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PubMed1993

A case of periodic sweating associated with a subarachnoid cyst and multifocal dystonia.

A case of periodic sweating with multifocal dystonia is reported in a 60-year-old woman. At the age of 48 years, she presented with involuntary twisting of the lower face on the right. Six months later she noticed similar movements in the head and right arm. Four years later she began having attacks of generalized sweating over the whole face, anterior region of the trunk and both arms. The attacks occurred hourly each and every day. They lasted for about 10 min and were followed by voluntary urinary voiding. The biochemical and laboratory investigations showed no abnormalities except for the luteinizing hormone and follicle-stimulating hormone values that were below normal. The computerized tomography and magnetic resonance imaging scans revealed a suprasellar cyst. Clonazepam was introduced with partial improvement of the dystonic movements but not of the sweating attacks. The patient refused surgery. Acetazolamide was added and reduced the sweating attacks. We speculate that the periodic sweating may be related to cerebrospinal fluid production and cyst enlargement, hence the ability of acetazolamide, which reduces cerebrospinal fluid production, to reduce attacks.

Arachnoid Cysts↗

PubMed1994

Sweating and vascular responses in the face: normal regulation and dysfunction in migraine, cluster headache and harlequin syndrome.

At least four neural mechanisms influence facial blood flow. Firstly, sympathetic vasoconstrictor fibres exert a tonic constrictor influence on the vasculature of the ears, lips and nose, and sparsely supply other parts of the face. Secondly, the sympathetic nervous system actively dilates the cutaneous vasculature of the face during heat stress and emotion. Thirdly, parasympathetic vasodilator reflexes in the facial and glossopharyngeal nerves increase blood flow to the exocrine glands and tissues of the eyes, nose and mouth when these tissues are irritated. Fourthly, axon reflexes release vasoactive peptides from sensory fibres, which participate in local inflammatory responses. The sympathetic nervous system normally controls facial sweating. However, after injury to postganglionic sympathetic fibres, parasympathetic fibres sometimes make functional connections with sweat glands, so that parasympathetic reflexes provoke pathological sweating. In this review, new information about the neural pathways and stimuli which influence facial sweating and blood flow is summarized, and this is followed by a discussion of the pathophysiology of extracranial vascular disturbances and facial sweating in migraine, cluster headache and harlequin syndrome.

Blood Vessels↗

PubMed1979

The significance of drug analysis of sweat in respect to rapid screening for drug abuse.

Morphine and methamphetamine, which are excreted in the sweat, are detected by the use of routine serological and physicochemical techniques for urinary examinations. Screening for drug abuse can be done with the same accuracy of that of urine. Rapid excretion of the drug via kidney (within one day) is followed by a slow but steady excretion of the sweat gland. Methamphetamine given orally in a dose of 10 mg is excreted in the sweat at a constant rate (1.4 microgram/ml). No significant difference of the amount excreted by both systems is found. Alveolar lining seems to prevent the elimination of the volatile methamphetamine via respiration. Not only narcotics and stimulants, but also many alkaloids and barbituarates are excreted in the sweat and detected quantitatively by the same principles. The toxicological analysis of the sweat promises a new scope of forensic investigation.

Forensic Medicine↗

PubMed1997

Clonidine decreases vasoconstriction and shivering thresholds, without affecting the sweating threshold.

PURPOSE: This study was conducted to test the hypothesis that clonidine produces a dose-dependent increase in the sweating threshold and dose-dependent decreases in vasoconstriction and shivering thresholds. METHODS: Six healthy subjects (two female) were studied on four days after taking clonidine in oral doses of either 0 (control), 3, 6 or 9 micrograms.kg-1. The order followed a balanced design in a double-blind fashion. Oesophageal temperature and mean skin temperature (from 12 sites) were measured. Subjects were seated in 37 degrees C water which was gradually warmed until sweating occurred (sweat rate increased above 50 g.m-2.h-1). The water was then cooled gradually until thresholds for vasoconstriction (onset of sustained decrease in fingertip blood flow) and shivering (sustained elevation in metabolism) were determined. Thresholds were then referred to as the core temperature, adjusted to a designated mean skin temperature of 33 degrees C. RESULTS: High dose clonidine similarly decreased the adjusted core temperature thresholds for vasoconstriction by 1.16 +/- 0.30 degrees C and for shivering by 1.63 +/- 0.23 degrees C (P < 0.01). The dose response effects were linear for both cold responses with vasoconstriction and shivering thresholds decreasing by 0.13 +/- 0.05 and 0.19 +/- 0.09 degree C.microgram-1 respectively (P < 0.0001). The sweating threshold was unaffected by clonidine, however the interthreshold range between sweating and vasoconstriction thresholds increased from control (0.19 +/- 0.48 degree C) to high dose clonidine (1.31 +/- 0.54 degrees C). CONCLUSION: The decreases in core temperature thresholds for cold responses and increased interthreshold range are consistent with the effects of several anaesthetic agents and opioids and is indicative of central thermoregulatory inhibition.

Adrenergic alpha-Agonists↗

PubMed2003

Monitoring sweat calcium using skin patches.

The purpose of this study was to determine whether a simple noninvasive sweat collection method using skin patches would be useful in monitoring sweat Ca and to determine changes in dermal Ca loss during a bed rest study testing a resistive exercise countermeasure. The study showed that the technique was highly reproducible: the mean intra-subject variation approached zero and the inter-individual variability (%CV) varied from 18% to 32% for the three anatomical regions (arm, chest, and back) tested. There was less than 10% difference in sweat Ca excretion from different skin regions within the same individual at a given time point. A calculated estimate of total body sweat excretion for 12 bed rest subjects was 35 +/- 4 mg/day (mean +/- SE), close to published whole body measurements. Bed rest testing showed no significant differences with or without exercise when conducted in a temperature-controlled environment. We conclude that the skin patch technique is useful for monitoring changes in sweat Ca.

Adult↗

PubMed2004

Heat and water vapour transfer of protective clothing systems in a cold environment, measured with a newly developed sweating thermal manikin.

A moveable sweating thermal manikin has recently been developed. Thermal and water-vapour resistances of three kinds of cold-protective clothing ensembles, laminated with polytetrafluoroethylene, polyurethane and without a laminate were measured, with the aid of the manikin in a cold environment of 5 degrees C with a relative humidity of 70% and an air velocity of around 1.5 m s(-1). Two sweating rates of 65 and 130 g m(-2) h(-1) were employed. Supplied heat fluxes in both of the sweat rates ranged from 350 W m(-2) to 400 W m(-2). To maintain a comfortable condition, the skin wettedness (w) (mean weighted value) had to be kept at < or = 0.6. The measurements obtained from the manikin when testing the three ensembles were w=0.3 (approximately) for the low sweat rate and w > or = 0.6 for the high sweat rate, irrespective of the property differences among the ensembles. In addition, the condensation in the ensembles in comparison with those calculated from an analytical equation is discussed. Condensation mass fluxes in the ensembles obtained by experiment and those from the calculation agreed sufficiently well. Thus, distribution of the condensation in the ensembles was estimated using the equation.

Cold Temperature↗

PubMed2005

Sex- and menstrual cycle-related differences in sweating and cutaneous blood flow in response to passive heat exposure.

To examine sex- and menstrual cycle-related differences in thermoregulatory responses to heat exposure, ten young women and six young men were heated passively by immersing their legs in water heated to 42 degrees C for 60 min (in ambient conditions of 30 degrees C and 45% relative humidity). The women underwent heat exposure during the mid-follicular (F) and mid-luteal (L) phases of the menstrual cycle, which were confirmed by assaying plasma female reproductive hormones. The rectal and mean body (T(b)) temperatures of women in the L phase were significantly greater than those of women in the F phase and of men during a pre-heating equilibration period (28 degrees C) and during heat exposure. During heat exposure, the local sweat rates (m(sw)) on the forehead, chest, back, and forearm of women in either phase were significantly lower than those of men, but the thigh (m(sw)) was similar to that of men. The m(sw) did not change at any site during the different phases of the menstrual cycle. The cutaneous blood flow (%LDF) was significantly greater on the thigh for women in either phase compared with men, but no difference was found at any other site (forehead, chest, back, and forearm). The %LDF on the back was significantly greater for women in the L phase than in the F phase, but those at other sites were similar in both phases. We conclude that, compared with men, heat loss from women depends more on cutaneous vasodilation (especially on the thigh) than on sweating, irrespective of the phase of the menstrual cycle. This phenomenon was due to peripheral mechanisms, as reflected in the greater slope of the relationship between %LDF and T(b) lower slope of the relationship between m(sw)) and frequency of sweat expulsion, and lower sweat output per gland. The menstrual cycle modified the T(b) threshold for vasodilation and sweat onset in women. Therefore, the sex difference in the T(b) threshold was more marked for women during the L phase than during the F phase. Moreover, the menstrual cycle modified the slope of the relationship between %LDF on the back and T(b).

Adult↗

PubMed1997

The effect of change in skin temperature due to evaporative cooling on sweating response during exercise.

The purpose of this study was to investigate whether there are any effects of skin temperature changes on sweating response in the first few minutes of mild exercise. Six healthy males performed a bicycle exercise at 100 W (50 rpm) for 30 min under an ambient temperature of 23 degrees C (40% RH). Esophageal temperature (Tes), mean skin temperature (Tsk), local skin temperature at the lower left scapula (Tsl), local sweating rate (Msw) and cutaneous blood flow by laser-Doppler flowmetry (LDF) were measured continuously. Although Tsl decreased markedly just after the onset of sweating, Tsk did not change. Msw did not increase constantly in the early stages of exercise, and there was a temporary interruption in the increase of Msw. This interruption in sweating was affected by the rate of change in Tsl rather than by the absolute value of Tsl, since there was a positive and significant correlation between the time of the interruption in the increase of Msw and the rate of decrease in Tsl (y = 6.47 x +0.04; r = 0.86, P < 0.05). The results suggest that sweating response in the early stages of exercise may be influenced by changes in local skin temperature due to evaporative cooling.

Adult↗

PubMed2004

[Botulinum toxin for treatment of gustatory sweating. A prospective randomized study].

BACKGROUND: Botulinum toxin A has meanwhile become a proven method for treatment of gustatory sweating (focal hyperhidrosis, Frey's syndrome). Clear-cut recommendations regarding dosage of botulinum toxin A in Frey's syndrome are currently not available. The aim of this prospective randomized study therefore was to investigate botulinum toxin A with respect to its efficacy in Frey's syndrome, the ideal dose yielding maximal duration of the effect, and patient contentedness as well as unwanted side effects in patients of the Clinic of OMF Surgery at the Ruhr-University of Bochum. PATIENTS AND METHOD: Twenty patients suffering from severe Frey's syndrome as a result of operations of the parotid gland were examined with the starch iodine test according to Minor. The gustatory skin areas were re-examined after intracutaneous injection of botulinum toxin A for up to 1 year. The patients ( n=20) were randomly assigned to two different treatment groups (group I: 2 MU/cm(2), n=10; group II: 3 MU/cm(2), n=10). RESULTS: Mean sweating skin areas in the two treatment groups ranged between 39+/-9 and 32+/-12 cm(2), respectively. A single injection of 3 MU botulinum toxin A resulted in a nearly complete blockade of gustatory sweating for the observation period of 1 year. In the group treated with 2 MU botulinum toxin A, 44% of the total gustatory skin areas were still sweating, thus necessitating a second injection of botulinum toxin A in these patients. CONCLUSION: Intracutaneous injection of botulinum toxin A represents a highly effective and minimally invasive procedure for the treatment of Frey's syndrome. This study shows for the first time that a dosage of 3 MU/cm(2) of botulinum toxin A achieves a complete and reliable blockade of gustatory sweating lasting for at least 12 months. This dose may therefore be recommended for treatment of this syndrome.

Adult↗

PubMed1985

Neonatal treatment with nerve growth factor antiserum eliminates cholinergic sympathetic innervation of rat sweat glands.

Most mammalian sympathetic neurons are noradrenergic, and their dependence upon nerve growth factor (NGF) for survival during development is well established. A minor population of sympathetic neurons, including those that innervate sweat glands, is cholinergic. To determine whether cholinergic sympathetic neurons, like their noradrenergic counterparts, require NGF during development, neonatal rats were treated with NGF-antiserum and 3 weeks later their sweat glands were examined for the presence of innervation. Acetylcholinesterase (AChE) staining and vasoactive intestinal polypeptide-like immunoreactivity (VIP-IR) which mark the mature sweat gland innervation were absent from the sweat glands of the anti-NGF treated animals. Further, when the glands were examined with the electron microscope, no axons or nerve terminals were evident. These observations indicate that the elaboration of the sweat gland plexus is NGF-dependent and suggest that at least one population of cholinergic sympathetic neurons in the rat requires NGF for survival. Our findings are consistent with the idea that during development NGF is a required trophic factor not only for noradrenergic sympathetic but also for cholinergic sympathetic neurons.

Acetylcholinesterase↗

PubMed1988

Evidence for neurotransmitter plasticity in vivo. II. Immunocytochemical studies of rat sweat gland innervation during development.

Previous studies of the cholinergic sympathetic innervation of rat sweat glands provide evidence for a change in neurotransmitter phenotype from noradrenergic to cholinergic during development. To define further the developmental history of cholinergic sympathetic neurons, we have used immunocytochemical techniques to examine developing and mature sweat gland innervation for the presence of the catecholamine synthetic enzymes tyrosine hydroxylase (TH) and dopamine beta-hydroxylase (DBH) and for two neuropeptides present in the mature cholinergic innervation, vasoactive intestinal peptide (VIP) and calcitonin gene-related peptide (CGRP). In 7-day old animals, intensely TH- and DBH-immunoreactive axons were closely associated with the forming glands. The intensity of both the TH and DBH immunofluorescence decreased as the glands and their innervation developed. Neither TH-IR nor DBH-IR disappeared entirely; faint immunoreactivity for both enzymes was reproducibly detected in mature animals. In contrast to noradrenergic properties, the expression of peptide immunoreactivities appeared relatively late. No VIP-IR or CGRP-IR was detectable in the sweat gland innervation at 4 or 7 days. In some glands VIP-IR first appeared in axons at 10 days, and was evident in all glands by 14 days. CGRP-IR was detectable only after 14 days. In addition to VIP-IR and CGRP-IR, we examined the sweat gland innervation for several neuropeptides which have been described in noradrenergic sympathetic neurons including neuropeptide Y, somatostatin, substance P, and leu- and met-enkephalin; these peptides were not evident in either developing or mature sweat gland axons. Our observations provide further evidence for the early expression and subsequent modulation of noradrenergic properties in a population of cholinergic sympathetic neurons in vivo. In addition, the asynchronous appearance during development of the two neuropeptide immunoreactivities raises the possibility that the expression of peptide phenotypes may be controlled independently.

Animals↗

PubMed1991

Lead in sweat and its relationship to salivary and urinary levels in normal healthy subjects.

Sweat was collected from the arms of 24 normal healthy subjects while they sat in a hot chamber. Blood, urine and saliva samples were also collected. These were analyzed for lead by atomic absorption spectrophotometry. Sweat lead levels recorded in this study are lower than those previously reported. Subjects with mean blood lead levels of 8.62 micrograms dl-1 (range 6-13.6) had mean sweat levels of 5.2 micrograms l-1 (range 1.5-13.0), approximately 25% of their urinary levels. Although salivary lead levels with a mean of 4.8 micrograms l-1 (range 2.5-10) are comparable to sweat levels, their relationship to blood lead levels is poor (r = -0.186 compared with r values of 0.7208 and 0.234 for sweat and urinary levels, respectively).

Calcium↗

PubMed1995

Mechanisms of physiological gustatory sweating and flushing in the face.

Mechanisms of physiological gustatory sweating and flushing were investigated in 21 patients with a facial nerve lesion compromising parasympathetic outflow to the lacrimal gland, and in 13 patients undergoing diagnostic blockade of the stellate ganglion. Vascular responses and electrodermal activity (which reflects sweating) were monitored on each side of the forehead before and during gustatory stimulation with chillies or Tabasco sauce (derived from chillies). Vascular responses in the cheeks were also monitored in 14 patients with a facial nerve lesion. Sympathetic blockade increased gustatory vasodilatation but prevented gustatory sweating on the blocked side of the forehead. A facial nerve lesion did not affect gustatory sweating in the forehead or vasodilatation in the cheeks. However, a facial nerve lesion impaired vasodilatation in the forehead in all six patients who ate chillies, and also in four of five patients whose blood vessels dilated extensively on the normally-innervated side of the forehead when the patients tasted Tabasco sauce. These findings suggest that sympathetic sudomotor activity mediates physiological gustatory sweating in the forehead, whereas sympathetic vasoconstrictor tone inhibits gustatory vasodilatation in the forehead. A parasympathetic vasodilator reflex in the facial nerve contributes actively to gustatory flushing in the forehead, but some other unidentified mechanism influences vascular responses in the cheeks.

Adrenergic Fibers↗

PubMed1986

Receptors for vasoactive intestinal peptide on isolated human sweat glands.

Human sweat gland function is predominantly under cholinergic control. Sweat secretion may also be regulated by Vasoactive Intestinal Peptide (VIP), which coexists with acetylcholine in nerves to sweat gland acini and ducts. We have examined the expression of VIP receptors on isolated human eccrine sweat glands. Two classes of specific binding sites for VIP were demonstrated: one with high affinity (Kd = 0.58-2.4 nM), and another with low affinity (Kd = 175-288 nM). The data suggest a physiological regulatory role for VIP in sweat gland function.

Eccrine Glands↗

PubMed1992

Cholinergic sensitivity of the eccrine sweat gland in trained and untrained men.

The purpose of this study was to compare the cholinergic responsiveness of the human sweat gland in trained and untrained men. Eighteen healthy male volunteers (9 trained, 9 sedentary) served as subjects. Pilocarpine concentration vs. sweat rate dose-response curves were obtained from each subject using iontophoresis. From these measurements, maximal iontophoretic sweat rate (SRmax) was determined and correlated with each subject's maximal oxygen uptake (VO2max). The trained group had a significantly (P less than 0.05) greater mean SR max and their mean dose-response curve was shifted up and to the left, as compared to the sedentary controls. Furthermore, VO2max was significantly correlated with SRmax (r = 0.76). These findings suggest that the modification occurring in the human sweat gland after training may include improvements in both SRmax and cholinergic sensitivity, and support the hypothesis that the potentiation in sweating following training is achieved via a peripheral mechanism.

Adult↗

PubMed2004

Chemically and electrically induced sweating and flare reaction.

Both thin afferent (nociceptors) and efferent (sympathetic sudomotor) nerve fibers can be activated electrically and chemically, resulting in neurogenic erythema and sweating. These reactions have been used before to assess the impairment of sympathetic and nociceptor fibers in humans. In this study, electrically induced sweating and erythema were assessed simultaneously in the foot dorsum and thigh, and were compared to chemically induced activation. Reproducible intensity-response relations (stimulation intensities 0-30 mA, 1 Hz) were obtained from 32 subjects. The steepest increase of the sweat response was induced at lower intensities as compared to that of the erythema (18.3 mA vs. 25.7 mA, p<0.01) and reached a plateau for intensities above 25 mA, suggesting lower electrical thresholds for sudomotor fibers. Maximum flare areas induced electrically with 30 mA were smaller than those evoked chemically (flare size: 4.5 cm2 vs. 10.6 cm2). In contrast, the electrically evoked sweating rate was higher than that evoked chemically (acetylcholine, or ACh; sweating rate 0.31 vs. 0.21 microl/cm2/min, p<0.01), which might be attributed to an increased effectiveness of synchronized discharge in sympathetic fibers upon electrical stimulation.

Acetylcholine↗

PubMed2004

Sweat gland morphology and periglandular innervation in essential palmar hyperhidrosis before and after treatment with intradermal botulinum toxin.

BACKGROUND: Intradermal botulinum toxin (Btx) produces long-lasting relief of focal hyperhidrosis, but its mechanism of action is poorly understood. OBJECTIVE: To study the effect of Btx A on the size and innervation of sweat glands in patients with palmar hyperhidrosis. METHODS: Palmar skin biopsy was performed in 26 hyperhidrotic patients before scheduled Btx treatment and in 11 controls. Twelve of the patients also underwent biopsy 1 to 6 months after the Btx injections. Sweat gland morphology was investigated by light microscopy; the cross-sectional area of the secretory tubule and its lumen was measured by image analysis. Immunofluorescence (IF) with antibodies to the neural markers protein gene product 9.5 (PGP 9.5) and growth-associated protein 43 (GAP 43), and to vasoactive intestinal peptide (VIP) and calcitonin gene-related peptide (CGRP), was used to analyze the periglandular innervation. RESULTS: The gross morphology of the sweat glands was similar in patients and controls, with no significant differences in tubular and luminal areas between the groups. After Btx treatment, the tubular dimensions remained unchanged, but the lumen tended to be smaller ( P = .07). Around the glands, increased GAP 43 staining indicating sprouting was seen within 3 months after Btx treatment ( P = .016); whereas the PGP 9.5 staining was decreased in most specimens ( P = .09) indicating lack of functional nerve growth. No change in VIP or CGRP immunoreactivity was observed. CONCLUSIONS: The sweat glands appear structurally normal in hyperhidrotic patients before Btx therapy, whereas after therapy the luminal area of the gland is frequently diminished. The IF data GAP 43/PGP 9.5 suggest that Btx therapy induces long-standing functional denervation of the sweat glands, which might explain its anti-transpiratory efficacy.

Adolescent↗

PubMed2002

Detection of dermcidin-derived peptides in sweat by ProteinChip technology.

Recently, a novel antimicrobial peptide DCD-1, derived from the Dermcidin (DCD) gene and secreted by sweat glands, has been described by Schittek et al. [Nat. Immunol. 2 (2001) 1133.]. Here we describe the application of the surface-enhanced laser desorption/ionisation (SELDI) technology for the detection of DCD-1 and other dermcidin-derived peptides directly from microlitre amounts of human sweat. The advantages of the technique are as follows: (a) it can be carried out with ease and rapidity; (b) multiple samples can be processed simultaneously; (c) prior purification is not required; and (d) only a limited sample volume is necessary for both protein profiling and semiquantitation. Profiling of human sweat from various donors revealed that in addition to DCD-1, other DCD-derived peptide species were also present in significant quantities. Four of five identified peptides were DCD-1 related, while the fifth corresponded to a portion of the DCD protein outside the DCD-1 core. This provides clues as to how the novel protein is processed to its active form, though further work remains to elucidate this fully. Thus, we have demonstrated the applicability of such technology to the detection of DCD-1 and for the protein profiling of sweat in general. Such studies could reveal valuable new biomarkers for diagnosis and treatment of skin and sweat gland disorders.

Amino Acid Sequence↗