--since my neural investigations included a major component of looking for causes of central pain syndrome, such as MS and seizure damage . . .

Central Pain Syndrome is possible as an adjunct to any of a number of conditions that cause pain--neural or otherwise. But perhaps it is good, for the sake of argument, to divide central pain into the kind that comes from central sensitization--that is, when long term-pain signals from damage in other parts of the body cause trophic changes in the neural network and a perpetuation of "painful" firing patterns, such as is assumed to be happening in reflex sympathetic dystrophy/complex regional pain syndrome--and that caused by direct traumatic damage to the spinothalamic sensory tracts. The latter, which is what the painonline.com people usually refer to (I'm a member of the CPS alliance) simply has a different starting point--the initial damage is in those spinothalamic tracts, due to stroke, MS, HIV infection, B12 deficiency, seizure damage, and a number of other possible causes. The symptoms, though, may be body-wide, and may be indistinguishable from those of widespread, diffuse peripheral neuropathies, or from those of RSD/CRPS or other central sensitization syndromes.

There are, supposedly, some clinical observations that can distinguish Central Pain from direct spinothalamic damage. The symptom of "temporal summation" is allegedly one; this occurs when initial slight stimulatin is not immediately parasthetic or painful, but becomes so over some seconds in an increasingly intense manner, and then fades slowly over seconds to minutes. Supposedly, peripherally damaged nerves are painful immediately to touch. But, I have spoken with people with no central pain signs, but evidence of peripheral neuropathy, who have this temporal summation symptom, and there are people who've experienced both types of sensations.

Moreover, I suspect Kathi's report of her drug responses may not be universal, either. While the mechanisms of Neurontin and Lyrica are not fully understood, it is surmised that they work by making the inhibitory neurotransmitter GABA more available to the central nervous system, stopping or at least slowing erroneous propogation of pain signals. So, since they have CNS actions, they might work on both peripheral and central syndromes--indeed, the anti-epileptics are prescribed for people with central pain such as from MS and for those with pain from peripheral damage.

What I do suspect is that anyone with long-term, chronic pain probably experiences some degree of the first type of central sensitization. In that case, nontraditonal therapies to re-train the neural firing patterns--visualization, meditation, targeted exercise--would seem to have a very good chance of succeeding. I speculate they would be somewhat less effective for the second kind of Central Pain (primary spinothalamic damage).