There is no evidence whatsoever that the sympathetic ganglia have any regulatory function on sweating

There is no "signal that tells the body to sweat excessively". The nervous system doesn't work like that. Worse, it implies that there is some separate signal that tells the body to sweat "normally" which, again, is implied to be unaffected by the surgery. It's nonsense and an affront to all that is known about neuroanatomy and neurophysiology.

Of all the lies and distortions, this is the one that pisses me off the most. Not only is it demonstrably false, it is criminally misleading in terms of what it leads the patient to expect. There no evidence whatsoever that the sympathetic ganglia have any regulatory function. Regulation if sympathetic activity occurs in the brain, not the sympathetic ganglia.

Why the hell don't they call it what it is?: sympathetic denervation surgery (which is a fancy name for a particular type of nerve injury). It eliminates excessive sweating by eliminating the ability to sweat at all (anhidrosis) over a large area. It achieves this end in the most brutal way possible: by permanently destroying the neural pathways. Any statement or implication that sympathectomy reduces sweating to normal levels or improves the regulation of sweating in any way is a boldfaced lie.

So numerous are the possible variations that the outcome of a sympathectomy is unpredictable

The sympathetic pathways to the heart are extremely variable in their topography, and the diversity of arrangements encountered accounts for the morphological contradictions in the literature. So numerous are the possible variations that the outcome of a sympathectomy is unpredictable. Where denervation is incomplete, collateral sprouting and regeneration of nerves could even lead to hyperstimulation via the sympathetic pathways.
http://onlinelibrary.wiley.com/doi/10.1002/aja.1001240203/abstract

sympathectomy created imbalance of autonomic activity and functional changes of the intrathoracic organs - yet it is heavily advertised on the internet as the best elective procedure for sweaty hands or blushing

Surgical thoracic sympathectomy such as ESD (endoscopic thoracic sympathectic denervation) or heart transplantation can result in an imbalance between the sympathetic and parasympathetic activities and result in functional changes in the intrathoracic organs.
Therefore, the procedures affecting sympathetic nerve functions, such as epidural anesthesia, ESD, and heart transplantation, may cause an imbalance between sympathetic and parasympathetic activities (1, 6, 16, 17). Recently, it has been reported that ESD results in functional changes of the intrathoracic organs.


In conclusion, our study demonstrated that ESD adversely affected lung function early after surgery and the BHR was affected by an imbalance of autonomic activity created by bilateral ESD in patients with primary focal hyperhidrosis.
Journal of Asthma, 46:276–279, 2009
http://informahealthcare.com/doi/abs/10.1080/02770900802660949

important relationship among cognitive performance, HRV, and prefrontal neural function

These findings in total suggest an important relationship among cognitive performance, HRV, and prefrontal neural function that has important implications for both physical and mental health. Future studies are needed to determine exactly which executive functions are associated with individual differences in HRV in a wider range of situations and populations.
http://www.ncbi.nlm.nih.gov/pubmed/19424767

Low HRV is a risk factor for pathophysiology and psychopathology

The intimate connection between the brain and the heart was enunciated by Claude Bernard over 150 years ago. In our neurovisceral integration model we have tried to build on this pioneering work. In the present paper we further elaborate our model. Specifically we review recent neuroanatomical studies that implicate inhibitory GABAergic pathways from the prefrontal cortex to the amygdala and additional inhibitory pathways between the amygdala and the sympathetic and parasympathetic medullary output neurons that modulate heart rate and thus heart rate variability. We propose that the default response to uncertainty is the threat response and may be related to the well known negativity bias. We next review the evidence on the role of vagally mediated heart rate variability (HRV) in the regulation of physiological, affective, and cognitive processes. Low HRV is a risk factor for pathophysiology and psychopathology. Finally we review recent work on the genetics of HRV and suggest that low HRV may be an endophenotype for a broad range of dysfunctions.
http://www.ncbi.nlm.nih.gov/pubmed/18771686

Surgical sympathectomy is the gold standard of treatment for this disease, by which all other treatments must be judged

http://www.fortishospitals.com/heart-care/treatments-and-procedures/vats-sympathetectomy.html

acute response to surgical denervation and abrupt release of sympathetic tone

Intraoperative predictability of successful outcome depends on monitoring of the acute response to surgical denervation and abrupt release of sympathetic tone.

Information on the long-term physiological sequelae is emerging rapidly. Preoperatively, in addition to abnormal sudomotor control, sympathetic cardiovascular regulation may be affected mildly in severe cases of hyperhidrosis. A blunted reflex bradycardia response to parasympathomimetic maneuvers such as Valsalva maneuver or cold water face immersion, as well as an increased heart rate response
to orthostatic stress, suggests a hyperfunctioning sympathetic discharge that is reversed after ETS.25,69 Because sympathetic cardiac accelerator fibers exit the spinal cord from segments T1 to T4, ETS is believed to simulate a mild physiological !-adrenergic blockade.70 This is because the heart rate at rest and during maximal exercise is lower 6 weeks postoperatively

DIAGNOSIS AND TREATMENT OF HYPERHIDROSIS,  CONCISE REVIEW FOR CLINICIANS
Mayo Clin Proc.     •     May 2005;80(5):657-666