Friday, May 25, 2007
Thursday, April 19, 2007
Electrodermal recordings during human orgasm
Abstract
We tested the hypothesis that palmar sweat glands activation is expressed every time a mass sympathetic activation takes place. We performed 11 palmar electrodermal recordings during sexual intercourse and orgasm of one male and one female student, and 4 palmar electrodermal plus heart rate recordings during sexual intercourse and orgasm of the same couple. High palmar electrodermal activity was recorded during sexual intercourse but low during orgasm. In opposition, the highest value of heart rate was recorded at the moment of orgasm. We concluded that palmar sweat glands activation may not be considered an indiscriminate consequent of sympathetic discharge.
Introduction
The sweating of palms is not controlled by the same thermoregulatory mechanism which activate the sweat glands of the rest of the body skin areas (Kerassidis, 1994). It can accompany fear, anxiety, tension, discomfort, exploratory and sexual behaviour and it can be triggered by novel stimuli, pain, sudden exposure to cold, emotionally loaded words, and every kind of physical or intellectual effort (Edelberg, 1973; Fowles, 1986). Thus, if the electodermal activity (EDA) can accompany almost everything, the Fowles’ (1986) question whether this function is a complex and noisy manifestation of non-specific activity must be considered justified.
If the non-specific activity hypothesis is true, the palmar sweat glands activation must somehow follow the activity of sympathetic nervous system, since sweat glands are innervated only by sympathetic fibers. It is very possible that palmar and plantar sweating is a residue of the evolution and follows mass sympathetic activation at fight and flight reactions (Cannon's theory). Obviously, if the activation of palmar-plantar sweat glands is an indiscriminate consequent of any mass sympathetic discharge, it carries no specific message about inner processes and the question ‘’why is this local sweating expressed?’’ becomes almost meaningless.
We have to clarify that in this work we do not search the capacity for specificity of the sympathetic nervous system. We consider that it has been approved by many works, like the following: (i) the experiments of Lacey (1967) and Miller (1969a, 1969b), (ii) the establishment that autonomic manifestations differ among anxiety disorders (Hoehn-Saric & McLeod, 1988; Ost, Sterner & Lindahl, 1984), or are not correlated; for example Dawson, Schell, Braaten & Catania (1985) found that depressed patients exhibit higher tonic heart rate levels in parallel with lower tonic skin conductance levels, (iii) the recordings during the REM phase of sleep, where EDA was eliminated, in contrast to all other sympathetic functions which remained at the same levels as in awakening (Johnson & Lubin, 1966; Lester, Burch, & Dossett, 1967; Kushniruk, Rustenburg & Ogilvie, 1985), (iv) the intraneural recordings of sympathetic nerve traffic which have shown that "the view of a diffusely acting system led to the term sympathetic tone is not tenable" (Wallin, 1992; Wallin & Elam, 1994).
However, the capacity for specificity of the sympathetic nervous system does not exclude the possibility that the palmoplantar sweating, a residual of evolution function for humans, is nowadays a non-specific response and it follows the mass sympathetic discharges. Chrousos (1992) mentioned that, to a certain threshold, stressors elicit adaptive responses specific to the nature of the stressor; however, once a certain threshold has been exceeded, a systemic reaction takes place. Probably the EDA is noisy and non-specific to the threshold, and follows mass sympathetic discharges, over that threshold. The study of Shih, Wu & Lin (1983) supports the sympathetic activation theory. In this, it is suggested that subjects hyperhidrotic in their palms have an over-functioning of the sympathetic nervous fibres passing through the 2 and 3 thoracic (T2,3) ganglia, which leads to autonomic dysfunction elsewhere.
In order to check whether palmar sweating follows a mass sympathetic activation that takes place when no benefit of palmar wetting exists, we performed recordings of EDA during orgasm. Orgasm could be considered as a mass sympathetic discharge because (i) the neuronal firing in orgasm is initiated within the L1, L2 sympathetic ganglia (Chusid, 1979; Guyton, 1990) which innervate the low extremities, (ii) the augmentation of heart rate that takes place during orgasm, indicates that fibers passing through upper sympathetic ganglia (which innervate the heart and the upper extremities) are also activated and, (iii) the augmentation of blood pressure is an indication of vasoconstrictor activity and/or of elevation of cardiac output that means sympathetic activation also. Additionally, at the moment of orgasm no benefit for the action of palmar wetting exists, because neither friction improvement (Adelman, Taylor, & Meglung, 1975) nor abrasion prevention (Wilcott 1966) of the palms is demanded. This way, if palmar sweat glands activation takes place at the moment of orgasm, it may be considered as a consequent of mass sympathetic discharge.
It must be mentioned, that the choice of orgasm as a mass sympathetic activation was rather inevitable, in spite of the obvious difficulties that implies. The huge emotional interindividual differences, as response to a stimulus, did not permit any certainty that a chosen stimulus could cause high sympathetic activation without causing a reaction in which palmar wetting could be beneficial to the tested subjects.
Methods
Participants
Obviously, subjects recruitment for recordings of this kind is very difficult. We found only a couple of 1 male and 1 female student. These individuals participated to another work (Kerassidis, Haristou, Kohiadakis, Tzagournissakis & Bitzaraki, 1997), in which they responded to any stimulus (startling, mental, physical) and they were successfully subjected to many clinical and laboratory tests.
We realized that two subjects were very few, but we decided to take the recordings hoping that extended and repeated recordings during sexual intercourse and orgasm would give us the potentiality to compare the moments of high and low EDA with that of orgasm, and that simultaneous recordings of heart rate could reveal whether the moment of orgasm was indeed a moment of high sympathetic activation for the specific individuals or not.
Materials
The first recordings were performed at home with portable recording apparatuses. The chart recorder of Philip-Harris and an Hg battery (E=1.35 V) as an electric source were used. The applied voltage on the students’ fingers was about 0.5-1 V and the current was less than 10 μA cm-2. The electrodes displayed a surface of 1 cm2 and were covered by silver-silver chloride. A cream prepared according to the published recommendations of Fowles, Christie, Edelberg, Grings, Lykken & Venables (1981) based on neutral ointment cream mixed with saline (2:1) was used as the electrolytic media. For simultaneous recordings of EDA and heart rate (HR), a Beckman R 511A was used.
Procedure
Eleven recordings of the EDA of the couple of students were performed in their house, in a long period of time, at different moments of the day. Electrodes were placed on the first phalanxes of the fingers of the left palm of one participant, after cleaning with a cotton immersed to water with alcohol. The person with the recording electrodes lay in bed and held the arm with the electrodes still during the sexual intercourse; she/he removed one out of the two electrodes, as event-marker, after orgasm.
Four additional recordings of palmar EDA and HR, during the sexual intercourse of the same couple, were performed. The HR recording was used as an indicator of the upper sympathetic chain ganglia activity. For these recordings, Beckman recorder was carried in students’ house. The signals for HR recordings were carried through electrodes attached to the left and right forearm and to the chest (ground). At preparatory sessions, it was completely confirmed that no kind of interaction between EDA and HR recordings occurred. The person with the recording electrodes and wires lay in bed and held a passive attitude during the sexual intercourse and gave immediately after orgasm the Beckman's event-marker signal.
Results
The first 11 recordings of sexual intercourse showed that during orgasm, of both participants, the EDA was small or negligible, the skin conductance level (SCL) of the palm was decreased, and when a skin conductance response (SCR) occurred, it was small in relation to the great SCRs during sexual intercourse. In the case shown in Fig.1, for example, during orgasm the SCR is 0,2 μS, but during sexual intercourse, many SCRs, up to 0,6 μS, were recorded. In the case shown in Fig. 2, huge SCRs were recorded at moments of discomfort due to real life problems, while no SCR was recorded during orgasm.
The finding that EDA during orgasm was small in relation to EDA of other moments during sexual intercourse was very important. However, it could not undoubtedly be interpreted as a demonstration that EDA does not indiscriminately follow mass sympathetic activity, because the moments during sexual intercourse of higher recorded EDA could be of higher sympathetic activity in relation to the moment of orgasm. This way, the EDA during orgasm could have been masked.
The simultaneous recording of EDA and HR, of the same couple during sexual intercourse and orgasm, confirmed the previous findings that the EDA during orgasm was small or negligible. However, the value of HR recorded at the moment of orgasm was the highest. In the recordings of the male student, the HR was elevated to 125 pulses min-1 during orgasm (both times) but his EDA was negligible. In the recordings of the female student the HR was elevated to about 100 pulses min-1 during orgasm (both times). The HR of both students was varied (about 60-83 pulses min-1 for the female, and 60-100 pulses min-1 for the male), during sexual intercourse.
Discussion
From the first recordings during sexual intercourse and orgasm it was found that the palmar sweat glands activation was weak during orgasm, for both male and female students, but it was strong, especially at moments of discomfort, during sexual intercourse. The recordings of EDA plus HR during sexual intercourse and orgasm confirmed that the sweat glands activation was weak during orgasm and showed that the recorded HR was maximum at that time.
In general, findings deriving from only two subjects are not rightfully considered enough to sustain a conclusion. The idiosyncrasy of any kind is avoided only by large and representative number of subjects. But in the case of sexual intercourse and orgasm the recruitment of a large number of subjects is very difficult. Of course, the difficulty does not justify the violation of the rule of the large numbers. However, we think that the performed recordings have not brought to light any idiosyncrasy. Everybody can observe that the palms and soles do not sweat at the moments of orgasm as it happens at the moments of discomfort in real life. In addition, the HR recordings showed that the individuals of the present work presented a high sympathetic activation at the moment of orgasm, normally, and as it was theoretically expected. These individuals were subjected to tests like general hematological, blood glucose concentration as well as levels of thyroid hormones (FT3, FT4, TSH) and electrolytes (Na, K, P, Ca, Mg), and neurological examination, and no abnormality was revealed. In addition, as it was mentioned above, they responded to all kind of stimuli that normally cause EDA. It is reasonable to accept that they normally did not present a significant EDA during orgasm, and unjustified that they did not. In the second case, we must explain why especially in these individuals the verified high sympathetic activity during orgasm was not followed by EDA.
The simple and reasonable explanation of the findings is that the mass sympathetic activation which indeed took place at the moment of orgasm did not activate the sweat glands of the palm. Undoubtedly, the sympathetic nervous system may act as a unit: faster heart rate, vasoconstriction, increased blood sugar, discharge of adrenaline, erection of the hairs, sweat glands activation, in ‘’fight’’ and ‘’flight’’ reactions (Cannon’s theory). The capability of mass activation may be the reason of its anatomical unity. But the findings show that the sympathetic nervous system has also the capability of specificity (probably, a later creation of the evolution). As Wallin (1992) mentioned "... the degree of sympathetic differentiation is even greater than previously known; it occurs not only between different tissues but may also occur between different regions of the same tissue. Probably such differences may originate both at spinal and supraspinal levels." In the palmar sweat glands activation, structures of all the levels of the central nervous system are involved (Ladpli & Wang, 1960; Isamat, 1961; Wilcott, 1969; Wilcott & Bradley, 1970; Venables & Christie, 1973; Edelberg, 1973; Delerm, Delsaut & Roy, 1982; Fowles, 1986; Sato, Kang, Saga & Sato, 1989; Weitkunat, Buhrer & Sparrer, 1990; Venables, 1991; Turkstra, 1995). Probably, the highest centers control the palmar sweat glands activation unless otherwise prevented (Venables, 1991) and the whole expression of the function is more complicate than the simple scheme of the general sympathetic arousal view implies.
The recordings showed that the mass and high sympathetic discharge, which takes place in orgasm, did not activate the sweat glands of the palm, and we conclude that palmar EDA may not be considered as an indiscriminate consequent of sympathetic discharge.
References
Adelman, S., Taylor, C.R., & Meglung, N.C. (1975). Sweating on paws and palms: what is its function? American Journal of Psychology, 229(5), 1400-1402.
Chusid, J.G. (1979). The Autonomic Nervous System. In Correlative neuroanatomy & functional neurology. Los Altos, California: LANGE Medical Publications.
Chrousos, G.P. (1992). Regulation and dysregulation of the hypothalamic-pituitary-adrenal axis. Endocrinology and Metabolism Clinics of North America, 21(4), 833-858.
Delerm, B., Delsaut, M., & Roy, J.C. (1982). Mesencephalic and bulbar reticular control of skin potential responses in kittens. Experimental Brain Research, 46, 209-214.
Dawson, M.E., Schell, A.M., Braaten, J.R., & Catania, J.J. (1985). Diagnostic utility of autonomic measures for major depressive disorders. Psychiatry Research, 15, 261-270.
Edelberg, R. (1973). Mechanisms of electrodermal adaptations for locomotion, manipulation, or defence. In: E. Stellar & J.M. Sprague (Eds). Progress in physiological psychology (Vol. 5, pp. 155-209). New York: Academic Press.
Fowles, D.C. (1986). The eccrine system and electrodermal activity. In M.G.H. Coles, E. Donchin & S.W. Porges (Eds). Psychophysiology: Systems, Processes and Applications (pp. 51-96). New York: The Guilford Press.
Fowles, D.C., Christie, M.J., Edelberg, R., Grings, W.W., Lykken, D.T., & Venables, P.H. (1981). Publication recommendations for electrodermal measurements (committee report). Psychophysiology, 18, 232-239.
Guyton, A.C. (1990). Reproductive functions of man. In Human Physiology and Mechanisms of Disease (pp. 716-727). Athens: Litsas Medical Publications.
Hoehn-Saric, R., & McLeod, D.R. (1988). The peripheral sumpathetic nervous system. Its role in normal and pathological anxiety. Psychiatric Clinics of North America, 11(2), 375-386.
Isamat, F. (1961). Galvanic skin response from stimulation of limbic cortex. Journal of Neurophysiology, 24, 176-181.
Johnson, L.C., & Lubin, A. (1966). Spontaneous electrodermal activity during waking and sleeping. Psychophysiology, 3(1), 8-17.
Kerassidis, S. (1994). Is palmar and plantar sweating thermoregulatory? Acta Physiologica Scandinavica, 152, 259-263.
Kerassidis, S., Haristou, A., Kohiadakis, G., Tzagournissakis, M., & Bitzaraki, K. (1997). Palmar hyperhidrosis. Manuscript submitted for publication.
Kushniruk, A., Rustenburg, J., & Ogilvie, R. (1985). Psychological correlates of electrodermal activity during REM sleep. Sleep, 8(2), 146-154.
Lacey, J.I. (1967). Somatic response patterning and stress: Some revisions of activation theory. In M.H. Appley & R. Trumbull (Eds). Psychological Stress (Issues in research) (pp. 15-42). New York: Appleton-Century-Crofts.
Ladpli, R., & Wang, G.H. (1960). Spontaneous variations of skin potentials in footpads of normal, striatal and spinal cats. Journal of Neurophysiology, 23, 448-452.
Lester, B.K., Burch, N.R., & Dossett, R.C. (1967). Nocturnal EEG-GSR profiles: the influence of presleep states. Psychophysiology, 3, 238-248.
Miller, N.E. (1969a). Learning of visceral and glandular responses. Science, 163, 434-445.
Miller, N.E. (1969b). Psychosomatic effects of specific types of training. Annals of the New York Academy of Sciences, 159, 1025-1040.
Ost, L., Sterner, U., & Lindahl, I. (1984). Physiological responses in blood phobics. Behaviour Research and Therapy, 22(2), 109-117.
Sato, K.T., Kang, W.H., Saga, K., & Sato, K.T. (1989). Biology of sweat glands and their disorders. 1. Normal sweat gland function. Journal of the American Academy of Dermatology, 20(4), 537-563.
Shih, C.J., Wu, J.J., & Lin, M.T. (1983). Autonomic dysfunction in palmar hyperhidrosis. Journal of Autonomic Nervous System, 8, 33-43.
Turkstra, L.S. (1995). Electrodermal response and outcome from severe brain injury. Brain Injury, 9(1), 61-80.
Venables, P.H. (1991). Autonomic activity. Annals of the New York Academy of Sciences, 620, 191-207.
Venables, P.H., & Christie, M.J. (1973). Mechanisms, Instructions, Recording Techniques, and Quantification of Responses. In W.F. Prokasy & D.C. Raskin (Eds). Electrodermal activity in psychological research (pp. 1-123). New York: The Academic Press.
Wallin, B.G. (1992). Intraneural recordings of normal and abnormal sympathetic activity in man. In R. Bannister & C.J. Mathias (Eds). Autonomic Failure. A textbook of clinical disorders of the autonomic nervous system (pp. 359-377). Oxford: Oxford Medical Publications.
Wallin, B.G., & Elam, M. (1994). Insights from intraneural recordings of sympathetic nerve traffic in humans. American Physiological Society, 9, 203-207.
Weitkunat, R., Buhrer, M., & Sparrer, B. (1990). Cortical initiation of phasic electrodermal activity. International Journal of Psychophysiology, 9, 303-314.
Wilcott, R.C. (1966). Adaptive value of arousal sweating and the epidermal mechanism related to skin potential and skin resistance. Psychophysiology, 2(3), 249-262.
Wilcott, R.C. (1969). Electrical stimulation of the anterior cortex and skin- potential responses in the cat. Journal of Comparative Physiology and Psychology, 69(3), 465-472.
Wilcott, R.C., & Bradley, H.H. (1970). Low-frequency electrical stimulation of the cat's anterior cortex and inhibition of skin potential responses. Journal of Comparative Physiology and Psychology, 72(3), 351-355.
We tested the hypothesis that palmar sweat glands activation is expressed every time a mass sympathetic activation takes place. We performed 11 palmar electrodermal recordings during sexual intercourse and orgasm of one male and one female student, and 4 palmar electrodermal plus heart rate recordings during sexual intercourse and orgasm of the same couple. High palmar electrodermal activity was recorded during sexual intercourse but low during orgasm. In opposition, the highest value of heart rate was recorded at the moment of orgasm. We concluded that palmar sweat glands activation may not be considered an indiscriminate consequent of sympathetic discharge.
Introduction
The sweating of palms is not controlled by the same thermoregulatory mechanism which activate the sweat glands of the rest of the body skin areas (Kerassidis, 1994). It can accompany fear, anxiety, tension, discomfort, exploratory and sexual behaviour and it can be triggered by novel stimuli, pain, sudden exposure to cold, emotionally loaded words, and every kind of physical or intellectual effort (Edelberg, 1973; Fowles, 1986). Thus, if the electodermal activity (EDA) can accompany almost everything, the Fowles’ (1986) question whether this function is a complex and noisy manifestation of non-specific activity must be considered justified.
If the non-specific activity hypothesis is true, the palmar sweat glands activation must somehow follow the activity of sympathetic nervous system, since sweat glands are innervated only by sympathetic fibers. It is very possible that palmar and plantar sweating is a residue of the evolution and follows mass sympathetic activation at fight and flight reactions (Cannon's theory). Obviously, if the activation of palmar-plantar sweat glands is an indiscriminate consequent of any mass sympathetic discharge, it carries no specific message about inner processes and the question ‘’why is this local sweating expressed?’’ becomes almost meaningless.
We have to clarify that in this work we do not search the capacity for specificity of the sympathetic nervous system. We consider that it has been approved by many works, like the following: (i) the experiments of Lacey (1967) and Miller (1969a, 1969b), (ii) the establishment that autonomic manifestations differ among anxiety disorders (Hoehn-Saric & McLeod, 1988; Ost, Sterner & Lindahl, 1984), or are not correlated; for example Dawson, Schell, Braaten & Catania (1985) found that depressed patients exhibit higher tonic heart rate levels in parallel with lower tonic skin conductance levels, (iii) the recordings during the REM phase of sleep, where EDA was eliminated, in contrast to all other sympathetic functions which remained at the same levels as in awakening (Johnson & Lubin, 1966; Lester, Burch, & Dossett, 1967; Kushniruk, Rustenburg & Ogilvie, 1985), (iv) the intraneural recordings of sympathetic nerve traffic which have shown that "the view of a diffusely acting system led to the term sympathetic tone is not tenable" (Wallin, 1992; Wallin & Elam, 1994).
However, the capacity for specificity of the sympathetic nervous system does not exclude the possibility that the palmoplantar sweating, a residual of evolution function for humans, is nowadays a non-specific response and it follows the mass sympathetic discharges. Chrousos (1992) mentioned that, to a certain threshold, stressors elicit adaptive responses specific to the nature of the stressor; however, once a certain threshold has been exceeded, a systemic reaction takes place. Probably the EDA is noisy and non-specific to the threshold, and follows mass sympathetic discharges, over that threshold. The study of Shih, Wu & Lin (1983) supports the sympathetic activation theory. In this, it is suggested that subjects hyperhidrotic in their palms have an over-functioning of the sympathetic nervous fibres passing through the 2 and 3 thoracic (T2,3) ganglia, which leads to autonomic dysfunction elsewhere.
In order to check whether palmar sweating follows a mass sympathetic activation that takes place when no benefit of palmar wetting exists, we performed recordings of EDA during orgasm. Orgasm could be considered as a mass sympathetic discharge because (i) the neuronal firing in orgasm is initiated within the L1, L2 sympathetic ganglia (Chusid, 1979; Guyton, 1990) which innervate the low extremities, (ii) the augmentation of heart rate that takes place during orgasm, indicates that fibers passing through upper sympathetic ganglia (which innervate the heart and the upper extremities) are also activated and, (iii) the augmentation of blood pressure is an indication of vasoconstrictor activity and/or of elevation of cardiac output that means sympathetic activation also. Additionally, at the moment of orgasm no benefit for the action of palmar wetting exists, because neither friction improvement (Adelman, Taylor, & Meglung, 1975) nor abrasion prevention (Wilcott 1966) of the palms is demanded. This way, if palmar sweat glands activation takes place at the moment of orgasm, it may be considered as a consequent of mass sympathetic discharge.
It must be mentioned, that the choice of orgasm as a mass sympathetic activation was rather inevitable, in spite of the obvious difficulties that implies. The huge emotional interindividual differences, as response to a stimulus, did not permit any certainty that a chosen stimulus could cause high sympathetic activation without causing a reaction in which palmar wetting could be beneficial to the tested subjects.
Methods
Participants
Obviously, subjects recruitment for recordings of this kind is very difficult. We found only a couple of 1 male and 1 female student. These individuals participated to another work (Kerassidis, Haristou, Kohiadakis, Tzagournissakis & Bitzaraki, 1997), in which they responded to any stimulus (startling, mental, physical) and they were successfully subjected to many clinical and laboratory tests.
We realized that two subjects were very few, but we decided to take the recordings hoping that extended and repeated recordings during sexual intercourse and orgasm would give us the potentiality to compare the moments of high and low EDA with that of orgasm, and that simultaneous recordings of heart rate could reveal whether the moment of orgasm was indeed a moment of high sympathetic activation for the specific individuals or not.
Materials
The first recordings were performed at home with portable recording apparatuses. The chart recorder of Philip-Harris and an Hg battery (E=1.35 V) as an electric source were used. The applied voltage on the students’ fingers was about 0.5-1 V and the current was less than 10 μA cm-2. The electrodes displayed a surface of 1 cm2 and were covered by silver-silver chloride. A cream prepared according to the published recommendations of Fowles, Christie, Edelberg, Grings, Lykken & Venables (1981) based on neutral ointment cream mixed with saline (2:1) was used as the electrolytic media. For simultaneous recordings of EDA and heart rate (HR), a Beckman R 511A was used.
Procedure
Eleven recordings of the EDA of the couple of students were performed in their house, in a long period of time, at different moments of the day. Electrodes were placed on the first phalanxes of the fingers of the left palm of one participant, after cleaning with a cotton immersed to water with alcohol. The person with the recording electrodes lay in bed and held the arm with the electrodes still during the sexual intercourse; she/he removed one out of the two electrodes, as event-marker, after orgasm.
Four additional recordings of palmar EDA and HR, during the sexual intercourse of the same couple, were performed. The HR recording was used as an indicator of the upper sympathetic chain ganglia activity. For these recordings, Beckman recorder was carried in students’ house. The signals for HR recordings were carried through electrodes attached to the left and right forearm and to the chest (ground). At preparatory sessions, it was completely confirmed that no kind of interaction between EDA and HR recordings occurred. The person with the recording electrodes and wires lay in bed and held a passive attitude during the sexual intercourse and gave immediately after orgasm the Beckman's event-marker signal.
Results
The first 11 recordings of sexual intercourse showed that during orgasm, of both participants, the EDA was small or negligible, the skin conductance level (SCL) of the palm was decreased, and when a skin conductance response (SCR) occurred, it was small in relation to the great SCRs during sexual intercourse. In the case shown in Fig.1, for example, during orgasm the SCR is 0,2 μS, but during sexual intercourse, many SCRs, up to 0,6 μS, were recorded. In the case shown in Fig. 2, huge SCRs were recorded at moments of discomfort due to real life problems, while no SCR was recorded during orgasm.
The finding that EDA during orgasm was small in relation to EDA of other moments during sexual intercourse was very important. However, it could not undoubtedly be interpreted as a demonstration that EDA does not indiscriminately follow mass sympathetic activity, because the moments during sexual intercourse of higher recorded EDA could be of higher sympathetic activity in relation to the moment of orgasm. This way, the EDA during orgasm could have been masked.
The simultaneous recording of EDA and HR, of the same couple during sexual intercourse and orgasm, confirmed the previous findings that the EDA during orgasm was small or negligible. However, the value of HR recorded at the moment of orgasm was the highest. In the recordings of the male student, the HR was elevated to 125 pulses min-1 during orgasm (both times) but his EDA was negligible. In the recordings of the female student the HR was elevated to about 100 pulses min-1 during orgasm (both times). The HR of both students was varied (about 60-83 pulses min-1 for the female, and 60-100 pulses min-1 for the male), during sexual intercourse.
Discussion
From the first recordings during sexual intercourse and orgasm it was found that the palmar sweat glands activation was weak during orgasm, for both male and female students, but it was strong, especially at moments of discomfort, during sexual intercourse. The recordings of EDA plus HR during sexual intercourse and orgasm confirmed that the sweat glands activation was weak during orgasm and showed that the recorded HR was maximum at that time.
In general, findings deriving from only two subjects are not rightfully considered enough to sustain a conclusion. The idiosyncrasy of any kind is avoided only by large and representative number of subjects. But in the case of sexual intercourse and orgasm the recruitment of a large number of subjects is very difficult. Of course, the difficulty does not justify the violation of the rule of the large numbers. However, we think that the performed recordings have not brought to light any idiosyncrasy. Everybody can observe that the palms and soles do not sweat at the moments of orgasm as it happens at the moments of discomfort in real life. In addition, the HR recordings showed that the individuals of the present work presented a high sympathetic activation at the moment of orgasm, normally, and as it was theoretically expected. These individuals were subjected to tests like general hematological, blood glucose concentration as well as levels of thyroid hormones (FT3, FT4, TSH) and electrolytes (Na, K, P, Ca, Mg), and neurological examination, and no abnormality was revealed. In addition, as it was mentioned above, they responded to all kind of stimuli that normally cause EDA. It is reasonable to accept that they normally did not present a significant EDA during orgasm, and unjustified that they did not. In the second case, we must explain why especially in these individuals the verified high sympathetic activity during orgasm was not followed by EDA.
The simple and reasonable explanation of the findings is that the mass sympathetic activation which indeed took place at the moment of orgasm did not activate the sweat glands of the palm. Undoubtedly, the sympathetic nervous system may act as a unit: faster heart rate, vasoconstriction, increased blood sugar, discharge of adrenaline, erection of the hairs, sweat glands activation, in ‘’fight’’ and ‘’flight’’ reactions (Cannon’s theory). The capability of mass activation may be the reason of its anatomical unity. But the findings show that the sympathetic nervous system has also the capability of specificity (probably, a later creation of the evolution). As Wallin (1992) mentioned "... the degree of sympathetic differentiation is even greater than previously known; it occurs not only between different tissues but may also occur between different regions of the same tissue. Probably such differences may originate both at spinal and supraspinal levels." In the palmar sweat glands activation, structures of all the levels of the central nervous system are involved (Ladpli & Wang, 1960; Isamat, 1961; Wilcott, 1969; Wilcott & Bradley, 1970; Venables & Christie, 1973; Edelberg, 1973; Delerm, Delsaut & Roy, 1982; Fowles, 1986; Sato, Kang, Saga & Sato, 1989; Weitkunat, Buhrer & Sparrer, 1990; Venables, 1991; Turkstra, 1995). Probably, the highest centers control the palmar sweat glands activation unless otherwise prevented (Venables, 1991) and the whole expression of the function is more complicate than the simple scheme of the general sympathetic arousal view implies.
The recordings showed that the mass and high sympathetic discharge, which takes place in orgasm, did not activate the sweat glands of the palm, and we conclude that palmar EDA may not be considered as an indiscriminate consequent of sympathetic discharge.
References
Adelman, S., Taylor, C.R., & Meglung, N.C. (1975). Sweating on paws and palms: what is its function? American Journal of Psychology, 229(5), 1400-1402.
Chusid, J.G. (1979). The Autonomic Nervous System. In Correlative neuroanatomy & functional neurology. Los Altos, California: LANGE Medical Publications.
Chrousos, G.P. (1992). Regulation and dysregulation of the hypothalamic-pituitary-adrenal axis. Endocrinology and Metabolism Clinics of North America, 21(4), 833-858.
Delerm, B., Delsaut, M., & Roy, J.C. (1982). Mesencephalic and bulbar reticular control of skin potential responses in kittens. Experimental Brain Research, 46, 209-214.
Dawson, M.E., Schell, A.M., Braaten, J.R., & Catania, J.J. (1985). Diagnostic utility of autonomic measures for major depressive disorders. Psychiatry Research, 15, 261-270.
Edelberg, R. (1973). Mechanisms of electrodermal adaptations for locomotion, manipulation, or defence. In: E. Stellar & J.M. Sprague (Eds). Progress in physiological psychology (Vol. 5, pp. 155-209). New York: Academic Press.
Fowles, D.C. (1986). The eccrine system and electrodermal activity. In M.G.H. Coles, E. Donchin & S.W. Porges (Eds). Psychophysiology: Systems, Processes and Applications (pp. 51-96). New York: The Guilford Press.
Fowles, D.C., Christie, M.J., Edelberg, R., Grings, W.W., Lykken, D.T., & Venables, P.H. (1981). Publication recommendations for electrodermal measurements (committee report). Psychophysiology, 18, 232-239.
Guyton, A.C. (1990). Reproductive functions of man. In Human Physiology and Mechanisms of Disease (pp. 716-727). Athens: Litsas Medical Publications.
Hoehn-Saric, R., & McLeod, D.R. (1988). The peripheral sumpathetic nervous system. Its role in normal and pathological anxiety. Psychiatric Clinics of North America, 11(2), 375-386.
Isamat, F. (1961). Galvanic skin response from stimulation of limbic cortex. Journal of Neurophysiology, 24, 176-181.
Johnson, L.C., & Lubin, A. (1966). Spontaneous electrodermal activity during waking and sleeping. Psychophysiology, 3(1), 8-17.
Kerassidis, S. (1994). Is palmar and plantar sweating thermoregulatory? Acta Physiologica Scandinavica, 152, 259-263.
Kerassidis, S., Haristou, A., Kohiadakis, G., Tzagournissakis, M., & Bitzaraki, K. (1997). Palmar hyperhidrosis. Manuscript submitted for publication.
Kushniruk, A., Rustenburg, J., & Ogilvie, R. (1985). Psychological correlates of electrodermal activity during REM sleep. Sleep, 8(2), 146-154.
Lacey, J.I. (1967). Somatic response patterning and stress: Some revisions of activation theory. In M.H. Appley & R. Trumbull (Eds). Psychological Stress (Issues in research) (pp. 15-42). New York: Appleton-Century-Crofts.
Ladpli, R., & Wang, G.H. (1960). Spontaneous variations of skin potentials in footpads of normal, striatal and spinal cats. Journal of Neurophysiology, 23, 448-452.
Lester, B.K., Burch, N.R., & Dossett, R.C. (1967). Nocturnal EEG-GSR profiles: the influence of presleep states. Psychophysiology, 3, 238-248.
Miller, N.E. (1969a). Learning of visceral and glandular responses. Science, 163, 434-445.
Miller, N.E. (1969b). Psychosomatic effects of specific types of training. Annals of the New York Academy of Sciences, 159, 1025-1040.
Ost, L., Sterner, U., & Lindahl, I. (1984). Physiological responses in blood phobics. Behaviour Research and Therapy, 22(2), 109-117.
Sato, K.T., Kang, W.H., Saga, K., & Sato, K.T. (1989). Biology of sweat glands and their disorders. 1. Normal sweat gland function. Journal of the American Academy of Dermatology, 20(4), 537-563.
Shih, C.J., Wu, J.J., & Lin, M.T. (1983). Autonomic dysfunction in palmar hyperhidrosis. Journal of Autonomic Nervous System, 8, 33-43.
Turkstra, L.S. (1995). Electrodermal response and outcome from severe brain injury. Brain Injury, 9(1), 61-80.
Venables, P.H. (1991). Autonomic activity. Annals of the New York Academy of Sciences, 620, 191-207.
Venables, P.H., & Christie, M.J. (1973). Mechanisms, Instructions, Recording Techniques, and Quantification of Responses. In W.F. Prokasy & D.C. Raskin (Eds). Electrodermal activity in psychological research (pp. 1-123). New York: The Academic Press.
Wallin, B.G. (1992). Intraneural recordings of normal and abnormal sympathetic activity in man. In R. Bannister & C.J. Mathias (Eds). Autonomic Failure. A textbook of clinical disorders of the autonomic nervous system (pp. 359-377). Oxford: Oxford Medical Publications.
Wallin, B.G., & Elam, M. (1994). Insights from intraneural recordings of sympathetic nerve traffic in humans. American Physiological Society, 9, 203-207.
Weitkunat, R., Buhrer, M., & Sparrer, B. (1990). Cortical initiation of phasic electrodermal activity. International Journal of Psychophysiology, 9, 303-314.
Wilcott, R.C. (1966). Adaptive value of arousal sweating and the epidermal mechanism related to skin potential and skin resistance. Psychophysiology, 2(3), 249-262.
Wilcott, R.C. (1969). Electrical stimulation of the anterior cortex and skin- potential responses in the cat. Journal of Comparative Physiology and Psychology, 69(3), 465-472.
Wilcott, R.C., & Bradley, H.H. (1970). Low-frequency electrical stimulation of the cat's anterior cortex and inhibition of skin potential responses. Journal of Comparative Physiology and Psychology, 72(3), 351-355.
ABOUT THE MALADAPTIVE NATURE OF PALMAR SWEATING AND HYPERHIDROSIS
ABSTRACT
In this work, the influence of the benefit of palmar wetting in the intensity of palmar sweating was examined. The electrodermal activity (EDA) of hyperhidrotic and normal subjects was compared, in a leafing (palmar wetting is desirable) and fingerprinting (palmar wetting is unwanted) tasks. Hyperhidrotic, in the same degree as normal subjects, presented a higher EDA during leafing than fingerprinting. We concluded that the ability of a beneficial manifestation of palmar sweating does not be lost in the case of palmar hyperhidrosis. This finding may implies that It must be questioned the unsophisticated view for the maladaptive nature of palmar hyperhidrosis or the neurotic manifestation of a function in general.
INTRODUCTION
Many times a day, the electrodermal activity (EDA) of a subject seems to be pointless, since there is no benefit of palmar wetting (friction improvement or abrasion prevention Adelman et al. 1975, Wilcott 1966) for the subject's action. These times, the manifestation of palmar sweating offers no adaptation to the action demands, probably it complicates that, and could be considered maladaptive. Fowles' (1986) question of whether this function is simply a complex and noisy manifestation of non-specific activity is absolutelly justifiable from this side of view.
The isolation of palmar sweating from the action's demands of palmar wetting can be understandable if palmar and plantar sweating, as a residue of the evolution, follows mass sympathetic discharge, at fight and flight reactions (Cannon's theory) and there is no kind of a special regulation for this. However, the following findings, coming from different fields of the research, challenge this view: (i) the sympathetic nervous system has been approved that has a greater capacity for specificity than has usually been attributed to it (Lacey 1967, Miller 1969a, Miller 1969b), (ii) autonomic manifestations differ considerably among anxiety disorders (Saric and McLeod 1988, Ost et al. 1984), e.g. depressed patients exhibit higher tonic heart rate levels in parallel with lower tonic skin conductance levels (Dawson 1985), (iii) EDA was eliminated during the REM phase of sleep, in contrast to all other sympathetic functions which remained at the same levels as in awakening (Johnson and Lubin 1966, Lester et al. 1967, Kushniruk et al. 1985), (iv) intraneural recordings of sympathetic nerve traffic have shown that the view of a diffusely acting system led to the term "sympathetic tone" is not tenable (Wallin 1992, Wallin and Elam 1994), (v) we have found from recordings during sexual intercourse and orgasm that palmar sweating is not augmented in the moment of orgasm when a mass sympathetic activation takes place. These findings led us to the conclusion that palmar sweating is not manifested as an indistinct concomitant of sympathetic discharge.
In order to exlore the way of the palmar sweating regulation, we had posed the question of how far the intensity of palmar sweating is influenced by the usefulness of palmar wetting in action. In an experiment special designed to give an answer to this quuestion, we found that palmar sweating was significantly higher in leafing (palmar wetting was desirable) than weighing a hydrophilic substance (palmar wetting was unwanted), although both tasks designed to involve, within the bounds of possibility, the same movement's demands and emotional load. Normal palmar sweating subjects were participated to this experiment. This finding was an indication that the usefulness of palmar wetting influence the intensity of palmar sweating, an indication that probably a cognitive appreciatory mechanism contributes to the regulation of palmar sweating in a purposeful way.
After that the problem could be placed in new terms: what happens to this appreciatory mechanism when excessive palmar sweating takes place and no benefit of palmar wetting in action can be found (examinations, social relationships, writing, etc.)? The most clear-cut case of pointless palmar sweating is observed in the palmar hypehidrosis. We posed the question of whether a disruption of the appreciatory of the benefit of palmar wetting mechanism take place in palmar hyperhidrosis.
The answer to this question may be of greater interest for the neurotic manifestation of a function in general. Neurotic manifestation of a function is predominately considered maladaptive (Eysenck 1979) and we have collected the following findings which support the hypothesis that palmar hyperhidrosis is indeed a neurotic manifestation of palmar sweating: (i) palmar hyperhidrosis is not controlled by a thermoregulatory mechanism (Kerassidis 1994), (ii) clinical and laboratory test, general haematological, levels of thyroid hormones, glucose and electrolytes, heart rate variability (performed after 24 hours electrocardiogram recording as an estimate of autonomic balance), neurological examinations, estimation of the density of sweat glands on palms of hyperhidrotics, etc. failed to reveal any type of organic disease as an antecedent of palmar hyperhidrosis (papers submitted for publication). (iii) hyperhidrosis is expressed in discomfort and some individuals had manifested hyperhidrosis for a trancient hard period of their life, which was dissapeared when the problems were overcame (from interviews with hyperhidrotic in palms subjects, attracted by local mass media for the research) (iv) personality's tests (Eysenck's Personality Questionnaire and Minnesota Multiphasic Personality Inventory) revealed significant differences between hyperhidrotic and normal subjects in neuroticism traits. We have concluded that the neuroticism probably makes hyperhidrotics more prone to identify stressors as discomfort producing.
MATERIALS AND METHODS
Subjects
Twenty: 10 hyperhidrotic in palms, mean age 33 years old (range 18-56) and 10 normal palmar sweating subjects, mean age 30 years old (range 20-62), participated in this experiment. Males were 5 and females also 5, in each group.
Materials
J&J Modules of Unicomp was used for the recording of conductivity of right palm. The electrodes were of Ag-AgCl. Day books were used for leafing. An ink-pad and sheets were used for fingerprints.
Procedure
Subjects read instructions for leafing. They were reminded that leafing would be facilitated if their forefinger could sweat. They made a leafing rehearsal in order to familiarise with the procedure. So their electrodermal responses (EDRs) during leafing would not be part of startling or novelty reaction. They had to turn the pages of a day book only by the forefinger and stay still the fingers with electrodes (thumb and middle finger), in order to avoid artifacts, for 100 seconds. No conversation was permitted.
After leafing, electrodes were not removed, in order to prevent artificial changes to the level of conductivity (LC). Subjects read the instructions to make continuously fingerprints of the fingers of both palms. They were reminded that they had to avoid palmar sweating for good quality fingerprints. They performed this task for 100 seconds too.
The order of execution of the tasks in this procedure was opposite of that of our previous experiment where only normal subjects participated. Now, the leafing (palmar wetting was desirable) was performed first and fingerprinting (palmar wetting is unwanted) followed. In the previous experiment the weighing of the hydrophilic substance was performed first (palmar wetting was unwanted) and leafing followed. We reversed the order of the execution of the tasks in order to check how the result of the previous experiment could be caused by some kind of sensitisation. We changed the weighing of the hydrophilic substance with the fingerprinting in order to make more similar the tasks, since in both leafing and fingerprinting the fingers tuch paper (if a somatosensory feedback would be important).
RESULTS
We compared the number of electodermal responses (EDRs) and the mean skin conductance level (SCL) between leafing and fingerprinting. As EDR we accepted any increase in palmar conductivity over 0.3 μS and the mean SCL was calculated by the computer as the mean value of 20 mean values of SCL for 5 sec each one.
One tail paired t-test revealed that the number of EDRs of normal palmar sweating subjects was significantly higher (P<.002) during leafing than fingerprinting. Hyperhidrotics, similarly, had significantly higher (P<.002) EDRs during leafing than fingerprinting. In both groups the number of EDRs during fingerprinting was diminished about in the half of those during leafing. A two factor (sex, hyperhidrosis) analysis of variance (ANOVA) on the number of EDRs during leafing and fingerprinting did not reveal any significant difference, although hyperhidrotics had, in both tasks, a higher number of EDRs than normal subjects.
One tail paired t-test revealed that the mean SCL of normal palmar sweating subjects was significantly higher (P<.003) during leafing than fingerprinting. Hyperhidrotics, similarly, had significantly higher (P<.005) mean SCL during leafing than fingerprinting. The diminution of mean SCL from leafing to fingerprinting was about 30% for both groups. A two factor (sex, hyperhidrosis) analysis of variance (ANOVA) on mean SCL during the two tasks revealed that hyperhidrotics had a significantly higher (P<.02) mean SCL during leafing than normal subjects, and a significantly higher (P<.01) mean SCL during fingerprinting. Females had a significantly higher (P<.05) mean SCL during both tasks and the interaction of the factors (sex, hyperhidrosis) was also significant (P<.05) in both tasks.
DISCUSSION
We found that both hyperhidrotic in palms and normal palmar sweating subjects expressed higher EDA during leafing (palmar sweating is desirable) than fingerprinting (palmar sweating is unwanted). The diminution of palmar sweating from the first to the second task was about the same for both hyperhidrotic and normal subjects. The mean palmar SCL of hyperhidrotics and females was higher than normal subjects and males respectively, in both tasks. The finding for normal subjects replicated the finding of our previous similar experiment and confirmed the suggestion that the magnitude of palmar sweating is influenced from the usefulness of palmar wetting in action. As far as the hyperhidrotics are concerned, it was expected that the influence of the palmar wetting usefulness to the magnitude of palmar sweating would be lesser than normal subjects or it would not exist at all. However, the fact that palmar sweating of hyperhidrotics is differentiated between tasks analogously to the benefit of palmar wetting, indicates that no disruption of the appreciatory of usefulness mechanism takes place, even in the case of excessive-neurotic manifestation of palmar sweating. This finding challenges the unsophisticated view about the maladaptive nature of excessive sweating and hyperhidrosis, perhaps and for the neurotic function in general.
But how can be explained that palmar sweating is manifested in examinations, social relationships, writing, etc. when no benefit of palmar wetting in action can be found? We faced this phenomenon in the second task when the palmar sweating of both groups was not zero, despite that it was absolutely undesirable. Two interpretations can be given. The first is that the impact of the appreciatory mechanism is limited and it is superimposed to the impact of other, more automatically influenced the palmar sweating factors. The second is that the benefit from palmar wetting is only one of the elements of the appreciatory mechanism in its regulation of palmar sweating. In order to judge these interpretations we have to remind that since a sound may in general cause an EDR to a subject, a weak noise in a danger environment may cause a strong EDR and no EDR may be caused by a loud noise in a disco. Obviously, there is a strong determination of the electrodermal behaviour by an appreciatory mechanism for a wide limited area of stimuli and conditions. Perhaps this is in other words the same with the tendency for electrodermal reflexes to involve control by the highest centers unless otherwise prevented (Venables 1991).
We suggest that a nonword appreciatory mechanism is still working in these cases when palmar sweating takes place and no benefit of palmar wetting in action can be found. However, the estimation of this mechanism may not only rely on how useful is the palmar wetting. Palmar sweating may be useful for other reasons to the organism beyond mechanical facilitation of the action. There is a large piece of evidence in the research of EDA which permits making a suggestion about that, but it must be in a review article.
REFERENCES
Adelman, S., Taylor, C. R. and Meglung, N. C. (1975) Sweating on paws and palms: what is its function? Am. J. Psychol., 229(5): 1400-1402.
Dawson, M. E.et al (1985) Diagnostic utility of autonomic measures for major depressive disorders. Psychiatry Res., 15: 261-270.
Eysenck, H. J. (1979) The conditioning model of neurosis. Behav. Brain Sci., 2: 155-199.
Fowles, D. C. 1986. The eccrine system and electrodermal activity. In: M. G. H. Coles, E. Donchin, S. W. Porges (Eds), Psychophysiology : Systems, Processes, and Applications., Elsevier, Amsterdam, pp. 51-96.
Hoehn-Saric, R. and McLeod, D. R. (1988) The peripheral sumpathetic nervous system. Its role in normal and pathological anxiety. Psychiatr. Clin. North Am., 11(2): 375-386.
Johnson, L. C. and Lubin, A. (1966) Spontaneous electrodermal activity during waking and sleeping. Psychophysiology., 3(1): 8-17.
Kerassidis, S. (1994) Is palmar and plantar sweating thermoregulatory? Acta Physiol. Scand., 152: 259-263.
Kushniruk, A., Rustenburg, J. and Ogilvie, R. (1985) Psychological correlates of electrodermal activity during REM sleep. Sleep., 8(2): 146-154.
Lacey, J. I. (1967) Somatic response patterning and stress: Some revisions of activation theory.In: M.H. Appley and R. Trumbull (Eds), Psychological Stress (Issues in research), Chapter 2, ACC, New York, pp. 15-42.
Lester, B. K., Burch, N. R. and Dossett, R. C. (1967) Nocturnal EEG-GSR profiles : the influence of presleep states. Psychophysiology, 3: 238-248.
Miller, N. E. (1969) Psychosomatic effects of specific types of training. Ann. N. Y. Acad. Sci., 159: 1025-1040.
Miller, N. E. (1969) Learning of visceral and glandural responses. Science. 163: 434-445.
Ost, L., Sterner, U., Lindahl, I. (1984) Physiological responses in blood phobics. Behav Res Ther. 22(2): 109-117.
Venables, P. H. (1991) Autonomic activity. Ann. N. Y. Acad. Sci., 620: 191-207.
Wallin, B. G.(1992) Intraneural recordings of normal and abnormal sympathetic activity in man. In: R. Bannister, C. J. Mathiaw (Eds), Autonomic Failure. A textbook of clinical disorders of the autonomic nervous system, Oxford Medical Publications, Oxford, pp. 359-377.
Wallin, B. G. and Elam, M. (1994) Insights from intraneural recordings of sympathetic nerve traffic in humans. Am. Physiol .Soc., 9: 203-207.
Wilcott, R. C. (1966) Adaptive value of arousal sweating and the epidermal mechanism related to skin potential and skin resistance. Psychophysiology, 2(3): 249-262.
In this work, the influence of the benefit of palmar wetting in the intensity of palmar sweating was examined. The electrodermal activity (EDA) of hyperhidrotic and normal subjects was compared, in a leafing (palmar wetting is desirable) and fingerprinting (palmar wetting is unwanted) tasks. Hyperhidrotic, in the same degree as normal subjects, presented a higher EDA during leafing than fingerprinting. We concluded that the ability of a beneficial manifestation of palmar sweating does not be lost in the case of palmar hyperhidrosis. This finding may implies that It must be questioned the unsophisticated view for the maladaptive nature of palmar hyperhidrosis or the neurotic manifestation of a function in general.
INTRODUCTION
Many times a day, the electrodermal activity (EDA) of a subject seems to be pointless, since there is no benefit of palmar wetting (friction improvement or abrasion prevention Adelman et al. 1975, Wilcott 1966) for the subject's action. These times, the manifestation of palmar sweating offers no adaptation to the action demands, probably it complicates that, and could be considered maladaptive. Fowles' (1986) question of whether this function is simply a complex and noisy manifestation of non-specific activity is absolutelly justifiable from this side of view.
The isolation of palmar sweating from the action's demands of palmar wetting can be understandable if palmar and plantar sweating, as a residue of the evolution, follows mass sympathetic discharge, at fight and flight reactions (Cannon's theory) and there is no kind of a special regulation for this. However, the following findings, coming from different fields of the research, challenge this view: (i) the sympathetic nervous system has been approved that has a greater capacity for specificity than has usually been attributed to it (Lacey 1967, Miller 1969a, Miller 1969b), (ii) autonomic manifestations differ considerably among anxiety disorders (Saric and McLeod 1988, Ost et al. 1984), e.g. depressed patients exhibit higher tonic heart rate levels in parallel with lower tonic skin conductance levels (Dawson 1985), (iii) EDA was eliminated during the REM phase of sleep, in contrast to all other sympathetic functions which remained at the same levels as in awakening (Johnson and Lubin 1966, Lester et al. 1967, Kushniruk et al. 1985), (iv) intraneural recordings of sympathetic nerve traffic have shown that the view of a diffusely acting system led to the term "sympathetic tone" is not tenable (Wallin 1992, Wallin and Elam 1994), (v) we have found from recordings during sexual intercourse and orgasm that palmar sweating is not augmented in the moment of orgasm when a mass sympathetic activation takes place. These findings led us to the conclusion that palmar sweating is not manifested as an indistinct concomitant of sympathetic discharge.
In order to exlore the way of the palmar sweating regulation, we had posed the question of how far the intensity of palmar sweating is influenced by the usefulness of palmar wetting in action. In an experiment special designed to give an answer to this quuestion, we found that palmar sweating was significantly higher in leafing (palmar wetting was desirable) than weighing a hydrophilic substance (palmar wetting was unwanted), although both tasks designed to involve, within the bounds of possibility, the same movement's demands and emotional load. Normal palmar sweating subjects were participated to this experiment. This finding was an indication that the usefulness of palmar wetting influence the intensity of palmar sweating, an indication that probably a cognitive appreciatory mechanism contributes to the regulation of palmar sweating in a purposeful way.
After that the problem could be placed in new terms: what happens to this appreciatory mechanism when excessive palmar sweating takes place and no benefit of palmar wetting in action can be found (examinations, social relationships, writing, etc.)? The most clear-cut case of pointless palmar sweating is observed in the palmar hypehidrosis. We posed the question of whether a disruption of the appreciatory of the benefit of palmar wetting mechanism take place in palmar hyperhidrosis.
The answer to this question may be of greater interest for the neurotic manifestation of a function in general. Neurotic manifestation of a function is predominately considered maladaptive (Eysenck 1979) and we have collected the following findings which support the hypothesis that palmar hyperhidrosis is indeed a neurotic manifestation of palmar sweating: (i) palmar hyperhidrosis is not controlled by a thermoregulatory mechanism (Kerassidis 1994), (ii) clinical and laboratory test, general haematological, levels of thyroid hormones, glucose and electrolytes, heart rate variability (performed after 24 hours electrocardiogram recording as an estimate of autonomic balance), neurological examinations, estimation of the density of sweat glands on palms of hyperhidrotics, etc. failed to reveal any type of organic disease as an antecedent of palmar hyperhidrosis (papers submitted for publication). (iii) hyperhidrosis is expressed in discomfort and some individuals had manifested hyperhidrosis for a trancient hard period of their life, which was dissapeared when the problems were overcame (from interviews with hyperhidrotic in palms subjects, attracted by local mass media for the research) (iv) personality's tests (Eysenck's Personality Questionnaire and Minnesota Multiphasic Personality Inventory) revealed significant differences between hyperhidrotic and normal subjects in neuroticism traits. We have concluded that the neuroticism probably makes hyperhidrotics more prone to identify stressors as discomfort producing.
MATERIALS AND METHODS
Subjects
Twenty: 10 hyperhidrotic in palms, mean age 33 years old (range 18-56) and 10 normal palmar sweating subjects, mean age 30 years old (range 20-62), participated in this experiment. Males were 5 and females also 5, in each group.
Materials
J&J Modules of Unicomp was used for the recording of conductivity of right palm. The electrodes were of Ag-AgCl. Day books were used for leafing. An ink-pad and sheets were used for fingerprints.
Procedure
Subjects read instructions for leafing. They were reminded that leafing would be facilitated if their forefinger could sweat. They made a leafing rehearsal in order to familiarise with the procedure. So their electrodermal responses (EDRs) during leafing would not be part of startling or novelty reaction. They had to turn the pages of a day book only by the forefinger and stay still the fingers with electrodes (thumb and middle finger), in order to avoid artifacts, for 100 seconds. No conversation was permitted.
After leafing, electrodes were not removed, in order to prevent artificial changes to the level of conductivity (LC). Subjects read the instructions to make continuously fingerprints of the fingers of both palms. They were reminded that they had to avoid palmar sweating for good quality fingerprints. They performed this task for 100 seconds too.
The order of execution of the tasks in this procedure was opposite of that of our previous experiment where only normal subjects participated. Now, the leafing (palmar wetting was desirable) was performed first and fingerprinting (palmar wetting is unwanted) followed. In the previous experiment the weighing of the hydrophilic substance was performed first (palmar wetting was unwanted) and leafing followed. We reversed the order of the execution of the tasks in order to check how the result of the previous experiment could be caused by some kind of sensitisation. We changed the weighing of the hydrophilic substance with the fingerprinting in order to make more similar the tasks, since in both leafing and fingerprinting the fingers tuch paper (if a somatosensory feedback would be important).
RESULTS
We compared the number of electodermal responses (EDRs) and the mean skin conductance level (SCL) between leafing and fingerprinting. As EDR we accepted any increase in palmar conductivity over 0.3 μS and the mean SCL was calculated by the computer as the mean value of 20 mean values of SCL for 5 sec each one.
One tail paired t-test revealed that the number of EDRs of normal palmar sweating subjects was significantly higher (P<.002) during leafing than fingerprinting. Hyperhidrotics, similarly, had significantly higher (P<.002) EDRs during leafing than fingerprinting. In both groups the number of EDRs during fingerprinting was diminished about in the half of those during leafing. A two factor (sex, hyperhidrosis) analysis of variance (ANOVA) on the number of EDRs during leafing and fingerprinting did not reveal any significant difference, although hyperhidrotics had, in both tasks, a higher number of EDRs than normal subjects.
One tail paired t-test revealed that the mean SCL of normal palmar sweating subjects was significantly higher (P<.003) during leafing than fingerprinting. Hyperhidrotics, similarly, had significantly higher (P<.005) mean SCL during leafing than fingerprinting. The diminution of mean SCL from leafing to fingerprinting was about 30% for both groups. A two factor (sex, hyperhidrosis) analysis of variance (ANOVA) on mean SCL during the two tasks revealed that hyperhidrotics had a significantly higher (P<.02) mean SCL during leafing than normal subjects, and a significantly higher (P<.01) mean SCL during fingerprinting. Females had a significantly higher (P<.05) mean SCL during both tasks and the interaction of the factors (sex, hyperhidrosis) was also significant (P<.05) in both tasks.
DISCUSSION
We found that both hyperhidrotic in palms and normal palmar sweating subjects expressed higher EDA during leafing (palmar sweating is desirable) than fingerprinting (palmar sweating is unwanted). The diminution of palmar sweating from the first to the second task was about the same for both hyperhidrotic and normal subjects. The mean palmar SCL of hyperhidrotics and females was higher than normal subjects and males respectively, in both tasks. The finding for normal subjects replicated the finding of our previous similar experiment and confirmed the suggestion that the magnitude of palmar sweating is influenced from the usefulness of palmar wetting in action. As far as the hyperhidrotics are concerned, it was expected that the influence of the palmar wetting usefulness to the magnitude of palmar sweating would be lesser than normal subjects or it would not exist at all. However, the fact that palmar sweating of hyperhidrotics is differentiated between tasks analogously to the benefit of palmar wetting, indicates that no disruption of the appreciatory of usefulness mechanism takes place, even in the case of excessive-neurotic manifestation of palmar sweating. This finding challenges the unsophisticated view about the maladaptive nature of excessive sweating and hyperhidrosis, perhaps and for the neurotic function in general.
But how can be explained that palmar sweating is manifested in examinations, social relationships, writing, etc. when no benefit of palmar wetting in action can be found? We faced this phenomenon in the second task when the palmar sweating of both groups was not zero, despite that it was absolutely undesirable. Two interpretations can be given. The first is that the impact of the appreciatory mechanism is limited and it is superimposed to the impact of other, more automatically influenced the palmar sweating factors. The second is that the benefit from palmar wetting is only one of the elements of the appreciatory mechanism in its regulation of palmar sweating. In order to judge these interpretations we have to remind that since a sound may in general cause an EDR to a subject, a weak noise in a danger environment may cause a strong EDR and no EDR may be caused by a loud noise in a disco. Obviously, there is a strong determination of the electrodermal behaviour by an appreciatory mechanism for a wide limited area of stimuli and conditions. Perhaps this is in other words the same with the tendency for electrodermal reflexes to involve control by the highest centers unless otherwise prevented (Venables 1991).
We suggest that a nonword appreciatory mechanism is still working in these cases when palmar sweating takes place and no benefit of palmar wetting in action can be found. However, the estimation of this mechanism may not only rely on how useful is the palmar wetting. Palmar sweating may be useful for other reasons to the organism beyond mechanical facilitation of the action. There is a large piece of evidence in the research of EDA which permits making a suggestion about that, but it must be in a review article.
REFERENCES
Adelman, S., Taylor, C. R. and Meglung, N. C. (1975) Sweating on paws and palms: what is its function? Am. J. Psychol., 229(5): 1400-1402.
Dawson, M. E.et al (1985) Diagnostic utility of autonomic measures for major depressive disorders. Psychiatry Res., 15: 261-270.
Eysenck, H. J. (1979) The conditioning model of neurosis. Behav. Brain Sci., 2: 155-199.
Fowles, D. C. 1986. The eccrine system and electrodermal activity. In: M. G. H. Coles, E. Donchin, S. W. Porges (Eds), Psychophysiology : Systems, Processes, and Applications., Elsevier, Amsterdam, pp. 51-96.
Hoehn-Saric, R. and McLeod, D. R. (1988) The peripheral sumpathetic nervous system. Its role in normal and pathological anxiety. Psychiatr. Clin. North Am., 11(2): 375-386.
Johnson, L. C. and Lubin, A. (1966) Spontaneous electrodermal activity during waking and sleeping. Psychophysiology., 3(1): 8-17.
Kerassidis, S. (1994) Is palmar and plantar sweating thermoregulatory? Acta Physiol. Scand., 152: 259-263.
Kushniruk, A., Rustenburg, J. and Ogilvie, R. (1985) Psychological correlates of electrodermal activity during REM sleep. Sleep., 8(2): 146-154.
Lacey, J. I. (1967) Somatic response patterning and stress: Some revisions of activation theory.In: M.H. Appley and R. Trumbull (Eds), Psychological Stress (Issues in research), Chapter 2, ACC, New York, pp. 15-42.
Lester, B. K., Burch, N. R. and Dossett, R. C. (1967) Nocturnal EEG-GSR profiles : the influence of presleep states. Psychophysiology, 3: 238-248.
Miller, N. E. (1969) Psychosomatic effects of specific types of training. Ann. N. Y. Acad. Sci., 159: 1025-1040.
Miller, N. E. (1969) Learning of visceral and glandural responses. Science. 163: 434-445.
Ost, L., Sterner, U., Lindahl, I. (1984) Physiological responses in blood phobics. Behav Res Ther. 22(2): 109-117.
Venables, P. H. (1991) Autonomic activity. Ann. N. Y. Acad. Sci., 620: 191-207.
Wallin, B. G.(1992) Intraneural recordings of normal and abnormal sympathetic activity in man. In: R. Bannister, C. J. Mathiaw (Eds), Autonomic Failure. A textbook of clinical disorders of the autonomic nervous system, Oxford Medical Publications, Oxford, pp. 359-377.
Wallin, B. G. and Elam, M. (1994) Insights from intraneural recordings of sympathetic nerve traffic in humans. Am. Physiol .Soc., 9: 203-207.
Wilcott, R. C. (1966) Adaptive value of arousal sweating and the epidermal mechanism related to skin potential and skin resistance. Psychophysiology, 2(3): 249-262.
What provokes palmar hyperhidrosis?
ABSTRACT
In this work, we try to find out why some types of physical or mental effort of the every day life activities provoke excessive sweating in hyperhidrotic individuals but other types do not. We compared (i) the palmar and forearm electrodermal activity (EDA) of hyperhidrotic in palms and normal individuals when they performed mental arithmetic: a. in recumbent position, without moving or speaking, and b. in standing position, while they vocalized the solutions to the same mental arithmetic task (ii) the amount of palmar and forearm sweat of the same individuals while they were bicycling a. normally, b. with distress, and c. after reducing the distress. Forearm EDA was recorded in order to check the supposition that an over-function of sympathetic nervous fibers, which innervate both palmar and forearm sweat glands, is responsible for palmar hyperhidrosis. The lack of forearm electrodermal responses during mental arithmetic for both groups, as well as the insignificant correlation between palmar and forearm sweating, especially for hyperhidrotics, indicate that the theory of over-function of sympathetic nervous fibers is not tenable. The finding that palmar EDA of both hyperhidrotic and normal individuals in standing position was much higher than that in recumbent position indicate that the muscle tension is a decisive factor for the magnitude of palmar sweating during mental effort. The finding that the amount of palmar sweat of hyperhidrotics was increased during the second and decreased during the third bicycling task, indicate that the distress is a decisive factor for hyperhidrotic sweating during physical effort. We concluded that the necessary and effective ingredient of a mental or physical effort, in order to provoke palmar hyperhidrosis, is the combination of distress with muscle tension.
INTRODUCTION
From our investigation on palmar hyperhidrosis, we already know that: (i) it is not controlled by a thermoregulatory mechanism [1], (ii) extended clinical and laboratory tests did not reveal any type of organic disease (hematological abnormality, electrolytic or glucose imbalance, thyroid gland dysfunction, neurological abnormality, autonomic imbalance, etc.) or a higher density of sweat glands on palm, but only a higher score in Neuroticism scale of Eysenck's Personality Questionnaire of hyperhidrotics as compared to normal palmar sweating individuals (unpublished data), (iii) hyperhidrotics presented higher scores in Psychasthenia, Social Introversion, and Depression of Minnesota Multiphasic Personality Inventory [2]. These findings were in agreement with those of Lerer, Jacobowitz and Wahba [3] and of Lerer and Jacobowitz [4] that hyperhidrotic individuals are characterized by lower overall ability to cope with stress and a strong proclivity to avoid problems, in the sense that they suggest that personality traits may be responsible for palmar hyperhidrosis.
From extended interviews about everyday life of hyperhidrotics we know that in many cases mental efforts do not cause hyperhidrosis and that hyperhidrotics may not sweat at all on their palms when they perform calm a hard handiwork. In the present work, we try to determine what is effective, what is necessary for palmar hyperhidrosis expression. This information could help in the understanding of the nature of the disorder as well as in its treatment, given the lack of investigation on the etiology of palmar hyperhidrosis (see the reviews by Sato, Kang, Saga, and Sato [5] on the disorders of sweat glands, by Lerer [6], Lerer, Jacobowitz and Wahba [3] on the psychological aspects of palmar hyperhidrosis, and by Fotopoulos and Sunderland [7] on the treatment of psychophysiological disorders). We subjected hyperhidrotic and normal palmar sweating individuals to 2 mental arithmetic (mental effort) and 3 bicycling (physical effort) tasks. The mental arithmetic tasks aimed to check the role of muscle tension on palmar sweating caused by the same mental effort. The bicycling tasks aimed to check the role of the distress on palmar sweating caused by the same physical effort.
Electrodermal recordings of forearm have been also performed in order to check the theory of Shih, Wu and Lin [19], that the over-function of sympathetic fibers passing through T2,3 ganglia is responsible for palmar hyperhidrosis. Since these ganglia innervate both palmar and forearm sweat glands, a kind of forearm hyperhidrosis, or at least a significant correlation between palmar and forearm sweating should be expected in the case of hyperhidrotics.
Before the presentation of the work, we should mention that the old view of general or sympathetic arousal, according to which palmar hyperhidrosis follows mass sympathetic discharge at fight and flight reactions (Cannon's theory), must not be considered as an answer to the question concerning the palmar hyperhidrosis expression. Former and recent studies [8-12] from different fields of research have challenged the view of a diffusely acting sympathetic system. Besides, it is well known that autonomic manifestations (and EDA) differ considerably among psychological disorders [13-15] and also in relation to stimulus presentation, or condition of performance [16-18], which means that no arousal theory can overcome the question why a specific sympathetic function is triggered under specific conditions. In addition, we repeatedly recorded slight or no palmar sweat glands activation during human orgasm (mass sympathetic activation took place), and we concluded that palmar sweating cannot be considered as a simple following of sympathetic discharge (unpublished data).
METHODS
PARTICIPANTS
Forty individuals participated in the present work. Twenty individuals were hyperhidrotic in their palms (and, usually, in their soles as well), whereas the remaining 20 individuals were normal in terms of palmar sweating. Twelve females and 8 males were included in each group. The mean age of the hyperhidrotic females was 31.4 (17-63) and of the normal females was 27.3 (20-42) years. The mean age of the hyperhidrotic males was 35 (21-56) and of the normal males was 34.3 (22-61) years. The mean body weight of the hyperhidrotic females was 60.3 (50-73) and of the normal females was 56.4 (45-70) kg. The mean body weight of the hyperhidrotic males was 75.6 (62-87) and of the normal males was 76.2 (62-102) kg. The educational level of hyperhidrotics/normals was: 11/12 higher education, 3/4 students, and 6/4 secondary-lower.
Individuals with palmar hyperhidrosis were recruited by advertisements in the local mass media. They participated voluntarily in the research. Six persons who manifested excessive sweating all over the body, or predominantly in other areas of the body, like the forehead and the armpits, were not included in this study. The authors from people who reported never having suffered from excessive palmar sweating selected normal palmar sweating individuals. Attention was paid to the equivalence on gender, age, and educational level to the hyperhidrotic group.
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 was 3.1 mg (S.D. 2.3, range 0-7). We did not exclude any individual from the research. The participation of 2 individuals, one from the hyperhidrotic group with 4 mg palmar sweating and one from the normal group with 12 mg palmar sweating, confirmed that they did not have the electrodermal behavior they had declared. Their scores in the tests were excluded from the analysis. This way, the simple method of measuring the palmar sweating during writing was proved to be a good confirmation tool of the declared by the participants’ electrodermal behavior.
MATERIALS
We used the voltage coupler 9878 of the Beckman R 511A polygraph for chart recording of palmar skin conductance, during mental arithmetic tests. The recorded voltage was received from the ends of a resistor (1000 Ω) which was in series connection with the individual and an external stabilized voltage source (0.5 V). The J&J Modules, designed to support the B45 biofeedback program of Unicomp, were used for the recording of palmar and forearm skin conductance. German 3M, Ag-AgCl electrodes, 8 mm diameter were used; after each session their polarity was changed and they were replaced after two sessions, in order to prevent polarization. Electrolytic paste of Hewlett Packard was used as electrolytic medium.
A gravimetric method was used during bicycling task, because the profuse sweating, especially of hyperhidrotics, and the movement demands of the task, could cause artificial recordings. Sweat collecting plasters were attached on the palm and forearm during bicycling. The sweat collecting plaster consisted of a leucoplast (5Χ5) cm with a small sponge (2Χ2) cm attached to its center. A waterproof membrane on its outer surface was used to prevent any evaporation of the collected sweat. The sweat collecting plaster weighed about 580 mg and could absorb more than 500 mg of sweat almost immediately. The weight of plasters was measured by an electronic balance (Shimadzu) with 1 mg readability and 340 g weighing capacity.
DESIGN AND PROCEDURE
All participants washed their hands. Each individual was asked to read the instructions describing the procedure and to avoid speaking until completion of the tasks. Electrodes for skin conductance recording were attached on the two palms as well as on the forearm of the right hand, while the individual was laid on an examination table. The electrodes were not removed during the mental arithmetic tasks, in order to avoid artificial differences in skin conductance levels. The blood pressure and heart rate measurements, which were interposed, will not be presented in this work.
Three minutes after relaxing on the examination table, the participant was asked to perform the first out of the two mental arithmetic tasks, that is, to add continuously the number 7 for 72 s, without speaking or contracting any muscle. The participant reported the found sum at the end of the 72 s period. After this task and during the 3 min intertask break that followed, the participant was asked to sit for 2 min and then to stand for 1 min, in order to accustom to the standing position before performing the second mental arithmetic task. This second task was the same with the previous one in terms of mental effort, starting from another number. The two mental arithmetic tasks were designed to be the same, apart from the body posture and speaking, in order to check the role of muscle tension in palmar sweating caused by the same mental effort.
Some min later, the participant performed 3 bicycling tasks. During the first task, the participants bicycled for 4 min, in order to compare the palmar sweating of hyperhidrotic and normal individuals during physical exercise. Sweat collecting plasters were attached (after wiping the area) on the palm (hypothenar eminence) and forearm of the individual's left hand. The plasters were weighed immediately before and after each bicycling task. A clothing support around the neck prevented sweat secreted by other areas from reaching the plasters. The participant was asked to keep bicycling at a constant rate of 10-15 miles per hour, using a tachometer. Before the second bicycling task, which was identical to the first one in terms of physical exercise, the shoes and the socks of the participant were taken off by the experimenter, in order to investigate the influence of distress in the EDA caused by physical effort. The unwarned removal of the shoes and socks caused psychological distress, especially in hyperhidrotics (they all mentioned that, after a relevant question at the end of the tasks), because of the revelation of their wet soles, soaked socks with probably unpleasant odor, and of the difficulty in bicycling with naked their wet soles. Before the third bicycling task, socks and shoes were replaced and absorbing gloves were put on both palms, in order the distress of profuse sweating to be eliminated.
STATISTICS
We compared the number of electrodermal responses (EDRs) and the skin conductance level (SCL) in mental arithmetic, and weight of sweat in bicycling, using three factor ANOVA, with sex and hyperhidrosis as between-subject factors and repeated measures as within subject factor.
RESULTS
Mental arithmetic tasks: The hyperhidrotics presented a significantly higher number of palmar EDRs as compared to normal individuals during the performance of the mental arithmetic tasks F=9.62, DF=1, P<.004. No statistically significant differences were found between males and females. A significantly higher number of palmar EDRs was found during the performance of mental arithmetic in standing position as compared to recumbent position, for hyperhidrotics F=36.40, DF=1, P<.000, and for normal individuals F=21,28, DF=1, P<.000. The number of EDRs was about 70% higher in the standing position than in the recumbent one, in both hyperhidrotic and normal individuals, indicating that muscular tension causes a marked augmentation in the number of EDRs. Seven hyperhidrotics presented a smaller number of EDRs than the average of that of normal individuals, during the performance of mental arithmetic task in the recumbent position, but no one in the standing position. Forearm did not present any EDR during the performance of the mental arithmetic tasks.
Mean SCL was calculated by the computer every 4 s, while the SCL over the experimental period was taken as the average of 18 periods. Τhe hyperhidrotics presented significantly higher palmar SCL as compared to control individuals during the performance of the mental arithmetic F=32,42, DF=1, P<.000. No statistically significant differences were found between males and females. Significantly higher palmar SCL was observed during the execution of mental arithmetic in standing position in relation to that in recumbent position, for hyperhidrotics F=22.56, DF=1, P<.000, and for normal individuals F=20.26, DF=1, P<.000. The interaction of hyperhidrosis X execution position was also significant F=6.31, DF=1, P<.02. The augmentation of SCL of palms in the standing position in relation to SCL in the recumbent position was about 30% for hyperhidrotic and 43% for normal individuals. The higher augmentation of palmar SCL of normal individuals (in spite of the same augmentation of EDRs) in relation to that of hyperhidrotics was due to the smaller prior wetting of their palmar stratum corneum. Only one hyperhidrotic presented a smaller palmar SCL than the average of normal individuals SCL, during the performance of mental arithmetic task in the recumbent position but no one in the standing position.
Significantly higher forearm SCL was found in hyperhidrotic as compared to normal palmar sweating individuals during the performance of the mental arithmetic tasks F=8.78, DF=1, P<.005. This finding was probably the result of higher thermoregulatory sweating in the whole body of hyperhidrotics, because when the heat load in the bicycling tasks induced profuse thermoregulatory sweating in both groups, sweat product of forearm of hyperhidrotic and normal individuals was the same, while sweat product of palms was very different. There was no significant difference between forearm SCL during the execution of mental arithmetic in standing position in relation to that in recumbent position, in either group. The correlation between palmar and forearm SCL was significant (P<.05) only for normal individuals (r1=.468 and r2=.487) and insignificant for hyperhydrotic individuals (r1=.386 and r2=.09) in both tasks, respectively.
Bicycling: The weight of palmar sweat secreted during the performance of all 3 bicycling tasks was significantly higher in hyperhidrotic as compared to normal individuals F=14.41, DF=1, P<.001 (Fig. 1). Gender differences on palmar sweat were not significant, but the interaction of hyperhidrosis X sex was significant F=4.98, DF=1, P<.032. No significant difference was found in forearm weight of sweat between hyperhidrotic and normal individuals (Fig. 2). The weight of forearm sweat of males was higher than that of females during the bicycling tasks F=7.08, DF=1, P<.01. Palmar sweating of hyperhidrotics was significantly higher than forearm sweating during all 3 bicycling tasks. Palmar sweating of normal individuals was significantly higher than forearm sweating only during the first bicycling task.
Palmar sweating of hyperhidrotics was augmented from the first to the second bicycling task and was significantly reduced from the second to the third F=16.49, DF=1, P<.001 (Fig. 1). Palmar sweating of normal individuals was augmented significantly during the second bicycling task F=10.32, DF=1, P<.005 and remained at the same level during the third. Forearm sweating was augmented significantly from one to the next bicycling task for both hyperhidrotic (F=38.54, DF=1, P<.000, F=11.90, DF=1, P<.003), and normal individuals (F=44.54, DF=1, P<.000, F=13.93, DF=1, P<.002).
As expected from a thermoregulatory aspect, forearm sweating was augmented within the total bicycling time in both hyperhidrotic and normal individuals. In contrast, palmar sweating of hyperhidrotics displayed a maximum during the second bicycling task when physical exercise was combined with distress, and a significant diminution during the third bicycling task after reducing the distress (Figure 1). It is also noteworthy that all hyperhidrotics displayed higher values of weight of palmar sweat than the average of that of normal individuals, during only the second bicycling task.
Females displayed more palmar sweating than males during all 3 bicycling tasks (with the difference being significant in the second task) and less forearm sweating during all 3 bicycling tasks (with significant differences in the second and third task). Correlation analysis indicated a lack of general pattern of correlation between palmar and forearm sweating in either hyperhidrotic and normal or male and female individuals
CONCLUSIONS
From the forearm electrodermal recordings and sweating we have to stress that: (i) the forearm did not present measurable EDRs during mental arithmetic tasks, (ii) the sweating of forearm, for both normal and hyperhidrotic individuals, was augmented from the first to the third bicycling task, following the heat load, which indicate a thermoregulatory pattern of activation (iii) the sweating of forearm was not correlated to palmar sweating of hyperhidrotics in any task. These findings clearly demonstrate that palmar and forearm sweating is under of different central nervous control and do not support the theory of over-functioning sympathetic fibers, passing through the T2,3 ganglia (which, according to Shih, Wu and Lin [19] "play an important role in the elaboration or modulation of autonomic function elsewhere"), as the cause of palmar hyperhidrosis. It is worth mentioned that these authors have reported the following results which are in disagreement with their own theory: T2,3 ganglionectomized individuals displayed much less sweating, during physical exercise, in their forehead, upper chest, and upper extremities than normal individuals (indicating that fibers passing through T2,3 ganglia innervate all these areas), while hyperhidrotics displayed palmar but not forehead and chest hyperhidrosis. Obviously, the sweat glands of all these areas, especially for hyperhidrotics, are not activated by the sympathetic nervous system as a unit. Findings on the pathophysiology of palmar hyperhidrosis (and especially heart rate and blood pressure recordings, and heart rate variability analysis, as a quantitative assessment of autonomic balance) do not also give support to the over-functioning sympathetic fibers theory of palmar hyperhidrosis (unpublished data).
Based on the palmar EDA recordings, both hyperhidrotic and normal groups presented significantly higher palmar sweating during the mental arithmetic in the standing than in the recumbent position. This increase cannot be considered as thermoregulatory, since forearm sweating was not respectively augmented. This finding indicates that the muscular tension increases palmar sweating (both normal and hyperhidrotic) caused by mental process. It was also found that seven hyperhidrotics presented a smaller number of EDRs than the average number of normal individuals, during the performance of mental arithmetic task in the recumbent position, but no one in the standing position. This finding questions the ability of mental effort to cause palmar hyperhidrosis by itself, showing that the tension of the muscles may be a determinative factor for the magnitude of palmar sweating.
In the other side, the significant decrease of palmar sweating of hyperhidrotics in the third bicycling task (when the distress was reduced) questions the ability of physical effort, and therefore of muscle tension, to cause palmar hyperhidrosis by itself. Among the three bicycling tasks, all hyperhidrotics expressed excessive sweating (over the average of normal individuals) only during the second one, when the physical effort was combined with distress.
These findings suggest that neither mental nor physical effort may alone provoke hyperhidrosis. Considering the distress as the active ingredient of mental effort in provoking hyperhidrosis (a pleasant or calm thought has never been mentioned as sudorific) and the muscle tension as the active ingredient of physical effort, we consider that the combination of distress with muscle tension is the necessary and efficient factor for palmar hyperhidrosis expression. This conclusion is additionally supported by the following elements: (i) the relaxation is the active ingredient in the biofeedback treatment of palmar hyperhidrosis [20] (ii) the relation between palmar sweating and muscular tension is justified from a developmental point of view, because friction improvement [21] and abrasion prevention [22], which are the mechanical purposes of plantar sweating in mammals, are necessary only to the moving animal (iii) the hyperhidrotics may not sweat at all on their palms when they perform calm a hard handiwork or mental activity. Even in the case of a mentally acting hyperhidrotic individual, when facing difficulties of no handiwork demand, its excessive palmar sweating may also be considered as the result of the combination of mental effort or distress with muscle tension, since hidden muscular activity may accompany the mental processes [23].
In this point, we have to remind that the hyperhidrotics scored significantly higher than normal individuals on the Neuroticism scale of the Eysenck Personality Questionnaire (unpublished data) and in the scales of Depression, Social Introversion, and Psychasthenia of the Minnesota Multiphase Personality Inventory (MMPI) [2]. In agreement with the suggestion of Lerer, Jacobowitz and Wahba [3] and of Lerer and Jacobowitz [4] that hyperhidrotic individuals are characterized by lower overall ability to cope with stress and a strong proclivity to avoid problems, they may be more prone to distress feelings in their everyday life activities.
Conclusively, this work, in agreement with findings of former ones, suggests that (i) palmar hyperhidrosis is not caused by over-functioning of sympathetic fibers passing through T2,3 ganglia, and (ii) the combination of distress with muscle tension is the necessary and effective condition for palmar hyperhidrosis expression. Hyperhidrotics may be individuals who feel more easily distress, and perhaps produce higher tension of muscles (caused by the distress), than normal palmar sweating individuals.
REFERENCES
1. Kerassidis S: Is palmar and plantar sweating thermoregulatory? Acta Physiol Scand 1994;52:259-263.
2. Κερασίδης Σ, Μπιτζαράκη Κ: Στοιχεία της προσωπικότητας των υπεριδρωτικών στις παλάμες [Personality traits of hyperhidrotics in palms]. Ψυχιατρική 1997;8:181-187
3. Lerer Β, Jacobowitz J, Wahba A: Personality features in essential hyperhidrosis. Int J Psychiatry Med 1980;10(1):59-67.
4. Lerer Β, Jacobowitz J: Τreatment of essential hyperhidrosis by psychotherapy. Psychosomatics 1981;22(6):536-538.
5. Sato K, Kang W, Saga K, Sato KT: Biology of sweat glands and their disorders: 2. Disorders of sweat gland function. J Am Acad Dermatol 1989;20:713-726.
6. Lerer Β: Hyperhidrosis: A review of its psychological aspects. Psychosomatics 1977;18:28-31.
7. Fotopoulos SS, Sunderland WP: Biofeedback in the treatment of psychophysiologic disorders. Biofeedback Self Regul 1978;3(4):331-361.
8. Lacey JI: Somatic response patterning and stress: Some revisions of activation theory; in Appley MH & Trumbull R (eds): Psychological Stress (Issues in research) New York: ACC., 1967, pp 15-42
9. Miller NE: Learning of visceral and glandular responses. Science 1969a;163:434-445.
10. Miller NE: Psychosomatic effects of specific types of training. Ann N Y Acad Science 1969b;159:1025-1040.
11. Wallin BG: Intraneural recordings of normal and abnormal sympathetic activity in man; in Bannister R & Mathiaw CJ (eds): Autonomic Failure. A textbook of clinical disorders of the autonomic nervous system. Oxford: Oxford Medical Publications, 1992, pp 359-377.
12. Wallin G, Elam M: Insights from intraneural recordings of sympathetic nerve traffic in humans. NIPS 1994; 9:203-207.
13. Hoehn-Saric R, McLeod DR: The peripheral sympathetic nervous system. Its role in normal and pathological anxiety. Psychiatr Clin North Am 1988;11(2):375-386.
14. Ost L, Sterner U, Lindahl I: Physiological responses in blood phobics. Behav Res Ther 1984;22(2):109-117.
15. Dawson ME, Schell AM, Braaten J, Catania JJ: Diagnostic utility of autonomic measures for major depressive disorders. Psychiatry Res 1985;15:261-270.
16. Edelberg R: Mechanisms of electrodermal adaptations for locomotion, manipulation, or defense; in Stellar E & Sprague JM (eds): Progress in physiological psychology. New York: Academic Press, 1973, pp 155-209.
17. Venables PH, Christie MJ: Mechanisms, Instructions, Recording Techniques, and Quantification of Responses; in Prokasy WF & Raskin DC (eds): Electrodermal activity in psychological research New York: Academic Press, 1973, pp 1-124.
18. Fowles DC: The eccrine system and electrodermal activity. In M. G. H. Coles, Donchin E & Porges SW (eds.): Psychophysiology: Systems, Processes, and Applications. Oxford: The Guilford Press, 1986, pp 51-96.
19. Shih CJ, Wu JJ, Lin MT: Autonomic dysfunction in palmar hyperhidrosis. J Auton Nerv Syst 1983;8:33-43.
20. Duller P, Doyle Gentry W: Use of biofeedback in treating chronic hyperhidrosis: a preliminary report. Br J Dermatol 1980;103:143-146.
21. Adelman S, Taylor C, Meglung N: Sweating on paws and palms: what is its function? Am J Physiol 1975;229:1400-1402.
22. Wilcott RC: Adaptive value of arousal sweating and the epidermal mechanism related to skin potential and skin resistance. Psychophysiology 1966:2(3):249-262.
23. Cacciopo JT, Petty RE: Electromyograms as measures of extent affectivity of information processing. Am Psychol 1981;36:441-456.
In this work, we try to find out why some types of physical or mental effort of the every day life activities provoke excessive sweating in hyperhidrotic individuals but other types do not. We compared (i) the palmar and forearm electrodermal activity (EDA) of hyperhidrotic in palms and normal individuals when they performed mental arithmetic: a. in recumbent position, without moving or speaking, and b. in standing position, while they vocalized the solutions to the same mental arithmetic task (ii) the amount of palmar and forearm sweat of the same individuals while they were bicycling a. normally, b. with distress, and c. after reducing the distress. Forearm EDA was recorded in order to check the supposition that an over-function of sympathetic nervous fibers, which innervate both palmar and forearm sweat glands, is responsible for palmar hyperhidrosis. The lack of forearm electrodermal responses during mental arithmetic for both groups, as well as the insignificant correlation between palmar and forearm sweating, especially for hyperhidrotics, indicate that the theory of over-function of sympathetic nervous fibers is not tenable. The finding that palmar EDA of both hyperhidrotic and normal individuals in standing position was much higher than that in recumbent position indicate that the muscle tension is a decisive factor for the magnitude of palmar sweating during mental effort. The finding that the amount of palmar sweat of hyperhidrotics was increased during the second and decreased during the third bicycling task, indicate that the distress is a decisive factor for hyperhidrotic sweating during physical effort. We concluded that the necessary and effective ingredient of a mental or physical effort, in order to provoke palmar hyperhidrosis, is the combination of distress with muscle tension.
INTRODUCTION
From our investigation on palmar hyperhidrosis, we already know that: (i) it is not controlled by a thermoregulatory mechanism [1], (ii) extended clinical and laboratory tests did not reveal any type of organic disease (hematological abnormality, electrolytic or glucose imbalance, thyroid gland dysfunction, neurological abnormality, autonomic imbalance, etc.) or a higher density of sweat glands on palm, but only a higher score in Neuroticism scale of Eysenck's Personality Questionnaire of hyperhidrotics as compared to normal palmar sweating individuals (unpublished data), (iii) hyperhidrotics presented higher scores in Psychasthenia, Social Introversion, and Depression of Minnesota Multiphasic Personality Inventory [2]. These findings were in agreement with those of Lerer, Jacobowitz and Wahba [3] and of Lerer and Jacobowitz [4] that hyperhidrotic individuals are characterized by lower overall ability to cope with stress and a strong proclivity to avoid problems, in the sense that they suggest that personality traits may be responsible for palmar hyperhidrosis.
From extended interviews about everyday life of hyperhidrotics we know that in many cases mental efforts do not cause hyperhidrosis and that hyperhidrotics may not sweat at all on their palms when they perform calm a hard handiwork. In the present work, we try to determine what is effective, what is necessary for palmar hyperhidrosis expression. This information could help in the understanding of the nature of the disorder as well as in its treatment, given the lack of investigation on the etiology of palmar hyperhidrosis (see the reviews by Sato, Kang, Saga, and Sato [5] on the disorders of sweat glands, by Lerer [6], Lerer, Jacobowitz and Wahba [3] on the psychological aspects of palmar hyperhidrosis, and by Fotopoulos and Sunderland [7] on the treatment of psychophysiological disorders). We subjected hyperhidrotic and normal palmar sweating individuals to 2 mental arithmetic (mental effort) and 3 bicycling (physical effort) tasks. The mental arithmetic tasks aimed to check the role of muscle tension on palmar sweating caused by the same mental effort. The bicycling tasks aimed to check the role of the distress on palmar sweating caused by the same physical effort.
Electrodermal recordings of forearm have been also performed in order to check the theory of Shih, Wu and Lin [19], that the over-function of sympathetic fibers passing through T2,3 ganglia is responsible for palmar hyperhidrosis. Since these ganglia innervate both palmar and forearm sweat glands, a kind of forearm hyperhidrosis, or at least a significant correlation between palmar and forearm sweating should be expected in the case of hyperhidrotics.
Before the presentation of the work, we should mention that the old view of general or sympathetic arousal, according to which palmar hyperhidrosis follows mass sympathetic discharge at fight and flight reactions (Cannon's theory), must not be considered as an answer to the question concerning the palmar hyperhidrosis expression. Former and recent studies [8-12] from different fields of research have challenged the view of a diffusely acting sympathetic system. Besides, it is well known that autonomic manifestations (and EDA) differ considerably among psychological disorders [13-15] and also in relation to stimulus presentation, or condition of performance [16-18], which means that no arousal theory can overcome the question why a specific sympathetic function is triggered under specific conditions. In addition, we repeatedly recorded slight or no palmar sweat glands activation during human orgasm (mass sympathetic activation took place), and we concluded that palmar sweating cannot be considered as a simple following of sympathetic discharge (unpublished data).
METHODS
PARTICIPANTS
Forty individuals participated in the present work. Twenty individuals were hyperhidrotic in their palms (and, usually, in their soles as well), whereas the remaining 20 individuals were normal in terms of palmar sweating. Twelve females and 8 males were included in each group. The mean age of the hyperhidrotic females was 31.4 (17-63) and of the normal females was 27.3 (20-42) years. The mean age of the hyperhidrotic males was 35 (21-56) and of the normal males was 34.3 (22-61) years. The mean body weight of the hyperhidrotic females was 60.3 (50-73) and of the normal females was 56.4 (45-70) kg. The mean body weight of the hyperhidrotic males was 75.6 (62-87) and of the normal males was 76.2 (62-102) kg. The educational level of hyperhidrotics/normals was: 11/12 higher education, 3/4 students, and 6/4 secondary-lower.
Individuals with palmar hyperhidrosis were recruited by advertisements in the local mass media. They participated voluntarily in the research. Six persons who manifested excessive sweating all over the body, or predominantly in other areas of the body, like the forehead and the armpits, were not included in this study. The authors from people who reported never having suffered from excessive palmar sweating selected normal palmar sweating individuals. Attention was paid to the equivalence on gender, age, and educational level to the hyperhidrotic group.
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 was 3.1 mg (S.D. 2.3, range 0-7). We did not exclude any individual from the research. The participation of 2 individuals, one from the hyperhidrotic group with 4 mg palmar sweating and one from the normal group with 12 mg palmar sweating, confirmed that they did not have the electrodermal behavior they had declared. Their scores in the tests were excluded from the analysis. This way, the simple method of measuring the palmar sweating during writing was proved to be a good confirmation tool of the declared by the participants’ electrodermal behavior.
MATERIALS
We used the voltage coupler 9878 of the Beckman R 511A polygraph for chart recording of palmar skin conductance, during mental arithmetic tests. The recorded voltage was received from the ends of a resistor (1000 Ω) which was in series connection with the individual and an external stabilized voltage source (0.5 V). The J&J Modules, designed to support the B45 biofeedback program of Unicomp, were used for the recording of palmar and forearm skin conductance. German 3M, Ag-AgCl electrodes, 8 mm diameter were used; after each session their polarity was changed and they were replaced after two sessions, in order to prevent polarization. Electrolytic paste of Hewlett Packard was used as electrolytic medium.
A gravimetric method was used during bicycling task, because the profuse sweating, especially of hyperhidrotics, and the movement demands of the task, could cause artificial recordings. Sweat collecting plasters were attached on the palm and forearm during bicycling. The sweat collecting plaster consisted of a leucoplast (5Χ5) cm with a small sponge (2Χ2) cm attached to its center. A waterproof membrane on its outer surface was used to prevent any evaporation of the collected sweat. The sweat collecting plaster weighed about 580 mg and could absorb more than 500 mg of sweat almost immediately. The weight of plasters was measured by an electronic balance (Shimadzu) with 1 mg readability and 340 g weighing capacity.
DESIGN AND PROCEDURE
All participants washed their hands. Each individual was asked to read the instructions describing the procedure and to avoid speaking until completion of the tasks. Electrodes for skin conductance recording were attached on the two palms as well as on the forearm of the right hand, while the individual was laid on an examination table. The electrodes were not removed during the mental arithmetic tasks, in order to avoid artificial differences in skin conductance levels. The blood pressure and heart rate measurements, which were interposed, will not be presented in this work.
Three minutes after relaxing on the examination table, the participant was asked to perform the first out of the two mental arithmetic tasks, that is, to add continuously the number 7 for 72 s, without speaking or contracting any muscle. The participant reported the found sum at the end of the 72 s period. After this task and during the 3 min intertask break that followed, the participant was asked to sit for 2 min and then to stand for 1 min, in order to accustom to the standing position before performing the second mental arithmetic task. This second task was the same with the previous one in terms of mental effort, starting from another number. The two mental arithmetic tasks were designed to be the same, apart from the body posture and speaking, in order to check the role of muscle tension in palmar sweating caused by the same mental effort.
Some min later, the participant performed 3 bicycling tasks. During the first task, the participants bicycled for 4 min, in order to compare the palmar sweating of hyperhidrotic and normal individuals during physical exercise. Sweat collecting plasters were attached (after wiping the area) on the palm (hypothenar eminence) and forearm of the individual's left hand. The plasters were weighed immediately before and after each bicycling task. A clothing support around the neck prevented sweat secreted by other areas from reaching the plasters. The participant was asked to keep bicycling at a constant rate of 10-15 miles per hour, using a tachometer. Before the second bicycling task, which was identical to the first one in terms of physical exercise, the shoes and the socks of the participant were taken off by the experimenter, in order to investigate the influence of distress in the EDA caused by physical effort. The unwarned removal of the shoes and socks caused psychological distress, especially in hyperhidrotics (they all mentioned that, after a relevant question at the end of the tasks), because of the revelation of their wet soles, soaked socks with probably unpleasant odor, and of the difficulty in bicycling with naked their wet soles. Before the third bicycling task, socks and shoes were replaced and absorbing gloves were put on both palms, in order the distress of profuse sweating to be eliminated.
STATISTICS
We compared the number of electrodermal responses (EDRs) and the skin conductance level (SCL) in mental arithmetic, and weight of sweat in bicycling, using three factor ANOVA, with sex and hyperhidrosis as between-subject factors and repeated measures as within subject factor.
RESULTS
Mental arithmetic tasks: The hyperhidrotics presented a significantly higher number of palmar EDRs as compared to normal individuals during the performance of the mental arithmetic tasks F=9.62, DF=1, P<.004. No statistically significant differences were found between males and females. A significantly higher number of palmar EDRs was found during the performance of mental arithmetic in standing position as compared to recumbent position, for hyperhidrotics F=36.40, DF=1, P<.000, and for normal individuals F=21,28, DF=1, P<.000. The number of EDRs was about 70% higher in the standing position than in the recumbent one, in both hyperhidrotic and normal individuals, indicating that muscular tension causes a marked augmentation in the number of EDRs. Seven hyperhidrotics presented a smaller number of EDRs than the average of that of normal individuals, during the performance of mental arithmetic task in the recumbent position, but no one in the standing position. Forearm did not present any EDR during the performance of the mental arithmetic tasks.
Mean SCL was calculated by the computer every 4 s, while the SCL over the experimental period was taken as the average of 18 periods. Τhe hyperhidrotics presented significantly higher palmar SCL as compared to control individuals during the performance of the mental arithmetic F=32,42, DF=1, P<.000. No statistically significant differences were found between males and females. Significantly higher palmar SCL was observed during the execution of mental arithmetic in standing position in relation to that in recumbent position, for hyperhidrotics F=22.56, DF=1, P<.000, and for normal individuals F=20.26, DF=1, P<.000. The interaction of hyperhidrosis X execution position was also significant F=6.31, DF=1, P<.02. The augmentation of SCL of palms in the standing position in relation to SCL in the recumbent position was about 30% for hyperhidrotic and 43% for normal individuals. The higher augmentation of palmar SCL of normal individuals (in spite of the same augmentation of EDRs) in relation to that of hyperhidrotics was due to the smaller prior wetting of their palmar stratum corneum. Only one hyperhidrotic presented a smaller palmar SCL than the average of normal individuals SCL, during the performance of mental arithmetic task in the recumbent position but no one in the standing position.
Significantly higher forearm SCL was found in hyperhidrotic as compared to normal palmar sweating individuals during the performance of the mental arithmetic tasks F=8.78, DF=1, P<.005. This finding was probably the result of higher thermoregulatory sweating in the whole body of hyperhidrotics, because when the heat load in the bicycling tasks induced profuse thermoregulatory sweating in both groups, sweat product of forearm of hyperhidrotic and normal individuals was the same, while sweat product of palms was very different. There was no significant difference between forearm SCL during the execution of mental arithmetic in standing position in relation to that in recumbent position, in either group. The correlation between palmar and forearm SCL was significant (P<.05) only for normal individuals (r1=.468 and r2=.487) and insignificant for hyperhydrotic individuals (r1=.386 and r2=.09) in both tasks, respectively.
Bicycling: The weight of palmar sweat secreted during the performance of all 3 bicycling tasks was significantly higher in hyperhidrotic as compared to normal individuals F=14.41, DF=1, P<.001 (Fig. 1). Gender differences on palmar sweat were not significant, but the interaction of hyperhidrosis X sex was significant F=4.98, DF=1, P<.032. No significant difference was found in forearm weight of sweat between hyperhidrotic and normal individuals (Fig. 2). The weight of forearm sweat of males was higher than that of females during the bicycling tasks F=7.08, DF=1, P<.01. Palmar sweating of hyperhidrotics was significantly higher than forearm sweating during all 3 bicycling tasks. Palmar sweating of normal individuals was significantly higher than forearm sweating only during the first bicycling task.
Palmar sweating of hyperhidrotics was augmented from the first to the second bicycling task and was significantly reduced from the second to the third F=16.49, DF=1, P<.001 (Fig. 1). Palmar sweating of normal individuals was augmented significantly during the second bicycling task F=10.32, DF=1, P<.005 and remained at the same level during the third. Forearm sweating was augmented significantly from one to the next bicycling task for both hyperhidrotic (F=38.54, DF=1, P<.000, F=11.90, DF=1, P<.003), and normal individuals (F=44.54, DF=1, P<.000, F=13.93, DF=1, P<.002).
As expected from a thermoregulatory aspect, forearm sweating was augmented within the total bicycling time in both hyperhidrotic and normal individuals. In contrast, palmar sweating of hyperhidrotics displayed a maximum during the second bicycling task when physical exercise was combined with distress, and a significant diminution during the third bicycling task after reducing the distress (Figure 1). It is also noteworthy that all hyperhidrotics displayed higher values of weight of palmar sweat than the average of that of normal individuals, during only the second bicycling task.
Females displayed more palmar sweating than males during all 3 bicycling tasks (with the difference being significant in the second task) and less forearm sweating during all 3 bicycling tasks (with significant differences in the second and third task). Correlation analysis indicated a lack of general pattern of correlation between palmar and forearm sweating in either hyperhidrotic and normal or male and female individuals
CONCLUSIONS
From the forearm electrodermal recordings and sweating we have to stress that: (i) the forearm did not present measurable EDRs during mental arithmetic tasks, (ii) the sweating of forearm, for both normal and hyperhidrotic individuals, was augmented from the first to the third bicycling task, following the heat load, which indicate a thermoregulatory pattern of activation (iii) the sweating of forearm was not correlated to palmar sweating of hyperhidrotics in any task. These findings clearly demonstrate that palmar and forearm sweating is under of different central nervous control and do not support the theory of over-functioning sympathetic fibers, passing through the T2,3 ganglia (which, according to Shih, Wu and Lin [19] "play an important role in the elaboration or modulation of autonomic function elsewhere"), as the cause of palmar hyperhidrosis. It is worth mentioned that these authors have reported the following results which are in disagreement with their own theory: T2,3 ganglionectomized individuals displayed much less sweating, during physical exercise, in their forehead, upper chest, and upper extremities than normal individuals (indicating that fibers passing through T2,3 ganglia innervate all these areas), while hyperhidrotics displayed palmar but not forehead and chest hyperhidrosis. Obviously, the sweat glands of all these areas, especially for hyperhidrotics, are not activated by the sympathetic nervous system as a unit. Findings on the pathophysiology of palmar hyperhidrosis (and especially heart rate and blood pressure recordings, and heart rate variability analysis, as a quantitative assessment of autonomic balance) do not also give support to the over-functioning sympathetic fibers theory of palmar hyperhidrosis (unpublished data).
Based on the palmar EDA recordings, both hyperhidrotic and normal groups presented significantly higher palmar sweating during the mental arithmetic in the standing than in the recumbent position. This increase cannot be considered as thermoregulatory, since forearm sweating was not respectively augmented. This finding indicates that the muscular tension increases palmar sweating (both normal and hyperhidrotic) caused by mental process. It was also found that seven hyperhidrotics presented a smaller number of EDRs than the average number of normal individuals, during the performance of mental arithmetic task in the recumbent position, but no one in the standing position. This finding questions the ability of mental effort to cause palmar hyperhidrosis by itself, showing that the tension of the muscles may be a determinative factor for the magnitude of palmar sweating.
In the other side, the significant decrease of palmar sweating of hyperhidrotics in the third bicycling task (when the distress was reduced) questions the ability of physical effort, and therefore of muscle tension, to cause palmar hyperhidrosis by itself. Among the three bicycling tasks, all hyperhidrotics expressed excessive sweating (over the average of normal individuals) only during the second one, when the physical effort was combined with distress.
These findings suggest that neither mental nor physical effort may alone provoke hyperhidrosis. Considering the distress as the active ingredient of mental effort in provoking hyperhidrosis (a pleasant or calm thought has never been mentioned as sudorific) and the muscle tension as the active ingredient of physical effort, we consider that the combination of distress with muscle tension is the necessary and efficient factor for palmar hyperhidrosis expression. This conclusion is additionally supported by the following elements: (i) the relaxation is the active ingredient in the biofeedback treatment of palmar hyperhidrosis [20] (ii) the relation between palmar sweating and muscular tension is justified from a developmental point of view, because friction improvement [21] and abrasion prevention [22], which are the mechanical purposes of plantar sweating in mammals, are necessary only to the moving animal (iii) the hyperhidrotics may not sweat at all on their palms when they perform calm a hard handiwork or mental activity. Even in the case of a mentally acting hyperhidrotic individual, when facing difficulties of no handiwork demand, its excessive palmar sweating may also be considered as the result of the combination of mental effort or distress with muscle tension, since hidden muscular activity may accompany the mental processes [23].
In this point, we have to remind that the hyperhidrotics scored significantly higher than normal individuals on the Neuroticism scale of the Eysenck Personality Questionnaire (unpublished data) and in the scales of Depression, Social Introversion, and Psychasthenia of the Minnesota Multiphase Personality Inventory (MMPI) [2]. In agreement with the suggestion of Lerer, Jacobowitz and Wahba [3] and of Lerer and Jacobowitz [4] that hyperhidrotic individuals are characterized by lower overall ability to cope with stress and a strong proclivity to avoid problems, they may be more prone to distress feelings in their everyday life activities.
Conclusively, this work, in agreement with findings of former ones, suggests that (i) palmar hyperhidrosis is not caused by over-functioning of sympathetic fibers passing through T2,3 ganglia, and (ii) the combination of distress with muscle tension is the necessary and effective condition for palmar hyperhidrosis expression. Hyperhidrotics may be individuals who feel more easily distress, and perhaps produce higher tension of muscles (caused by the distress), than normal palmar sweating individuals.
REFERENCES
1. Kerassidis S: Is palmar and plantar sweating thermoregulatory? Acta Physiol Scand 1994;52:259-263.
2. Κερασίδης Σ, Μπιτζαράκη Κ: Στοιχεία της προσωπικότητας των υπεριδρωτικών στις παλάμες [Personality traits of hyperhidrotics in palms]. Ψυχιατρική 1997;8:181-187
3. Lerer Β, Jacobowitz J, Wahba A: Personality features in essential hyperhidrosis. Int J Psychiatry Med 1980;10(1):59-67.
4. Lerer Β, Jacobowitz J: Τreatment of essential hyperhidrosis by psychotherapy. Psychosomatics 1981;22(6):536-538.
5. Sato K, Kang W, Saga K, Sato KT: Biology of sweat glands and their disorders: 2. Disorders of sweat gland function. J Am Acad Dermatol 1989;20:713-726.
6. Lerer Β: Hyperhidrosis: A review of its psychological aspects. Psychosomatics 1977;18:28-31.
7. Fotopoulos SS, Sunderland WP: Biofeedback in the treatment of psychophysiologic disorders. Biofeedback Self Regul 1978;3(4):331-361.
8. Lacey JI: Somatic response patterning and stress: Some revisions of activation theory; in Appley MH & Trumbull R (eds): Psychological Stress (Issues in research) New York: ACC., 1967, pp 15-42
9. Miller NE: Learning of visceral and glandular responses. Science 1969a;163:434-445.
10. Miller NE: Psychosomatic effects of specific types of training. Ann N Y Acad Science 1969b;159:1025-1040.
11. Wallin BG: Intraneural recordings of normal and abnormal sympathetic activity in man; in Bannister R & Mathiaw CJ (eds): Autonomic Failure. A textbook of clinical disorders of the autonomic nervous system. Oxford: Oxford Medical Publications, 1992, pp 359-377.
12. Wallin G, Elam M: Insights from intraneural recordings of sympathetic nerve traffic in humans. NIPS 1994; 9:203-207.
13. Hoehn-Saric R, McLeod DR: The peripheral sympathetic nervous system. Its role in normal and pathological anxiety. Psychiatr Clin North Am 1988;11(2):375-386.
14. Ost L, Sterner U, Lindahl I: Physiological responses in blood phobics. Behav Res Ther 1984;22(2):109-117.
15. Dawson ME, Schell AM, Braaten J, Catania JJ: Diagnostic utility of autonomic measures for major depressive disorders. Psychiatry Res 1985;15:261-270.
16. Edelberg R: Mechanisms of electrodermal adaptations for locomotion, manipulation, or defense; in Stellar E & Sprague JM (eds): Progress in physiological psychology. New York: Academic Press, 1973, pp 155-209.
17. Venables PH, Christie MJ: Mechanisms, Instructions, Recording Techniques, and Quantification of Responses; in Prokasy WF & Raskin DC (eds): Electrodermal activity in psychological research New York: Academic Press, 1973, pp 1-124.
18. Fowles DC: The eccrine system and electrodermal activity. In M. G. H. Coles, Donchin E & Porges SW (eds.): Psychophysiology: Systems, Processes, and Applications. Oxford: The Guilford Press, 1986, pp 51-96.
19. Shih CJ, Wu JJ, Lin MT: Autonomic dysfunction in palmar hyperhidrosis. J Auton Nerv Syst 1983;8:33-43.
20. Duller P, Doyle Gentry W: Use of biofeedback in treating chronic hyperhidrosis: a preliminary report. Br J Dermatol 1980;103:143-146.
21. Adelman S, Taylor C, Meglung N: Sweating on paws and palms: what is its function? Am J Physiol 1975;229:1400-1402.
22. Wilcott RC: Adaptive value of arousal sweating and the epidermal mechanism related to skin potential and skin resistance. Psychophysiology 1966:2(3):249-262.
23. Cacciopo JT, Petty RE: Electromyograms as measures of extent affectivity of information processing. Am Psychol 1981;36:441-456.
Is the hyperhidrotic palmar sweating unrelated to the action demands on palmar wetting?
ABSTRACT
In this work, the influence of the benefit of palmar wetting in the intensity of palmar sweating was examined. The electrodermal activity (EDA) of hyperhidrotic and normal subjects was compared, in leafing (turning sheets by rubbing the finger, so palmar wetting was desirable) and fingerprinting (making ink prints of fingers on a paper sheet, so palmar wetting was unwanted) tasks. Hyperhidrotic, in the same degree as normal subjects, presented a higher EDA during leafing than fingerprinting, although both tasks designed to involve the same movement and emotional load. We concluded that the ability of a beneficial manifestation of palmar sweating is retained in the case of palmar hyperhidrosis. This finding, in addition to the further investigation on palmar hyperhidrosis, contributes also to the clarification of what the maladaptive nature of a neurotic function means.
DESCRIPTOR TERMS
Hyperhidrosis, palmar sweating, electrodermal, maladaptive, neurotic.
Is the hyperhidrotic palmar sweating unrelated to the action demands on
palmar wetting?
Stelios Kerassidis
INTRODUCTION
Trying to find out what is behind palmar hyperhidrosis we already know that: (i) it is not controlled by a thermoregulatory mechanism (Kerassidis 1994), (ii) extended clinical and laboratory tests, did not reveal any type of organic disease (Kerassidis et al. 1997), nor a higher density of sweat glands on palm of hyperhidrotics (kerassidis & Haristou 1997), (iii) hyperhidrotic presented higher score in Neuroticism scale of Eysenck's Personality Questionnaire (Kerassidis et al.) and in Psychasthenia, Social Introversion, and Depression of Minnesota Multiphasic Personality Inventory (kerassidis & Bitzaraki, 1996), (iv) in agreement with the suggestion of Lerer et al. (1980) and of Lerer and Jacobowitz (1981) that hyperhidrotic individuals are characterised by lower overall ability to cope with stress and a strong proclivity to avoid problems, we found that excessive palmar sweating is provoked by feelings of discomfort (no relaxed subjects) and we concluded that personality traits may make hyperhidrotics more prone to identify stressors as discomfort-producing (Kerassidis et al.).
The above findings leads to the conclusion that palmar hyperhidrosis may be a neurotic manifestation of normal palmar sweating, a disorder of the type of psychosomatic ones. Since neurotic manifestation of a function is predominately considered maladaptive (Eysenck 1979), we wondered how wrongly excessive palmar sweating is expressed. Many times a day, the electrodermal activity (EDA) of an individual, (not only of a hyperhidrotic one), seems to be pointless, since there is no benefit of palmar wetting (friction improvement Adelman et al. 1975, or abrasion prevention Wilcott 1966) in action. During examinations, social relationships, writing, etc., the manifestation of palmar sweating offers no adaptation to the action demands, it rather troubles them, and could be considered maladaptive. Fowles' (1986) questioned whether this function is simply a complex and noisy manifestation of non-specific activity.
To answer this question, we designed a series of special experiments and we found that palmar sweating of non-hyperhidrotic individuals, was significantly higher in leafing (turning sheets by rubbing the finger, so palmar wetting was desirable) than weighing a hydrophilic substance (palmar wetting was unwanted), although both tasks designed to involve the same demand of movement and emotional load (unpublished). This finding indicated that the usefulness of palmar wetting influence the intensity of palmar sweating, so in normal individuals, an appreciatory of the benefit of palmar sweating mechanism was seen to exists.
In the present work we try to give an answer to the question of how the palmar sweating is influenced by the usefulness of palmar wetting in the case of palmar hyperhidrosis, hoping that it could be useful to the discussion about the maladaptive nature of the condition.
We have to note that the old view of general arousal or general sympathetic arousal must not be considered as an answer to the question of the way the palmar hyperhidrosis is expressed. Namely, that it simply follows mass sympathetic discharge, at fight and flight reactions (Cannon's theory). Former and recent studies from different fields of research, have challenged the view of a diffusely acting sympathetic system (Lacey 1967, Miller 1969a, Miller 1969b, Wallin 1992, Wallin and Elam 1994). Besides, it is well known that autonomic manifestations differ considerably among psychological disorders (Saric and McLeod 1988, Ost et al. 1984, Dawson 1985), stimulus presentation, or condition of performance (Edelberg, Venables, Fowles), that means that no theory of general or sympathetic arousal can overcome the question why the specific function is triggered under specific conditions. Finally, we recorded a slight or not a bit palmar sweat glands activation during human orgasm (when a mass sympathetic activation was taking place), and we concluded that palmar sweating cannot be considered as a simple following of sympathetic discharge (Kerassidis 1997).
METHODS
PARTICIPANTS
Twenty: 10 hyperhidrotic in palms, mean age 33 years old (range 18-56) and 10 normal palmar sweating individuals, mean age 30 years old (range 20-62), participated in this experiment. Males were 5 and females also 5, in each group. These subjects had participated to our previous work on pathophysiology of palmar hyperhidrosis (kerassidis et al...). From the beginning of that work, 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 and from that of normal individuals 3.1 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 research. The 20 subjects of the present work (out of the 42 subjects of the previous) were undoubtedly well defined as hyperhidrotic or normal not only because of the writing test, but because the tasks of the previous work approved that as well.
MATERIALS
J&J Modules of Unicomp were used for the recording of conductivity of right palm. Electrodes of Ag-AgCl, 8 mm in diameter and electrolytic paste of Hewelett Packard were used. Frequent change of polarity and replacement of electrodes were used in order to prevent polarisation of the electrodes. An ink-pad and sheets of paper were used for fingerprinting.
PROCEDURE
Subjects read instructions for leafing. They were reminded that leafing would be facilitated if their forefinger could sweat. They made a leafing rehearsal in order to familiarise with the procedure. So their electrodermal responses (EDRs) during leafing would not be part of startling or novelty reaction. They had to turn the pages of a day book only by the forefinger and to keep motionless the fingers with electrodes (thumb and middle finger), for 100 s. No conversation was permitted.
After leafing, electrodes were not removed, in order to prevent artificial changes to the level of conductivity (LC). Subjects read the instructions to make continuously fingerprints of the fingers of both palms. They were reminded that they had to avoid palmar sweating for good quality fingerprints. They performed this task for 100 seconds too.
The order of execution of the tasks in this procedure was opposite of that of our previous experiment where only normal subjects participated. Now, the leafing (palmar wetting was desirable) was performed first and fingerprinting (palmar wetting is unwanted) followed. In the previous experiment the weighing of the hydrophilic substance was performed first (palmar wetting was unwanted) and leafing followed. We reversed the order of the execution of the tasks in order to check how the result of the previous experiment could be caused by some kind of sensitisation. We changed the weighing of the hydrophilic substance with the fingerprinting in order to make more similar the tasks, since in both leafing and fingerprinting the fingers touch paper (if a somatosensory feedback would be important).
Data analysis
We compared the number of electodermal responses (EDRs) and the mean skin conductance level (SCL), during every task. As EDR we accepted any increase in palmar conductivity over 0.03 μS, the mean SCL was calculated by the computer as the mean value of 20 mean values of SCL for 5 s each one. Analysis of variance (ANOVA)-Repeated Measures design was used. Namely, three factor ANOVA/MANOVA (multivariate ANOVA) with sex and hyperhidrosis as between-subject factors and repeated measures as within subject factor (2X2X2) were performed.
RESULTS
At first, we have to mention that the artefacts were kept at minimum despite the use of the palm, the recording of which was made, especially for 3 reasons: (i) during leafing the participants used only the forefinger but the recording electrodes attached to the thumb and the middle finger, (ii) during fingerprinting, when the participants made fingerprints of the recorded fingers they instructed to pouch carefully, and (iii) the .03 μS criterion for an EDR is slightly high (Levinson and Edelberg, 1985) so small alterations in skin conductance due to palm movement did not count as an EDR.
The results of the analysis are given on tables 1,2. As we can see, hyperhidrotics and females presented significantly higher SCL, during tasks, than normal and male individuals respectively. Group differences were due to the higher wetting of palmar stratum corneum of hyperhidrotics and sex differences to the thinner epidermis resulting to higher conductivity of woman palmar skin. No significant difference was revealed for EDRs either between hyperhidrotic and normal or between male and female individuals, during both tasks.
Within subjects differences caused by the two tasks was very significant. In both groups the number of EDRs during fingerprinting was decreased about in the half of those during leafing. The decrease of mean SCL from leafing to fingerprinting was about 30% for both groups.
DISCUSSION
We found that both hyperhidrotic in palms and normal palmar sweating subjects expressed significantly higher EDA during leafing (palmar wetting is desirable) than fingerprinting (palmar wetting is unwanted). Knowing that the differences in SCL may due to the prior of the tasks wetting of palmar stratum corneum, we can say that the electrodermal behaviour of hyperhidrotic and normal individuals was surpassingly comparable.
The finding for normal subjects replicated the finding of our previous similar experiment and confirmed the hypothesis that the magnitude of palmar sweating is influenced from the usefulness of palmar wetting in action. The fact that although the order between desirable and unwanted wetting of palms tasks was different than that of the previous experiment, the difference in palmar sweating between task was almost the same, indicate that this difference cannot be attributed to the order of the performance of the tasks. In addition, the fact that in both tasks of the present work, the fingers attached sheets of paper, indicate that the difference of the EDA between tasks cannot be attributed to an automatically activated, via a somatosensory feedback pathway, mechanism. That means that probably a cognitive appreciatory mechanism is responsible for the difference of EDA between tasks. It must be noted that for the present work is uninterested whether it was the belief of an individual (amplified by our instructions) or a conditioned response formed by its prior experience, about the functional significance of the wetting of palm, that caused the higher EDA. That was important to be determined was the potentiality of a purposeful modification of palmar sweating, beyond emotional load or sympathetic arousal.
For the hyperhidrotics, it was expected that the influence of the palmar wetting usefulness to the magnitude of palmar sweating would be lesser than normal subjects or it would not exist at all. However, the fact that palmar sweating of hyperhidrotics is differentiated between tasks analogously to the differentiation of palmar sweating of normal individuals, indicates that no disruption of the appreciatory of usefulness mechanism takes place in the case of palmar hyperhidrosis. May that means that palmar hyperhidrosis is not a neurotic phenomenon, or that the muladaptiveness of the neurotic expression does not simply implies that the function is not related with the needs of action? We believe that the findings of the works mentioned in the introduction, in combination with the finding of this work, suggest the second view as correct.
But then, how can we explain the excessive palmar sweating of hyperhidrotics, during examinations, social relationships, writing, etc. when no benefit of palmar wetting in action exists? Even in the case of normal group, we faced this phenomenon in the second task when the palmar sweating of both groups was not zero, despite that it was absolutely undesirable. Obviously, the impact of the appreciatory mechanism is limited and it is superimposed to the impact of another, probably triggering more automatically the palmar sweating. The question is: does this triggering the palmar sweating mechanism activate the palmar sweat glands blindly, in the context of a general or sympathetic arousal, or a benefit beyond the palmar wetting is accomplished for the organism? Many findings of EDA research suggest that palmar sweating may be useful for other reasons to the organism beyond mechanical facilitation of the action, but since it cannot be supported by the findings of the present work, it must be the issue of another one.
What we can clearly concluded from the findings of this work is that palmar sweating is not unrelated to the action demands on palmar wetting, even in the case of palmar hyperhidrosis, and this obviously means that palmar sweating may not be considered a noisy manifestation of a non-specific activity (Fowles, 1986),.
REFERENCES
Adelman, S., Taylor, C. R. and Meglung, N. C. (1975) Sweating on paws and palms: what is its function? Am. J. Psychol., 229(5): 1400-1402.
Dawson, M. E.et al (1985) Diagnostic utility of autonomic measures for major depressive disorders. Psychiatry Res., 15: 261-270.
Eysenck, H. J. (1979) The conditioning model of neurosis. Behav. Brain Sci., 2: 155-199.
Fowles, D. C. 1986. The eccrine system and electrodermal activity. In: M. G. H. Coles, E. Donchin, S. W. Porges (Eds), Psychophysiology : Systems, Processes, and Applications., Elsevier, Amsterdam, pp. 51-96.
Hoehn-Saric, R. and McLeod, D. R. (1988) The peripheral sympathetic nervous system. Its role in normal and pathological anxiety. Psychiatr. Clin. North Am., 11(2): 375-386.
Johnson, L. C. and Lubin, A. (1966) Spontaneous electrodermal activity during waking and sleeping. Psychophysiology., 3(1): 8-17.
Kerassidis, S. (1994) Is palmar and plantar sweating thermoregulatory? Acta Physiol. Scand., 152: 259-263.
Kushniruk, A., Rustenburg, J. and Ogilvie, R. (1985) Psychological correlates of electrodermal activity during REM sleep. Sleep., 8(2): 146-154.
Lacey, J. I. (1967) Somatic response patterning and stress: Some revisions of activation theory.In: M.H. Appley and R. Trumbull (Eds), Psychological Stress (Issues in research), Chapter 2, ACC, New York, pp. 15-42.
Lester, B. K., Burch, N. R. and Dossett, R. C. (1967) Nocturnal EEG-GSR profiles : the influence of presleep states. Psychophysiology, 3: 238-248.
Miller, N. E. (1969) Psychosomatic effects of specific types of training. Ann. N. Y. Acad. Sci., 159: 1025-1040.
Miller, N. E. (1969) Learning of visceral and glandular responses. Science. 163: 434-445.
Ost, L., Sterner, U., Lindahl, I. (1984) Physiological responses in blood phobics. Behav Res Ther. 22(2): 109-117.
Venables, P. H. (1991) Autonomic activity. Ann. N. Y. Acad. Sci., 620: 191-207.
Wallin, B. G.(1992) Intraneural recordings of normal and abnormal sympathetic activity in man. In: R. Bannister, C. J. Mathiaw (Eds), Autonomic Failure. A textbook of clinical disorders of the autonomic nervous system, Oxford Medical Publications, Oxford, pp. 359-377.
Wallin, B. G. and Elam, M. (1994) Insights from intraneural recordings of sympathetic nerve traffic in humans. Am. Physiol .Soc., 9: 203-207.
Wilcott, R. C. (1966) Adaptive value of arousal sweating and the epidermal mechanism related to skin potential and skin resistance. Psychophysiology, 2(3): 249-262.
In this work, the influence of the benefit of palmar wetting in the intensity of palmar sweating was examined. The electrodermal activity (EDA) of hyperhidrotic and normal subjects was compared, in leafing (turning sheets by rubbing the finger, so palmar wetting was desirable) and fingerprinting (making ink prints of fingers on a paper sheet, so palmar wetting was unwanted) tasks. Hyperhidrotic, in the same degree as normal subjects, presented a higher EDA during leafing than fingerprinting, although both tasks designed to involve the same movement and emotional load. We concluded that the ability of a beneficial manifestation of palmar sweating is retained in the case of palmar hyperhidrosis. This finding, in addition to the further investigation on palmar hyperhidrosis, contributes also to the clarification of what the maladaptive nature of a neurotic function means.
DESCRIPTOR TERMS
Hyperhidrosis, palmar sweating, electrodermal, maladaptive, neurotic.
Is the hyperhidrotic palmar sweating unrelated to the action demands on
palmar wetting?
Stelios Kerassidis
INTRODUCTION
Trying to find out what is behind palmar hyperhidrosis we already know that: (i) it is not controlled by a thermoregulatory mechanism (Kerassidis 1994), (ii) extended clinical and laboratory tests, did not reveal any type of organic disease (Kerassidis et al. 1997), nor a higher density of sweat glands on palm of hyperhidrotics (kerassidis & Haristou 1997), (iii) hyperhidrotic presented higher score in Neuroticism scale of Eysenck's Personality Questionnaire (Kerassidis et al.) and in Psychasthenia, Social Introversion, and Depression of Minnesota Multiphasic Personality Inventory (kerassidis & Bitzaraki, 1996), (iv) in agreement with the suggestion of Lerer et al. (1980) and of Lerer and Jacobowitz (1981) that hyperhidrotic individuals are characterised by lower overall ability to cope with stress and a strong proclivity to avoid problems, we found that excessive palmar sweating is provoked by feelings of discomfort (no relaxed subjects) and we concluded that personality traits may make hyperhidrotics more prone to identify stressors as discomfort-producing (Kerassidis et al.).
The above findings leads to the conclusion that palmar hyperhidrosis may be a neurotic manifestation of normal palmar sweating, a disorder of the type of psychosomatic ones. Since neurotic manifestation of a function is predominately considered maladaptive (Eysenck 1979), we wondered how wrongly excessive palmar sweating is expressed. Many times a day, the electrodermal activity (EDA) of an individual, (not only of a hyperhidrotic one), seems to be pointless, since there is no benefit of palmar wetting (friction improvement Adelman et al. 1975, or abrasion prevention Wilcott 1966) in action. During examinations, social relationships, writing, etc., the manifestation of palmar sweating offers no adaptation to the action demands, it rather troubles them, and could be considered maladaptive. Fowles' (1986) questioned whether this function is simply a complex and noisy manifestation of non-specific activity.
To answer this question, we designed a series of special experiments and we found that palmar sweating of non-hyperhidrotic individuals, was significantly higher in leafing (turning sheets by rubbing the finger, so palmar wetting was desirable) than weighing a hydrophilic substance (palmar wetting was unwanted), although both tasks designed to involve the same demand of movement and emotional load (unpublished). This finding indicated that the usefulness of palmar wetting influence the intensity of palmar sweating, so in normal individuals, an appreciatory of the benefit of palmar sweating mechanism was seen to exists.
In the present work we try to give an answer to the question of how the palmar sweating is influenced by the usefulness of palmar wetting in the case of palmar hyperhidrosis, hoping that it could be useful to the discussion about the maladaptive nature of the condition.
We have to note that the old view of general arousal or general sympathetic arousal must not be considered as an answer to the question of the way the palmar hyperhidrosis is expressed. Namely, that it simply follows mass sympathetic discharge, at fight and flight reactions (Cannon's theory). Former and recent studies from different fields of research, have challenged the view of a diffusely acting sympathetic system (Lacey 1967, Miller 1969a, Miller 1969b, Wallin 1992, Wallin and Elam 1994). Besides, it is well known that autonomic manifestations differ considerably among psychological disorders (Saric and McLeod 1988, Ost et al. 1984, Dawson 1985), stimulus presentation, or condition of performance (Edelberg, Venables, Fowles), that means that no theory of general or sympathetic arousal can overcome the question why the specific function is triggered under specific conditions. Finally, we recorded a slight or not a bit palmar sweat glands activation during human orgasm (when a mass sympathetic activation was taking place), and we concluded that palmar sweating cannot be considered as a simple following of sympathetic discharge (Kerassidis 1997).
METHODS
PARTICIPANTS
Twenty: 10 hyperhidrotic in palms, mean age 33 years old (range 18-56) and 10 normal palmar sweating individuals, mean age 30 years old (range 20-62), participated in this experiment. Males were 5 and females also 5, in each group. These subjects had participated to our previous work on pathophysiology of palmar hyperhidrosis (kerassidis et al...). From the beginning of that work, 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 and from that of normal individuals 3.1 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 research. The 20 subjects of the present work (out of the 42 subjects of the previous) were undoubtedly well defined as hyperhidrotic or normal not only because of the writing test, but because the tasks of the previous work approved that as well.
MATERIALS
J&J Modules of Unicomp were used for the recording of conductivity of right palm. Electrodes of Ag-AgCl, 8 mm in diameter and electrolytic paste of Hewelett Packard were used. Frequent change of polarity and replacement of electrodes were used in order to prevent polarisation of the electrodes. An ink-pad and sheets of paper were used for fingerprinting.
PROCEDURE
Subjects read instructions for leafing. They were reminded that leafing would be facilitated if their forefinger could sweat. They made a leafing rehearsal in order to familiarise with the procedure. So their electrodermal responses (EDRs) during leafing would not be part of startling or novelty reaction. They had to turn the pages of a day book only by the forefinger and to keep motionless the fingers with electrodes (thumb and middle finger), for 100 s. No conversation was permitted.
After leafing, electrodes were not removed, in order to prevent artificial changes to the level of conductivity (LC). Subjects read the instructions to make continuously fingerprints of the fingers of both palms. They were reminded that they had to avoid palmar sweating for good quality fingerprints. They performed this task for 100 seconds too.
The order of execution of the tasks in this procedure was opposite of that of our previous experiment where only normal subjects participated. Now, the leafing (palmar wetting was desirable) was performed first and fingerprinting (palmar wetting is unwanted) followed. In the previous experiment the weighing of the hydrophilic substance was performed first (palmar wetting was unwanted) and leafing followed. We reversed the order of the execution of the tasks in order to check how the result of the previous experiment could be caused by some kind of sensitisation. We changed the weighing of the hydrophilic substance with the fingerprinting in order to make more similar the tasks, since in both leafing and fingerprinting the fingers touch paper (if a somatosensory feedback would be important).
Data analysis
We compared the number of electodermal responses (EDRs) and the mean skin conductance level (SCL), during every task. As EDR we accepted any increase in palmar conductivity over 0.03 μS, the mean SCL was calculated by the computer as the mean value of 20 mean values of SCL for 5 s each one. Analysis of variance (ANOVA)-Repeated Measures design was used. Namely, three factor ANOVA/MANOVA (multivariate ANOVA) with sex and hyperhidrosis as between-subject factors and repeated measures as within subject factor (2X2X2) were performed.
RESULTS
At first, we have to mention that the artefacts were kept at minimum despite the use of the palm, the recording of which was made, especially for 3 reasons: (i) during leafing the participants used only the forefinger but the recording electrodes attached to the thumb and the middle finger, (ii) during fingerprinting, when the participants made fingerprints of the recorded fingers they instructed to pouch carefully, and (iii) the .03 μS criterion for an EDR is slightly high (Levinson and Edelberg, 1985) so small alterations in skin conductance due to palm movement did not count as an EDR.
The results of the analysis are given on tables 1,2. As we can see, hyperhidrotics and females presented significantly higher SCL, during tasks, than normal and male individuals respectively. Group differences were due to the higher wetting of palmar stratum corneum of hyperhidrotics and sex differences to the thinner epidermis resulting to higher conductivity of woman palmar skin. No significant difference was revealed for EDRs either between hyperhidrotic and normal or between male and female individuals, during both tasks.
Within subjects differences caused by the two tasks was very significant. In both groups the number of EDRs during fingerprinting was decreased about in the half of those during leafing. The decrease of mean SCL from leafing to fingerprinting was about 30% for both groups.
DISCUSSION
We found that both hyperhidrotic in palms and normal palmar sweating subjects expressed significantly higher EDA during leafing (palmar wetting is desirable) than fingerprinting (palmar wetting is unwanted). Knowing that the differences in SCL may due to the prior of the tasks wetting of palmar stratum corneum, we can say that the electrodermal behaviour of hyperhidrotic and normal individuals was surpassingly comparable.
The finding for normal subjects replicated the finding of our previous similar experiment and confirmed the hypothesis that the magnitude of palmar sweating is influenced from the usefulness of palmar wetting in action. The fact that although the order between desirable and unwanted wetting of palms tasks was different than that of the previous experiment, the difference in palmar sweating between task was almost the same, indicate that this difference cannot be attributed to the order of the performance of the tasks. In addition, the fact that in both tasks of the present work, the fingers attached sheets of paper, indicate that the difference of the EDA between tasks cannot be attributed to an automatically activated, via a somatosensory feedback pathway, mechanism. That means that probably a cognitive appreciatory mechanism is responsible for the difference of EDA between tasks. It must be noted that for the present work is uninterested whether it was the belief of an individual (amplified by our instructions) or a conditioned response formed by its prior experience, about the functional significance of the wetting of palm, that caused the higher EDA. That was important to be determined was the potentiality of a purposeful modification of palmar sweating, beyond emotional load or sympathetic arousal.
For the hyperhidrotics, it was expected that the influence of the palmar wetting usefulness to the magnitude of palmar sweating would be lesser than normal subjects or it would not exist at all. However, the fact that palmar sweating of hyperhidrotics is differentiated between tasks analogously to the differentiation of palmar sweating of normal individuals, indicates that no disruption of the appreciatory of usefulness mechanism takes place in the case of palmar hyperhidrosis. May that means that palmar hyperhidrosis is not a neurotic phenomenon, or that the muladaptiveness of the neurotic expression does not simply implies that the function is not related with the needs of action? We believe that the findings of the works mentioned in the introduction, in combination with the finding of this work, suggest the second view as correct.
But then, how can we explain the excessive palmar sweating of hyperhidrotics, during examinations, social relationships, writing, etc. when no benefit of palmar wetting in action exists? Even in the case of normal group, we faced this phenomenon in the second task when the palmar sweating of both groups was not zero, despite that it was absolutely undesirable. Obviously, the impact of the appreciatory mechanism is limited and it is superimposed to the impact of another, probably triggering more automatically the palmar sweating. The question is: does this triggering the palmar sweating mechanism activate the palmar sweat glands blindly, in the context of a general or sympathetic arousal, or a benefit beyond the palmar wetting is accomplished for the organism? Many findings of EDA research suggest that palmar sweating may be useful for other reasons to the organism beyond mechanical facilitation of the action, but since it cannot be supported by the findings of the present work, it must be the issue of another one.
What we can clearly concluded from the findings of this work is that palmar sweating is not unrelated to the action demands on palmar wetting, even in the case of palmar hyperhidrosis, and this obviously means that palmar sweating may not be considered a noisy manifestation of a non-specific activity (Fowles, 1986),.
REFERENCES
Adelman, S., Taylor, C. R. and Meglung, N. C. (1975) Sweating on paws and palms: what is its function? Am. J. Psychol., 229(5): 1400-1402.
Dawson, M. E.et al (1985) Diagnostic utility of autonomic measures for major depressive disorders. Psychiatry Res., 15: 261-270.
Eysenck, H. J. (1979) The conditioning model of neurosis. Behav. Brain Sci., 2: 155-199.
Fowles, D. C. 1986. The eccrine system and electrodermal activity. In: M. G. H. Coles, E. Donchin, S. W. Porges (Eds), Psychophysiology : Systems, Processes, and Applications., Elsevier, Amsterdam, pp. 51-96.
Hoehn-Saric, R. and McLeod, D. R. (1988) The peripheral sympathetic nervous system. Its role in normal and pathological anxiety. Psychiatr. Clin. North Am., 11(2): 375-386.
Johnson, L. C. and Lubin, A. (1966) Spontaneous electrodermal activity during waking and sleeping. Psychophysiology., 3(1): 8-17.
Kerassidis, S. (1994) Is palmar and plantar sweating thermoregulatory? Acta Physiol. Scand., 152: 259-263.
Kushniruk, A., Rustenburg, J. and Ogilvie, R. (1985) Psychological correlates of electrodermal activity during REM sleep. Sleep., 8(2): 146-154.
Lacey, J. I. (1967) Somatic response patterning and stress: Some revisions of activation theory.In: M.H. Appley and R. Trumbull (Eds), Psychological Stress (Issues in research), Chapter 2, ACC, New York, pp. 15-42.
Lester, B. K., Burch, N. R. and Dossett, R. C. (1967) Nocturnal EEG-GSR profiles : the influence of presleep states. Psychophysiology, 3: 238-248.
Miller, N. E. (1969) Psychosomatic effects of specific types of training. Ann. N. Y. Acad. Sci., 159: 1025-1040.
Miller, N. E. (1969) Learning of visceral and glandular responses. Science. 163: 434-445.
Ost, L., Sterner, U., Lindahl, I. (1984) Physiological responses in blood phobics. Behav Res Ther. 22(2): 109-117.
Venables, P. H. (1991) Autonomic activity. Ann. N. Y. Acad. Sci., 620: 191-207.
Wallin, B. G.(1992) Intraneural recordings of normal and abnormal sympathetic activity in man. In: R. Bannister, C. J. Mathiaw (Eds), Autonomic Failure. A textbook of clinical disorders of the autonomic nervous system, Oxford Medical Publications, Oxford, pp. 359-377.
Wallin, B. G. and Elam, M. (1994) Insights from intraneural recordings of sympathetic nerve traffic in humans. Am. Physiol .Soc., 9: 203-207.
Wilcott, R. C. (1966) Adaptive value of arousal sweating and the epidermal mechanism related to skin potential and skin resistance. Psychophysiology, 2(3): 249-262.
Is palmar hyperhidrosis caused by a positive feedback loop of
ABSTRACT
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.
INTRODUCTION
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.
METHODS
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.
It 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.
RESULTS
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.
DISCUSSION
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.
REFERENCES
Boucsein, W. Electrodermal activity. New York: Plenum Press; 1992.
Duller, P.; Doyle Gentry, W. Use of biofeedback in treating chronic hyperhidrosis: a preliminary report. Br. J. Dermatol. 103:143-146; 1980.
Edelman, R. Effects of differential afferent feedback on instrumental GSR conditioning. J. Physiol. 74:3-14; 1970.
Kerassidis, S. Is palmar and plantar sweating thermoregulatory? Acta Physiol. Scand. 52:259-263; 1994.
Kerassidis, S.; Charistou, A. Nonresponders among hyperhidrotics. Biological Psychology. 52:85-90; 2000.
Klinge, V. Effects of exteroceptive feedback and instructions on control of spontaneous galvanic skin responses. Psychophysiology. 9(3):305-317; 1972.
Lerer, Β.; Jacobowitz, J., Wahba, A. Personality features in essential hyperhidrosis. Int. J. Psychiatry Med. 10(1):59-67; 1980.
Lerer, Β. Hyperhidrosis: A review of its psychological aspects. Psychosomatics. 18:28-31; 1977.
Russel, C.; Davey, G.C.L. The effects of false response feedback on human "fear" conditioning. Behav. Res. Ther. 29:191-196; 1991.
Sato, K.; Kang, W.; Saga, K.; Sato, K.T. Biology of sweat glands and their disorders: 2. Disorders of sweat gland function. J. Am. Acad. Dermatol. 20:713-726; 1989.
Κερασίδης, Σ.; Μπιτζαράκη, Κ. Στοιχεία της προσωπικότητας των υπεριδρωτικών στις παλάμες [Personality traits of hyperhidrotics in palms]. Ψυχιατρική. 8:181-187; 1977.
Κερασίδης, Σ.; Κοχιαδάκης, Γ. Ανάλυση της μεταβλητότητας του καρδιακού ρυθμού σε άτομα με υπεριδρωσία παλαμών [Heart-rate variability analysis in hyperhidrotics in palms]. Ελληνική καρδιολογική επιθεώρηση. 39(6):474-478; 1998.
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.
INTRODUCTION
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.
METHODS
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.
It 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.
RESULTS
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.
DISCUSSION
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.
REFERENCES
Boucsein, W. Electrodermal activity. New York: Plenum Press; 1992.
Duller, P.; Doyle Gentry, W. Use of biofeedback in treating chronic hyperhidrosis: a preliminary report. Br. J. Dermatol. 103:143-146; 1980.
Edelman, R. Effects of differential afferent feedback on instrumental GSR conditioning. J. Physiol. 74:3-14; 1970.
Kerassidis, S. Is palmar and plantar sweating thermoregulatory? Acta Physiol. Scand. 52:259-263; 1994.
Kerassidis, S.; Charistou, A. Nonresponders among hyperhidrotics. Biological Psychology. 52:85-90; 2000.
Klinge, V. Effects of exteroceptive feedback and instructions on control of spontaneous galvanic skin responses. Psychophysiology. 9(3):305-317; 1972.
Lerer, Β.; Jacobowitz, J., Wahba, A. Personality features in essential hyperhidrosis. Int. J. Psychiatry Med. 10(1):59-67; 1980.
Lerer, Β. Hyperhidrosis: A review of its psychological aspects. Psychosomatics. 18:28-31; 1977.
Russel, C.; Davey, G.C.L. The effects of false response feedback on human "fear" conditioning. Behav. Res. Ther. 29:191-196; 1991.
Sato, K.; Kang, W.; Saga, K.; Sato, K.T. Biology of sweat glands and their disorders: 2. Disorders of sweat gland function. J. Am. Acad. Dermatol. 20:713-726; 1989.
Κερασίδης, Σ.; Μπιτζαράκη, Κ. Στοιχεία της προσωπικότητας των υπεριδρωτικών στις παλάμες [Personality traits of hyperhidrotics in palms]. Ψυχιατρική. 8:181-187; 1977.
Κερασίδης, Σ.; Κοχιαδάκης, Γ. Ανάλυση της μεταβλητότητας του καρδιακού ρυθμού σε άτομα με υπεριδρωσία παλαμών [Heart-rate variability analysis in hyperhidrotics in palms]. Ελληνική καρδιολογική επιθεώρηση. 39(6):474-478; 1998.
ON THE ANTECEDENTS OF PALMAR HYPERHIDROSIS
ABSTRACT
We compared hyperhidrotic and normal individuals on the parameters that have been related, or could be, to excessive sweating, in order to fill the research gap on the antecedents of palmar hyperhidrosis. We performed neurological examination, general hematological test, and measurements of blood levels of thyroid hormones FT3, FT4, TSH, glucose, and electrolytes Na, K, P, Ca, Mg. The participants also fill in the Eysenck Personality, as well as a laboratory constructed Questionnaire. In addition, we compared the palmar sweat glands density of the participants using the iontophoresis of pilocarpine technique. We found that palmar hyperhidrosis cannot be attributed to any of the examined pathological parameters, or to higher density of palmar sweat glands. However hyperhidrotics scored significantly higher in Neuroticism scale of personality test. We concluded that the dysfunction is possibly related to personality traits while a genetic predisposition is also possible.
Key words: hyperhidrotic, palmar sweating, sweat glands.
Stelios Kerassidis
INTRODUCTION
Palmar hyperhidrosis refers to excessive local sweating on the palms of the hands. Although the disorder is a socially and an occupationally distressing, and sometimes disabling, condition [1], there is minimal research data on this, probably because it has not life threatening consequences. The reviews by Sato et al. [1) on the disorders of sweat glands, by Lerer [2], Lerer et al. [3] on the psychological aspects of palmar hyperhidrosis, and by Fotopoulos & Sunderland [4] on the treatment of psychophysiological disorders, underline the lack of publications on the etiology of palmar hyperhidrosis. In opposition to this lack, and probably because of this, some one can find plenty of “public opinions”. Actually, every physician, dermatologist and psychiatrist treats the patients having in mind her/his own theory concerning the antecedents of palmar hyperhidrosis. In the present work we compare hyperhidrotic and normal individuals on any of the parameters which have been related, or could be, to excessive sweating (not only of the palms) as a possible antecedent of palmar hyperhidrosis.
Laboratory and clinical tests, including the following, were performed:
1. standard neurological examination, in order to check for dysautonomy or neurological damage,
2. general hematological, investigating for a possible association of palmar hyperhidrosis with a blood abnormality,
3. measurement of blood levels of hormones FT3, FT4, TSH, investigating for a possible association of palmar hyperhidrosis with thyroid gland over-function (which can cause excessive sweating by accelerating the metabolic process),
4. measurement of blood glucose levels, in order to check for a possible association of palmar hyperhidrosis with hypoglycemia (and to exclude diabetic individuals),
5. measurement of blood levels of Na, K, P, Ca, Mg, investigating for a possible association of palmar hyperhidrosis with electrolyte imbalance [Edelberg [5] suggested that skin may have a role as an accessory kidney in control of water and electrolyte balance], or parathyroidism,
6. filling in of the Eysenck Personality Questionnaire (EPQ), in order to examine whether personality traits could differentiate hyperhidrotics from normal individuals,
7. filling in of a laboratory constructed questionnaire, in order to examine whether some habits, diseases or heredity could differentiate hyperhidrotics from normal individuals,
8. palmar sweat glands count, in order to examine whether palmar hyperhidrosis is the result of a higher sweat glands density on the palms. (The greater skin conductance activity at the distal, relative to the medial, phalanx had been attributed by Freedman et al. [6] to the greater density of sweat glands at the distal, relative to the medial, site. They suggested that there is a positive relationship between sweat glands count and skin conductance activity. This relationship holds for different areas within the palm but it could not be excluded that differences in palmar sweating between hyperhidrotic and normal individuals are caused by differences in the density of their palmar sweat glands.)
MATERIAL AND METHODS
Participants
Forty individuals participated in the tests. Twenty individuals were hyperhidrotic in their palms (and, usually, in their soles as well), whereas the remaining 20 individuals were normal in terms of palmar sweating. Twelve females and 8 males were included in each group. The mean age of the hyperhidrotic females was 31.4 and of the normal females was 27.3 years. The mean age of the hyperhidrotic males was 35 and of the normal males was 34.3 years. The mean body weight of the hyperhidrotic females was 60.3 (50-73) kg and of the normal females was 56.4 (45-70) kg. The mean body weight of the hyperhidrotic males was 75.6 (62-87) kg and of the normal males was 76.2 (62-102) kg. The educational level of hyperhidrotics/normal was: 11/12 higher education, 3/4 students, 6/4 secondary-lower. No individual of our study was alcohol or drug addicted, or under medication.
Twenty-four individuals (out of the previous forty) participated in the sweat gland density measurement. Twelve were hyperhidrotic and 12 normal palmar sweating individuals. Seven females and 5 males were included in each group. The mean age of the hyperhidrotic females was 28 and of the normal females was 28 years also. The mean age of the hyperhidrotic males was 33 and of the normal males was 23 years.
Individuals with palmar hyperhidrosis were recruited by the local mass media. Among those who volunteered to participate, six persons who manifested excessive sweating all over the body, or predominantly in other areas of the body, like the forehead and the armpits, were excluded of the research. Normal palmar sweating individuals were selected by the authors, among people who reported never having suffered from excessive palmar sweating. In order to confirm the participants' estimation of the degree of their palmar sweating, a sweat collecting plaster was attached to 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 mg (S.D. 2.3, range 0-7). Out of the 42 individuals who were subjected to this confirmation test, one from the hyperhidrotic group had 4 mg palmar sweat and one from the normal group had 12 mg palmar sweat. The scores of these two persons were excluded from the analysis.
Design and materials
The participants underwent a standard neurological examination and were subjected to the laboratory blood tests: general hematological, blood glucose concentration as well as blood levels of thyroid hormones (FT3, FT4, TSH) and electrolytes (Na, K, P, Ca, Mg). The participants answered many kinds of questions including: alcohol and drug consuming, medication, habits of sleep, state of digestive system, feelings of palpitation, suffocation, dizziness, skin problems, diseases in general, the time of the first appearance of hyperhidrosis, its expression in every day life, relatives suffering from hyperhidrosis etc. The Greek translation of the Eysenck Personality Questionnaire [7], comprising 84 questions and 4 scales (Neuroticism, Psychotism, Extroversion and Lying), was completed after the end of the tests.
For the sweat glands density count, the iontophoresis of pilocarpine technique [8, 9] was used as it is described below. A 3x5 cm sheet of blotting paper was soaked in 4% w/v pilocarpine chloride in benzalkonium chloride (Alkon-Courreur, Sterile ophthalmic solution) and applied to the test area of the palmar skin. Two 2x3 cm gauze pads soaked in sterile normal saline served as conductive materials. One was placed over the blotting paper, on the hypothenar eminence of the left palm and the other on the exterior side of the palm of the same hand. Two 1.5x2.5 cm copper pieces served as electrodes. The electrodes were placed over the gauze pads so that the positive electrode was over the pilocarpine. A current of 1 mA was applied for 5 min. We used 3 batteries (9V each one), connected in series, to form an electric source. The regulation of current at the value of 1 mA (provided that the individuals did not present the same value of palmar resistance due to the different thickness and wetting of stratum cormeum) was accomplished by a potentiometer connected in series with palmar resistance. After a 5 min iontophoresis of pilocarpine in the hypothenar eminence of the left palm of the individual, the palm was dried, painted with alcohol iodine and dried again. At this time the palm was placed on a paper sheet and it was firmly placed on a sloping glass, so that the testing area was laid over the paper. The experimenter looked carefully at the opposite side of the glass so that she could watch spots appearing on the paper (which turned black in the presence of sweat and iodine, because of the containing polysaccharides) in the points the sweat came out of the pores of the testing area. When it was estimated that the sweat spots were clearly distinguished, the individual was asked to remove carefully its palm from the paper sheet. This procedure of taking an imprint of the testing area on the paper sheet was repeated. Four imprints of the testing area were taken for each individual (see Fig.). Then, the paper sheets were clearly photocopied on transparent membranes and counted using the Microcomputer Imaging Device (MCID, Imaging Research INC). (The photostats were additionally necessary because fainting of the imprints on the papers would happen a few weeks later.)
The time between the placement of the palm on the paper and its removal from it was different for each individual. In order to see if there were sweat glands that they had not produced sweat till the removal of the palm (because they may have been less activated), we occasionally left the palm on the paper sheet, for longer time than that we estimated as necessary. Many sweat traces joined this way and the imprint became muddy, but no increase in the number of spots was observed.
Statistics
Two factor (sex and hyperhidrosis) analysis of variance (ANOVA) was used for comparisons between hyperhidrotic and normal individuals and between females and males in clinical tests.
The counting of the spots was accomplished via the Microcomputer Imaging Device. The device could count the spots in any selected area. We measured and compared areas of any magnitude, but we present the comparison on 1 cm2 area of hypothenar eminence (near the sulcus, indicated by the arrow in Fig.). This was the area with the higher density of spots for all individuals. The differences in the density of spots on this area (and the very adjacent) between the 4 imprints of the same individual were small (0-5%) and the higher measured value was selected for the statistical analysis. We compared the number of spots (active sweat glands) in the counted area of hypothenar eminence, by a two factor (sex and hyperhidrosis) Analysis of Variance (ANOVA).
RESULTS
Eight out of the 20 hyperhidrotics and 1 out of the 20 normal individuals declared that they had at least one close relative suffering from palmar or plantar hyperhidrosis. This difference is significant, F=6.40, P<.004. No other systematic difference between hyperhidrotic and normal individuals was revealed by the laboratory constructed questionnaire .
The neurological examination did not reveal any neurological damage or dysautonomy to any individual of both groups. No significant differences were found between hyperhidrotic and normal individuals in the general blood test, or in blood concentrations of thyroid hormones, glucose, or electrolytes. However, hyperhidrotics displayed higher scores than normal individuals (13.35 / 9.75) in EPQ Neuroticism scale (F=6.352, P<.01). There was no significant difference in any of the 3 other EPQ scales (Psychotism, Extroversion and Lying). Differences between females and males were not significant.
The mean values and standard deviations of the number of active sweat glands in the counted area of hypothenar eminence are shown in the Table. The two factor ANOVA revealed no statistically significant difference between hyperhidrotic and normal individuals (F=1.7, P<.20). Females presented a higher number of active sweat glands on the counted area (425 s.g./ cm2) than males (383 s.g./ cm2), but the difference was not statistically significant (F=3.1, P<0.09). This difference may due to the more injuries of the male palm which probably cause more destroys of sweat glands. The correlation coefficient between age and number of sweat glands count was also insignificant (r=0.079), probably because of the narrow range of the ages of participants.
DISCUSSION
The finding that significantly more hyperhidrotics than normal individuals had a close relative suffering from palmar hyperhidrosis (40% of hyperhidrotics, and only 5% of normal individuals) suggests that a genetic predisposition to excessive palmar sweating may exists. This conclusion is also supported by works like that of Adar et al in which 53% of the patients had some family history of hyperhidrosis, while 21% had first-degree hyperhidrotic, of Kwon et al. [12] in which hyperhidrotics had 30.9% familial hyperhidrosis in first degree relatives while James et al [........] studied “a family with hereditary emotional hyperhidrosis”.
According to our laboratory tests, there was no indication that the hyperhidrotics were characterised by neurological damage, dysautonomy, hematological abnormality, electrolytic or blood glucose imbalance, and thyroid gland dysfunction. We also found no statistically significant difference in the density of palmar sweat glands between hyperhidrotic and normal individuals. The hypothenar eminence is the area that touches the paper when an individual writes. It is well known that hyperhidrotics sweat so much in this area that usually need to use a napkin for writing. In the confirmation test of the participants' estimate of the degree of their palmar sweating (methods section), we found that the mean weight of palmar sweat of hyperhidrotic was 6-7 times more than that of normal individuals. If this difference was due to higher density of palmar active sweat glands, hyperhidrotics should have 6-7 times higher density compared to normal individuals. Our finding suggests that the difference in palmar sweating between hyperhidrotic and normal individuals cannot, by any means, be attributed to a difference of sweat gland density.
However, hyperhidrotics displayed higher scores than normal individuals in Neuroticism scale of Eysenck Personality Questionnaire. In another work (10), we have also found higher scores for hyperhidrotics than normal individuals in Psychotism, Depression and Social Introversion of Minnesota Multifasic Personality Inventory. We consider that these findings are in line with the suggestion of Lerer, et al. [3] and of Lerer and Jacobowitz [11] that hyperhidrotic individuals are characterized by lower overall ability to cope with stress and a strong proclivity to avoid problems, in the sense that they all suggest that personality traits may be responsible for the palmar hyperhidrosis disorder. There is also the alternative view, that individuals who suffer from palmar hyperhidrosis may develop pathological personality traits as a consequence of this condition. Of course, the possibility of a feedback influence of hyperhidrosis on the personality of hyperhidrotic cannot be excluded, but we suggest that this is a secondary effect. The fact that some individuals started to exhibit excessive palmar sweating when they faced a serious problem, and other expressed palmar hyperhidrosis only for a transient, limited, hard period of their life (data from interviews), indicates that psychological stressors may be responsible for the disorder.
We have to mention that Kwon et al. [12] found no evidence of abnormal personality features using the EPQ on hyperhidrotics on palms, soles, and axillae. We suppose that the discrepancy between this and the present work is deceptive and it is due to the different methodology which was used. Kwon et al. [12] used only hyperhidrotics without any control group, while we used a normal palmar sweating group, matched to the group of hyperhidrotics, for comparisons. The higher score on EPQ Neuroticism scale between our matched groups of hyperhidrotic and normal individuals, do not automatically put hyperhidrotics in a psychiatric patients group, and for this reason there is not discrepancy between our work and that of Kwon et al. This difference cannot also be considered accidental. Hyperhidrotic in relation to normal individuals may probably are more anxious, with more intense emotional reactions, and a proclivity in psychosomatic disorders [13]. It is somehow like a test group to present statistically significant higher blood pressure values than a control group, without the test group to be hypertensive.
Conclusively, the findings indicate that palmar hyperhidrosis cannot be attributed either to the pathological parameters, which could be considered to be related to excessive sweating, or to higher density of palmar sweat glands. The dysfunction is possibly related to personality traits, while a genetic predisposition is also possible.
ACKNOWLEDGEMENT
The present work is one of a series of studies on palmar sweating and hyperhidrosis conducted at the Laboratory of Physiology, School of Health Sciences, University of Crete, in collaboration and with the support of the University Hospital of Crete. The present work was especially supported by the Laboratories of Clinical Chemistry and Biochemistry as well as the Nuclear Medicine of the University Hospital of Crete.
REFERENCES
1. Sato K, Kang W, Saga K, Sato KT. Biology of sweat glands and their disorders: 2. Disorders of sweat gland function. J Am Acad Dermatol. 1989;20:713-726.
2. Lerer Β. Hyperhidrosis: A review of its psychological aspects. Psychosomatics. 1977;18:28-31.
3. Lerer Β, Jacobowitz J, Wahba A. Personality features in essential hyperhidrosis. Int J Psychiatry Med. 1980;10(1):59-67.
4. Fotopoulos SS, Sunderland WP. Biofeedback in the treatment of psychophysiologic disorders. Biofeedback Self Regul. 1978;3(4):331-361.
5. Edelberg R. Mechanisms of electrodermal adaptations for locomotion, manipulation, or defense. In: Stellar E, Sprague JM, eds. Progress in physiological psychology. New York: Academic Press; 1973:155-209.
6. Freedman LW, Scerbo AS, Dawson ME, et al. The relationship of sweat gland count to electrodermal activity. Psychophysiology. 1994;1:196-200.
7. Δημητρίου EΧ. Το ερωτηματολόγιο προσωπικότητας (Eysenck Personality Questionnaire): στάθμιση στον ελληνικό πληθυσμό, ενήλικο και παιδικό [The Eysenck Personality Questionnaire (EPQ): The validity of the Greek, adult and junior, version]. Εγκέφαλος. 1986;23:41-54.
8. Kennedy W, Sakuta M, Sutherland D, Goets F. The sweating deficiency in diabetes mellitus: Methods of quantitation and clinical correlation. Neurology. 1984;34:758-763.
9. Morris J, Dische S, Mott G. A pilot study of a method of estimating the number of functional eccrine sweat glands in irradiated human skin. Radiother Oncol. 1992;25:49-55.
10. Κερασίδης Σ, Μπιτζαράκη Κ. Στοιχεία της προσωπικότητας των υπεριδρωτικών στις παλάμες [Personality traits of hyperhidrotics in palms]. Ψυχιατρική. 1997;8(3):196-202.
11. Lerer Β, Jacobowitz J. Τreatment of essential hyperhidrosis by psychotherapy. Psychosomatics. 1981;22(6):536-538.
12. Kwon OS, Kim BS, Cho KH, Kwon JS, Shin MS, Youn JI, Chung JH. Essential hyperhydrosis: no evidence of abnormal personality features. Clin Exp Dermatol. 1998;23(1): 45-6.
13. Eysenck HJ, Eysenck SBG. Manual of the EPQ (Personality Questionaire). London: Hodder and Stoughton Educational; 1975.
TABLE
Mean values and standard deviations (in parentheses) of the number of active sweat glands on an area 1 cm2 of the hypothenar eminence of the palm.
Hyperhidrotics Normal Total
Female 420 (62) 429 (57) 425 (58)
Male 356 (11) 410 (78) 383 (60)
Total 393 (57) 421 (64)
We compared hyperhidrotic and normal individuals on the parameters that have been related, or could be, to excessive sweating, in order to fill the research gap on the antecedents of palmar hyperhidrosis. We performed neurological examination, general hematological test, and measurements of blood levels of thyroid hormones FT3, FT4, TSH, glucose, and electrolytes Na, K, P, Ca, Mg. The participants also fill in the Eysenck Personality, as well as a laboratory constructed Questionnaire. In addition, we compared the palmar sweat glands density of the participants using the iontophoresis of pilocarpine technique. We found that palmar hyperhidrosis cannot be attributed to any of the examined pathological parameters, or to higher density of palmar sweat glands. However hyperhidrotics scored significantly higher in Neuroticism scale of personality test. We concluded that the dysfunction is possibly related to personality traits while a genetic predisposition is also possible.
Key words: hyperhidrotic, palmar sweating, sweat glands.
Stelios Kerassidis
INTRODUCTION
Palmar hyperhidrosis refers to excessive local sweating on the palms of the hands. Although the disorder is a socially and an occupationally distressing, and sometimes disabling, condition [1], there is minimal research data on this, probably because it has not life threatening consequences. The reviews by Sato et al. [1) on the disorders of sweat glands, by Lerer [2], Lerer et al. [3] on the psychological aspects of palmar hyperhidrosis, and by Fotopoulos & Sunderland [4] on the treatment of psychophysiological disorders, underline the lack of publications on the etiology of palmar hyperhidrosis. In opposition to this lack, and probably because of this, some one can find plenty of “public opinions”. Actually, every physician, dermatologist and psychiatrist treats the patients having in mind her/his own theory concerning the antecedents of palmar hyperhidrosis. In the present work we compare hyperhidrotic and normal individuals on any of the parameters which have been related, or could be, to excessive sweating (not only of the palms) as a possible antecedent of palmar hyperhidrosis.
Laboratory and clinical tests, including the following, were performed:
1. standard neurological examination, in order to check for dysautonomy or neurological damage,
2. general hematological, investigating for a possible association of palmar hyperhidrosis with a blood abnormality,
3. measurement of blood levels of hormones FT3, FT4, TSH, investigating for a possible association of palmar hyperhidrosis with thyroid gland over-function (which can cause excessive sweating by accelerating the metabolic process),
4. measurement of blood glucose levels, in order to check for a possible association of palmar hyperhidrosis with hypoglycemia (and to exclude diabetic individuals),
5. measurement of blood levels of Na, K, P, Ca, Mg, investigating for a possible association of palmar hyperhidrosis with electrolyte imbalance [Edelberg [5] suggested that skin may have a role as an accessory kidney in control of water and electrolyte balance], or parathyroidism,
6. filling in of the Eysenck Personality Questionnaire (EPQ), in order to examine whether personality traits could differentiate hyperhidrotics from normal individuals,
7. filling in of a laboratory constructed questionnaire, in order to examine whether some habits, diseases or heredity could differentiate hyperhidrotics from normal individuals,
8. palmar sweat glands count, in order to examine whether palmar hyperhidrosis is the result of a higher sweat glands density on the palms. (The greater skin conductance activity at the distal, relative to the medial, phalanx had been attributed by Freedman et al. [6] to the greater density of sweat glands at the distal, relative to the medial, site. They suggested that there is a positive relationship between sweat glands count and skin conductance activity. This relationship holds for different areas within the palm but it could not be excluded that differences in palmar sweating between hyperhidrotic and normal individuals are caused by differences in the density of their palmar sweat glands.)
MATERIAL AND METHODS
Participants
Forty individuals participated in the tests. Twenty individuals were hyperhidrotic in their palms (and, usually, in their soles as well), whereas the remaining 20 individuals were normal in terms of palmar sweating. Twelve females and 8 males were included in each group. The mean age of the hyperhidrotic females was 31.4 and of the normal females was 27.3 years. The mean age of the hyperhidrotic males was 35 and of the normal males was 34.3 years. The mean body weight of the hyperhidrotic females was 60.3 (50-73) kg and of the normal females was 56.4 (45-70) kg. The mean body weight of the hyperhidrotic males was 75.6 (62-87) kg and of the normal males was 76.2 (62-102) kg. The educational level of hyperhidrotics/normal was: 11/12 higher education, 3/4 students, 6/4 secondary-lower. No individual of our study was alcohol or drug addicted, or under medication.
Twenty-four individuals (out of the previous forty) participated in the sweat gland density measurement. Twelve were hyperhidrotic and 12 normal palmar sweating individuals. Seven females and 5 males were included in each group. The mean age of the hyperhidrotic females was 28 and of the normal females was 28 years also. The mean age of the hyperhidrotic males was 33 and of the normal males was 23 years.
Individuals with palmar hyperhidrosis were recruited by the local mass media. Among those who volunteered to participate, six persons who manifested excessive sweating all over the body, or predominantly in other areas of the body, like the forehead and the armpits, were excluded of the research. Normal palmar sweating individuals were selected by the authors, among people who reported never having suffered from excessive palmar sweating. In order to confirm the participants' estimation of the degree of their palmar sweating, a sweat collecting plaster was attached to 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 mg (S.D. 2.3, range 0-7). Out of the 42 individuals who were subjected to this confirmation test, one from the hyperhidrotic group had 4 mg palmar sweat and one from the normal group had 12 mg palmar sweat. The scores of these two persons were excluded from the analysis.
Design and materials
The participants underwent a standard neurological examination and were subjected to the laboratory blood tests: general hematological, blood glucose concentration as well as blood levels of thyroid hormones (FT3, FT4, TSH) and electrolytes (Na, K, P, Ca, Mg). The participants answered many kinds of questions including: alcohol and drug consuming, medication, habits of sleep, state of digestive system, feelings of palpitation, suffocation, dizziness, skin problems, diseases in general, the time of the first appearance of hyperhidrosis, its expression in every day life, relatives suffering from hyperhidrosis etc. The Greek translation of the Eysenck Personality Questionnaire [7], comprising 84 questions and 4 scales (Neuroticism, Psychotism, Extroversion and Lying), was completed after the end of the tests.
For the sweat glands density count, the iontophoresis of pilocarpine technique [8, 9] was used as it is described below. A 3x5 cm sheet of blotting paper was soaked in 4% w/v pilocarpine chloride in benzalkonium chloride (Alkon-Courreur, Sterile ophthalmic solution) and applied to the test area of the palmar skin. Two 2x3 cm gauze pads soaked in sterile normal saline served as conductive materials. One was placed over the blotting paper, on the hypothenar eminence of the left palm and the other on the exterior side of the palm of the same hand. Two 1.5x2.5 cm copper pieces served as electrodes. The electrodes were placed over the gauze pads so that the positive electrode was over the pilocarpine. A current of 1 mA was applied for 5 min. We used 3 batteries (9V each one), connected in series, to form an electric source. The regulation of current at the value of 1 mA (provided that the individuals did not present the same value of palmar resistance due to the different thickness and wetting of stratum cormeum) was accomplished by a potentiometer connected in series with palmar resistance. After a 5 min iontophoresis of pilocarpine in the hypothenar eminence of the left palm of the individual, the palm was dried, painted with alcohol iodine and dried again. At this time the palm was placed on a paper sheet and it was firmly placed on a sloping glass, so that the testing area was laid over the paper. The experimenter looked carefully at the opposite side of the glass so that she could watch spots appearing on the paper (which turned black in the presence of sweat and iodine, because of the containing polysaccharides) in the points the sweat came out of the pores of the testing area. When it was estimated that the sweat spots were clearly distinguished, the individual was asked to remove carefully its palm from the paper sheet. This procedure of taking an imprint of the testing area on the paper sheet was repeated. Four imprints of the testing area were taken for each individual (see Fig.). Then, the paper sheets were clearly photocopied on transparent membranes and counted using the Microcomputer Imaging Device (MCID, Imaging Research INC). (The photostats were additionally necessary because fainting of the imprints on the papers would happen a few weeks later.)
The time between the placement of the palm on the paper and its removal from it was different for each individual. In order to see if there were sweat glands that they had not produced sweat till the removal of the palm (because they may have been less activated), we occasionally left the palm on the paper sheet, for longer time than that we estimated as necessary. Many sweat traces joined this way and the imprint became muddy, but no increase in the number of spots was observed.
Statistics
Two factor (sex and hyperhidrosis) analysis of variance (ANOVA) was used for comparisons between hyperhidrotic and normal individuals and between females and males in clinical tests.
The counting of the spots was accomplished via the Microcomputer Imaging Device. The device could count the spots in any selected area. We measured and compared areas of any magnitude, but we present the comparison on 1 cm2 area of hypothenar eminence (near the sulcus, indicated by the arrow in Fig.). This was the area with the higher density of spots for all individuals. The differences in the density of spots on this area (and the very adjacent) between the 4 imprints of the same individual were small (0-5%) and the higher measured value was selected for the statistical analysis. We compared the number of spots (active sweat glands) in the counted area of hypothenar eminence, by a two factor (sex and hyperhidrosis) Analysis of Variance (ANOVA).
RESULTS
Eight out of the 20 hyperhidrotics and 1 out of the 20 normal individuals declared that they had at least one close relative suffering from palmar or plantar hyperhidrosis. This difference is significant, F=6.40, P<.004. No other systematic difference between hyperhidrotic and normal individuals was revealed by the laboratory constructed questionnaire .
The neurological examination did not reveal any neurological damage or dysautonomy to any individual of both groups. No significant differences were found between hyperhidrotic and normal individuals in the general blood test, or in blood concentrations of thyroid hormones, glucose, or electrolytes. However, hyperhidrotics displayed higher scores than normal individuals (13.35 / 9.75) in EPQ Neuroticism scale (F=6.352, P<.01). There was no significant difference in any of the 3 other EPQ scales (Psychotism, Extroversion and Lying). Differences between females and males were not significant.
The mean values and standard deviations of the number of active sweat glands in the counted area of hypothenar eminence are shown in the Table. The two factor ANOVA revealed no statistically significant difference between hyperhidrotic and normal individuals (F=1.7, P<.20). Females presented a higher number of active sweat glands on the counted area (425 s.g./ cm2) than males (383 s.g./ cm2), but the difference was not statistically significant (F=3.1, P<0.09). This difference may due to the more injuries of the male palm which probably cause more destroys of sweat glands. The correlation coefficient between age and number of sweat glands count was also insignificant (r=0.079), probably because of the narrow range of the ages of participants.
DISCUSSION
The finding that significantly more hyperhidrotics than normal individuals had a close relative suffering from palmar hyperhidrosis (40% of hyperhidrotics, and only 5% of normal individuals) suggests that a genetic predisposition to excessive palmar sweating may exists. This conclusion is also supported by works like that of Adar et al in which 53% of the patients had some family history of hyperhidrosis, while 21% had first-degree hyperhidrotic, of Kwon et al. [12] in which hyperhidrotics had 30.9% familial hyperhidrosis in first degree relatives while James et al [........] studied “a family with hereditary emotional hyperhidrosis”.
According to our laboratory tests, there was no indication that the hyperhidrotics were characterised by neurological damage, dysautonomy, hematological abnormality, electrolytic or blood glucose imbalance, and thyroid gland dysfunction. We also found no statistically significant difference in the density of palmar sweat glands between hyperhidrotic and normal individuals. The hypothenar eminence is the area that touches the paper when an individual writes. It is well known that hyperhidrotics sweat so much in this area that usually need to use a napkin for writing. In the confirmation test of the participants' estimate of the degree of their palmar sweating (methods section), we found that the mean weight of palmar sweat of hyperhidrotic was 6-7 times more than that of normal individuals. If this difference was due to higher density of palmar active sweat glands, hyperhidrotics should have 6-7 times higher density compared to normal individuals. Our finding suggests that the difference in palmar sweating between hyperhidrotic and normal individuals cannot, by any means, be attributed to a difference of sweat gland density.
However, hyperhidrotics displayed higher scores than normal individuals in Neuroticism scale of Eysenck Personality Questionnaire. In another work (10), we have also found higher scores for hyperhidrotics than normal individuals in Psychotism, Depression and Social Introversion of Minnesota Multifasic Personality Inventory. We consider that these findings are in line with the suggestion of Lerer, et al. [3] and of Lerer and Jacobowitz [11] that hyperhidrotic individuals are characterized by lower overall ability to cope with stress and a strong proclivity to avoid problems, in the sense that they all suggest that personality traits may be responsible for the palmar hyperhidrosis disorder. There is also the alternative view, that individuals who suffer from palmar hyperhidrosis may develop pathological personality traits as a consequence of this condition. Of course, the possibility of a feedback influence of hyperhidrosis on the personality of hyperhidrotic cannot be excluded, but we suggest that this is a secondary effect. The fact that some individuals started to exhibit excessive palmar sweating when they faced a serious problem, and other expressed palmar hyperhidrosis only for a transient, limited, hard period of their life (data from interviews), indicates that psychological stressors may be responsible for the disorder.
We have to mention that Kwon et al. [12] found no evidence of abnormal personality features using the EPQ on hyperhidrotics on palms, soles, and axillae. We suppose that the discrepancy between this and the present work is deceptive and it is due to the different methodology which was used. Kwon et al. [12] used only hyperhidrotics without any control group, while we used a normal palmar sweating group, matched to the group of hyperhidrotics, for comparisons. The higher score on EPQ Neuroticism scale between our matched groups of hyperhidrotic and normal individuals, do not automatically put hyperhidrotics in a psychiatric patients group, and for this reason there is not discrepancy between our work and that of Kwon et al. This difference cannot also be considered accidental. Hyperhidrotic in relation to normal individuals may probably are more anxious, with more intense emotional reactions, and a proclivity in psychosomatic disorders [13]. It is somehow like a test group to present statistically significant higher blood pressure values than a control group, without the test group to be hypertensive.
Conclusively, the findings indicate that palmar hyperhidrosis cannot be attributed either to the pathological parameters, which could be considered to be related to excessive sweating, or to higher density of palmar sweat glands. The dysfunction is possibly related to personality traits, while a genetic predisposition is also possible.
ACKNOWLEDGEMENT
The present work is one of a series of studies on palmar sweating and hyperhidrosis conducted at the Laboratory of Physiology, School of Health Sciences, University of Crete, in collaboration and with the support of the University Hospital of Crete. The present work was especially supported by the Laboratories of Clinical Chemistry and Biochemistry as well as the Nuclear Medicine of the University Hospital of Crete.
REFERENCES
1. Sato K, Kang W, Saga K, Sato KT. Biology of sweat glands and their disorders: 2. Disorders of sweat gland function. J Am Acad Dermatol. 1989;20:713-726.
2. Lerer Β. Hyperhidrosis: A review of its psychological aspects. Psychosomatics. 1977;18:28-31.
3. Lerer Β, Jacobowitz J, Wahba A. Personality features in essential hyperhidrosis. Int J Psychiatry Med. 1980;10(1):59-67.
4. Fotopoulos SS, Sunderland WP. Biofeedback in the treatment of psychophysiologic disorders. Biofeedback Self Regul. 1978;3(4):331-361.
5. Edelberg R. Mechanisms of electrodermal adaptations for locomotion, manipulation, or defense. In: Stellar E, Sprague JM, eds. Progress in physiological psychology. New York: Academic Press; 1973:155-209.
6. Freedman LW, Scerbo AS, Dawson ME, et al. The relationship of sweat gland count to electrodermal activity. Psychophysiology. 1994;1:196-200.
7. Δημητρίου EΧ. Το ερωτηματολόγιο προσωπικότητας (Eysenck Personality Questionnaire): στάθμιση στον ελληνικό πληθυσμό, ενήλικο και παιδικό [The Eysenck Personality Questionnaire (EPQ): The validity of the Greek, adult and junior, version]. Εγκέφαλος. 1986;23:41-54.
8. Kennedy W, Sakuta M, Sutherland D, Goets F. The sweating deficiency in diabetes mellitus: Methods of quantitation and clinical correlation. Neurology. 1984;34:758-763.
9. Morris J, Dische S, Mott G. A pilot study of a method of estimating the number of functional eccrine sweat glands in irradiated human skin. Radiother Oncol. 1992;25:49-55.
10. Κερασίδης Σ, Μπιτζαράκη Κ. Στοιχεία της προσωπικότητας των υπεριδρωτικών στις παλάμες [Personality traits of hyperhidrotics in palms]. Ψυχιατρική. 1997;8(3):196-202.
11. Lerer Β, Jacobowitz J. Τreatment of essential hyperhidrosis by psychotherapy. Psychosomatics. 1981;22(6):536-538.
12. Kwon OS, Kim BS, Cho KH, Kwon JS, Shin MS, Youn JI, Chung JH. Essential hyperhydrosis: no evidence of abnormal personality features. Clin Exp Dermatol. 1998;23(1): 45-6.
13. Eysenck HJ, Eysenck SBG. Manual of the EPQ (Personality Questionaire). London: Hodder and Stoughton Educational; 1975.
TABLE
Mean values and standard deviations (in parentheses) of the number of active sweat glands on an area 1 cm2 of the hypothenar eminence of the palm.
Hyperhidrotics Normal Total
Female 420 (62) 429 (57) 425 (58)
Male 356 (11) 410 (78) 383 (60)
Total 393 (57) 421 (64)
Subscribe to:
Posts (Atom)