Compensatory Changes
From Corposcindosis
Contents |
Compensatory Hyperhidrosis
The most well-documented symptom of corposcindosis is “compensatory hyperhidrosis”. While patients cannot sweat at all above the nipple line, they tend to sweat profusely on the rest of the body.
Compensatory Hyperhidrosis The most common areas for compensatory hyperhidrosis are the abdomen, lower back, crotch, and the backs of the legs. Complaints of soaked underwear or shirts are common. Patients report sweating at lower temperatures than before surgery, greater volumes of perspiration, and longer times waiting for sweating to stop.
Mechanism for Compensatory Hyperhidrosis
Compensatory hyperhidrosis is also referred to as “compensatory sweating” and “reflex sweating”. The mechanism of this surgically-induced excessive lower body sweating is “poorly understood” (Kopelman et al. 2000). Some hypotheses have been advanced:
The "compensatory cooling" hypothesis
The body cannot sweat on part of the body, so it compensates for the loss of evaporative cooling in that area by creating more evaporative cooling in another area.
Given the nature of the autonomic nervous system to maintain homeostasis by compensating in response to stressors, this hypothesis has an immediate plausibility. However, under this hypothesis, simply wetting the head and shoulders with water (imitating the lost sweating) would be expected to relieve compensatory hyperhidrosis. Several ETS patients have reported that compensatory hyperhidrosis occurs regardless of putting water on the head and shoulders.
The "reflex" hypothesis
Nerve impulses from the lower body travel upwards along the sympathetic chain and encounter dead ends and scar tissue, which causes a rebounding or reflexive signal to be sent back down the chain, stimulating excessive lower-body sweating.
The CS model generates a third hypothesis that may explain or at least contribute to the phenomenon:
The “false message” hypothesis
“The local and mean skin temperature are important for providing sensory input [to the control center]” (Kenney). Recall that thermoreceptors located in the denerved area are surrounded by skin that is up to 12 degrees F hotter than normal (see Gyftokostas et al. 1992). Messages about environment temperature are exaggerated, leading to exaggerated sweating response.
We call for more empirical research on total body sweating, and the etiology of compensatory hyperhidrosis. Patients should be warned about compensatory hyperhidrosis.
Total Body Perspiration
While historically used to treat a variety of complaints, currently the most common indication for ETS surgery is “hyperhidrosis”, that is excessive sweating. Patient consent is ordinarily premised around a desire to “reduce” the excessive sweating. (see Addenbrooke consent form). A natural curiosity would lead us to wonder whether the surgery actually reduced the total amount of sweating, or in fact increased it. Thusfar, only one study has attempted to answer that question.
“The effect of upper dorsal thoracoscopic sympathectomy on the total amount of body perspiration.” (Kopelman et al. 2000)
By 2000, Israeli surgeons Hashmonai, Kopelman and colleagues had noticed that “compensatory hyperhidrosis is a disturbing sequela of this operation”. (Kopelman et al. 2000, emphasis added). They conducted a very straightforward test on their ETS patients. They weighed the subjects, then sent them into the sauna to sweat for 10 minutes, then weighed them again to see how much water had been lost. This process was done before and after surgery.
“The amount of perspiration induced by the sauna bath ranged from 60 to 480 g, with a mean value of 185.29 +/- 125.80 g, before the operation, and from 60 to 540 g, with a mean value of 265.88 +/- 154.05 g, after the operation (P = 0.0113).” (Kopelman et al. 2000).
Total body sweating has increased 43% on average.
Let’s see what these numbers actually describe. Body sweating has been divided into two distinct regions, an upper region comprising about 1/3 of total body surface which can no longer sweat at all, and a lower region comprising the remaining 2/3 of total body surface which now sweats so hyperactively that total body sweating is 43% higher than it was initially. Since the 43% total increase is being generated by only 67% of the body surface, that part of the body must have increased its sweating by 113%. (67% x 213% = 143%). In other words, the lower body now sweats more than twice as much as it did before surgery.
Thus Koppelman casts serious doubt on the efficacy of ETS as hyperhidrosis treatment. If the goal is reduced sweating, thoracic sympathectomy is highly unlikely to achieve that. Research on total body sweating is called for. Patients should be warned that total body sweating is expected to go up, not down.
Sexual Function
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.:
“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)
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.
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.
Other Compensatory Hyperactivity
While the exact mechanics of compensatory hyperactivity are not known, the phenomenon exists without a doubt in regard to sweating. Thus we can suppose that, whatever the mechanism, other sympathetically innervated effectors in the still-innervated zone may exhibit a similar hyperactive response, especially if those effectors are similar to sweat glands in that they are either
- distributed throughout the innervated and denervated areas and/or
- innervated only by the SNS, and not the PSNS
Blood vessels are distributed throughout the body, and most of them have only sympathetic innervation. Adipose Tissue is also widely distributed. Will either of these exhibit compensatory hyperactivity in the still-innervated areas? If so, what would sympathetic hyperactivity cause?
The kidneys are thought to only have sympathetic innervation, not parasympathetic. They are expected to remain fully innervated after ETS, but could they experience sympathetic hyperactivity? If so, how might that affect their function?
