Efficacy of Ketamine in Anesthetic Dosage for the Treatment of Refractory Complex Regional Pain Syndrome: An Open-Label Phase II Study

Kiefer, Ralph-Thomas; Rohr, P.; Ploppa, Annette; Dieterich, Hans-Jürgen; Grothusen, John R.; Koffler, Sandra P.; Altemeyer, K.-H.; Unertl, K.; Schwartzman, Robert J.

doi:10.1111/j.1526-4637.2007.00402.x

Cited by 146 publications

(140 citation statements)

References 64 publications

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“…Our study not only reveals a new post-translational mechanism underlying sustained KCC2 down-regulation in the spinal cord after nerve injury but also opens new avenues for research into signaling mechanisms of synaptic plasticity and neuropathic pain. Normalizing calpain activity may represent an important mechanism through which NMDAR antagonists produce long-lasting analgesic effects in patients with neuropathic pain caused by nerve injury (60,61). On the basis of our evidence, reducing abnormal calpain activity could represent a new strategy for restoring Cl Ϫ homeostasis and for treatment of chronic neuropathic pain.…”

Section: Discussionmentioning

confidence: 96%

N-Methyl-d-aspartate Receptor- and Calpain-mediated Proteolytic Cleavage of K+-Cl− Cotransporter-2 Impairs Spinal Chloride Homeostasis in Neuropathic Pain

Zhou

Chen

Byun

et al. 2012

Journal of Biological Chemistry

131

159

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Section: Discussionmentioning

confidence: 96%

N-Methyl-d-aspartate Receptor- and Calpain-mediated Proteolytic Cleavage of K+-Cl− Cotransporter-2 Impairs Spinal Chloride Homeostasis in Neuropathic Pain

Zhou

Chen

Byun

et al. 2012

Journal of Biological Chemistry

131

159

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“…Both clinical and animal studies have shown that ketamine can be applied for treating many kinds of chronic pain, such as neuropathic pain, cancer pain, and complex regional pain syndrome [4,5,37] . The present results show that a low dose of ketamine (30 g/kg) administration did not affect the pain threshold of the neuropathic rats, while 100 g/kg ketamine showed obvious effects on mechanical allodynia.…”

Section: Discussionmentioning

confidence: 99%

Ketamine Depresses Toll-Like Receptor 3 Signaling in Spinal Microglia in a Rat Model of Neuropathic Pain

et al. 2011

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Reports suggest that microglia play a key role in spinal nerve ligation (SNL)-induced neuropathic pain, and toll-like receptor 3 (TLR3) has a substantial role in the activation of spinal microglia and the development of tactile allodynia after nerve injury. In addition, ketamine application could suppress microglial activation in vitro, and ketamine could inhibit proinflammatory gene expression possibly by suppressing TLR-mediated signal transduction. Therefore, the present study was designed to disclose whether intrathecal ketamine could suppress SNL-induced spinal microglial activation and exert some antiallodynic effects on neuropathic pain by suppressing TLR3 activation. Behavioral results showed that intrathecal ketamine attenuated SNL-induced mechanical allodynia, as well as spinal microglial activation, in a dose-dependent manner. Furthermore, Western blot analysis displayed that ketamine application downregulated SNL-induced phosphorylated-p38 (p-p38) expression, which was specifically expressed in spinal microglia but not in astrocytes or neurons. Besides, ketamine could reverse TLR3 agonist (polyinosine-polycytidylic acid)-induced mechanical allodynia and spinal microglia activation. It was concluded that intrathecal ketamine depresses TLR3-induced spinal microglial p-p38 mitogen-activated protein kinase pathway activation after SNL, probably contributing to the antiallodynic effect of ketamine on SNL-induced neuropathic pain.

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“…Unlike high-dose opioid analgesics, respiratory depression is not seen with ketamine. & Clinical trials to date have been limited, but recently published studies have addressed three forms of ketamine treatment: intravenous subanesthetic dosing [67,68], intravenous high-dose anesthesia ("ketamine coma") [69], and topical administration [70•]. Although intravenous ketamine is used routinely by anesthesiologists intraoperatively as an anesthetic agent, its use in treating CRPS is considered off-label.…”

Section: Spinal Cord Stimulationmentioning

confidence: 99%

Complex Regional Pain Syndrome: State of the Art Update

Henson

Bruehl

2010

Curr Treat Options Cardio Med

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Although the pathophysiology of complex regional pain syndrome (CRPS) is not fully understood, it appears to reflect multiple interacting mechanisms. In addition to altered autonomic function, a role for inflammatory mechanisms and altered somatosensory and motor function in the brain is increasingly suggested. Several possible risk factors for development of CRPS, including genetic factors, have been identified. Few treatments have been proven effective for CRPS in well-designed clinical trials. However, recent work suggests that bisphosphonates may be useful in CRPS management and that the N-methyl-D: -aspartate receptor antagonist ketamine significantly reduces CRPS pain when administered topically or intravenously at subanesthetic dosages. Extended use of ketamine at anesthetic dosages ("ketamine coma") remains a controversial and unproven treatment for CRPS. Spinal cord stimulation may be effective for reducing pain in approximately two thirds of CRPS patients not responding to other treatments, but its efficacy appears to diminish over time.

show abstract

Efficacy of Ketamine in Anesthetic Dosage for the Treatment of Refractory Complex Regional Pain Syndrome: An Open-Label Phase II Study

Abstract: This open-label trial suggests benefit in pain reduction, associated CRPS symptoms, improved quality of life and ability to work following anesthetic ketamine in previously refractory CRPS patients. However, a randomized controlled trial will be necessary to prove its efficacy.

Cited by 146 publications

References 64 publications

N-Methyl-d-aspartate Receptor- and Calpain-mediated Proteolytic Cleavage of K+-Cl− Cotransporter-2 Impairs Spinal Chloride Homeostasis in Neuropathic Pain

N-Methyl-d-aspartate Receptor- and Calpain-mediated Proteolytic Cleavage of K+-Cl− Cotransporter-2 Impairs Spinal Chloride Homeostasis in Neuropathic Pain

Ketamine Depresses Toll-Like Receptor 3 Signaling in Spinal Microglia in a Rat Model of Neuropathic Pain

Complex Regional Pain Syndrome: State of the Art Update

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