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Purpose When performing endoscopic thoracic sympathectomy (ETS) in palmar hyperhidrosis patients, a device can be used to measure sweat volume pre- and postoperatively in order to assess indications and treatment effects. In this study, we measured changes in the dynamics of sweating in hyperhidrosis patients pre- and postoperatively and compared the values with those in healthy subjects without hyperhidrosis. Methods The patient group comprised 25 persons with palmar hyperhidrosis who were scheduled for ETS. The dynamics of sweating was measured at 1 day prior to surgery and at 2 days postoperatively, in 18 patients at > 1 year postoperatively in another palmar hyperhidrosis group, and in 20 healthy subjects without hyperhidrosis. A device for measuring local sweat volume was applied at the thenar eminence of both palms. Indicators established were basal sweat rate (BSR; mg/min/cm2), peak sweat rate (PSR; mg/min/cm2) during mental stress (sympathetic sweating response), sweat volume (SV), and sweat time (ST; s). Results After surgery, all of the indicators were significantly reduced in hyperhidrosis patients and there was very little response to mental stress. The subgroup of these patients assessed at > 1 year after ETS showed a trend of increased BSR similar to that of healthy subjects. These changes did not correlate with the extent of the removal surgery. Preoperatively, hyperhidrosis patients had significantly greater BSR, PSR, and SV and longer ST than healthy subjects. Conclusion All of the sweating parameters were increased in palmar hyperhidrosis patients prior to surgery. Immediately after ETS, all these parameters were significantly reduced. At > 1 year after ETS, the BSR had increased to a level similar to that of the healthy volunteers, although PSR did not respond to mental stress.

The aim of this study was to report a method that quantifies axon reflex sweating from individual sweat glands with nanoliter precision. Measurement of the axon reflex is generally expressed as a single variable (e.g., the flare area or total sweat volume). High-definition videography enables precise measurement of sweating from single, axon reflex-stimulated sweat glands (SGs). The sudomotor axon reflex was activated in healthy subjects and subjects with peripheral neuropathy by iontophoresis of 10% acetylcholine. Sweating was simultaneously imaged for 5 min in a 2.5-cm2 area of iodine-coated skin to one side of the stimulus, using a customized high-resolution camera with starch-coated transparent tape over a rigid viewing screen. A second video then imaged the directly stimulated sweating. The indirect sweat response was quantified in terms of sweat gland number and distance from the stimulation site (radius), sweat rate per gland, and total sweat. Fifty-two healthy control and twenty subjects with neuropathy underwent testing at the foot, calf, thigh, and hand. Normal ranges were calculated for SG density, mean sweat rate per SG, and total sweat volume. Neuropathy subjects demonstrated reduced sweating, and values differed between body sites. The described method precisely measures the total and individual sweat output of hundreds of SGs in response to a standard, axon reflex-mediated stimulus, and quantifies alterations in axon reflex sweating seen in peripheral neuropathy.

Purpose: The aim of this study was to review the evidenceon the epidemiology, physiopathology, categorization, andmanagement of cholinergic urticaria. We specificallyfocused on several subtypes of cholinergic urticaria andinvestigated the relationship between cholinergic urticariaand idiopathic anhidrosis.Methods: Using an integrative approach, we reviewedpublications addressing the epidemiology, clinical features,diagnostic approach, physiopathology, subtype classifica-tion, and therapeutic approach to cholinergic urticaria.Results: Multiple mechanisms were found to contribute tothe development of cholinergic urticaria. This disordershould be classified based on the pathogenesis and clinicalcharacteristics of each subtype. Such a classification sys-tem would lead to better management of this resistantcondition. In particular, sweating function should be givenmore attention when examining patients with cholinergicurticaria.Conclusions: Because cholinergic urticaria is not a homo-geneous disease, its subtype classification is essential forselection of the most suitable therapeutic method

Currently available techniques for the evaluation of small fiber neuropathy and related sudomotor function remain suboptimal. Electrochemical skin conductance (ESC) has recently been introduced as a simple noninvasive and fast method for the detection of sudomotor dysfunction. The purpose of this review is to synthesize and appraise research using ESC measurements for sudomotor evaluation in adults. Electronic databases including MEDLINE and Google Scholar were searched (up to March 13, 2017). The search strategy included the following terms: "electrochemical skin conductance,” “Sudoscan,” and “EZSCAN.” Evidence was graded according to defined quality indicators including (1) level of evidence; (2) use of established tests as reference tests (e.g., quantitative sudomotor axon test [QSART], sympathetic skin responses [SSR], thermoregulatory sweat test [TST], and skin biopsies to assess sudomotor and epidermal small fibers); (3) use of consecutive/non-consecutive subjects; and (4) study design (prospective/retrospective). A total of 24 studies met the inclusion criteria. These were classified into preclinical, normative, comparative/diagnostic, or interventional. ESC measurement properties, diagnostic accuracy, and similarities to and differences from established tests were examined. ESC measurements expand the arsenal of available tests for the evaluation of sudomotor dysfunction. The advantages and disadvantages of ESC versus established tests for evaluating sudomotor/small fiber function reviewed herein should be used as evidence to inform future guidelines on the assessment of sudomotor function.

To examine symptoms indicating central nervous system (CNS) autonomic dysfunction in pediatric patients with migraine and tension-type headache.A retrospective chart review assessed six symptoms (i.e. constipation, insomnia, dizziness, blurry vision, abnormal blood pressure, and cold and clammy palms and soles) indicating central nervous system (CNS) autonomic dysfunction in 231 patients, ages 5-18 years, diagnosed with migraine, tension-type headache (TTH), or Idiopathic Scoliosis (IS).Higher frequencies of "insomnia," "dizziness," and "cold and clammy palms and soles" were found for both migraine and TTH patients compared to the IS control group (P 0.001). Frequencies of all six symptoms were greater in TTH than migraine patients with "cold and clammy palms and soles" reaching significance (P 0.001).The need for prospective research investigating autonomic dysfunction in pediatric headache patients is discussed.

© 2015, Springer-Verlag Berlin Heidelberg. Objective: Research has suggested that the autonomic nervous system (ANS) is involved in the experience of vasomotor symptoms (VMS) during menopause. We examined the relationship of VMS intensity and heart rate variability (HRV), a measure of ANS function. Methods: Women (n = 282) were recruited from three American states for a clinical trial of yoga, exercise, and omega-3 fatty acid supplements for VMS. To be eligible, women had to report at least 14 VMS per week, with some being moderate to severe. Sitting electrocardiograms were recorded for 15 min using Holter monitors at both baseline and 12-week follow-up. Time and frequency domain HRV measures were calculated. Women completed daily diary measures of VMS frequency and intensity for 2 weeks at baseline and for 1 week at the follow-up assessment 12 weeks later. Multivariable linear regression was used to assess the relationship between VMS and baseline HRV measures and to compare change in HRV with change in VMS over the 12 weeks. Results: Baseline HRV was not associated with either VMS frequency or intensity at baseline. Change in HRV was not associated with change in VMS frequency or intensity across the follow-up. Interpretation: Heart rate variability (HRV) was not associated with basal VMS frequency or intensity in perimenopausal and postmenopausal women experiencing high levels of VMS. Autonomic function may be associated with the onset or presence of VMS, but not with the number or intensity of these symptoms.

Endoscopic thoracic sympathectomy/sympathotomy for the treatment of palmar hyperhidrosis is generally performed by either cutting or clamping the sympathetic chain. However, it remains unclear as to which of these methods is more effective and has fewer side effects. This study was conducted to compare the effects of sympathotomy by cutting or clamping at T3 on two outcomes—postoperative palmar sweating and compensatory sweating; it also evaluated postoperative patient satisfaction. The participants were among 289 patients who underwent bilateral sympathotomy at T3 for palmar hyperhidrosis. These patients were sent questionnaires by mail to assess their self-reported degree of postoperative palmar sweating and compensatory sweating, as well as their level of satisfaction. Of the 92 patients who responded to the questionnaire, 54 had undergone sympathotomy by cutting (cutting group) and 38 by clamping (clamping group). The degree of postoperative palmar sweating was significantly lower in the cutting group than in the clamping group. However, compensatory sweating was significantly more severe in the cutting group than in the clamping group. No significant difference was observed in the degree of patient satisfaction between the groups. Sympathotomy by clamping at T3 was less effective in reducing the primary symptom of postoperative palmar sweating, but induced less compensatory sweating than did sympathotomy by cutting at T3. However, both methods were similar with regard to patient satisfaction. The degree of postoperative palmar sweating and the severity of compensatory sweating were inversely correlated with the degree of patient satisfaction.

In mammals, sweating is a multifunctional response that aids in locomotion, thermal regulation, self-protection, and communication of psychological state. Humans possess three types of sweat glands (apocrine, eccrine, and apoeccrine) that are differentially distributed on the body surface and make unique contributions to these distinct functions of the sweating response. In humans, eccrine glands, which are widely distributed on hairy skin, play an important role in thermoregulation. They are also found on the glabrous skin of the palm and sole, where they are not usually activated by heat, but rather by deep respiration, mental stress, and local tactile stimulation. Sweating on the palm and sole, so-called "emotional sweating", acts to prevent slippage while grasping or performing a delicate task using the fingertips. Although the central pathways of emotional sweating are not yet elucidated in detail, it is thought that the amygdala, cingulate cortex, and medulla participate via efferent fibers that descend through the spinal cord and connect to preganglionic sympathetic neurons in the nucleus intermediolateralis. The limbic system, including the amygdala and cingulate cortex, is critical for emotional processing and many cognitive functions. Thus, measurement of sweat output on the palm or sole is useful for evaluating sympathetic function and limbic activity in autonomic and psychiatric disorders.

We report a case of idiopathic pure sudomotor failure (IPSF) in which serum carcinoembryonic antigen (CEA) levels elevated at onset, and remained high while anhidrosis lasted. We considered that changes in serum levels of CEA were related to the disease activity of IPSF.

Objective Though hyperhidrosis is generally considered a subjectively perceived disease, it seems more and more doubtful that merely subjective evaluation is sufficient to qualify the patient to surgery. The aim of this study was to develop further gravimetry as a method of evaluation of sweating intensity and determination of the applicability of it in post-operative follow-up of primary hyperhidrosis (PHH) patients. Methods Total of 1,485 gravimetry assays has been performed in 343 patients treated for hyperhidrosis and in 220 healthy volunteers. In all of the subjects the measurements were taken from four localizations (face, hands, armpits and trunk) and normalized by body surface of the participant. The measurements were taken twice for every participant to obtain test–retest correlations. Mean values and standard deviations (SD) have been evaluated and on that basis reference values were quantified. Thresholds for diagnosis of hyperhidrosis were quantified on the basis of normal distribution theory as healthy population mean +2 SD. Results In healthy volunteers, mean value of gravimetrically evaluated intensity of sweating were: facial: 19.15 ± 14.97 mg/min/m2, palmar: 18.49 ± 14.06 mg/min/m2, axillary: 42.39 ± 47.08 mg/min/m2 and plantar: 15.77 ± 16.87 mg/min/m2. Thresholds for diagnosis of hyperhidrosis were quantified, respectively as: 49, 46, 136 and 50 mg/min/m2. The overall test–retest correlation was 0.71. Interpretation Gravimetry is easy, reproducible and fast method of evaluation of sweating. The reference values are stable and can serve as a qualifying and follow-up tool for evaluation of the patients with PHH in any localization.

The biochemical mechanisms by which hyperglycemia causes microvascular disease and neuropathy are poorly understood. Experimental studies have established that oxidative stress is present in diabetic rodents with neuropathy, and that antioxidant therapy is protective. Oxidative stress is also present in human diabetes, but its clinical importance is uncertain. We examined several biochemical measures of oxidative stress in 37 patients with recent-onset (less than 2 years) type 1 diabetes annually in a 3-year longitudinal study. We also performed a comprehensive annual evaluation of somatosensory and autonomic nerve function. A total of 41 control subjects were studied. Malondialdehyde excretion, a measure of lipid peroxidation, was 1.5l ± .1 μmol/g creatinine in the control subjects, but 2.43 ± . 3 in the diabetic patients in year one, 2.39 ± .2 in year two and 1.92 ± .15 in year three, which was different from controls across all years; p

Autonomic nervous system (ANS) activity may play an important role in the development of lower urinary tract symptoms (LUTS). Men with severe LUTS and men with mild or no LUTS completed the Valsalva maneuver, quantitative sudomotor axon reflex test, tilt-table, and deep breathing tests. There were no differences between men with severe LUTS compared to men with mild or no LUTS (all P values > 0.05). Systemic ANS tests may not be useful in detecting the underlying physiologic changes that lead to LUTS in aging men.

Sudomotor dysfunction is common in many subtypes of neuropathy but is one of the earliest detectable neurophysiologic abnormalities in distal small fiber neuropathy. Clinical assessments of sudomotor function include thermoregulatory sweat testing (TST), quantitative sudomotor axon reflex testing (QSART), silicone impressions, the sympathetic skin response (SSR), the acetylcholine sweat-spot test and quantitative direct and indirect axon reflex testing (QDIRT). These testing techniques, when used in combination, can detect and localize pre- and postganglionic lesions, can provide early diagnosis of sudomotor dysfunction and can monitor disease progression or disease recovery. In this article, we describe many of the common clinical tests available for evaluation of sudomotor function with focus on the testing methodology and limitations while providing concrete examples of test results.

Postural tachycardia syndrome (POTS) is a fairly common condition that may or may not be associated with autonomic neuropathy. In a retrospective analysis, we compared two groups of patients based on clinical and autonomic criteria, those with POTS in isolation (POTS-Alone), and POTS with evidence of autonomic neuropathy (POTS-AN). Of 260 records reviewed, 57 patients met the criteria for POTS; 38 (67%) patients assigned to the POTS-Alone group and 19 (33%) patients assigned to the POTS-AN group. A decreased sweat output on the quantitative sudomotor axon reflex test is the most frequent abnormal finding in the POST-AN group suggesting sympathetic cholinergic neuropathy. Clinically, headache and gastrointestinal symptoms were more frequent among the POTS-AN group. Therefore, POTS may exist in isolation and may differ from those associated with AN.

Compensatory sweating (CS) is the most common adverse event and the main cause of dissatisfaction among patients undergoing a VATS sympathectomy for the treatment of primary hyperhidrosis. It has been described that obese individuals experience more sweating than thinner ones. The aim of this study is to identify the Body Mass Index (BMI) and the level of resection as predictive factors for CS and its relation to levels of patient satisfaction following the procedure.From October 1998 to June 2003, 102 patients undergoing VATS sympathectomies (51 for palmar hyperhidrosis, PH, and 51 for axillary hyperhidrosis, AH) were prospectively surveyed. They were divided into three groups according to their BMI: Group I was composed of 19 patients with BMI20 (9 patients with PH and 10 with AH); Group II was composed of 52 patients with 20or =BMI25 (25 with PH and 27 with AH); and Group III was composed of 31 patients with BMIor =25 (17 with PH and 14 with AH). Each procedure was simultaneously and bilaterally performed under general anesthesia using two 5.5 mm trocars and a 30 degrees optic system.Patients treated for PH (resection of T2-T3) had more severe CS than those with AH (resection of T3-T4) (p=0.007) and the greater the BMI, the greater the severity of the CS (p0.001). No statistically significant difference was found between the BMI bands in relation to the degree of satisfaction (p=0.644), nor when we compared the degree of satisfaction to the degree of CS (p=0.316).The greater the BMI, the more severe the CS, but this did not correlate with the patients' level of satisfaction. Avoiding the resection of T2 sympathetic ganglia is also important in reducing the intensity of CS.

The aim of this study was to determine whether the sympathetic skin response (SSR) recorded from the big toe is more sensitive than standard SSR recorded from the sole for the detection of sudomotor fiber dysfunction in diabetic neuropathy. We recorded big toe SSR (SSRBT) and plantar SSR (SSRP) in 17 diabetic patients with non-disabling neuropathy (group A), 13 patients with disabling neuropathy (group B) and 30 age-matched normal controls. With regard to controls, SSRP amplitude was reduced only in group B. In contrast, SSRBT amplitude was reduced in both groups of patients (p

Although thermoregulatory sweat testing is commonly used to assess the autonomic nervous system, the power of this stimulus to induce sweating has not been studied. In 8 healthy male subjects, the authors quantitated sweat rates, core temperature, heart rate, and blood pressure during clinical thermoregulatory sweat testing, a separate exercise protocol, and with exercise added to thermal conditions. The authors found that (1) the addition of exercise to the thermal environment produced no further increase in sweat rate (3,841+/-948 versus 3,888+/-866 nl/mn - cm2); (2) maximum sweat rates closely corresponded to the theoretical maximum (6,000 nl/mn - cm2) derived from single gland studies; (3) sweat rates vary across subjects, but are similar across sites in any one individual; (4) core temperature rise is a major determinant of cardiovascular load in both thermal and exercise settings; (5) blood pressure decreased 28/11 mm Hg during thermal load, but increased 26/10 mm Hg with exercise, in agreement with current understanding of muscle and skin vascular physiology. The authors conclude that clinical thermoregulatory testing conditions produce maximum sweat rates in humans.

We compared quantitative sudomotor axon-reflex test responses in persons with normal and impaired glucose tolerance (IGT). Responses were significantly impaired in those with IGT, which may be indicative of early distal small fiber neuropathy.

The objective of the present investigation was to describe and localize autonomic dysfunction in acute and chronic stages of complex regional pain syndrome (CRPS). Patients were investigated twice: the first investigation was performed as soon as diagnosis was established during the acute stage of CRPS and the second investigation was performed about 2 years later. Twenty-one patients completed the follow-up investigation. The median duration of CRPS was 5 (range 2–21) weeks at first investigation and 94 weeks (22–148) at follow-up. Skin temperature was recorded by thermography, sudomotor function was assessed by thermoregulatory sweat test (TST) and quantitative sudomotor axon reflex test (QSART). Skin temperature was warmer on the affected side at the first investigation (P

A total of 114 patients with various sympathetic disorders underwent endoscopic sympathetic block over different thoracic ganglions by the clipping method. The advantages of this method include the recognition of the clipped level, changeability, and reversibility. However, 4.4% of patients were unilaterally clipped at the wrong level.

Centrally and locally mediated sympathetic vasoconstrictor responses in skeletal muscle and subcutaneous tissue were studied in six patients with definite multiple sclerosis and severely affected thermoregulatory sweating. The purpose of the study was to evaluate vasomotor function in patients with pronounced thermoregulatory dysfunction and to differentiate between locally and centrally elicited vasomotor reflexes in two different tissues. The method used, the 133-Xenon washout technique, makes such a distinction possible. In spite of the severe sweating disturbances, we found centrally and locally mediated sympathetic vasomotor reflexes to be preserved in skeletal muscle and subcutaneous tissue. The results support the view that sudomotor and vasomotor functions are independently controlled. Previously described differences in sympathetic vasoconstrictor responses in skeletal muscle and subcutaneous tissue in several other neurological disorders are not present in patients with multiple sclerosis, based on our results.

Forehead sweating developed in 78% of medical students when they attempted tracheal intubation on a simulator, and increased during subsequent attempts if the first attempt was not successful. Thus, forehead sweating may be a useful index of mental strain.

QSART (quantitative sudomotor axon reflex testing) was performed in a patient with idiopathic pure sudomotor failure. Generalized reduction in thermoregulatory sweating and complete absence of axon reflex sweating were observed, suggesting a deficit of sweat gland cholinergic synaptic transmission or receptors. QSART responded promptly to treatment. Putative pathophysiological mechanisms are discussed.

The neurohumoral, peptidergic and biochemical responses to supine leg exercise were studied in two groups with primary autonomic failure: Shy-Drager syndrome (SDS, n = 15) and pure autonomic failure (PAF, n = 15), to determine if these accounted for exercise-induced hypotension and the greater blood pressure (BP) fall in PAF. Responses were compared to normal subjects (controls, n = 15), in whom BP rose with exercise. Resting plasma noradrenaline (NA) was higher in controls than SDS, and was lowest in PAF. With exercise, NA increased in controls, with a small rise in SDS, but no change in PAF. Resting plasma adrenaline (A) was higher in controls and SDS than PAF, with no change during exercise. Plasma dopamine was unrecordable at all stages in all groups. Resting plasma renin activity (PRA) was higher in controls than SDS and PAF, and was unchanged with exercise in all groups. Plasma insulin, C-peptide and serum growth hormone (GH) were similar at rest and with exercise in the three groups. Plasma glucose was higher at rest in SDS and PAF, and increased with exercise in all three groups. In conclusion, neither exercise-induced hypotension, nor the differences between SDS and PAF could be related to abnormalities in the release of A, PRA, insulin, glucose or GH. The abnormal NA response to exercise was consistent with the BP fall being due to inadequate compensatory sympathetic activity. In SDS, the small NA increase, in the presence of supersensitivity, may have reduced their BP fall as compared to PAF. These results suggest that impaired sympathetic neural activity is a key factor in exercise-induced hypotension.

The sweatspot test assesses the local sweat response to an intradermal injection of acetylcholine. It has been reported as a more sensitive indicator of autonomic dysfunction in impotent diabetic men than either pupillary or cardiovascular tests, and has been used to establish the presence of autonomic dysfunction in patients with idiopathic chronic constipation. However, the usefulness of this test as a simple and quick method of diagnosing autonomic dysfunction in an elderly population has not been established. This is important given the high prevalence of reduced autonomic function with ageing and hypertension. We compared the age-associated responses in the sweatspot test and its relation to cardiovascular autonomic function in elderly normotensive and hypertensive subjects. We studied eleven normotensive and 24 untreated hypertensive elderly subjects (mean age 75.7 years, range 63–85) and compared the results of the sweatspot test to a young control group (n = 11, mean age 32.0 years, range 25–41), and to a standard battery of cardiovascular autonomic function tests. The median sweatspot score was significantly lower in the elderly compared with young subjects (1.9 vs. 12.0, p < 0.0001) although there was no difference between elderly normotensive and hypertensive subjects (1.6 vs. 2.4, p = 0.8). No correlation was demonstrated between the median sweatspot score and the number of abnormal cardiovascular tests. The sweatspot test was grossly abnormal in all elderly subjects and was not correlated to changes in cardiovascular autonomic function. Its diagnostic use in the elderly is therefore of very limited value.

Vasoactive intestinal polypeptide (VIP) and substance P (SP) immunoreactivity are reduced in the cutaneous nerves of diabetic patients with peripheral neuropathy. The functional significance of this finding was studied by measuring the forearm sweat response to intradermal methacholine and the effect of coadministration of VIP and SP in six normal subjects, and in six diabetic patients with neuropathy and eight without. Flare responses to the two peptides were also measured. Methacholine-induced sweat output was significantly greater in neuropathic patients compared with the other groups (p < 0.05), suggesting upper limb denervation supersensitivity. VIP and SP alone did not evoke sweating in any subject. Injection of VIP or SP reduced methacholine-induced sweating to a similar degree in all groups, except that the reduction was smaller in the non-neuropathic group than in the others (p = 0.028 versus normal subjects, p = 0.014 versus neuropathic diabetic patients). Flare responses to the peptides were markedly reduced in the neuropathic patients compared with the other groups (p < 0.01). In neuropathic patients, increased sweat responses and decreased flare coexist with diminished neurophysiological measurements; cutaneous sweating and flare responses provide valuable additional information to conventional methods of neurological assessment in diabetic neuropathy.

Immunoreactivity to various peptides has been demonstrated in nerve terminals around the sweat glands, suggesting a regulatory function for these peptides on sweating. The present study evaluated the calcitonin-gene related peptide and substance P related regulation of sweating in man. Both calcitonin-gene related peptide and substance P, when administered alone, failed to cause sweat secretion, whereas sweating induced by methacholine chloride alone was four times greater when administered with calcitonin-gene related peptide and suppressed by 70% when administered with substance P. The degree of calcitonin-gene related peptide dependent augmentation and substance P dependent suppression of the methacholine chloride induced sweating was dependent on the concentration of calcitonin-gene related peptide and substance P. These findings suggest that calcitonin-gene related peptide enhances cholinergic sweating and substance P inhibits it.

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.

Electrodermal activity (EDA) increases during arousal, emotional stimuli or thermoregulatory sweating and is sometimes apparent in unfiltered ECG recordings. We hypothesized that changes in EDA precede any change in blood pressure (BP) or cerebral blood velocity (CBV) observed at syncope. Data from 70 patients referred for recurrent syncope were retrospectively analyzed. 400Hz continuous waveforms were recorded of BP (Finapres), CBV (transcranial Doppler), expired CO(2) (PCO(2)) and ECG at rest and during 80 degrees head-up tilt (HUT). Two independent investigators determined the onset and termination of EDA in relation to syncope using the raw and a low pass filtered ECG trace. Of the 53 patients who experienced syncope during HUT, 33 (62 %) increased EDA 257 +/- 357s prior to syncope that continued for 75 +/- 73s following syncope. Seven patients (13%) had EDA only after syncope for 208 +/- 213s. In 13 patients (25 %), EDA was not detectable. In most cases, EDA preceded any change in BP, PCO(2) or CBV and persisted past the hemodynamic recovery following syncope. Although variable, EDA may be an objective correlate to the clinical observation that patients' symptoms precede any measurable change in cerebral perfusion. The actual relationship between EDA and symptoms of presyncope requires further investigation.

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.

A 45-year-old woman presented with a 10 year history of asymmetrical facial flushing and sweating after exertion or in hot weather. During these episodes the right side of her face remained dry and white, while the left side normally flushed. Sweating was impaired on the left side in the limbs and trunk. She also had areflexia in the lower limbs and slow pupillary reactions to light and darkness, as seen in Adie's syndrome. The topography of the sweating disorder suggested that the lesion involved the sympathetic pathways at the level of spinal cord. The relationship with the harlequin syndrome and related disorders is discussed.

Compensatory sweating is a major complaint following endoscopic thoracic sympathetic surgery in treatment of palmar hyperhidrosis. T3 ramicotomy was applied in order to decrease compensatory sweating. From Oct 1999 to June 2002, forty patients underwent T3 sympathetic clipping (group I), and 68 patients underwent T3 ramicotomy (group II) to treat palmar hyperhidrosis. We retrospectively analyzed the rate of satisfaction, result of operation, and grade of compensatory sweating. In group I, 36 patients (90%) showed decreased sweating on both hands, 4 patients (10 %) persistent sweating on both hands. In group II, 46 patients (67.6%) had decreased sweating on both hands, 14 patients (23.5 %) had persistent sweating on both hands, and 8 patients (8.9 %) had persistent sweating in one hand. The rate of satisfaction was 82.5 % (33/40) in group I and 67.6 % (46/68) in group II with no significant statistic difference (p = 0.067). Excluding patients with persistent sweating postoperatively, the rate of compensatory sweating in group II was 67.4%, which was significantly lower than in group I 94.1%, with a p value of 0.003. Although the rate of persisting sweating after operation was high, T3 ramicotomy resulted in lower rate of compensatory sweating compared to T3 sympathetic clipping.