Intravenous Ketamine in Neuropathic Pain
What can intravenous Ketamine do for neuropathic pain patients? Treatment of refractory neuropathic pain is a clinical challenge.
However, many new case reports and small clinical trials suggest that the N-methyl-D-aspartic acid (NMDA) receptor antagonists Ketamine may be clinically useful in treating cases of neuropathic pain.
This case report supports the idea that Ketamine can be useful in the reduction of refractory chronic neuropathic pain. And that the effect of Ketamine can persist for many weeks after treatment.
Low dose Ketamine infusion for neuropathic pain
A 59-year-old treatment resistant male patiënt with neuropathic pain secondary to chronic idiopathic axonal polyneuropathy (CIAP) was treated with a continuous intravenous administration of low dose Ketamine. With 20 mg/h for 5 days. This resulted in an almost complete pain relief without significant side effects.
The analgesic effect lasted 10–12 weeks after which the Ketamine infusion was repeated, and the patiënt remained responsive to this treatment regime during 3.5 years. NO side effects were reported.
This case supports the growing body of evidence that Ketamine may be useful in the management of refractory chronic neuropathic pain. In our hands the same effects seem to be possible by administering Ketamine in a topical cream.
Ketamine might have glia as target for neuropathic pain
Other news: Glia is a new target in the treatment of neuropathic pain. Ketamine might have a mode of action related to glia hyperactivity.
The acute analgesic effects of Ketamine are generally believed to be mediated by the inhibition of NMDA receptors in nociceptive neurons. The authors explored the possible effect of Ketamine on spinal microglia.
They found that S-Ketamine preferentially suppressed the nerve injury-induced development of tactile allodynia and hyper activation of spinal microglia.
NS1619-induced tactile allodynia was completely inhibited by S-Ketamine, suggesting that S-Ketamine preferentially suppresses the nerve injury-induced hyper activation and migration of spinal microglia through the blockade of BK channels.[1]
, December 2011
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References
Analgesic Effect of Subanesthetic Intravenous Ketamine in Refractory Neuropathic Pain: A Case ReportOsama Elsewaisy, MBBS,* Barry Slon, FANZCA, † and John Monagle, FANZCA † Pain MedicineISSN: 1526-4637 (Online)ISSN: 1526-2375 (Print)Volume 11, Issue 6, 2010.Pages: 946–950
Studies about the efficacy of oral Ketamine in neuropathic pain, [Eide and Stubhaug, 1997] , [Klepsad and Borchgrevink, 1997] , [Nikolajsen et al., 1997] , [Enarson et al., 1999] , [Fisher and Hagen, 1999] and [Rabben et al., 1999]
[1] Hayashi Y, Kawaji K, Sun L, Zhang X, Koyano K, Yokoyama T, Kohsaka S, Inoue K, Nakanishi H. | Microglial Ca2+-Activated K+ Channels Are Possible Molecular Targets for the Analgesic Effects of S-Ketamine on Neuropathic Pain. | J Neurosci. | 2011 Nov 30;31(48):17370-17382.