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Effects of repetitive high intensity stimulation on electrodermal responsivity in male alcoholics and normal controls
AddictiveBehaviors,
0306-4603/85 $3.00 + .OO Copyright Q 1985 Pergamon Press Ltd
Vol. 10, pp. 181-185, 1985 Printed in the USA. All rights reserved.
BRIEF REPORT EFFECTS OF REPETITIVE HIGH INTENSITY STIMULATION ON ELECTRODERMAL RESPONSIVITY IN MALE ALCOHOLICS AND NORMAL CONTROLS VERNER J. KNOTT Royal Ottawa Hospital
DAVID R. BULMER Institute of Living, Adult Outpatient Department Abstract-Relative to nonalcoholics, alcoholics exhibited minimal changes in resting skin conductance levels and spontaneous responses with the onset of high intensity stimulation. Alcoholics also evidenced fewer responses and faster habituation to these stimuli.
INTRODUCTION
The tension reduction hypothesis (TRH) postulates that excessive consumption of alcohol is an attempt to reduce a chronic state of tension and stress exhibited by alcoholics (Appel & Herman, 1972). Definitive evaluation of the first corollary of the TRH, namely, that alcohol exhibits tension-reducing properties, is prevented by a confusing and discrepant pattern of findings on acute/chronic alcohol effects (Higgins, 1972). Evaluation of the TRH is made more complex when attempts to evaluate the experimental literature pertaining to its second corollary, that alcoholics are hyper-aroused. Naitoh’s review (1972) of the psychophysiological literature fails to offer consistent support for this position and on the contrary, recent studies by Rubin and colleagues (1977, 1978, 1980), employing pupillometric indices of autonomic nervous system (ANS) activity, argue not for a hyper-aroused, but for a hypo-aroused endogenous ANS state, and in particular, a dampened sympathetic state, as being characteristic of alcoholics. The consistency of these findings seriously question the TRH and they merit further study, specifically with respect to psychophysiological indices which are sensitive both to stress and to sympathetic activity. Eccrine sweat gland function is mediated through a cholinergic, sympathetic innervation (Venables & Christie, 1973) and non-invasive measurement of eccrine activity via skin conductance has been employed in both normal and psychiatric populations (Prokasy & Raskin, 1973) as a measure of arousal/ stress to physical/psychic stimulation. The purpose of this investigation was to examine further ANS responsivity in alcoholics in relation to skin conductance activity to repeated presentations of high intensity auditory stimuli with specific interest being focused on the hypothesis that alcoholics would exhibit lower resting tonic levels and reduced nonspecific responsivity together with attenuated phasic responses and faster response habituation. Requests for reprints should be sent to Verner J. Knott, patient Dept., 1145 Carling Avenue, Ottawa, Canada, KlZ 7K4. 181
Royal Ottawa Hospital,
Adult Out-
182
VERNER J. KNOTT and DAVID R. BULMER
METHOD
Subjects The nonalcoholics were 15 healthy male adults who were receiving no medication and drank only modest quantities of alcohol on social occasions. Their mean age was 35.9 years (range: 25 to 52). All subjects were required to refrain from tobacco, food and beverages 12 hours prior to test time (9:00 a.m.-12:OO p.m.) The 15 male alcoholics were inpatients at the Alcohol and Drug Treatment Unit of the Royal Ottawa Hospital. The mean age was 40.0 years (range: 24 to 56 years). To qualify for study, all patients had to have been free from alcohol and prescribed medication for a minimum of 2 weeks prior to testing and have had no history of drug abuse. The alcoholics’ drinking histories were positive with respect to one or more of the following characteristics: previous imprisonment or hospitalization for drinking; spree drinking within the last 5 years; interrupted work history due to excessive drinking, and family strife due to drinking. All had evidence of physical dependence on alcohol as indicated by amnesia, blackouts and a history of one or more episodes of severe alcohol withdrawal syndrome. All patients had a withdrawal syndrome on admission to the unit consisting of tremor, agitation, sweating, gastrointestinal disturbance and some had a brief period of hallucinations or delirium. All had raised levels of liver enzymes at the time of admission. The results of neurological, psychiatric and psychological examination were carefully screened to exclude alcoholics exhibiting signs of neurological disease or psychotic disorders. Attempts were also made to exclude alcoholics with medical complications such as hepatic, renal, pulmonary, cardiac, gastrointestinal, genitourinary or serious nutritional or metabolic disorders. Apparatus Electrodermal activity was measured with the aid of a Beckman R-61 1 polygraph and an associated 9844 skin conductance coupler. Skin conductance was recorded directly in umhos by applying a constant 0.5-volt source to a pair of miniature Beckman Biopotential Ag/AgCl skin electrodes, which were attached with adhesive collars to the mid-phalangeal sites of the third and fourth fingers of the nondominant hand. A 0.5% potassium chloride paste mixed with agar was used as the external electrolyte. An additional electrode was placed on the forehead to serve as a ground. The maximum amplifier gain setting was 0.05 uhmos/cm. Stimuli were presented through headphones via a tone generator, which was triggered by a tape-recorded series of 400 Hz triggers with quasirandomised intervals between 20 and 60 sec. The first 12 stimuli were 1-set duration, 1000 Hz tones, with rise and decay times of 5 msec and an intensity setting of 100 dB (re: .002 dyne/cm*). Stimulus 13 was a “dishabituation” tone and was identical to the previous 12 stimuli with the exception that it was set at a lower frequency of 500 Hz and it was inserted in order to examine re-orientation following reduced responsivity to repeated identical stimuli. Procedure Immediately following electrode application subjects were placed in a reclining chair and were instructed to remain relaxed and to ignore the tones. For all recordings a 5-minute interval preceded the onset of the first stimulus. Data reduction Tonic skin conductance levels (SCL) were measured at the onset of each of the 13 stimuli. Phasic stimulus-specific skin conductance responses (SCR) to each stimuli
183
Repetitive high intensity stimulation
were measured with a response being defined as an increase in conductance greater or equal than 0.05 uhmos between 1 and 5 set after the stimulus onset. Amplitudes of SCRs were defined as the highest point within 4 set of response onset minus the SCL at response onset. In addition to the frequency of SCRs, frequency to habituation was also measured, and was defined as the number of responses until a criterion of three successive failures to respond. Dishabituation was assessed calculating the ratio of the response amplitudes to the 12th and 13th stimuli. Response fluctuations of .05 uhmos or greater appearing outside the period defined for SCRs were labelled non-specific skin conductance responses (NSSCR) and were counted for 1 min prior to the 1st stimulus and for the total stimulation period between stimuli 1 and 13. In addition to these measures, the following time-related measures were obtained for the 1st stimulus: latency, defined as the time elapsing between stimulus onset and response onset; rise time, the time elapsing from latency to peak response; recruitment, defined as the rate of response increase and calculated by dividing amplitude by rise time; half-recovery time, the time between the peak of the response and the point half way to the return to baseline. Statistical analysis of SCLs and SCRs were carried out by separate 2 (Group) x 13 (Stimuli) split-plot factorial ANOVAs. The remaining measures were subjected to t tests and a .05 (one-tailed) rejection region was adopted for all statistical tests. The functional relationship of SCLs and SCRs to stimuli was also examined by calculating the slope of these measures for each subject using a simple linear regression model. RESULTS
Mean resting skin conductance levels for alcoholics and controls are shown in Figure 1. Analysis of skin SCLs yielded significant stimulus (F = 2.59, df = 12/324,
.50
t
.45 .40 1
0
” 1
2
”
3
4
’ 5
1” 6 7
TRIALS
8
” 9
‘1’
10 111213
I
2
3
4
5
6
7
8
9
10 11 1213
TRIALS
Fig. 1. Mean skin conductance levels (XL: uhmos) and skin conductance responses @CR: uhmos) of alcoholics and normal controls across trials.
184
VERNER
J. KNOTT and DAVID R. BULMER
p < .003) and stimulus x Group interaction effects (F = 2.59, df = 12/324, p < .003). Additional t tests indicated that although significant differences were ap-
parent between groups prior to the first stimulus onset, normal controls exhibited significant increases in conductance levels at stimuli two (t = 3.8, df = 14, p < .OOS), three (t = 3.1, df = 14,~ < .005), four (t = 4.0, df = 14,~ < .OOS)and five (t = 1.84, df = 14, p < .05). Alcoholics did not exhibit any significant increases in tonic conductance levels throughout stimulus presentation. This was further substantiated with analysis of regression lines for SCL, in that significantly steeper XL slopes (t = 2.02, df = 27, p < .05) were observed for normal controls (mean - .041, f .Ol SD) than alcoholics (mean - .0007, f .02 SD) and in fact the average regression coefficient for the alcoholics did not significantly differ from zero. Similar results were shown with the analysis of NSSCRs. Although no significant differences were observed between groups prior to stimulus presentation, significant effects were observed during stimulation (t = 2.16, df = 27, p < .025) with normal controls exhibiting a greater number of spontaneous responses (mean 5.73, f 9.0 SD) than alcoholics (mean 1.25, f 3.2 SD) and in addition, a significantly greater number (x2 = 12.5, df = 1, p < .OOOS)of normal controls (80%) exhibited NSSCRs during stimulation than alcoholics (14.3%). Although normal controls appeared to exhibit larger responses than alcoholics, analysis of SCRs indicated a significant stimulus effect (F = 17.1, df = 12/324, p < .OOOl) but no Group or interaction effects. Analysis of response frequency and trials to habituation did however yield significant differences in that the average number of stimulus elicited responses was significantly greater (t = 1.75, df = 27, p < .05) for normal controls (mean 7.73 f 0.73 SD) than alcoholics (mean 4.29 f 1.20 SD) and the number of trials to habituation was significantly less (r = 2.1, df = 27, p < .05) for alcoholics (mean 4.36, f 1.19 SD) than for controls (mean 7.60, f 1.10 SD). Significant differences were also observed with the dishabituation index in that normal controls evidenced greater re-orientation than alcoholics (t = 2.03, df = 23, p < .05). No significant group differences were observed with the SCR regression measure. Analysis of temporal measures related to responsivity to the first stimulus indicated no significant differences for latency, rise time, recruitment or recovery indices. DISCUSSION
The present study attempted to determine whether electrodermal indices can differentiate alcoholics from normal controls. In general, there appeared to be a pattern of hypo-responsivity characterising alcoholics as they exhibited no significant changes in tonic levels with the onset of aversive stimulation and evidenced minimal changes in spontaneous fluctuations. In addition, although the groups did not differ with respect to magnitude or responsivity to the high intensity stimuli, alcoholics did differ from normal controls in that they responded with less frequency to the aversive stimuli and they took a fewer number of trials to habituate to these stimuli. This attenuated electrodermal responsivity in alcoholics supports the findings of reduced pupillometric responsivity observed by Rubin and colleagues (1977, 1978, 1980) and argues against the TRH which predicts alcoholics to be hyper-responsive. Finally, as there appears to be no doubt that sweating in man by eccrine sweat glands is mediated through a cholinergic sympathetic innervation (Venables & Christie, 1973), these findings seem to support those of Rubin and colleagues which emphasize the key role of reduced sympathetic activity in differentiating alcoholics and controls.
Repetitive high intensity stimulation
185
REFERENCES Cappel, H., & Herman, C.P. (1972). Alcohol and tension reduction: A review. Quarterly Journal of S&dies on Alcohol,
33, 33-64.
Higgins, R. (1976). Experimental investigations of tension-reduction models of alcoholism. In G. Goldstein & C. Neuringer (Eds.), Empirical studies in alcoholism. Cambridge: Ballinger. Naitoh, P. (1972). The effect of alcohol on the autonomic nervous system of humans; psychophysiological approach. In B. Kissin & H. Begleiter (Eds.), The biology of alcoholism, Vol. 2. Physiology and behavior. New York: Plenum. Rubin, LX, Gottheil, E., Roberts, A., Alterman, AI. & Holstine, J. (1977). Effects of stress on autonomic reactivity in alcoholics; pupillometric studies. I. Journal of Sfudieson Alcohol, 38, 2036-2048. Rubin, L.S., Gottheil, E., Roberts, A., Alterman, A.I. & Holstine, J. (1978). Autonomic nervous system concomitants of short-term abstinence in alcoholics; pupillometric studies. II. Journal of Studies on Alcohol, 39, 189551907. Rubin, L.S., Gottheil, E., Roberts, A., Alterman, A.I. & Holstine, J. (1980). Efects of alcohol on autonomic reactivity in alcoholics; pupillometric studies. III. Journal of Studieson Alcohol, 41, 61 l-622. Venables, P. & Christie, M. (1973). Mechanisms, instrumentation, recording techniques, and quantification of responses. In W. Prokasy & D. Raskin (Eds.), Electrodermal activity in psychological research. New York: Academic Press. Prokasy, W., & Raskin, D. (1973). Electrodermal activity in psychological research. New York: Academic Press.
0306-4603/85 $3.00 + .OO Copyright Q 1985 Pergamon Press Ltd
Vol. 10, pp. 181-185, 1985 Printed in the USA. All rights reserved.
BRIEF REPORT EFFECTS OF REPETITIVE HIGH INTENSITY STIMULATION ON ELECTRODERMAL RESPONSIVITY IN MALE ALCOHOLICS AND NORMAL CONTROLS VERNER J. KNOTT Royal Ottawa Hospital
DAVID R. BULMER Institute of Living, Adult Outpatient Department Abstract-Relative to nonalcoholics, alcoholics exhibited minimal changes in resting skin conductance levels and spontaneous responses with the onset of high intensity stimulation. Alcoholics also evidenced fewer responses and faster habituation to these stimuli.
INTRODUCTION
The tension reduction hypothesis (TRH) postulates that excessive consumption of alcohol is an attempt to reduce a chronic state of tension and stress exhibited by alcoholics (Appel & Herman, 1972). Definitive evaluation of the first corollary of the TRH, namely, that alcohol exhibits tension-reducing properties, is prevented by a confusing and discrepant pattern of findings on acute/chronic alcohol effects (Higgins, 1972). Evaluation of the TRH is made more complex when attempts to evaluate the experimental literature pertaining to its second corollary, that alcoholics are hyper-aroused. Naitoh’s review (1972) of the psychophysiological literature fails to offer consistent support for this position and on the contrary, recent studies by Rubin and colleagues (1977, 1978, 1980), employing pupillometric indices of autonomic nervous system (ANS) activity, argue not for a hyper-aroused, but for a hypo-aroused endogenous ANS state, and in particular, a dampened sympathetic state, as being characteristic of alcoholics. The consistency of these findings seriously question the TRH and they merit further study, specifically with respect to psychophysiological indices which are sensitive both to stress and to sympathetic activity. Eccrine sweat gland function is mediated through a cholinergic, sympathetic innervation (Venables & Christie, 1973) and non-invasive measurement of eccrine activity via skin conductance has been employed in both normal and psychiatric populations (Prokasy & Raskin, 1973) as a measure of arousal/ stress to physical/psychic stimulation. The purpose of this investigation was to examine further ANS responsivity in alcoholics in relation to skin conductance activity to repeated presentations of high intensity auditory stimuli with specific interest being focused on the hypothesis that alcoholics would exhibit lower resting tonic levels and reduced nonspecific responsivity together with attenuated phasic responses and faster response habituation. Requests for reprints should be sent to Verner J. Knott, patient Dept., 1145 Carling Avenue, Ottawa, Canada, KlZ 7K4. 181
Royal Ottawa Hospital,
Adult Out-
182
VERNER J. KNOTT and DAVID R. BULMER
METHOD
Subjects The nonalcoholics were 15 healthy male adults who were receiving no medication and drank only modest quantities of alcohol on social occasions. Their mean age was 35.9 years (range: 25 to 52). All subjects were required to refrain from tobacco, food and beverages 12 hours prior to test time (9:00 a.m.-12:OO p.m.) The 15 male alcoholics were inpatients at the Alcohol and Drug Treatment Unit of the Royal Ottawa Hospital. The mean age was 40.0 years (range: 24 to 56 years). To qualify for study, all patients had to have been free from alcohol and prescribed medication for a minimum of 2 weeks prior to testing and have had no history of drug abuse. The alcoholics’ drinking histories were positive with respect to one or more of the following characteristics: previous imprisonment or hospitalization for drinking; spree drinking within the last 5 years; interrupted work history due to excessive drinking, and family strife due to drinking. All had evidence of physical dependence on alcohol as indicated by amnesia, blackouts and a history of one or more episodes of severe alcohol withdrawal syndrome. All patients had a withdrawal syndrome on admission to the unit consisting of tremor, agitation, sweating, gastrointestinal disturbance and some had a brief period of hallucinations or delirium. All had raised levels of liver enzymes at the time of admission. The results of neurological, psychiatric and psychological examination were carefully screened to exclude alcoholics exhibiting signs of neurological disease or psychotic disorders. Attempts were also made to exclude alcoholics with medical complications such as hepatic, renal, pulmonary, cardiac, gastrointestinal, genitourinary or serious nutritional or metabolic disorders. Apparatus Electrodermal activity was measured with the aid of a Beckman R-61 1 polygraph and an associated 9844 skin conductance coupler. Skin conductance was recorded directly in umhos by applying a constant 0.5-volt source to a pair of miniature Beckman Biopotential Ag/AgCl skin electrodes, which were attached with adhesive collars to the mid-phalangeal sites of the third and fourth fingers of the nondominant hand. A 0.5% potassium chloride paste mixed with agar was used as the external electrolyte. An additional electrode was placed on the forehead to serve as a ground. The maximum amplifier gain setting was 0.05 uhmos/cm. Stimuli were presented through headphones via a tone generator, which was triggered by a tape-recorded series of 400 Hz triggers with quasirandomised intervals between 20 and 60 sec. The first 12 stimuli were 1-set duration, 1000 Hz tones, with rise and decay times of 5 msec and an intensity setting of 100 dB (re: .002 dyne/cm*). Stimulus 13 was a “dishabituation” tone and was identical to the previous 12 stimuli with the exception that it was set at a lower frequency of 500 Hz and it was inserted in order to examine re-orientation following reduced responsivity to repeated identical stimuli. Procedure Immediately following electrode application subjects were placed in a reclining chair and were instructed to remain relaxed and to ignore the tones. For all recordings a 5-minute interval preceded the onset of the first stimulus. Data reduction Tonic skin conductance levels (SCL) were measured at the onset of each of the 13 stimuli. Phasic stimulus-specific skin conductance responses (SCR) to each stimuli
183
Repetitive high intensity stimulation
were measured with a response being defined as an increase in conductance greater or equal than 0.05 uhmos between 1 and 5 set after the stimulus onset. Amplitudes of SCRs were defined as the highest point within 4 set of response onset minus the SCL at response onset. In addition to the frequency of SCRs, frequency to habituation was also measured, and was defined as the number of responses until a criterion of three successive failures to respond. Dishabituation was assessed calculating the ratio of the response amplitudes to the 12th and 13th stimuli. Response fluctuations of .05 uhmos or greater appearing outside the period defined for SCRs were labelled non-specific skin conductance responses (NSSCR) and were counted for 1 min prior to the 1st stimulus and for the total stimulation period between stimuli 1 and 13. In addition to these measures, the following time-related measures were obtained for the 1st stimulus: latency, defined as the time elapsing between stimulus onset and response onset; rise time, the time elapsing from latency to peak response; recruitment, defined as the rate of response increase and calculated by dividing amplitude by rise time; half-recovery time, the time between the peak of the response and the point half way to the return to baseline. Statistical analysis of SCLs and SCRs were carried out by separate 2 (Group) x 13 (Stimuli) split-plot factorial ANOVAs. The remaining measures were subjected to t tests and a .05 (one-tailed) rejection region was adopted for all statistical tests. The functional relationship of SCLs and SCRs to stimuli was also examined by calculating the slope of these measures for each subject using a simple linear regression model. RESULTS
Mean resting skin conductance levels for alcoholics and controls are shown in Figure 1. Analysis of skin SCLs yielded significant stimulus (F = 2.59, df = 12/324,
.50
t
.45 .40 1
0
” 1
2
”
3
4
’ 5
1” 6 7
TRIALS
8
” 9
‘1’
10 111213
I
2
3
4
5
6
7
8
9
10 11 1213
TRIALS
Fig. 1. Mean skin conductance levels (XL: uhmos) and skin conductance responses @CR: uhmos) of alcoholics and normal controls across trials.
184
VERNER
J. KNOTT and DAVID R. BULMER
p < .003) and stimulus x Group interaction effects (F = 2.59, df = 12/324, p < .003). Additional t tests indicated that although significant differences were ap-
parent between groups prior to the first stimulus onset, normal controls exhibited significant increases in conductance levels at stimuli two (t = 3.8, df = 14, p < .OOS), three (t = 3.1, df = 14,~ < .005), four (t = 4.0, df = 14,~ < .OOS)and five (t = 1.84, df = 14, p < .05). Alcoholics did not exhibit any significant increases in tonic conductance levels throughout stimulus presentation. This was further substantiated with analysis of regression lines for SCL, in that significantly steeper XL slopes (t = 2.02, df = 27, p < .05) were observed for normal controls (mean - .041, f .Ol SD) than alcoholics (mean - .0007, f .02 SD) and in fact the average regression coefficient for the alcoholics did not significantly differ from zero. Similar results were shown with the analysis of NSSCRs. Although no significant differences were observed between groups prior to stimulus presentation, significant effects were observed during stimulation (t = 2.16, df = 27, p < .025) with normal controls exhibiting a greater number of spontaneous responses (mean 5.73, f 9.0 SD) than alcoholics (mean 1.25, f 3.2 SD) and in addition, a significantly greater number (x2 = 12.5, df = 1, p < .OOOS)of normal controls (80%) exhibited NSSCRs during stimulation than alcoholics (14.3%). Although normal controls appeared to exhibit larger responses than alcoholics, analysis of SCRs indicated a significant stimulus effect (F = 17.1, df = 12/324, p < .OOOl) but no Group or interaction effects. Analysis of response frequency and trials to habituation did however yield significant differences in that the average number of stimulus elicited responses was significantly greater (t = 1.75, df = 27, p < .05) for normal controls (mean 7.73 f 0.73 SD) than alcoholics (mean 4.29 f 1.20 SD) and the number of trials to habituation was significantly less (r = 2.1, df = 27, p < .05) for alcoholics (mean 4.36, f 1.19 SD) than for controls (mean 7.60, f 1.10 SD). Significant differences were also observed with the dishabituation index in that normal controls evidenced greater re-orientation than alcoholics (t = 2.03, df = 23, p < .05). No significant group differences were observed with the SCR regression measure. Analysis of temporal measures related to responsivity to the first stimulus indicated no significant differences for latency, rise time, recruitment or recovery indices. DISCUSSION
The present study attempted to determine whether electrodermal indices can differentiate alcoholics from normal controls. In general, there appeared to be a pattern of hypo-responsivity characterising alcoholics as they exhibited no significant changes in tonic levels with the onset of aversive stimulation and evidenced minimal changes in spontaneous fluctuations. In addition, although the groups did not differ with respect to magnitude or responsivity to the high intensity stimuli, alcoholics did differ from normal controls in that they responded with less frequency to the aversive stimuli and they took a fewer number of trials to habituate to these stimuli. This attenuated electrodermal responsivity in alcoholics supports the findings of reduced pupillometric responsivity observed by Rubin and colleagues (1977, 1978, 1980) and argues against the TRH which predicts alcoholics to be hyper-responsive. Finally, as there appears to be no doubt that sweating in man by eccrine sweat glands is mediated through a cholinergic sympathetic innervation (Venables & Christie, 1973), these findings seem to support those of Rubin and colleagues which emphasize the key role of reduced sympathetic activity in differentiating alcoholics and controls.
Repetitive high intensity stimulation
185
REFERENCES Cappel, H., & Herman, C.P. (1972). Alcohol and tension reduction: A review. Quarterly Journal of S&dies on Alcohol,
33, 33-64.
Higgins, R. (1976). Experimental investigations of tension-reduction models of alcoholism. In G. Goldstein & C. Neuringer (Eds.), Empirical studies in alcoholism. Cambridge: Ballinger. Naitoh, P. (1972). The effect of alcohol on the autonomic nervous system of humans; psychophysiological approach. In B. Kissin & H. Begleiter (Eds.), The biology of alcoholism, Vol. 2. Physiology and behavior. New York: Plenum. Rubin, LX, Gottheil, E., Roberts, A., Alterman, AI. & Holstine, J. (1977). Effects of stress on autonomic reactivity in alcoholics; pupillometric studies. I. Journal of Sfudieson Alcohol, 38, 2036-2048. Rubin, L.S., Gottheil, E., Roberts, A., Alterman, A.I. & Holstine, J. (1978). Autonomic nervous system concomitants of short-term abstinence in alcoholics; pupillometric studies. II. Journal of Studies on Alcohol, 39, 189551907. Rubin, L.S., Gottheil, E., Roberts, A., Alterman, A.I. & Holstine, J. (1980). Efects of alcohol on autonomic reactivity in alcoholics; pupillometric studies. III. Journal of Studieson Alcohol, 41, 61 l-622. Venables, P. & Christie, M. (1973). Mechanisms, instrumentation, recording techniques, and quantification of responses. In W. Prokasy & D. Raskin (Eds.), Electrodermal activity in psychological research. New York: Academic Press. Prokasy, W., & Raskin, D. (1973). Electrodermal activity in psychological research. New York: Academic Press.