The Journal of Psychology

ISSN: 0022-3980 (Print) 1940-1019 (Online) Journal homepage: http://www.tandfonline.com/loi/vjrl20

Ethanol Induced Slowing of Human Reaction Time and Speed of Voluntary Movemen H. E. King To cite this article: H. E. King (1975) Ethanol Induced Slowing of Human Reaction Time and Speed of Voluntary Movemen, The Journal of Psychology, 90:2, 203-214, DOI: 10.1080/00223980.1975.9915777 To link to this article: http://dx.doi.org/10.1080/00223980.1975.9915777

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Published as a separate and in The Journal of Psychology, 1975, 90, 203-214.

ETHANOL INDUCED SLOWING OF HUMAN REACTION TIME AND SPEED OF VOLUNTARY MOVEMENT* University of Pittsburgh School of Medicine and Western Psychiatric Institute and Clinic

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SUMMARY This study tested the hypothesis that a CNS depressant (ethanol) would affect self-initiated psychomotor movement speed as much as the speed of an homologous movement made in response to an external stimulus. Four normal Ss (three male, one female, aged between 33-45 years) provided well-practiced measures of reaction time and a simple homologous traverse movement (a) in response to a signal from the E and (b) initiated at the S’s own discretion. Performance by each S under ethanol conditions (B. A. L. .22%) was compared with his own baseline (pre- and postdrug) scores. Traverse originated by the S was consistently faster in the nondrug condition. Under peak-ethanol, both forms of traverse were slowed significantly in all Ss. Speed reductions were similar but consistently greater for self-initiated movement. A single S who repeated the experimental sequence under a minimally effective dosage (B. A. L. .08%) showed no important reduction in reactive movement speed, but was slowed significantly in self-initiated traverse measured concomitantly. The selective sensitivity of self-initiated movement to ethanol provides added evidence that a higher level of neural organization underlies control of human voluntary action. A. INTRODUCTION Clinical neurology makes an important distinction between those human actions called “voluntary” and “involuntary” and has contributed extensive evidence on the different ways in which these broad classes of human behavior can be affected by disease or by trauma afflicting the central nervous system (2, 11). One looks in vain for further information on this distinction in modern texts on neurophysiology, psychiatry, or psychology,

* Received in the Editorial Office on April 7 , 1975, and published immediately at Provincetown, Massachusetts. Copyright b y The Journal Press. 203

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however, where a certain unease continues to surround the entire concept of volition-very probably the legacy of years of unresolved philosophic debate over questions of “free-will” versus “determinism” (1, 3, 10). Recent experimental work with animal subjects, such as that of Vanderwolf on the role of limbic-diencephalic mechanisms in the initiation of movement in the rat (13), reminds us that progress can yet be made with questions of the kind when experiments are kept within the range of the operationally definable and the temptation is resisted to solve every philosophic riddle ever posed about existence of “the will” by any single or simple experiment. The present study directs attention to one such facet of volitional control, in the normal human S, by comparing the maximum speeds attainable in executing active and reactive simple effector movements having exactly the same external form, under normal circumstances, at first, and again when the functioning of the central nervous system was momentarily depressed by alcohol. We interested ourselves, recently, in the question of whether an experimentally induced state of mild CNS depression (by means of an ethanol intoxication) would affect the speed of well-practiced voluntary (i. e., active or self-initiated) psychomotor movement in the same way that it would influence the speed of reactive movement (i. e., the identical movement made in response to an external stimulus given by the E ) . The increased latency of reaction time measures recorded during states of alcoholic intoxication is, of course, a well-known and much studied phenomenon (14, pp. 298-303). The causes underlying this regularly observed slowing of psychomotor responsiveness have been interpreted quite differently by different investigators, however, with some writers attributing a primary importance to the limiting effects that alcohol in the CNS may exert on the S’s ability to attend and to focus on signals to respond (14, pp. 298-300), while others have emphasized more the impact that ethanol in the brain may have on response mechanisms per se (14, pp. 300-303).

In the present experiment, reaction time measures were collected at all experimental sittings, but they were not regarded as the principal response under study. They provided, rather, a criterion variable to serve as an index of individual reactivity to the drug and to its dosage. They were systematically factored out of all calculations made of the speed of executing the simple thrust movements that were under scrutiny. Our interest lay in comparing identical space-traversing movements, timed only after they

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had actually begun, not including the interval elapsing between a signal to respond and the beginning of that movement.

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B.

METHOD

The data for each S were considered individually, comparing his speed of movement under ethanol conditions with his own baseline (pre- and postdrug) level of performance. Each volunteer was first instructed in making a simple ballistic thrust-response: an effector movement made with the preferred hand-and-arm, forward and 15” to the right, as quickly as possible on hearing an auditory signal (buzzer, 55 db). Two measures of elapsed time were recorded independently from this single movement: a response that is unitary from the S’s point of view. The interval between onset of the signal tone and lift of the responding hand from its starting position provided a standard measure of (lift) reaction time (4, pp. 16-18), while the interval elapsing between onset of the tone and closing a target key placed 26.6 cm distant yielded a standard measure of ballistic (or jump) reaction time (4, p. 18). A warning (ready) signal always preceded onset of the tone by an interval of 1.5 to 4.0 seconds, varied randomly. If the time taken by an individual S to complete his lift reaction is subtracted from the time needed to complete his ballistic response, the measure derived is called Traverse, Experimenter Cued, and the equation can be represented as follows: Traverse (E-C) = R T (ballistic) - R T (lift). This score represents the air-time, so to speak, of a simple reactive thrust movement: i. e., the interval elapsing between completing lift of the responding hand from the start postition and closure of the distant (target) key. * An identical physical arrangement was also used to record the minimal time taken by the same S to leave a starting position and to cross-and-press a target key, placed at an identical distance and angle, when initiating and executing the thrust movement were entirely at his own discretion. These measures were taken while the S worked at a different test board, at a different experimental sitting. The “stimulus” for making the response was something internal: the S’s voluntary beginning of an otherwise homologous motion. An identical auditory tone (buzzer, 55 db) automatically accompanied this active movement, the sound beginning only as the movement itself was launched (i. e., after lift of the hand from the starting I

The basis for deriving this measure has been more completely described elsewhere (6).

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position had been completed). This interval, called Traverse, Subject Cued, represents the air-time taken for the simple active thrust movement under study, as shown in the following equation: Traverse (S-C) = interval between lift from start key and closure of target key. Daily practice in performing each of these simple hand-and-arm movements allowed stable, baseline speeds to be established for each S on each measure. Very little learning is observed in the execution of movements of this kind, as a rule (4, 6), and the performance speeds of our normal, volunteer Ss (three male, one female, aged between 33-45 years) were observed to be reliable-in terms of both mean response and intraindividual variability-well before introduction of the experimental condition of ethanol intoxication. The desired level of blood alcohol (B. A. L. .22%) was achieved by carefully measured oral dosages, determined for each individual S by sex and by weight with use of Widmark’s formula for r (14,p. 44). The dose was 1.33 g/kg in isotonic solution, taken as rapidly as was comfortably possible (all Ss < 3 minutes), Ingestion was at 10 AM,the S fasting, except for a small portion of orange juice taken at least two hours earlier. All Ss were volunteers, medically examined and free of barbiturates or antihistamines in the body at the time of testing. Expected clearance time was about 300 minutes; all Ss were driven to their homes 7.5 hours postingestion. Test times were preselected to reflect phases of the ideal blood-alcohol curve, to sample (a) the absorption phase, ( b ) plateau, (c) diffusionequilibration, and ( d )elimination phase [see Wallgren and Barry (14,p. 45)]. One S repeated these procedures at a lower dose level (B. A. L. .08%) after a six month delay. The higher dosage was selected to produce an unequivocal state of intoxication in all Ss. The lower dose was calculated to produce a minimal, but significant, slowing of the criterion variable (lift reaction time), to allow an exploratory glimpse of the influence, if any, of a less disrupting quantity of ethanol in the bloodstream on the two kinds of space traversing movement under study.

C. RESULTS A systematic slowing of the criterion variable, lift reaction time (RT), was easily apparent in the performance of all Ss over the first hour (approximately) postingestion of alcohol, followed by a gradual return to the predrug baseline values over the succeeding six hours (Figure 1).2 The A notable exception to the pattern of recovery within the same test-day can be seen in the

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FIGURE 2 EXPERIMENTER-CUED (E-C) AND SUBJECT-CUED (S-c) TRAVERSE BEFORE,DURING,A N D AFTERTHE INGESTIONOF ETHANOL(B. A. L. .22%): TIME IN MILLISECONDS

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experimental intervals. When the data are displayed in this way, a visual impression can be gained of several salient features of these two measures: (a) baseline rates of speed, (b)intratest and intertest variability, (c) response slowing during peak-ethanol conditions, and (d) relative reduction of speed during ethanol conditions. All of the means recorded under peak-ethanol conditions differed significantly3 from the baseline performance for that individual for both forms of traverse movement observed. It is clear, from Figure 2, that the baseline (nondrug) speed of traverse for any given S was quite similar-whether the movement was cued by a signal from the E or initiated by the S himself. Traversing the identical physical distance was slightly, but consistently, faster when the S launched the movement himself. This was true for each individual in this small series, and the means for their combined performance reflected that difference as well. The slightly faster self-initiated traverse of space observed was in accord with the (reliably) lower mean speeds reported for the same measures when applied to a larger group of normal Ss (6, pp. 222-223). Although reductions in speed for both forms of traverse during peak ethanol conditions appeared to be of similar magnitude, the originally slightly faster measures of self-initiated traverse were somewhat more affected by ethanol conditions than was the same movement when cued by the E. Traverse (E-C) was slowed by 45%, overall, while Traverse (S-C) was reduced by 55%. No statistical test was applied to appraise the significance of this overall difference, as the focus of the experiment was on individual performance. The fact that all Ss were originally faster in traverse that they initiated themselves and were proportionately more slowed on self-initiated traverse under ethanol conditions would make it appear that this is the more sensitive of the two similar measures to disruption by alcohol in the body. The indices of intraindividual variability were also very similar for both measures for each S during the nondrug baseline condition and were similarly affected by ethanol conditions. Baseline intraindividual variability was consistently greater for E-cued traverse by a factor of approximately one and a half. The intraindividual variability of Traverse (E-C) trials was increased by a factor of 1.67, overall, during the ethanol condition-compared with a peak increase of 1.45, overall, for Traverse (S-C) trials. All mean speed scores were slowed to a value at least three times the standard deviation of that individual’s baseline performance calculated on the basis of his performance recorded the day before, preingestion on the test day, and again on the day after alcohol had been experimentally consumed.

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EXPERIMENTER-CUED (E-C) AND SUBJECT-CUED (s-c)TRAVERSE BEFORE, DURING, AND AFTER THE INGESTION OF ETHANOL (B. A. L. .08%): TIMEIN MILLISECONDS

The record of performance by the single S to receive a second, minimally effective ethanol dose (B. A. L. of .08%) is given in Figure 3. This amount of alcohol proved sufficient to produce a just-significant slowing of the criterion variable: lift reaction time. Traverse cued by the E showed no important change under this weakened ethanol condition, while the simultaneously observable slowing of self-initiated traverse departed significantly (by t test) from baseline. Although fewer trials were run at this reduced dose-level, and it was attempted with only a single S , the observation is consistent with the view that self-initiated traverse may be the more sensitive of the two measures to the action of ethanol on the CNS.

D. DISCUSSION What do these findings suggest about levels of psychomotor response organization that may exist within the normal, optimally functioning individual? The execution of specific, well-practiced, simple thrust movementsover a carefully predefined physical space-has shown that the speed of completing either response is much the same, whether the movement is initiated voluntarily or is made on cue from the E . The traverse times recorded were quite similar in the normal (nondrug) condition, but they were not identical. Traverse was consistently slightly faster when originated by the S himself. This relative advantage, in favor of the speed of active (voluntary) movement, has also been reported to typify the performance of a much larger sample of normal Ss studied earlier by the same

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simple test methods (6). Moreover, when the Ss in the present experiment were asked to continue to make the same, well-practiced thrust movements under experimentally induced suboptimal circumstances-ethanol in the body at a dose level sufficient to intoxicate them and to slow the latency of lift reaction reliably-both Traverse (E-C) and Traverse (S-C) were observed to be significantly slowed concomitantly. Self-initiated traverse was the more affected of the two, demonstrating (overall, for this small series) a 10 percent greater reduction in response completion time. This modest but consistent difference appeared to result primarily from a loss of the initial speed advantage shown by voluntary traverse (i. e., being slightly faster in the baseline, nondrug state). Under ethanol conditions, the maximum speeds attained by a given S became nearly identical for both forms of traverse movement observed (Figure 2). Lowering the dose of ethanol in the body-from an amount clearly intoxicating, to a blood-alcohol level barely adequate to slow the criterion variable reliably-produced a significant slowing of S-cued traverse time in the performance of the single S observed, but did not influence notably the speed of traverse cued by the E for that same S at that same time. These three summary statements (self-initiated response (a) is faster in the nondrug state, (b) is slowed more at high blood-alcohol levels, and (c) appears to be more sensitive to low dose-levels of blood-alcohol) accord well with Hughlings Jackson’s concept of a hierarchical functional arrangement of motor control within the CNS, in which a higher level of neural organization is required to control those actions that are called voluntary (12). Injury to the higher and phylogenetically younger levels of CNS organization is more likely, by the Jacksonian principle, to affect the voluntary actions of man than it is to influence his more routinized, overlearned, or automatic responses. The demonstration, in this experiment, of a differential effect of ethanol on active and reactive movement provides a (reversible) parallel to certain observations earlier made on patients afflicted with neurological disorders known to affect the voluntary movement system. When the same two forms of traverse measure described here were applied to paralysis agitans patients [Parkinson’s disease, characterized by muscular tremor, rigidity, and delay of voluntary movement (15)], an impairment of speed, when compared to the performance of matched control Ss, was evident for both forms of traverse, despite a virtually normal latency for lift reaction time. Traverse initiated by the S himself was severely disrupted (slowed by 50 percent), while homologous

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traverse movements cued by the E were reduced, simultaneously, only about half that much (slowed 25 percent) below the level of matched normal controls ( 5 ) . Finally, an attempt was made to discover the factorial loading of this new measure, within the domain of thefine psychomotor abilities (4, 7), by making an analysis of its pattern of infercorrelation with a number of other, more familiar tests of psychomotor and intellectual function. When applied to a sample of normal Ss as part of a larger battery of tests [including the Wechsler-Bellevue and Porteus Maze tests; measures of reaction time, tapping, and finger dexterity; the Trail-Making test; rated observations on test-taking behaviors; and measures of years of age and formal education (7)], a tentative identification was offered of its placement with regard to the three subfactors reported to typify fine psychomotor ability (in which speed or accuracy of movement, rather than strength or stamina, is in focus). Traverse movements initiated by the subject himself appeared to fall closest to Factor 11 (speed of stereotyped, wrist-arm movement), which is usually sampled by a test of tapping-speed (4). The relationship was a quite moderate one, however (a Pearson r of .43 with tapping-speed). There were even weaker bonds to Factor I (speed of initiating movement), an r of .28 with lift reaction time, and Factor 111 (precision in fingertip movement), an Y of .27 with the Assembly score on the Purdue Pegboard (7). The two forms of traverse are themselves certainly related (r = .61), but, it may be noted again, they are not identical measures. It appears that lift and jump reaction time (and the derived measure that they provide of traverse cued by the E ) sample some basic speed factor, which is typical of the speed that an individual shows in completing what Woodworth has termed “a prepared reflex” [in which the signal to respond triggers a preset response (16, pp. 305-306)]. Measures of S-cued traverse, in which the S provides both the set for response and the signal to release it, seem more akin to “what is ordinarily termed a willed act” (6, p. 225). Either form of measurement applies only to the “tail-end” of observable traverse motion, of course, and yields only a measure of the time elapsing between the external indication that a movement has actually begun and its specified end. And yet, these fragments of response appear to be sensitive to, and to differentiate between, more than one difference in conditions prevailing within the organism at the moment they are sampled. It is understandable that these two forms of traverse should resemble each other; what is unexpected is their difference. It will be necessary, of course,

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to probe further with these two measures into a variety of experimental and/or clinical conditions before any clear idea can be formed about just what aspects of psychomotor function they may actually represent. Despite a seeming simplicity, they have already shown appreciable promise as analytic tools by their selective sensitivity to pathologically or experimentally induced suboptimal conditions within the host. Tests of reactive psychomotor speed have served, over many years, as reliable and sensitive indicators of human suboptimal functioning, whether these states are brought about by physiological or pathological variables (8, 9). Continuing their use-while simultaneously extending our experimental observations into the realm of active, voluntary movement-should inform us more completely about the differing levels of neural organization that underlie the patterning of observable human movement.

REFERENCES ACH, N. Analyse des Willens. Berlin: Urban & Schwartzenberg, 1935. Abteilung VI, Teil E. 2. GARCIN,R. Coordination of voluntary movement. In P. Vinken & G. Bruyn (Eds.), Handbook of Clinical Neurology (Vol. 1). Amsterdam: North-Holland, 1969. 3. KIMBLE, G., & PERLMUTTER, L. The problem of volition. Psychol. Rev., 1970, 77, 1.

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KING, H. E. Psychomotor Aspects of Mental Disease. Cambridge, Mass.: Harvard Univ. Press, 1954. 5. . Defective psychomotor movement in Parkinson’s Disease: Exploratory observations. Percept. 6. Motor Skills, 1959, 9, 326. 6. . Reaction time and speed of voluntary movement by normal and psychotic subjects. J. of Psychol., 1965, 59, 219-227. 7. . Trail making performance as related to psychotic state, age, intelligence, education and fine psychomotor ability. Percept. 6.Motor Skills, 1967, 25, 649-658. 8. . Psychomotility: A dimension of behavior disorder. In J. Zubin & C. Shagass (Eds.), Neurobiological Aspects of Psychopathology. New York Grune & Stratton, 4.

1969.

9. 10. 11. 12. 13. 14.

. Psychomotor correlates of behavior disorder. In M. Kietzman, S. Sutton, & J. Zubin (Eds.), Experimental Approaches to Psychopathology. New York Academic Press, 1975. LANDIS,C., & BOLLES,M. Disorders of volition. In C. Landis & M. Bolles, Textbook of Abnormal Psychology (rev. ed.). New York Macmillan, 1950. LIVERSEDGE, L. Involuntary movements. In P. Vinken & G. Bruyn (Eds.), Handbook of Clinical Neurology (Vol. 1). Amsterdam: North-Holland, 1969. TAYLOR, J., Ed. Selected Writings of John Hughlings Jackson (2 vols.). London: Hodder & Stoughton, 1931. VANDERWOLF, C. Limbic-diencephalic mechanisms of voluntary movement. Psychol. Rev., 1971, 78, 83-113. WALLGREN,H., & BARRY,H. Actions of Alcohol (2 vols.). Amsterdam: Elsevier, 1970.

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WILSON,S. A. K. Neurology (2nd ed., Vol. 11). Baltimore, Md.: Williams & Wilkens,

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WOODWORTH, R. S. Experimental Psychology. New York: Holt, 1938.

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1955.

Western Psychiatric Institute and Clinic University of Pittsburgh 381 1 O’Hara Street Pittsburgh, Pennsylvania 15261