Sudomotor Activity Research Articles

Shoulder hand syndrome in hemispheric stroke

Shoulder hand syndrome in hemispheric stroke

Sympathetic cholinergic outflow using dynamic evaluation of postganglionic sudomotor activity (DEPSA)

Introduction: Sweating stimulation by iontophoresis of cholinergic agonists produces a sudomotor response not only in the stimulated area but also in adjacent regions. This property is due to the activation of the postganglionic axo-axonic reflex. It is particularly useful to detect peripheral autonomic neuropathies associated with the functional decrease of the activity of sympato-cholinergic postganglionic neurons.

Cardiorespiratory coupling of sympathetic outflow in humans: a comparison of respiratory and cardiac modulation of sympathetic nerve activity to skin and muscle

What is the central question of this study?Muscle sympathetic nerve activity (MSNA) is well known to be modulated by the arterial baroreceptors and respiration, but what are the magnitudes of cardiac and respiratory modulation of skin sympathetic nerve activity (SSNA), which primarily subserves thermoregulation?What is the main finding and what is its importance?Using direct microelectrode recordings of MSNA and SSNA in awake humans, we show that the magnitude of respiratory modulation of SSNA is identical to that of MSNA, the primary difference between the two sources of sympathetic outflow being the greater cardiac modulation of MSNA. This emphasises the role of the baroreceptors in entraining sympathetic outflow to muscle. It is well known that microelectrode recordings of skin sympathetic nerve activity (SSNA) in awake human subjects reveal spontaneous bursts of activity with no overt modulation by changes in blood pressure or respiration, in contrast to the clear cardiac and respiratory modulation of muscle sympathetic nerve activity (MSNA). However, cross-correlation analysis has revealed that, like individual muscle vasoconstrictor neurones, the firing of individual cutaneous vasoconstrictor neurones is temporally coupled to both the cardiac and respiratory rhythms during cold-induced cutaneous vasoconstriction, and the same is true of single sudomotor neurones during heat-induced sweating. Here, we used cross-correlation analysis to determine whether SSNA exhibits cardiac and respiratory modulation in thermoneutral conditions and to compare respiratory and cardiac modulation of SSNA with that of MSNA. Oligounitary recordings of spontaneous SSNA (n = 20) and MSNA (n = 18) were obtained during quiet, unrestrained breathing. Respiration was recorded by a strain-gauge transducer around the chest and ECG recorded by surface electrodes. Respiratory and cardiac modulation of SSNA and MSNA were quantified by fitting polynomial equations to the cross-correlation histograms constructed between the sympathetic spikes and respiration or ECG. The amplitude of the respiratory modulation (52.5 ± 3.4%) of SSNA was not significantly different from the amplitude of the cardiac modulation (46.6 ± 3.2%). Both were comparable to the respiratory modulation of MSNA (47.7 ± 4.2%), while cardiac modulation of MSNA was significantly higher (89.8 ± 1.5%). We conclude that SSNA and MSNA share similar levels of respiratory modulation, the primary difference between the two sources of sympathetic outflow being the marked cardiac modulation of MSNA provided by the baroreceptors.

Thermoreceptors in the upper gastrointestinal tract independently influence sudomotor activity

Warm and cool fluid ingestion during exercise has been previously shown to alter local sweat rate independently of core and skin temperatures. This study strove to identify the location of the thermoreceptors responsible. Six males cycled at 50% VO2max for 75 min in a 24.8 ± 0.7°C and 33.4 ± 3.5% RH environment, while either mouth‐swilling (SW) 1.5°C or 50°C water; or ingesting 1.5°C or 50°C water through a nasogastric (NG) tube in three 3.2 mL·kg−1 boluses after 15, 30, and 45 min of exercise. Mean skin temperature (Tsk), mean local sweat rate (MLSR) and rectal temperature (Tre) were measured continuously. For all trials, Tre and Tskwere similar throughout. In the NG trials, MLSR with 1.5°C water was lower than with 50°C water, after 30, 45, and 60 min (P<0.05), but not after 15 or 75 min (P>;0.05) of exercise. In contrast, during the SW trials, MLSR with 1.5°C and 50°C water was almost identical throughout exercise (P>;0.05). In conclusion, thermoreceptors in the stomach region, rather than thermoreceptors in the mouth, are responsible for the transient alterations of sudomotor activity previously observed following the ingestion of warm and cool water. Supported by NSERC Discovery Grant #386143–2010.

Quantitative assessment of cutaneous C‐fiber function in human skin via direct sudomotor activation

Small sympathetic cholinergic C‐fiber function was examined using intradermal electrical stimulation to activate sudomotor nerves in the forearm skin of healthy humans. We measured local sweat rate (SR) with a 0.7 cm2 capsule containing a humidity sensor and a thermocouple and flushed with dry gas. Two small stainless steel needles were place into the skin (7 mm apart, 2 mm deep) and stimulated at a constant current intensity of 2.5 mA for 30 s and 120 s at frequencies of 0.2, 1, 2, 4, 8, 16, 32, and 64 Hz. The stimulus‐response characteristics were evaluated using a non‐linear four‐parameter logistic curve fitting equation. Peak local SR occurred between 32 and 64 Hz and was similar for 30 and 120 s stimulus duration averaging 0.46 ± 0.2 and 0.49 ± 0.2 mg • min−1 • cm−2, respectively. The EC50 averaged 8.3 ± 0.3 Hz during the 30 sec stimulus but decreased to 3.6 ± 0.05 Hz (p<0.05) during the 120 s stimulus. The area under the SR‐time curve following atropine sulfate (2 μg/ml) was lower than control (p<0.05) and not different from zero. These data support the hypothesis that the SR response to intradermal electrical stimulation reflects, exclusively, the effect of direct depolarization of sympathetic cholinergic C‐fibers and release of acetylcholine. As such, this model can be used to provide a quantifiable assessment of small C‐fiber function in human skin.

Whole‐body sweat production during exercise: Evaporative heat loss requirement or percent VO2max?

Under conditions which permit full evaporation of the sweat produced, the evaporative heat loss requirement (Ereq) should determine whole‐body sweat production during exercise. Yet, most exercise temperature regulation studies employ a fixed percentage of maximum oxygen consumption (VO2max) when examining sweat production between independent groups. We therefore examined the relationship between sweat production and Ereq, as well as %VO2max during exercise. Twenty‐three males either performed exercise at different rates of metabolic heat production (200, 350, 500 W) at a fixed air temperature (30°C), or exercised at a fixed rate of metabolic heat production (290 W) at different air temperatures (30°C, 35°C, 40°C). Whole‐body sudomotor activity (i.e. evaporative heat loss, Esk) was measured directly by calorimetry. Stepwise multiple regression analysis revealed that end‐exercise values of Ereq significantly correlated with the variability in end‐exercise values of Esk (p<0.001), while %VO2max did not (p=0.690). Independently, end‐exercise Ereq explained ~95% of the variance in end‐exercise Esk values (adjusted R2=0.945). These data provide clear evidence that steady‐state sweat production during exercise is determined by Ereq, not percent of VO2max. Supported by NSERC grant RGPIN‐298159–2009 (held by GP Kenny).

Sex differences in postsynaptic sweating and cutaneous vasodilation

The current study aimed to determine whether a peripheral modulation of sweating contributes to the lower sudomotor thermosensitivity previously observed in females during exercise. We examined dose-response relationships in 12 males and 12 females to incremental doses of acetylcholine (ACh) and methylcholine (MCh) for sweating (ventilated capsule), as well as to ACh and sodium nitroprusside (SNP) for cutaneous vasodilation (laser-Doppler). All drugs were infused using intradermal microdialysis. On a separate day, potential sex differences in the onset threshold and/or thermosensitivity of heat loss responses were assessed during progressive increases in mean body temperature elicited by passive heating. Increases in sweating as a function of increasing concentration of ACh (P = 0.008) and MCh (P = 0.046) significantly differed between males and females. Although the concentration eliciting 50% of the maximal sweating response did not differ between sexes for either agonist (P > 0.1), maximum values were lower in females in response to ACh (0.34 ± 0.12 vs. 0.59 ± 0.19 mg·min(-1)·cm(-2), P = 0.04) and MCh (0.48 ± 0.12 vs. 0.78 ± 0.26 mg·min(-1)·cm(-2), P = 0.05). This observation was paralleled by a lower thermosensitivity of sudomotor activity in females during passive heating (1.29 ± 0.34 vs. 1.83 ± 0.33 mg·min(-1)·cm(-2)·°C(-1), P = 0.03), with no significant differences in the change in mean body temperature at which onset of sweating occurred (0.85 ± 0.19 vs. 0.67 ± 0.13°C, P = 0.10). No sex differences in cutaneous vasodilation were observed in response to ACh and SNP, as well as during passive heating (all P > 0.1). These findings provide direct evidence for a peripheral modulation of sudomotor activity in females. In contrast, sex does not modulate cutaneous vasodilation.

Does sex have an independent effect on thermoeffector responses during exercise in the heat?

Although a number of studies have examined potential differences in temperature regulation between males and females during heat stress, conclusions have remained limited as to whether reported differences are due to confounding physical characteristics or to actual differences in the physiological variables of temperature regulation. Recent observations suggest that sex differences in temperature regulation, particularly in sudomotor activity, go beyond those associated with physical characteristics. Females have recently been shown to have a lower sudomotor activity, as well as a lower thermosensitivity of the response compared to males during exercise performed at a fixed rate of metabolic heat production. Furthermore, sex differences in local and whole-body sudomotor activity are only evident above a certain combination of environmental conditions and rate of metabolic heat production. In contrast, both the onset threshold and thermosensitivity of cutaneous vasodilatation are similar between males and females. In theory, differences in the thermosensitivity of sudomotor activity could be related to either a central (neural activity/integration) and/or peripheral (effector organ) modulation of temperature regulation. Based on recent findings, sex differences in sudomotor activity appear to be mediated peripherally, although a central modulation has yet to be conclusively ruled out. Here we present a brief yet comprehensive review of the current state of knowledge pertaining to sex differences in temperature regulation during exercise in the heat.

Sudomotor function and sweat gland innervation in galanin knockout mice

The presence of galanin and galanin binding sites in sweat gland has been demonstrated previously. In order to investigate whether galanin can influence sweat gland function, we compared sweating induced in footpads of wild type and galanin knockout mice by cholinergic and thermal stimulation using the silicone impression technique. Pilocarpine injections resulted in a similar number of reactive sweat glands and non-significant difference in the amount of sweat secretion in wild type and galanin knockout mice. However, thermal stimulation led to a significant increase in the number of secreting sweat glands in galanin knockout mice. To further evaluate possible differences in the innervation of sweat glands that could explain differences in their secretory activity, immunohistochemical labeling of cutaneous and sudomotor innervations against protein gene product 9.5, vasoactive intestinal polypeptide and choline acetyltransferase in plantar pads was performed. Immunohistochemical analysis revealed no significant differences in the distribution and intensity of the innervations between wild type mice and galanin knockout mice. Although our results indicate normal cholinergic responses and innervation of the sweat glands in galanin knockout mice, they also demonstrate that galanin plays a role in regulating the sudomotor activity in response to thermal stimulation.

The cutaneous vascular response to heat stress does not explain sex‐related differences in sudomotor activity

Changes in skin blood flow can independently modulate changes in sweat production. These findings could explain the lower whole‐body sudomotor activity recently observed in females during exercise. We therefore examined potential sex‐differences in local cutaneous and whole‐limb vascular conductance during exercise in the heat (40°C). Eight males and eight females (follicular phase) performed three successive 30 min exercise bouts at fixed rates of metabolic heat production equal to 200, 250, and 300 W·m−2. Local sudomotor activity (ventilated capsule) and cutaneous vascular conductance (CVC, laser‐doppler) were measured on the back, chest, and forearm, while whole‐limb vascular conductance was measured at the forearm (FVC, venous occlusion plethysmography). Despite a similar requirement for heat loss during each exercise bout, increases in local sudomotor activity were significantly lower in females at each measurement site (p≤0.001). However, these differences were paralleled by similar CVC responses on the back (43 ± 2 vs. 47 ± 5%, p=0.195), chest (52 ± 5 vs. 48 ± 4%, p=0.705), and forearm (51 ± 3 vs. 60 ± 6%, p=0.212). Furthermore, FVC did not differ between sex throughout exercise (0.09 ± 0.01 vs. 0.10 ± 0.01 L·100 mL−1·min−1·mmHg−2, p=0.278). These results suggest that the lower sudomotor activity observed in females during exercise is not due to a different cutaneous vascular response. Supported by NSERC grant RGPIN‐298159‐2009.

Sudomotor activity and heat balance with serial cooling and heating of thermosensors in the esophagus and stomach

This study assessed heat balance parameters and characterized transient sweating responses on the forehead following graded changes in local temperature of the esophagus and stomach from ingesting water of different temperatures. Seven male participants cycled for 75‐min in a temperate environment while ingesting four 3.2 mL·kg−1 boluses of either 1.5°C, 10°C, 37°C or 50°C water, 5‐min before, and 15, 30 and 45‐min after the start of exercise at 50% VO2max. Whole‐body sweat loss (WBSL), rectal temperature (Tre), mean skin temperature (Tsk) and local sweat rate on the forehead (SRhead) were measured throughout. Evaporative heat loss from sweating (Esk), respiratory heat loss, dry heat losses and heat exchange with ingested water were subsequently calculated to estimate net body heat storage (S). Despite no differences in Tre or Tsk, the onset time for sudmotor activity on the forehead was significantly greater with declining fluid temperature (P<0.05), and both mean SRhead throughout exercise and WBSL was significantly lower with 1.5°C compared to 50°C water ingestion (P=0.002). Values for S were significantly greater following 1.5°C water ingestion relative to 50°C (P=0.033), indicating a disproportionate reduction of thermoregulatory sweating, and therefore Esk, relative to the internal heat transfer with 1.5°C water. It is proposed that these data present evidence of independent thermoafferent processes arising from changes in local temperature of the esophagus and/or stomach.Funding for the study was provided by a NSERC discovery grant.

Algodystrophie de la main

Algodystrophy or type I complex regional pain syndrome of the hand is characterized by regional vascular abnormalities with hyperpermeability, followed by a local colonization of fibroblasts after an initiating noxious event, e.g. the Pouteau-Colles fracture. Its typical natural clinical course is divided into three sequential stages: acute or pseudoinflammatory, then dystrophic, and at least atrophic. The pain is continuous and is accentuated with the use of the joints. Spontaneous pain, allodynia, hyperalgesia, and/or hyperpathia are outside the territory of a single peripheral nerve and disproportionate to the original event. There is regional evidence of edema, skin blood flow abnormality and abnormal sudomotor activity. Transient vascular hyperpermeability in the affected part is demonstrated by the three-bone scan features. 99mTechnetium EHDP bone scan provides an evaluation of the vascular abnormalities and of the osteoblastic activity. Some patients, especially female adolescent or young female patients, may have no bone edema in the affected extremity, and in these cases, bone scans reveal a low uptake in comparison with the other side and MRI signs are lacking. Local demineralization when present is demonstrated by X-rays, computed tomography, and bone mineral density and bone mineral content measurements. The amount of bone loss in algodystrophy in a few weeks or months can be very important. Trabecular fractures, or aseptic osteonecrosis are discussed in the differential diagnosis but their occurrence is rare in this localization. The best treatment against algodystrophy, especially of the hand remains to be discovered.

Autonomic markers of emotional processing: skin sympathetic nerve activity in humans during exposure to emotionally charged images

The sympathetic innervation of the skin primarily subserves thermoregulation, but the system has also been commandeered as a means of expressing emotion. While it is known that the level of skin sympathetic nerve activity (SSNA) is affected by anxiety, the majority of emotional studies have utilized the galvanic skin response as a means of inferring increases in SSNA. The purpose of the present study was to characterize the changes in SSNA when showing subjects neutral or emotionally charged images from the International Affective Picture System (IAPS). SSNA was recorded via tungsten microelectrodes inserted into cutaneous fascicles of the common peroneal nerve in ten subjects. Neutral images, positively charged images (erotica) or negatively charged images (mutilation) were presented in blocks of fifteen images of a specific type, each block lasting 2 min. Images of erotica or mutilation were presented in a quasi-random fashion, each block following a block of neutral images. Both images of erotica or images of mutilation caused significant increases in SSNA, but the increases in SSNA were greater for mutilation. The increases in SSNA were often coupled with sweat release and cutaneous vasoconstriction; however, these markers were not always consistent with the SSNA increases. We conclude that SSNA, comprising cutaneous vasoconstrictor and sudomotor activity, increases with both positively charged and negatively charged emotional images. Measurement of SSNA provides a more comprehensive assessment of sympathetic outflow to the skin than does the use of sweat release alone as a marker of emotional processing.

MRI Findings of Causalgia of the Lower Extremity Following Transsphenoidal Resection of Pituitary Tumor

Background. Causalgia is continuing pain, allodynia, or hyperalgesia after nerve injury with edema, changes in skin blood flow, or abnormal sudomotor activity. Here we report a case of lower extremity causalgia following elective transsphenoidal resection of a pituitary tumor in a young man. Clinical Presentation. A 33-year-old man with acromegaly underwent elective sublabial transsphenoidal resection of his pituitary tumor. During the three-hour surgery, the lower limbs were kept in a supine, neutral position with a pillow under the knees. The right thigh was slightly internally rotated with a tape to expose fascia lata, which was harvested to repair the sella. Postoperatively, he developed causalgia in a distal sciatic and common peroneal nerve distribution. Pain was refractory to several interventions. Finally, phenoxybenzamine improved his pain significantly. Conclusions. Malpositioning in the operating room resulted in causalgia in this young man. Phenoxybenzamine improved, and ultimately resolved, his symptoms. Improvement in his pain symptoms correlated with resolution of imaging changes in the distal sciatic and peroneal nerves on the side of injury.

Sympathetic skin response in Parkinson's disease before and after mental stress

This study aims to evaluate sympathetic sudomotor activity in Parkinson's disease (PD) by means of the sympathetic skin response (SSR) and explore its possible changes due to mental stress. Sudomotor function was evaluated using SSR in 29 patients with PD (Hoehn and Yahr stage I-IV) without any clinical evidence of autonomic dysfunction. Twenty-seven healthy matched controls were also evaluated. SSR was elicited by electrical stimulation of the right median nerve and simultaneously recorded on the palms of both hands. Arithmetic mental stress was evoked by means of the WAIS-R arithmetic subscale. Latency and amplitude of SSR were evaluated before and after arithmetic mental stress. The SSR was obtained in all patients and controls. There were no significant differences in its mean latency and amplitude between patients and controls. SSR parameters were significantly correlated with disease duration, UPDRS score, and disease stage. There were also significant correlations with rigidity and bradykinesia, but not with tremor. Mental stress had no effect on SSR parameters in any group. SSR parameters in PD without autonomic dysfunction were comparable to matched controls. Although PD patients are sensitive to mental stress, the arithmetic task had no effect on SSR parameters. Consequently, SSR as a method of evaluation of sympathetic sudomotor function is not sufficient for exploration of subclinical autonomic dysfunction in PD, but should be combined with other tests of autonomous nervous system.

Compensatory hyperhidrosis following thoracic sympathectomy: a biophysical rationale

A side-effect of endoscopic thoracic sympathectomy (ETS) is compensatory hyperhidrosis (CH), characterized by excessive sweating from skin areas with intact sudomotor function. The physiological mechanism of CH is unknown, but may represent an augmented local sweat rate from skin areas with uninterrupted sympathetic innervation based on evaporative heat balance requirements. For a given combination of activity and climate, the same absolute amount of evaporation (if any) is needed to balance the rate of metabolic heat production both pre- and post-ETS. However, the rate of local sweating per unit of skin surface area with intact sudomotor activity must be greater post-ETS as evaporation must be derived from a smaller skin surface area. Under conditions with high evaporative requirements, greater degradations in sweating efficiency associated with an increased dripping of sweat should also occur post-ETS, further pronouncing the sweat rate required for heat balance. In conclusion, in addition to the potential role of psychological stimuli for increased sudomotor activity, the existence of CH post-ETS can be described by the interplay between fundamental thermoregulatory physiology and altered heat balance biophysics and does not require a postoperative alteration in physiological control.

Caffeine Increases Sweating Sensitivity via Changes in Sudomotor Activity During Physical Loading

We assessed the effect of caffeine on sudomotor activity and sweating sensitivity during physical loading. Both physiological responses could occur due to energy expenditure. Subjects were 13 athletically trained males (22.1 ± 3.7 years old, 174.2 ± 5.4 cm tall, and weighing 70.9 ± 4.6 kg, with maximal oxygen consumption [VO(2)max] of 53.6 ± 4.4 mL/kg/minute). The study involved a within-subject, random, crossover design. Tests were performed following the ingestion of 3 mg/kg caffeine. The physical loading involved running for 30 minutes at 60% VO(2)max (24.0 ± 0.5°C, 40 ± 3.0% relative humidity). Tympanic temperature (TYMP) was significantly higher in the caffeine-consuming group (Caffe-I) at pre-exercise (40 minutes after caffeine intake and immediately before running) (P<.05). Mean body temperature (mT(b)) was significantly higher in the Caffe-I group at pre- and post-exercise (30 min after start of running) (P<.05). Onset time of localized sweating was significantly shorter in the Caffe-I group (P<.01), but localized sweat volume and active sweat gland output (per single gland) was significantly higher in the Caffe-I group (P<.001). Activated sweat gland density was significantly increased in the Caffe-I group on the abdomen and thigh (P<.01). In conclusion, caffeine ingestion caused not only increases in TYMP and mT(b) through thermogenesis, but also an increased sweating sensitivity via changes in sudomotor activity.

Large differences in peak oxygen uptake do not independently alter changes in core temperature and sweating during exercise

The independent influence of peak oxygen uptake (Vo(₂ peak)) on changes in thermoregulatory responses during exercise in a neutral climate has not been previously isolated because of complex interactions between Vo(₂ peak), metabolic heat production (H(prod)), body mass, and body surface area (BSA). It was hypothesized that Vo(₂ peak) does not independently alter changes in core temperature and sweating during exercise. Fourteen males, 7 high (HI) Vo(₂ peak): 60.1 ± 4.5 ml·kg⁻¹·min⁻¹; 7 low (LO) Vo(₂ peak): 40.3 ± 2.9 ml·kg⁻¹·min⁻¹ matched for body mass (HI: 78.2 ± 6.1 kg; LO: 78.7 ± 7.1 kg) and BSA (HI: 1.97 ± 0.08 m²; LO: 1.94 ± 0.08 m²), cycled for 60-min at 1) a fixed heat production (FHP trial) and 2) a relative exercise intensity of 60% Vo(₂ peak) (REL trial) at 24.8 ± 0.6°C, 26 ± 10% RH. In the FHP trial, H(prod) was similar between the HI (542 ± 38 W, 7.0 ± 0.6 W/kg or 275 ± 25 W/m²) and LO (535 ± 39 W, 6.9 ± 0.9 W/kg or 277 ± 29 W/m²) groups, while changes in rectal (T(re): HI: 0.87 ± 0.15°C, LO: 0.87 ± 0.18°C, P = 1.00) and aural canal (T(au): HI: 0.70 ± 0.12°C, LO: 0.74 ± 0.21°C, P = 0.65) temperature, whole-body sweat loss (WBSL) (HI: 434 ± 80 ml, LO: 440 ± 41 ml; P = 0.86), and steady-state local sweating (LSR(back)) (P = 0.40) were all similar despite relative exercise intensity being different (HI: 39.7 ± 4.2%, LO: 57.6 ± 8.0% Vo(2 peak); P = 0.001). At 60% Vo(2 peak), H(prod) was greater in the HI (834 ± 77 W, 10.7 ± 1.3 W/kg or 423 ± 44 W/m²) compared with LO (600 ± 90 W, 7.7 ± 1.4 W/kg or 310 ± 50 W/m²) group (all P < 0.001), as were changes in T(re) (HI: 1.43 ± 0.28°C, LO: 0.89 ± 0.19°C; P = 0.001) and T(au) (HI: 1.11 ± 0.21°C, LO: 0.66 ± 0.14°C; P < 0.001), and WBSL between 0 and 15, 15 and 30, 30 and 45, and 45 and 60 min (all P < 0.01), and LSR(back) (P = 0.02). The absolute esophageal temperature (T(es)) onset for sudomotor activity was ∼0.3°C lower (P < 0.05) in the HI group, but the change in T(es) from preexercise values before sweating onset was similar between groups. Sudomotor thermosensitivity during exercise were similar in both FHP (P = 0.22) and REL (P = 0.77) trials. In conclusion, changes in core temperature and sweating during exercise in a neutral climate are determined by H(prod), mass, and BSA, not Vo(₂ peak).

Electrophysiological Assessment of the Autonomic Nervous System in Male Patients with Acromegaly

Background/Aims: We aimed to electrophysiologically evaluate the autonomic function in acromegalic patients using sympathetic skin response (SSR) as a reflection of the sympathetic sudomotor activity and RR interval variation (RRIV) as an indicator of the cardiovagal autonomic function. Methods: The study group consisted of 18 male acromegalics, and the control group was composed of 18 age- and sex-matched healthy subjects. Participants underwent SSR and RRIV tests. Beginning latencies and amplitudes of the median and tibial SSRs were compared among the groups. The RRIV values recorded at rest and during hyperventilation were compared among the patients and controls. Results: Latencies of SSRs recorded from the palms (median) and soles (tibial) of acromegalics were significantly longer than in healthy subjects (p = 0.004, p < 0.001). The amplitude of SSR recorded from the sole (tibial) was significantly decreased (p = 0.028). The RRIVs obtained from acromegalics at rest and during hyperventilation were significantly decreased compared with those of controls (p < 0.001). The RRIVs obtained from controls prolonged significantly during hyperventilation (p < 0.001); however, in the acromegaly group, hyperventilation did not cause a significant change in RRIV (p = 0.983). Conclusions: The present study suggests that an autonomic dysfunction exists in patients with acromegaly. Dysautonomia in acromegalics may be documented by means of SSR and RRIV.

Complex regional pain syndrome

Complex regional pain syndrome (CRPS) is a rare condition. Two types of CRPS have been recognized: CRPS Ⅰ which occurs without a definite nerve lesion, and CRPS Ⅱ with the presence of definite nerve lesions. The prominent symptom of this disease is pain, and the pain is accompanied by skin color changes, abnormal skin temperature and sudomotor activity. This paper presents the clinical manifestation, pathogenesis, diagnosis, differential diagnosis and therapy of this entity. Key words: Complex regional pain syndrome ; Pain ;