Background: Different techniques of video-assisted thoracoscopic sympathetic surgery have become the radical treatments for palmar and axillary hyperhidrosis (AH). However, there is no consensus over which technique can make a minimal incidence of compensatory hyperhidrosis (CH). This study was designed to compare the incidence of CH after different techniques at the same sympathetic levels in the treatment of upper limb and facial hyperhidrosis (FH). Methods: The databases of PubMed, Web of Science, ScienceDirect, Ovid Medline, Embase, and Cochrane Library were searched to identify studies comparing different surgical techniques at the same sympathetic levels for upper limb and FH. The data was analyzed by Revman 5.3 software. Results: A total of ten studies involving 896 patients were included, of whom 149 underwent sympathectomy, 435 underwent sympathicotomy, and 312 under endoscopic sympathetic clip (ESC). Meta-analysis showed that the difference of incidence of CH and patients’ satisfaction was not significant between sympathectomy and sympathicotomy (P=0.05, 0.19, respectively). But, the incidence of CH is significant lower after ESC than after sympathicotomy (OR: 1.58, 95% CI: 1.04–2.38, P=0.03). However, the incidence of moderate/severe CH between these two groups is not significant different (OR: 1.49, 95% CI: 0.93–2.39, P=0.10). Conclusions: If only CH and the same sympathetic levels concerned, sympathectomy and sympathicotomy is equal for upper limb hyperhidrosis and FH. And, ESC should be recommended for a lower incidence of CH, comparing with sympathicotomy.

Copper is a trace element indispensable for cellular physiology, integral to cellular redox balance, and a constituent of enzyme active sites, thereby playing a pivotal role in cellular physiological function. Concerning the pathogenesis of Alzheimer’s disease (AD), the homeostatic balance of copper is perturbed both intracellularly and extracellularly. The copper–amyloid precursor protein (APP) complex facilitates the efflux of copper from cells, leading to intracellular copper depletion. Concurrently, extracellular copper associates with amyloid-beta (Aβ) plaques, precipitating copper-enriched Aβ deposition and augmenting reactive oxygen species (ROS) in the brain tissue, which finally culminates in oxidative brain damage. The interaction between copper and APP enhances the α-secretase pathway of APP processing while suppressing the β-secretase pathway, resulting in an increased production of soluble APP (sAPP), which contributes to neuroinflammation in the brain tissue. Utilizing the affinity of copper for Aβ plaques, the application of chelating agents to sequester copper within the brain can mitigate neurodegeneration associated with AD pathology. Furthermore, the use of metal imaging techniques to detect copper in the brain offers a potential diagnostic tool for the early identification of AD.