Hi Roz,

I came across it just the other day. I found an interesting site that explains things to about my basic level :
http://www.painonline.com/mt-archive...ntly_aske.html

"The NIH does not recognize any treatment as being satisfactory for the burning dysesthesia. By comparision, posterior column pain is likely to respond to various medications including opiates, anticonvulsants, or hypnotics. These same drugs may sedate the patient to the point where pain is less of a problem, but the levels required for dysesthesia are so high that the patient is usually sedated to the point of not being able to function. There is hope that some of the new N type Calcium channel blockers, such as Prialt or Ralfinamide will treat central pain. These drugs have been shown to benefit pain from injury to peripheral nerves, but no double blind studies exist to show that they are effective for pain of central origin."

Thanks for posting that, sounds like it may be the next research to keep a good eye on.
all the best,

Just Updating

Following is the abstract of the above paper (Stumman, et al., 2005) as well as the last paragraph from the discussion section:

Abstract:
Tetrodotoxin-resistant and tetrodotoxin-sensitive Na+ channels contribute to the abnormal spontaneous firing in dorsal root ganglion neurons associated with neuropathic pain. Effects of the anti-nociceptive agent ralfinamide on tetrodotoxin-resistant and tetrodotoxin-sensitive currents in rat dorsal root ganglion neurons were therefore investigated by patch clamp experiments. Ralfinamide inhibition was voltage-dependent showing highest potency towards inactivated channels. IC50 values for tonic block of half-maximal inactivated tetrodotoxin-resistant and tetrodotoxin-sensitive currents were 10 _M and 22 _M. Carbamazepine, an anticonvulsant used in the treatment of pain, showed significantly lower potency. Ralfinamide produced a hyperpolarising shift in the steady-state inactivation curves of both currents confirming the preferential interaction with inactivated channels. Additionally, ralfinamide use and frequency dependently inhibited both currents and significantly delayed repriming from inactivation. All effects were more pronounced for tetrodotoxin-resistant than tetrodotoxin-sensitive currents. The potency and mechanisms of actions of ralfinamide provide a hypothesis for the anti-nociceptive properties found in animal models.

From Discussion:
The overall conclusion is that the voltage-dependent inhibitory properties of ralfinamide against tetrodotoxin-resistant and tetrodotoxin-sensitive currents in dorsal root ganglion neurons provide a hypothesis to explain the anti-neuropathic properties demonstrated in animal models. The stronger anti-hyperalgesic and anti-allodynic effects in animal models of ralfinamide as compared to carbamazepine may arise from the ability of ralfinamide in clinical relevant doses to strongly attenuate both tetrodotoxin-resistant and tetrodotoxin-sensitive currents in dorsal root ganglion neurons, while clinical doses of carbamazepine may mainly influence tetrodotoxin-sensitive currents. The tetrodotoxin-sensitive and especially the tetrodotoxin-resistant blocking properties of ralfinamide are further increased when the currents are subjected to high frequency repetitive activation, as in hyperexcitability conditions.