Some interesting stuff lately.

We are indeed different in our Central Pains. This variation should indicate to physicians that we are consistent with research, not read as exposing some "inconsistency" that casts doubt on the reality of our pain.

The early comments by Ron Tasker that nerve injury pain is "similar" no matter where injury occurs, was brilliant for its time, but we are now advanced enough to refine matters further, and to note differences.

First, Frederick Lenz, a pain scientist famous for picking up abnormal currents in the CP thalamus, shows in June "Pain" that those of us with loss of cold discrimination are LESS likely to feel severe cold allodynia (pain from non noxious cold); whereas those with CP who RETAIN ability to sense slight cold differences are much MORE likely to have cold allodynia. This highlights the fact that one must retain some nerve function to have severe CP. Intermediate nerve injury is handled poorly by neurological testing. Praises to Lenz for having the sophistication to deal with INTERMEDIATE injury. Neurological pain states are not BLACK or WHITE, they are more subtle than that.

2. HOXA, a gene, when lost in knockout rats, causes degeneration of superficial layers in the cervical, but not the lumbar, spine. The superficial laminae contain the chronic pain tracts. Like any gene, some of us will have more active versions of it than others. Why nature designed a gene for the cervical cord pain tracts but not the lumbar pain tracts is mysterious.

3. MAGUK. It is now shown that NMDA, the chemical behind nerve injury pain, depends on membrane associated guanylate kinase (MAGUK) for its function. (See prior post on kinases, which attach high energy bonds to proteins to make them active). Once again, we will vary in our amounts of MAGUK, from person to person.

4. Alpha2delta. This is a gene produced component of the N-type Calcium channel. This channel is the place where conotoxins work. It has recently been discovered that alpha2delta is UPREGULATED in some, but not all, pain states. All humans vary in their inherited levels of alpha2delta. It also makes the scientists wonder if conotoxin will work mainly on those in whom alpha2delta is upregulated (produced by genes in increased amounts).

How grateful we are the scientists who do this work. The solution to CP will come from scientists who do not doubt for a second the reality of nerve injury pain because there are such excellent animal models. It is too bad clinicians continue to doubt CP, simply because they cannot see it with their eyes and we have no adequate vocabulary. If they will give us the words, we will tell them what is wrong with us. This gap in understanding affects patient care. If only MD's would inject capsaicin, or observe the predictable production of CP in rats in the lab, they would see with the eyes of the PhD scientists. Right now our hope lies not with the MD's but with the PhD's, although of course many of the PhD's have M.D.'s and justify our continued hopes for a cure.

[This message was edited by dejerine on 05-29-04 at 12:39 PM.]

[This message was edited by dejerine on 05-29-04 at 12:44 PM.]

[This message was edited by dejerine on 05-29-04 at 12:48 PM.]