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 hyperactivation of spinal microglia.

NS1619-induced tactile allodynia was completely inhibited by S-ketamine, suggesting that S-ketamine preferentially suppresses the nerve injury-induced hyperactivation and migration of spinal microglia through the blockade of BK channels.^[1]

There are some studies demonstrating 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] ).  

Jan M. Keppel Hesselink, MD, PhD, december 2011

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