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Sex hormones may influence multiple central nervous system pathways, including effects on the functioning of endogenous opioid systems, dopaminergic function, serotonergic activity, and other endogenous components involved in the nociceptive processing, as discussed below. Free testosterone (T) is transported into the cytoplasm of target tissue cells, where it can bind to the androgen receptor, or can be reduced to 5Ξ±-dihydrotestosterone (5Ξ±-DHT) by the cytoplasmic enzyme 5Ξ±-reductase. 5Ξ±-DHT binds to the same androgen receptor even more strongly than testosterone, so that its androgenic potency is about 5 times that of T.[147] The T-receptor or DHT-receptor complex undergoes a structural change that allows it to move into the cell nucleus and bind directly to specific nucleotide sequences of the chromosomal DNA.
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A study that assessed pain in patients who underwent arthroscopic anterior cruciate ligament (ACL) reconstruction at an outpatient facility in the United States did not find sex differences in pain at the immediate postoperative evaluation.398 However, on the first day after surgery, females had higher mean VAS pain scores than males. Rosseland345,346 assessed pain immediately after and 1-year after an arthroscopic ACL procedure. Two hours after the procedure, 84% of the females reported at least moderate pain compared with 57% for men.
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- Females reported less pain during the luteal versus the follicular phase.143 Jensen and Petersen198 used a model with both heat and capsaicin found that females exhibited greater dynamic tactile allodynia but responded similarly to males in subjective ratings of capsaicin pain and secondary hyperalgesia.
- The epidemiology of chronic pain in children has been reviewed by McGrath,272 but differences between boys and girls were only briefly discussed.
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The 46,XX testicular disorder of sex development (DSD), also known as 46,XX male syndrome, is a rare form of DSD and clinical phenotype shows complete sex reversal from female to male. The sex-determining region Y (SRY) gene can be identified in most 46,XX testicular DSD patients; however, approximately 20% of patients with 46,XX testicular DSD are SRY-negative. The SRY-box 9 (SOX9) gene has several important functions during testis development and differentiation in males, and overexpression of SOX9 leads to the male development of 46,XX gonads in the absence of SRY. In addition, SOX9 duplication has been found to be a rare cause of 46,XX testicular DSD in humans.
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This section was not included in Table 10 since only a limited number of studies have addressed this issue. Experimental manipulations have also been used to examine the influence of gender roles on pain perception. Levine and DeSimone248 reported that men reported less cold pressor pain in the presence of a female versus a male experimenter, whereas pain ratings for females were not influenced by experimenter sex. Similar findings were reported by Gijsbers and colleagues,160 who found that males showed a higher pressure pain threshold when tested by a female versus a male experimenter, whereas femalesβ pain threshold was not influenced by the sex of the experimenter. In addition to those alluded to above, several subsequent reviews of this rapidly expanding literature have been provided, often focusing on particular segments of research regarding sex, gender, and pain. We will conclude with a synopsis of the current state of the literature followed by a discussion of important issues to be addressed in future research.
Furthermore, duplications of the SOX3 locus were detected in three cases of 46,XX testicular DSD10). SOX3 analysis can be considered the next step for the diagnosis of 46,XX SRY-negative testicular DSD with normal copies of SOX9. A family study recently reported that 46,XY persons with a 178 kb duplication in a region about 500 kb upstream of SOX9 were completely normal fertile males, whereas 46,XX SRY-negative persons in the same family with duplications were clinically infertile males6). In this report, two of the three paternal cousins of their probands are known as infertile and the two probands share the same paternal haplotype for the SOX9 region, confirming the possibility that the father was indeed the carrier of the same triplication. Therefore, we should investigate family members of 46,XX male patients caused by SOX9 duplication. The 46,XX testicular disorder of sex development (DSD), also known as 46,XX male syndrome, is a rare condition with an estimated prevalence of one in 20,000 males1).
