimage 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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Section: Discussionmentioning

confidence: 68%

Spinal Glia and Proinflammatory Cytokines Mediate Mirror-Image Neuropathic Pain in Rats

et al. 2003

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“…Clinical relevance of reduced Na v 1.8 and Na v 1.9 expression The use of sodium channel blockers to treat both neuropathic and inflammatory pain in a clinical setting is well known to result in analgesia (Galer, 1995;McQuay et al, 1995;Clayton et al, 1997;Evans et al, 1997;Trezise and Xie, 1997). These include such treatments as topical creams (for example, lidocaine), anticonvulsants, and tricyclic antidepressants (reviewed in Rogers et al, 2006).…”

Section: Potential Mechanisms Of Modulation Of Sodium Channel Expressmentioning

confidence: 99%

Neurotrophin-3 significantly reduces sodium channel expression linked to neuropathic pain states

Wilson-Gerwing

Stucky

McComb

et al. 2008

Experimental Neurology

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Neuropathic pain resulting from chronic constriction injury (CCI) is critically linked to sensitization of peripheral nociceptors. Voltage gated sodium channels are major contributors to this state and their expression can be upregulated by nerve growth factor (NGF). We have previously demonstrated that neurotrophin-3 (NT-3) acts antagonistically to NGF in modulation of aspects of CCI-induced changes in trkA-associated nociceptor phenotype and thermal hyperalgesia. Thus, we hypothesized that exposure of neurons to increased levels of NT-3 would reduce expression of Na v 1.8 and Na v 1.9 in DRG neurons subject to CCI. In adult male rats, Na v 1.8 and Na v 1.9 mRNAs are expressed at high levels in predominantly small to medium size neurons. One week following CCI, there is reduced incidence of neurons expressing detectable Na v 1.8 and Na v 1.9 mRNA, but without a significant decline in mean level of neuronal expression, and similar findings observed immunohistochemically. There is also increased accumulation/redistribution of channel protein in the nerve most apparent proximal to the first constriction site. Intrathecal infusion of NT-3 significantly attenuates neuronal expression of Na v 1.8 and Na v 1.9 mRNA contralateral and most notably, ipsilateral to CCI, with a similar impact on relative protein expression at the level of the neuron and constricted nerve. We also observe reduced expression of the common neurotrophin receptor p75 in response to CCI that is not reversed by NT-3 in small to medium sized neurons and may confer an enhanced ability of NT-3 to signal via trkA, as has been previously shown in other cell types. These findings are consistent with an analgesic role for NT-3.

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“…Carbamazepine has been shown to be ine ective in CPSP, 23,27 but this has not greatly discouraged their use. Lamotrigine has been advocated for central pain, 28 and great hopes are held out for gabapentin, a release facilitator of endogenous GABA, which has been shown to be e ective in some painful neuropathies, and anecdotally in central pain.…”

Section: Treatment Of Central Painmentioning

confidence: 99%

Central pain following spinal and supraspinal lesions

Bowsher

1999

Spinal Cord

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Anticonvulsant drugs for management of pain: a systematic review

Cited by 655 publications

References 34 publications

Spinal Glia and Proinflammatory Cytokines Mediate Mirror-Image Neuropathic Pain in Rats

Spinal Glia and Proinflammatory Cytokines Mediate Mirror-Image Neuropathic Pain in Rats

Neurotrophin-3 significantly reduces sodium channel expression linked to neuropathic pain states

Central pain following spinal and supraspinal lesions

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