Reaction Times in Parkinson Disease Kenneth M.
\s=b\ Ten
Heilman, MD; Dawn Bowers, MA; Robert
hypokinetic parkinsonian pa-
tients and ten age- and sex-matched controls were tested, using reaction times with and without a warning signal. The time difference between each was used as a measure of phasic arousal. Both groups' reaction times improved with a warning signal, but there were no differences in reaction-time reduction between the parkinsonian and control groups. These results suggest either that hypokinesia in parkinsonism is not caused by an arousal defect or it is caused by a defect in the "autoevoked" arousal system. (Arch Neurol 33:139-140, 1976)
Although hypokinesia is often the most disabling symptom of Parkinson disease, little is known of its pathophysiology. While rigidity is often associated with hypokinesia,1 each can occur independently.2 Rigidity, therefore, cannot entirely explain the hypokinetic phenomenon. In normal subjects, reaction time is reduced if a warning signal is presented in time to produce alpha blocking (desynchronization) on the electroencephalogram before the re¬ action-time stimulus is presented.3 Thus, the warning signal appears to
reduce reaction time because it in¬ creases arousal,3 thereby making the sensory motor response more ef¬ ficient.34 Denny-Brown1 stated, "In severe degree of all these disorders, akinesia Accepted
for publication May 7, 1975. From the Veterans Administration Hospital (Drs Heilman, Watson, and Greer), and the Department of Neurology (Drs Heilman, Watson, and Greer and Ms Bowers), College of Medicine, University of Florida, Gainesville. Read by title before the 100th meeting of the American Neurological Association, New York, June 1975. Reprint requests to Department of Neurology, University of Florida, Gainesville, FL 32610 (Dr
Heilman).
Downloaded From: http://archneur.jamanetwork.com/ by a University of Pittsburgh User on 06/21/2015
T.
Watson, MD; Melvin Greer, MD
makes a gradual transition to akinet¬ ic mutism." It has been suggested that a defect in alerting or phasic arousal produces akinetic mutism (eg, after bilateral cingulate gyrus le¬ sions).5 This study ascertained whether hypokinetic parkinsonian pa¬ tients have a defect of arousal when tested by this reduction of the reac¬ tion-time paradigm. SUBJECTS AND METHODS Ten subjects with hypokinetic Parkinson disease were age- and sex-matched with ten controls. The warning signal was an 80-dB buzz emitted from a stimulus box for 0.5 second. The reaction-time stimulus was a quick-peak incandescent light. Sub¬ jects were asked to look at the lamp and keep their preferred finger on the tele¬
graph key. They were instructed not to press the key after the buzz, but to press as quickly as possible after the light. A timer started with the light and stopped when the key was depressed. There were three test conditions: (1) no warning signal, (2) a warning signal pre¬ ceding the reaction-time stimulus by 0.5 second, and (3) a warning signal preceding the reaction-time stimulus by one second. These three conditions were randomized during 75 reaction-time trials. The intertrial interval was approximately four sec¬ onds; the 75 trials were given in three blocks of 25 trials each.
RESULTS
The mean reaction times for the ex¬ perimental and control groups for the three test conditions are listed in Table 1. Each score was screened for outliers (anticipations or distractions) by the method of skewness.6 The screened and unscreened data were not different, so the unscreened data were used for the analysis of vari¬ ance. An analysis of variance for the reaction times was performed for the groups (parkinsonian and control)
and conditions (no warning 0.5-second, and 1.0-second
stimuli) (Table 2).
stimulus, warning
Main effects between both groups and warning stimuli conditions were important. Therefore, post hoc comparisons were made, using the Scheffé test.7 Although warning stim¬ uli significantly reduced reaction times (P< .01), there were no differ¬ ences between the 0.5- and 1.0-second warning stimuli. The hypokinetic par¬ kinsonian patients performed signifi¬ cantly more slowly (P < .01) than con¬ trols, with and without warning stimuli. Since performance on this reactiontime task depends, at least in part, on motor
performance,
any motor
or
arousal defect will cause slowing. Motorie slowing occurs not only in re¬ action times without warning signals but also in reaction times with warn¬ ing signals. Therefore, the preceding comparisons do not discriminate the arousal aspect from the visuomotor aspect. Since the same visuomotor processing is necessary for reaction times with and without warning sig¬ nals, the difference between the means of these reaction times should reflect the subjects' changes in arou¬ sal. The reduction of reaction time for hypokinetic patients was 127.1 msec with the 0.5-second warning signals and 125.8 msec with the 1.0-second warning signals; for controls, 120.0 msec with the 0.5-second warning sig¬ nals and 104.0 msec with the 1.0-sec¬ ond warning signals. Scheffé tests in¬ dicated no differences between any of these means. When patients given a regimen of
levodopa (seven) were compared to patients not receiving levodopa (three), reaction-time reductions were not different, but this may just reflect
Table 1.—Mean Reaction Times (in msec) of Parkinsonian and Control Groups for Warning Stimulus Conditions Condition No warning stimulus Warning stimuli 0.5 sec 1.0 Differences No warning stimulus to 0.5 sec No warning stimulus to 1.0 sec
Parkinsonian 487.5
Group
Control Group 377.0
360.4
257.0
sec_361.7_273.0
Table
127.1
120.0
125.8
104.0
2.—Analysis of Variance for Reaction Time Data of Parkinson and Control Groups forThree Warning Stimulus Conditions*
Source Warning stimulus
df 40
Group Subjects
1 18 900
Error Total
...
Sum of Squares
3.803,763.8 2,443,192.6 2,470,554.0 7,459,625.6 16,177,136.0
11.4f 294.7f 16.5f
No warning stimulus, 0.5-second interval between warning stimulus and reaction-time stimulus, and 1.0-second interval between warning stimulus and reaction-time stimulus. *
tP
\s=b\ Ten
Heilman, MD; Dawn Bowers, MA; Robert
hypokinetic parkinsonian pa-
tients and ten age- and sex-matched controls were tested, using reaction times with and without a warning signal. The time difference between each was used as a measure of phasic arousal. Both groups' reaction times improved with a warning signal, but there were no differences in reaction-time reduction between the parkinsonian and control groups. These results suggest either that hypokinesia in parkinsonism is not caused by an arousal defect or it is caused by a defect in the "autoevoked" arousal system. (Arch Neurol 33:139-140, 1976)
Although hypokinesia is often the most disabling symptom of Parkinson disease, little is known of its pathophysiology. While rigidity is often associated with hypokinesia,1 each can occur independently.2 Rigidity, therefore, cannot entirely explain the hypokinetic phenomenon. In normal subjects, reaction time is reduced if a warning signal is presented in time to produce alpha blocking (desynchronization) on the electroencephalogram before the re¬ action-time stimulus is presented.3 Thus, the warning signal appears to
reduce reaction time because it in¬ creases arousal,3 thereby making the sensory motor response more ef¬ ficient.34 Denny-Brown1 stated, "In severe degree of all these disorders, akinesia Accepted
for publication May 7, 1975. From the Veterans Administration Hospital (Drs Heilman, Watson, and Greer), and the Department of Neurology (Drs Heilman, Watson, and Greer and Ms Bowers), College of Medicine, University of Florida, Gainesville. Read by title before the 100th meeting of the American Neurological Association, New York, June 1975. Reprint requests to Department of Neurology, University of Florida, Gainesville, FL 32610 (Dr
Heilman).
Downloaded From: http://archneur.jamanetwork.com/ by a University of Pittsburgh User on 06/21/2015
T.
Watson, MD; Melvin Greer, MD
makes a gradual transition to akinet¬ ic mutism." It has been suggested that a defect in alerting or phasic arousal produces akinetic mutism (eg, after bilateral cingulate gyrus le¬ sions).5 This study ascertained whether hypokinetic parkinsonian pa¬ tients have a defect of arousal when tested by this reduction of the reac¬ tion-time paradigm. SUBJECTS AND METHODS Ten subjects with hypokinetic Parkinson disease were age- and sex-matched with ten controls. The warning signal was an 80-dB buzz emitted from a stimulus box for 0.5 second. The reaction-time stimulus was a quick-peak incandescent light. Sub¬ jects were asked to look at the lamp and keep their preferred finger on the tele¬
graph key. They were instructed not to press the key after the buzz, but to press as quickly as possible after the light. A timer started with the light and stopped when the key was depressed. There were three test conditions: (1) no warning signal, (2) a warning signal pre¬ ceding the reaction-time stimulus by 0.5 second, and (3) a warning signal preceding the reaction-time stimulus by one second. These three conditions were randomized during 75 reaction-time trials. The intertrial interval was approximately four sec¬ onds; the 75 trials were given in three blocks of 25 trials each.
RESULTS
The mean reaction times for the ex¬ perimental and control groups for the three test conditions are listed in Table 1. Each score was screened for outliers (anticipations or distractions) by the method of skewness.6 The screened and unscreened data were not different, so the unscreened data were used for the analysis of vari¬ ance. An analysis of variance for the reaction times was performed for the groups (parkinsonian and control)
and conditions (no warning 0.5-second, and 1.0-second
stimuli) (Table 2).
stimulus, warning
Main effects between both groups and warning stimuli conditions were important. Therefore, post hoc comparisons were made, using the Scheffé test.7 Although warning stim¬ uli significantly reduced reaction times (P< .01), there were no differ¬ ences between the 0.5- and 1.0-second warning stimuli. The hypokinetic par¬ kinsonian patients performed signifi¬ cantly more slowly (P < .01) than con¬ trols, with and without warning stimuli. Since performance on this reactiontime task depends, at least in part, on motor
performance,
any motor
or
arousal defect will cause slowing. Motorie slowing occurs not only in re¬ action times without warning signals but also in reaction times with warn¬ ing signals. Therefore, the preceding comparisons do not discriminate the arousal aspect from the visuomotor aspect. Since the same visuomotor processing is necessary for reaction times with and without warning sig¬ nals, the difference between the means of these reaction times should reflect the subjects' changes in arou¬ sal. The reduction of reaction time for hypokinetic patients was 127.1 msec with the 0.5-second warning signals and 125.8 msec with the 1.0-second warning signals; for controls, 120.0 msec with the 0.5-second warning sig¬ nals and 104.0 msec with the 1.0-sec¬ ond warning signals. Scheffé tests in¬ dicated no differences between any of these means. When patients given a regimen of
levodopa (seven) were compared to patients not receiving levodopa (three), reaction-time reductions were not different, but this may just reflect
Table 1.—Mean Reaction Times (in msec) of Parkinsonian and Control Groups for Warning Stimulus Conditions Condition No warning stimulus Warning stimuli 0.5 sec 1.0 Differences No warning stimulus to 0.5 sec No warning stimulus to 1.0 sec
Parkinsonian 487.5
Group
Control Group 377.0
360.4
257.0
sec_361.7_273.0
Table
127.1
120.0
125.8
104.0
2.—Analysis of Variance for Reaction Time Data of Parkinson and Control Groups forThree Warning Stimulus Conditions*
Source Warning stimulus
df 40
Group Subjects
1 18 900
Error Total
...
Sum of Squares
3.803,763.8 2,443,192.6 2,470,554.0 7,459,625.6 16,177,136.0
11.4f 294.7f 16.5f
No warning stimulus, 0.5-second interval between warning stimulus and reaction-time stimulus, and 1.0-second interval between warning stimulus and reaction-time stimulus. *
tP
