The hypothesis that palmar hyperhidrosis is due to a positive feedback loop of palmar sweating was examined. Hyperhidrotic in palms and normal palmar sweating individuals performed mental arithmetic tasks: 1. Control, 2. Experimental I: involving immersion of their palms and feet in warm water, and 3. Experimental II: as the former but watching their palmar conductivity alterations in a screen of computer. The immersion of palms and feet in warm water aimed to exclude the feeling of palmoplantar sweating and to prevent possible hypothermia caused by evaporation of sweat. The electrodermal activity (EDA) of hyperhidrotics was augmented from the first to the third task. The EDA of normal individuals was decreased from the first to the second and was slightly increased to the third task. The EDA augmentation of hyperhidrotics from the Control (having feedback of their palmoplantar sweating) to the Experimental I (without feedback of their palmoplantar sweating) indicate that for the excessive palmar sweating of hyperhidrotics a positive feedback loop of palmar sweating is not a necessary condition.
Key words: Hyperhidrosis, palmar sweating, electrodermal, feedback.
From our investigation on palmar hyperhidrosis, we already know that it is not controlled by a thermoregulatory mechanism (Kerassidis, 1994), it could not be considered as an orienting or defensive response after stimulation of startling kind (Kerassidis and Charistou, 2000) or as an indistinct concomitant of sympathetic discharge (Κερασίδης, Κοχιαδάκης, 1998), while extended clinical and laboratory tests did not reveal any type of organic disease (haematological abnormality, electrolytic or glucose imbalance, thyroid gland dysfunction, neurological abnormality, etc.) or a higher density of sweat glands on palm (unpublished data).
In addition to the negative pathophysiological findings, there are positive psychological findings (Lerer, Jacobowitz, Wahba, 1980; Lerer, 1977; Κερασίδης , Μπιτζαράκη, 1997) indicating that personality traits may be responsible for palmar hyperhidrosis. We have already found personality differences between hyperhidrotic and normal palmar sweating individuals, using Eysenck Personality Questionnaire and Minnesota Multiphasic Personality Inventory. After this, the better next research step is probably to clarify how personality traits could lead to palmar hyperhidrosis. The first answer to this question, which is emerged from the literature, is that a positive feedback process may be in the basis of this overfunctioning. Edelman (1970), Klinge (1972), Russel and Davey (1991) have demonstrated that the magnitude of palmar sweating is affected by the individual’s perception of this magnitude. Particularly, Russel and Davey (1991) mentioned that individuals who believed that they were exhibiting a strong electrodermal conditioning response did actually emit a response of a greater magnitude. Especially for palmar hyperhidrosis, Boucsein (1992) notices that the unpleasant feelings, produced by palmar sweating, elicit emotional excitement, thus forming a positive feedback loop for further sweating in hyperhidrotics. Beyond perception or emotion, but also involving a feedback process, Sato, et al. (1989) suggested that excessive palmoplantar sweating induces hypothermia which may increase the sympathetic outflow and aggravates hyperhidrosis. Duller and Doyle Gentry (1980) have reported successful treatment of chronic hyperhidrosis by the use of the method of biofeedback, which indicate that feedback processes are effective in modification of the magnitude of sweating. In the present work this last conclusion is not questioned. Our aim is to find out whether a positive feedback process, triggering from the sweating, is determinative factor of palmar hyperhidrosis expression. Namely, could palmar hyperhidrosis exist without the positive feedback process of palmar sweating? For this reason, we subjected hyperhidrotic and normal palmar sweating individuals to three mental arithmetic tasks: 1. Control: involving somatosensory feedback of their palmar and plantar sweating, 2. Experimental I: involving immersion of their palms and feet in warm water without feedback and prevention of their cooling, and 3. Experimental II: involving immersion of their palms and feet in warm water, with feedback regarding their palmar conductivity alterations, that is, having an instrumental but no somatosensory feedback of their palmar sweating.
Participants Twenty-six individuals, 13 hyperhidrotic in palms (5 male and 8 female), mean age 32 years old (range 17-40) and 13 normal palmar sweating (5 male and 8 female), mean age 28 years old (range 21-60), participated in this experiment. These subjects had participated in our previous work on pathophysiology of palmar hyperhidrosis (Kerassidis and Charistou, 2000) and they had been subjected to many clinical and laboratory tests. In order to confirm the participants’ estimate of the degree of their palmar sweating, a sweat collecting plaster was attached on each participant’s left palm, while she/he was writing for two minutes on a paper with the right hand. The mean weight of the sweat collected from the palm of hyperhidrotics was 20 mg (S.D. 14.9, range 7-65 mg) and from that of normal individuals 3.1 (S.D. 2.3, range 0-7) mg. Two subjects (one with 4 mg palmar sweating, who had declared hyperhidrotic and one with 12 mg, who had declared normal) were excluded from the analysis of the previous work and did not participated in the present work. The 26 individuals of the present work (out of the 42 individuals of the previous) were well confirmed as hyperhidrotic or normal also from their electrodermal behaviour in the tasks of previous works
.Materials J&J Modules of B45 biofeedback program of Unicomp were used for the recording of conductivity of the right palm of the individuals, as well as for the display in a graph form of the respective skin conductance value during the performance of the third task. Electrodes of Ag-AgCl, 8 mm in diameter and electrolytic paste of Hewlett Packard were used. Frequent change of polarity and replacement of electrodes were used in order to exclude any chance of polarization of the electrodes. The Polystat of Bioblock Scientific was used for heating and conservation of the temperature of the water at 30°C.
Procedure Individuals took off their shoes. Electrodes were placed on the first phalanx of the forefinger and the middle finger of the right palm. The electrodes were not removed until the end of the procedure in order to prevent artificial changes to the skin conductance level (SCL). The first, Control task was the continuous subtraction of the number 6 from a big number, for 72 seconds. The second, Experimental I task was also a continuous subtraction of the number 6 from another big number, for 72 seconds, but this time the palms and the soles of the individual were placed in two vessels with water in 30°C. The immersion of the palms and soles in the water aimed to exclude the feeling of their sweating. The heating of the water at 30°C aimed to prevent the vasoconstrictor activity and hypothermia, which could (according to Sato, et al., 1989 ) increase the sympathetic outflow and aggravate excessive sweating. Soles were also immersed in the water, because for many people, especially for hyperhidrotics, palmar sweating is often accompanied by sweating of the soles and this could be an indirect way for somatosensory perception. A very thin waterproof glove covered the right palm, with the electrodes, in order to avoid the short-circuiting of electrodes. This thin glove did not exclude the feeling of the warm water. In many rehearsals before the beginning of the experiment, we had ascertained that the two palms (with and without glove) had almost the same feeling of the water. The third, Experimental II task was the same as the Experimental I, but during that the individual watched her/his conductivity alterations in the screen of the computer in a real time graph. This way, the individual was informed about its palmar sweating by the instruments, without having any feeling of this. By the Experimental II task, we aimed to investigate the role of an external, not somatosensory, way of information about the magnitude of palmar sweating in the expression of palmar hyperhidrosis. I
Ιt must be noted that the order of the performance of the tasks was rather imperative, since (i) the Control mental arithmetic task should not be performed after the immersion of the palms and soles in the water, because the side effects of wetting and evaporation could not be estimated, (ii) the Experimental I and II tasks could not be respectively transferred, because if an individual during the second task, when the somatosensory perception was excluded, watched its EDA on the screen, the impact of this impression could not be avoided during the execution of the next task, where we had to examine the EDA with the individual having no suspicion about the degree of its palmar sweating
.Data analysis We compared the number of electrodermal responses (EDRs) and the mean skin conductance level (SCL) during every task. As EDR we accepted any increase in palmar conductivity over 0.02 micro-Siemens (μS), the mean SCL was calculated by the computer as the mean value of 18 mean values of SCL for 4 sec each one. The parameters were compared by the use of three factor ANOVA, with sex and hyperhidrosis as between-subject factors and repeated measures as within subject factor.
The results of the analysis are given on tables 1, 2. The mean values and standard deviations of EDRs and of SCLs, during the three tasks, for both groups, are given in Fig.1 and Fig. 2, respectively.Hyperhidrotics presented higher both EDRs and SCLs than normal individuals. The group differences on SCLs are much higher than those on EDRs, probably because of the higher wetting of palmar stratum corneum of hyperhidrotics as compared to normal individuals. Sex differences were significant only on SCLs and an interaction of group x sex on SCL was also found. The between tasks differences for each group show that the EDA of hyperhidrotics was increased from the first to the third task and that the EDA of normal individuals was decreased from the first to the second and was slightly increased to the third task.
The immersion of the palms and soles in the warm water aimed to exclude the feeling of the sweating as well as to prevent the vasoconstrictor activity and hypothermia. If the somatosensory feedback was a determinative factor for the manifestation of palmar hyperhidrosis, a significant decrease of the EDA of hyperhidrotics should have occurred during the Experimental I task. In contrast, the EDA of hyperhidrotics was increased during the Experimental I task and only that of normal individuals was decreased. During the Experimental II task, when the individuals were instrumentally informed about their EDA alterations, the EDA of hyperhidrotics was also increased (for normal individuals this increase was insignificant).This small increase of the EDA of normal individuals and the significant increase of EDA of hyperhidrotics from the Experimental I to the Experimental II task may indicate that the instrumental information of EDA partly substitutes the somatosensory one. But, it is also possible that this increase of EDA is simply the result of the greater difficulty of the Experimental II in relation to the Experimental I task, since the individuals during the Experimental II task had to watch the computer screen and simultaneously to perform the mental arithmetic task. For this reason, we consider that we cannot have a clear conclusion concerning the impact of the instrumental feedback of palmar sweating on the magnitude of it. However, that was not the main purpose of the present study, since previous works (Duller, Doyle Gentry, 1980; Edelman, 1970; Klinge, 1972; Russel, Davey, 1991; Boucsein, 1992) had already dealt with it. From the Control and Experimental I tasks, we can clearly conclude that the hyperhidrotic palmar sweating is not the result of a positive feedback loop, since increase and not decrease of palmar sweating of hyperhidrotics it is observed when the feedback was cut off. In this point, we have to clarify that the EDA increase of hyperhidrotics during the Experimental I task should not be considered thermoregulatory, caused by the immersion of hands in 30°C water (probably warmer than individual’s hands). We have already shown that even temperatures near to 60°C did not provoke thermoregulatory sweating in both hyperhidrotic and normal individuals’ palm when they were in relaxation, while profuse sweating was produced from almost any other skin areas (Kerassidis, 1994). The finding that the EDA of normal individuals was decreased from the Control to the Experimental I task is in agreement with previous works (Duller, Doyle Gentry, 1980; Edelman, 1970; Klinge, 1972; Russel, Davey, 1991; Boucsein, 1992), indicating that palmar sweating is influenced by the individual’s perception, since the exclusion of any perception may have resulted to this decrease. During the Experimental I task (when there was no feeling or information about palmar sweating, and when no palmar cooling took place), the successive performance of the same to the Control mental arithmetic task caused to hyperhidrotics even more palmar sweating than in the Control task (when the participants received somatosensory feedback and hypothermia could increase the sympathetic outflow). This finding clearly demonstrates that palmar hyperhidrosis may exist without any positive feedback process, which means that palmar hyperhidrosis cannot be considered as the result of such a process.
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