The literature have solid evidence that men and women experience pain differently, but do they experience CENTRAL pain differently?
When Dr. Wall endorsed conclusions of a lady researcher who spoke on female divergences in pain at a meeting in Portland in 1994, the conclusions were novel and the idea was so unexpected that attendees at the meeting asked few questions. Time has born her out, however,
Awareness of a feminine perspective on pain seemed a bit surprising at first, coming at a time when the trend was to deemphasize differences between the sexes. However, it was primarily female scientists who drew attention to the differences in male and female brains. First came the quantification of cells in the corpus callosum, which is the communicating area between the left and right hemispheres of the brain.
Objected to at first, there came an awareness that it was important not to overlook different ways in which pain handling might occur. Subsequent studies showed estrogen to have links to the cascade of pain chemicals. This stimulated more consideration as to how significant these differences might be.
Estrogen is actually synthesized in cells of the dorsal horn and rapidly regulates pain. Headache. 2007 Feb;47(2):326. Gupta et al have shown that release of enodmorphin 2 from the spinal cord is regulated by ovarian sex steroids. In models of peripheral pain, estrogen protected against inflammatory pain, as it did in alcoholic painful neuropathy linked both to protein kinase A and to protein kinase C. See Dina, Neuroscience. 2007 Mar 2;145(1):350-6. Other studies show that this if far from the whole story.
Making things more confusing was the finding by Claiborne et al in J Neurosci. 2006 Dec 13;26(50) that estrogen attenuates antinociception while testosterone facilitates it. Hagiwara et al in Neurosci Lett. 2007 Feb 2;412(3):264-7 showed that estrogen (17 B estradiol) treated female rats AND testosterone treated females rats showed significantly higher levels of pain behavior than castrated male rats. Once again, this was in a model of PERIPHERAL nerve injury pain. We still do not have tests for comparison in CENTRAL pain.
ERB 041, a a selective estrogen receptor-beta agonist is antihyperalgesic in both endometriosis and arthritis. See Leventhal et al, Eur J Pharmacol. 2006 Dec 28;553(1-3):146-8.
Timing is also important. You will recall that small cells in the superifical cord are thought to be C fibers, related to slow pain. Androgens are converted to estrogens in the body by aromatization. The enzyme which synthesizes estrogen is called, unsurprisingly, “aromatase”. Whereas there has been a presumption that any estrogenic control of pain probably has a genomic basis, Evrard found a nongenomic route, namely, that the injection of a blocker of aromatase in the superficial cord caused lessened pain almost immedately, within a minute. See Evrard, Am J Physiol Regul Integr Comp Physiol. 2006 Aug;291(2):R291-9
Thus, we are confident that central pain will also be ultimately shown to be impacted by the hormonal milieu.
These findings are sure to cause greater attention to therapies, and attention must be paid not only to which type of Central Pain is being discussed (burning dysesthesia, lancinating, muscle etc.), but also the sex of the subjects.