Carbamazepine and oxcarbazepine, the 10-keto analog of carbamazepine, have relatively similar pharmacological profiles. Both have been shown to block tetrodotoxin-resistant Na1 channels in brain tissue.1 Neuronal hyper-excitability, linked to accumulation of sodium channels in injured peripheral axons and cell bodies, is reduced by carbamazepine, as is similar excitability in dorsal horn neurons2, 3 and possibly elsewhere in the central nervous system (CNS) where sodium channel may be up-regulated.4 The selectivity of Na1 channel blockade remains to be determined, but interaction with a low activation state of Nav1.8 channels may be one of the key mechanisms of carbamazepine.5 In addition, both car-bamazepine and oxcarbazepine appear to antagonize the A1 adenosine receptor, increase dopaminergic transmission, and potentiate voltage-gated potassium channels, all potentially useful properties in chronic pain.1 Both drugs inhibit L-type voltage-gated calcium channels and presyn-aptic glutamate release, although it is uncertain whether this happens in sufficient concentrations in clinical conditions.1 Oxcarbazepine and its metabolites are also thought to modulate other calcium channels.6 Both car-bamazepine and oxcarbazepine have been shown to possess some antihyperalgesic effects in experimental models of inflammatory pain, probably mediated by indirect activation of adrenergic a2 receptors.7
Was this article helpful?
Do You Suffer From Chronic Pain? Do You Feel Like You Might Be Addicted to Pain Killers For Life? Are You Trapped on a Merry-Go-Round of Escalating Pain Tolerance That Might Eventually Mean That No Pain Killer Treats Your Condition Anymore? Have you been prescribed pain killers with dangerous side effects?