Quantification of eccrine sweat glands with acetylcholine sweat-spot test and anatomical redistribution of sweating after T2–T3 thoracoscopic sympathicolysis

Ramos, Ricard; Masuet, Cristina; Badía, M.; Pace, Valerio; Macía, Iván; Escobar, Ignacio; Villalonga, R.; Moya, Juan

doi:10.1007/s00464-008-9922-z

Cited by 6 publications

(4 citation statements)

References 21 publications

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“…The cause of this residual sweating is speculated to be the result of nerve regeneration through the stellate ganglia, increased neural traffic through existing pathways from the stellate, denervation supersensitivity of adrenergic or cholinergic receptors, or reorganization and up-regulation of the density of sweat glands. 23 These speculative mechanisms may also explain the 5 bilateral palmar hyperhidrosis failures; 3 patients experienced failure within 3 months postoperatively; 1 patient between 10 months and 12 months; and 1 patient between 16 and 18 months postoperatively. Two patients had mild increased compensatory hyperhidrosis on the trunk and thighs but did not seek postoperative treatment; the 3 other patients in whom surgery failed had no increased sweating elsewhere.…”

Section: Resultsmentioning

confidence: 99%

Endoscopic Transthoracic Limited Sympathotomy for Palmar-Plantar Hyperhidrosis: Outcomes and Complications During a 10-Year Period

Atkinson

Fode-Thomas

Fealey

et al. 2011

Mayo Clinic Proceedings

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Section: Resultsmentioning

confidence: 99%

Endoscopic Transthoracic Limited Sympathotomy for Palmar-Plantar Hyperhidrosis: Outcomes and Complications During a 10-Year Period

Atkinson

Fode-Thomas

Fealey

et al. 2011

Mayo Clinic Proceedings

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“…as few as 3 days in most subjects) of functional cholinergic denervation is sufficient to cause these responses in humans. Furthermore, in the aforementioned studies, responses were suppressed or inhibited 14,32,33 as opposed to the response being completely abolished in the present study (Figs 1 and 2).…”

Section: Discussionsupporting

confidence: 43%

“…On the other hand, cholinergic denervation decreases AQP5 expression in the rat submandibular glands, intraglandular injection of BTX reduces salivary secretion due in part to glandular atrophy, and surgical sympathectomy or spinal cord transection decreases sweat gland sensitivity 14,15,32,33 . Thus, as other possibilities, the inhibition of AQP5 expression, atrophy of the sweat gland, and/or reduced sweat gland sensitivity to cholinergic stimulation secondary to disruption of neuronal transmission following BTX administration may contribute to the responses shown in Figures 1 and 2, although it remains unknown whether < 10 days (e.g.…”

Section: Discussionmentioning

confidence: 99%

Botulinum toxin abolishes sweating via impaired sweat gland responsiveness to exogenous acetylcholine

Shibasaki

Davis

Cui

et al. 2009

British Journal of Dermatology

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Summary Background Botulinum toxin A (BTX) disrupts neurotransmitter release from cholinergic nerves. The effective duration of impaired sweat secretion with BTX is longer relative to that of impaired muscle contraction, suggesting different mechanisms in these tissues. Objectives The aim of this study was to test the hypothesis that BTX is capable of altering sweating by reducing the responsiveness of the sweat gland to acetylcholine. Methods BTX was injected into the dorsal forearm skin of healthy subjects at least 3 days before subsequent assessment. On the day of the experiment, intradermal microdialysis probes were placed within the BTX-treated area and in an adjacent untreated area. Incremental doses of acetylcholine were administered through the microdialysis membranes while the sweat rate (protocol 1; n = 8) or a combination of sweat rate and skin blood flow (protocol 2; n = 8) were assessed. Results A relative absence of sweating was observed at the BTX site for both protocols (protocol 1: 0·05 ± 0·09 mg cm−2 min−1; protocol 2: 0·03 ± 0·04 mg cm−2 min−1, both at the highest dose of acetylcholine), while the sweat rate increased appropriately at the control sites (protocol 1: 0·90 ± 0·46 mg cm−2 min−1; protocol 2: 1·07 ± 0·67 mg cm−2 min−1). Cutaneous vascular conductance increased to a similar level at both the BTX and control sites. Conclusions These results demonstrate that BTX is capable of inhibiting sweat secretion by reducing the responsiveness of the sweat gland to acetylcholine, while not altering acetylcholine-mediated cutaneous vasodilatation.

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“…Not including broader search terms such as “endocrine disrupting compound” in the abstract or keyword list may limit the ability of systematic reviews to identify them, particularly reviews which are not chemical specific. For example, as a follow-up exercise, a search using the terms “PFOA” and “hypothalamus” turned up only three papers, none of which were salient for the present review, but a search of “phthalate” and “hypothalamus” turned up 29, two of which had data on the pre-pubertal brain but were not identified in the initial search conducted for this review ((Ramos, Coesel et al 2008, Ramos, Masuet et al 2009); the first of which examined sex-specific effects and the second looked only at males). For the present review it was not feasible to search for papers chemical by chemical as there are literally hundreds of EDCs and searching for the most well-known ones (eg.…”

Section: Discussionmentioning

confidence: 99%

Assessment of sex specific endocrine disrupting effects in the prenatal and pre-pubertal rodent brain

Rebuli

Patisaul

2016

The Journal of Steroid Biochemistry and Molecular Biology

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Background Brain sex differences are found in nearly every region of the brain and fundamental to sexually dimorphic behaviors as well as disorders of the brain and behavior. These differences are organized during gestation and early adolescence and detectable prior to puberty. Endocrine disrupting compounds (EDCs) interfere with hormone action and are thus prenatal exposure is hypothesized to disrupt the formation of sex differences, and contribute to the increased prevalence of pediatric neuropsychiatric disorders that present with a sex bias. Objective Available evidence for the ability of EDCs to impact the emergence of brain sex differences in the rodent brain was reviewed here, with a focus on effects detected at or before puberty. Methods The peer-reviewed literature was searched using PubMed, and all relevant papers published by January 31, 2015 were incorporated. Endpoints of interest included molecular cellular and neuroanatomical effects. Studies on behavioral endpoints were not included because numerous reviews of that literature are available. Results The hypothalamus was found to be particularly affected by estrogenic EDCs in a sex, time, and exposure dependent manner. The hippocampus also appears vulnerable to endocrine disruption by BPA and PCBs although there is little evidence from the pre-pubertal literature to make any conclusions about sex-specific effects. Gestational EDC exposure can alter fetal neurogenesis and gene expression throughout the brain including the cortex and cerebellum. The available literature primarily focuses on a few, well characterized EDCs, but little data is available for emerging contaminants. Conclusion The developmental EDC exposure literature demonstrates evidence of altered neurodevelopment as early as fetal life, with sex specific effects observed throughout the brain even before puberty.

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Quantification of eccrine sweat glands with acetylcholine sweat-spot test and anatomical redistribution of sweating after T2–T3 thoracoscopic sympathicolysis

Cited by 6 publications

References 21 publications

Endoscopic Transthoracic Limited Sympathotomy for Palmar-Plantar Hyperhidrosis: Outcomes and Complications During a 10-Year Period

Endoscopic Transthoracic Limited Sympathotomy for Palmar-Plantar Hyperhidrosis: Outcomes and Complications During a 10-Year Period

Botulinum toxin abolishes sweating via impaired sweat gland responsiveness to exogenous acetylcholine

Assessment of sex specific endocrine disrupting effects in the prenatal and pre-pubertal rodent brain

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