Anecdotal complaints of loss of libido are quite common among both male and female ETS patients. Consider this blog entry from Kevan Wylie M.D.:
Perhaps the loss of libido is another example of compensatory hyperactivity of the SNS in the still-working lower part of the body. Unlike most blood vessels, which have only sympathetic innervation, the vessels in the sex organs also have parasympathetic. Sexual arousal is associated with co-activation of both the SNS and PSNS.
In men, an erection requires a surge of parasympathetic activity in the penis. Similarly, in women, clitoral erection and vaginal lubrication are initiated and maintained by parasympathetic dominance. If the SNS was operating hyperactively, this could prevent the PSNS dominance required for a strong erection and adequate lubrication. Even if sexual arousal is still mechanically possible, it is certainly plausible that a shift in the balance between SNS and PSNS could cause the patient to just “feel wrong” down there.
On the other hand, to achieve orgasm, the co-activation must shift to favor the SNS. If indeed SNS hyperactivity is present in the lower body, the CS model would predict greater difficulty achieving orgasm, but a more intense sensation if achieved.
A 1991 dog study entitled “The sympathetic role as antagonist of erection” stated “Our results suggest that an elevated central sympathetic tone may be one of the causes of psychogenic impotence.” (Diederichs et al. 1991)
Given the persistence of anecdotal complaints, human clinical study is warranted, provided patients are given adequate warning prior to surgical sympathectomy.
The MDs who responded to Dr. Wylie’s post suggested the patient’s loss of libido was due to purely psychological reasons, but this begs the question. Why would ETS lead to psychological problems? The CS model offers ample reasons for that, but there may be a purely physical explanation as well.“I have a patient who had a T2 sympathectomy and is now free of facial flushing, Goosebumps and sweating in the upper limbs. However, he also claims complete loss of libido. How can this be the case and has anyone any suggestions for managing this man in his early 30’s? His adrenal and pituitary function is normal other than a raised growth hormone of 34 (IGF-1 normal). Kind regards Kevan R Wylie MD Consultant in Sexual Medicine Porterbrook Clinic, Sheffield.” (Wylie)
Perhaps the loss of libido is another example of compensatory hyperactivity of the SNS in the still-working lower part of the body. Unlike most blood vessels, which have only sympathetic innervation, the vessels in the sex organs also have parasympathetic. Sexual arousal is associated with co-activation of both the SNS and PSNS.
In men, an erection requires a surge of parasympathetic activity in the penis. Similarly, in women, clitoral erection and vaginal lubrication are initiated and maintained by parasympathetic dominance. If the SNS was operating hyperactively, this could prevent the PSNS dominance required for a strong erection and adequate lubrication. Even if sexual arousal is still mechanically possible, it is certainly plausible that a shift in the balance between SNS and PSNS could cause the patient to just “feel wrong” down there.
On the other hand, to achieve orgasm, the co-activation must shift to favor the SNS. If indeed SNS hyperactivity is present in the lower body, the CS model would predict greater difficulty achieving orgasm, but a more intense sensation if achieved.
A 1991 dog study entitled “The sympathetic role as antagonist of erection” stated “Our results suggest that an elevated central sympathetic tone may be one of the causes of psychogenic impotence.” (Diederichs et al. 1991)
Given the persistence of anecdotal complaints, human clinical study is warranted, provided patients are given adequate warning prior to surgical sympathectomy.
