Patients with palmar hyperhidrosis have been reported to have a much
more complex dysfunction of autonomic nervous system, involving compensatory high parasympathetic
activity as well as sympathetic overactivity (13, 14), suggesting that sympathicotomy initially induces a
sympathovagal imbalance with a parasympathetic predominance, and that this is restored on a
long-term basis (14). Therefore, thoracic sympathicotomy may cause a temporary impairment of the
caudal-to-rostral hierarchy of thermoregulatory control and changes in microcirculation. The reduction
of finger skin temperature on the non-denervated side may be due to either a decrease in the cross-
inhibitory effect or the abnormal control of the inhibitory fibers by the sudomotor center (6).
Vasoconstrictor neurons have been found to be largely under the inhibitory control of various afferent
input systems from the body surface, whereas sudomotor neurons are predominantly under excitatory
control (15). The basic neuronal network for this reciprocal organization is probably located in the spinal
level (15). Therefore, the reduction in the contralateral skin temperature may be explained by cross-
inhibitory control of various afferent in the spinal cord.
In particular, our study showed that, following bilateral T3 sympathicotomy, the skin temperatures on
the hands increased whereas the skin temperatures on the feet decreased. These findings suggest a
cross-inhibitory control between the upper and lower extremities. However, the pattern of skin
temperature reduction on the feet differed from that on the contralateral hand. The skin temperature on
the feet did not decrease after right T3 sympathicotomy but decreased significantly after bilateral T3
sympathicotomy.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2722005/
