Just Updating

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.

I cannot tell you how perfectly this article describes me and probably a lot of others here, but most haven't had a chance to study it.
I did.
It is from one of the post above (THANK YOU!)
http://www.painonline.com/mt-archive...ntly_aske.html

I'll quote a few lines:
"Burning dysesthesia, "like acid under the skin", is the central symptom, but not all have it in a severe version. The same goes for ..... pains, which range from lancinating or shooting, electric like pains, to exaggerated pins and needles, cramping or tightening pain
in the muscles, overfulness in any hollow organ such as gut or bladder,
and marked increase in sensitivity to normal pain (hyperpathia)."

"..... pain cannot be seen on conventional MRI, on CT, and especially not on plain x-rays, yet many patients have been told they are malingering because these studies turn up negative. Consequently, many doctors, utterly without knowledge in the field, abuse nerve injury pain patients. This abuse can take the form of doubting that the pain exists or is severe, recommending surgery or medicines that are of no possible benefit, becoming insulting or angry if some medicine does not help, or refusing to treat CP adequately."

"What is loss of working memory?
.......similar to a computer attempting to run on less K." (K is memory...one K is very very little memory.

"What is hypersensitization?
It happens every day with common sunburn, or when we spill caustic drain cleaner on our hands. As everyone knows, sunburn is delayed. Central pain is also delayed and appears AFTER the initial injury." (sometimes my pain is worse tomorrrow because of what I did today.

"Are central pain subjects really still human?
Probably not fully. Who is fully human when in continual burning pain? However, if you will overlook the depression and flat emotional tone, and extend an increased measure of humanity to them, you will find it worth the effort for you and a blessing to them. The heart is softened but very heavy. You must not ask what they cannot give. No one with chronic severe pain is reeking with happiness. If they laugh or joke, do not assume they actually feel the humor. What they may be feeling is severe pain, but they desire human contact like anyone else. Don't ask too much of them socially. They will tire quickly of the act, and may be forced to retire even if they would prefer to continue to visit. If you are content to give, without expecting them to think and feel as normal people do, you will recognize the humanity in them, as you would in any other person. Severe pain is dehumanizing and exhausting, so family and friends must make adjustments and allowances for someone with severe central pain. Their little contribution to the conversation may be a "widow's mite" type of thing. (giving more than you really have to give)

"Is paralysis or central pain more disabling?
From the surveys, there is no hesitation in saying that severe c. pain is considerably more disabling than lack of mobility. This makes sense if one reflects on what inability to move means, and what agony means."

Even though most of this was copy / paste, it has taken the whole day to do this!!! or am I the only one who can relate to this? Hope

No, you're not. It's a wonderful site, beautifully written, that speaks volumes to me too, even though my RSD is nowhere near as severe as yours.
Thanks for that,
all the best.