[An attachment to the impulse stimulator ISE-O1 for the study of the critical frequency of the fusion of light flickers and phosphene].
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Accommodation, Ocular↗
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The different effects of aging on normal sensitivity in flicker and light-sense perimetry.
PURPOSE: To verify whether or not an accelerated loss at an older age for normal sensitivity in the central visual field is present when using the stimulus configuration of conventional white/white automated light-sense perimetry and the stimulus configuration of the automated flicker perimeter developed by one of the authors (BJL). METHODS: One hundred thirty eyes of 130 normal subjects aged 9 to 86 years were tested with the Humphrey-Field-Analyzer 640, program 30-2, and our automated flicker perimeter. In addition, short introductory learning programs were used for both techniques. All tests were performed in random order. RESULTS: Mean critical flicker fusion frequency shows a linear loss over the entire age range (r = -0.5546, P < 0.0001, slope a = -0.3820 dB/decade), whereas mean light difference sensitivity decreases only slightly up to 46 years of age (r = -0.0118, P = 0.9226, slope a = -0.0153 dB/decade), with a marked acceleration above 46 years of age (r = -0.7304, P < 0.0001, slope a = -2.0640 dB/decade). CONCLUSIONS: The absence of an accelerated loss at an older age for critical flicker fusion frequency (CFF) and the presence of such a loss for light-difference sensitivity (LDS) might be attributed to the independence of a flickering stimulus from distributing effects induced by the ocular media at an older age as proposed by one of the authors. The different age effects for CFF and LDS could also be explained by different age-related losses at different sites and for different neuronal populations throughout the visual pathways.
Adolescent↗
The effects of paroxetine, alone and in combination with alcohol on psychomotor performance and cognitive function in the elderly.
Fifteen healthy male volunteers aged over 60 years received acute and repeated doses of paroxetine 20 mg or placebo, and acute doses of lorazepam 1 mg (as a positive internal control) with or without alcohol (0.6 g/kg of body weight) administered openly in a double blind balanced crossover study in which each subject acted as his own control. Psychomotor performance and cognitive function were assessed using a test battery which included critical flicker fusion, choice reaction time, compensatory tracking, Stroop and memory scanning tests. Subjective ratings of mood and sleep were recorded using line analogue rating scales. The pattern of results indicated that paroxetine had little or no effect on most of the test variables, and in some instances (critical flicker fusion thresholds) improved information processing ability. This was in marked contrast to the lorazepam verum which produced sedation and disruption of performance. Paroxetine had a slight antagonistic effect on alcohol induced sedation whereas impairment of performance with lorazepam was potentiated by co-administration of alcohol. The low behavioural toxicity of paroxetine in elderly volunteers has important implications for the pharmacotherapy of depression.
Aged↗
The shape of the high frequency flicker sensitivity curve.
For a light flickering with a modulation amplitude delta L, there is a single frequency f above which the light appears steady (fused). The relationship between delta L and f has been measured often under a variety of conditions, but its mathematical form is disputed. Three candidate functions have been proposed: (1) log delta L alpha f [Ferry-Porter law], (2) log delta L alpha f1/2 [diffusion model], and (3) log delta L alpha log f [cascaded integrator model]. Although all three functions roughly fit flicker fusion data (after appropriate linear transformation), they differ in curvature. We compared these functions using the general expression (4) log delta L alpha f lambda, where lambda denotes a curvature parameter. Functions (1)-(3) are special cases of (4) with lambda = 1, 0.5, and 0 respectively. When applied to 35 sets of flicker fusion data, the mean values of the best fitting lambda for each data-set was 0.919 (95% confidence interval 1.027 to 0.812). We conclude that the Ferry-Porter law describes most data better than a diffusion model, and that an integrator model deviates consistently in every case.
Flicker Fusion↗
Effects of lorazepam on memory, attention and sedation in man: antagonism by Ro 15-1788.
In this study we examined the effects of lorazepam (2.0 mg PO) plus either placebo or one of three doses of the benzodiazepine antagonist Ro 15-1788 (0.3 mg, 1.0 mg or 3.0 mg IV) on measures of memory, attention and sedation. We found that lorazepam impaired verbal secondary memory performance, but also produced subjective and objective sedation; it increased reaction time, reduced critical flicker fusion thresholds and caused subjects to make more errors on a sustained attention task and rate themselves as drowsy. Ro 15-1788 dose dependently blocked the deficit in secondary memory produced by lorazepam, but also showed monotonic dose-related antagonism of its effects on indices of sedation (with the exception of the critical flicker fusion deficit, which was unaffected). These results demonstrate that lorazepam-induced cognitive deficits can be blocked by a benzodiazepine receptor antagonist. They also suggest that the memory deficits produced in this pharmacological model of organic amnesia are not readily dissociated from deficits in attention.
Adolescent↗
Diazepam suppresses the acquisition but not the expression of 'fear-potentiation' of the acoustic startle response in man.
Sudden auditory stimuli elicit a short-latency muscular response (acoustic startle response) which is enhanced during presentation of a Pavlovian conditioned stimulus (CS) that has previously been paired with an aversive unconditioned stimulus (US) ('fear-potentiation'). In rodents, acute treatment with benzodiazepines blocks both the acquisition of fear-potentiation and the expression of fear-potentiation induced by prior exposure to CS/US pairing. We examined the effect of diazepam on the acquisition and expression of fear-potentiation of the acoustic startle response in man. Forty-six male volunteers (18-30 years) participated in two sessions separated by 7 days. In session 1, they were exposed to 20 2-s presentations of a light (CS), 50% of which terminated with an electric shock to the wrist (1.8 mA, 50 ms: US). Somatosensory potentials evoked by the US were recorded from the scalp at Cz, and skin conductance responses from electrodes taped to the second and fourth fingers. In session 2, the CS was presented 20 times without the US; a random 50% of CS presentations terminated with a sound pulse (40-ms 115-dB 1-kHz); an equal number of sound pulses was presented without the CS. Electromyographic responses of the orbicularis oculi muscle to the acoustic stimuli were recorded from electrodes placed on the lower eyelid, late-latency auditory evoked potentials were recorded at Cz, and skin conductance responses from electrodes taped to the second and fourth fingers. In each session, alertness was measured using visual analogue self-rating scales and critical flicker fusion frequency. Subjects received placebo or diazepam 10mg in the two sessions in a double-blind protocol: group 1 (n 12) placebo/placebo; group 2 (n 11) placebo/diazepam; group 3 (n 12) diazepam/placebo; group 4 (n 11) diazepam/diazepam. Diazepam reduced alertness as measured by visual-analogue self-rating scales and critical flicker fusion frequency. In session 1, diazepam reduced the amplitude of the somatosensory potentials and skin conductance responses evoked by the CS. In session 2, the acoustic startle response, the N1/P2 auditory evoked response and the skin conductance response evoked by the sound stimuli were enhanced in the presence of the CS. This fear-potentiation was attenuated in subjects who received diazepam in session 1, but was not affected by the treatment given in session 2. The results indicate that diazepam blocks the acquisition of fear-potentiation of startle responses in man, as in animals, but does not prevent the expression of a previously learned response.
Acoustic Stimulation↗
The effects of acute doses of fexofenadine, promethazine, and placebo on cognitive and psychomotor function in healthy Japanese volunteers.
BACKGROUND: Genetic variations in cross-cultural metabolic capability may attenuate the lack of central nervous system effects of fexofenadine. OBJECTIVE: To compare the pharmacodynamics of fexofenadine and promethazine versus placebo in Japanese volunteers. METHODS: In this randomized, crossover, double-blind study, 24 subjects received single doses of fexofenadine 60 mg and 120 mg, promethazine 25 mg, and placebo, with a 6-day washout period between treatments. Objective measures included critical flicker fusion, choice reaction time, and a compensatory tracking task. A line analog rating scale evaluated self-rated sedation. A rapid visual information-processing task evaluated vigilance at baseline and at 2 hours. RESULTS: Fexofenadine was not significantly different from placebo on any test at any timepoint. In contrast, promethazine impaired critical flicker fusion thresholds (F[3,63] = 5.37, P = 0.0023); increased recognition reaction time (F[3,63] = 13.63, P < 0.0001) and total reaction time (F[3,63] = 12.23, P < 0.0001) components of the choice reaction time test; reduced tracking accuracy (F[3,63] = 14.25, P < 0.0001) and increased reaction times to peripheral stimuli (F[3,63] = 9.29, P < 0.0001) in the compensatory tracking task; reduced the number of valid responses (F[3,63] = 14.86, P < 0.0001) and impaired reaction times (F[3,63] = 12.02, P < 0.0001) in the rapid visual information-processing task test; and impaired subjective ratings of sedation (F[3,63] = 7.55, P = 0.0002), compared with placebo. CONCLUSIONS: A battery of tests sensitive to impairment by promethazine failed to show any negative cognitive or psychomotor effects with fexofenadine 60 and 120 mg. Fexofenadine is an intrinsically non-impairing antihistamine in Japanese subjects.
Adult↗
Effects of quetiapine and haloperidol on prepulse inhibition of the acoustic startle (eyeblink) response and the N1/P2 auditory evoked response in man.
Contraction of the orbicularis oculi muscle in response to a sudden loud sound (acoustic startle response) and the N1/P2 component of the auditory evoked potential are both attenuated when a brief low-intensity stimulus is presented 30-500 ms before the 'startle-eliciting' stimulus (PPI). Here, we report the effects of the 'atypical' antipsychotic drug quetiapine and the 'conventional' antipsychotic haloperidol on these responses. Sixteen males (aged 19-38 years) participated in four sessions at 7-day intervals, in which they received quetiapine 12.5 mg, quetiapine 25 mg, haloperidol 3 mg and placebo, according to a balanced double-blind design. Electromyographic (EMG) responses of the orbicularis oculi muscle and N1/P2 auditory evoked potentials were recorded in a 20-min session, 2 h after treatment. Subjects received 40 trials in which 1-kHz sounds were presented: (i) 40 ms, 115 dB ('pulse alone' trials) and (ii) 40 ms, 85 dB, followed after 120 ms by 40 ms, 115 dB ('prepulse/pulse' trials). Mean amplitudes of the EMG response and the N1/P2 potential were derived from the pulse-alone trials and, in each case, percentage PPI was calculated. Serum prolactin was measured after each treatment, and autonomic (heart rate, blood pressure, salivation) and psychological (visual analogue self-ratings of mood and alertness, critical flicker fusion frequency) measures were taken before and after each treatment. Quetiapine 12.5 mg and 25 mg significantly reduced the amplitude of the EMG response without altering its inhibition by prepulses; haloperidol had no effect on EMG response amplitude or PPI. Neither drug affected N1/P2 amplitude or PPI of this response. Quetiapine, but not haloperidol, reduced subjective alertness and critical flicker fusion frequency. Haloperidol, but not quetiapine, elevated serum prolactin level. The ability of quetiapine to attenuate the startle response may reflect its sedative action.
Acoustic Stimulation↗
[Therapy of the orthostatic syndrome. Studies using dimepropion-HCI].
We treated 30 patients between 22 to 30 years of age, who showed static labile circulatory disturbances of blood pressure. We carried out a double blind study following a two week schedule using for treatment an "indirect" sympathomimeticum Dimepropion-HCI. Control of therapy was achieved by a testing program which consisted in measuring systolic and diastolic blood pressure as well as the pulse rate. Also, we employed a flickers-fusion-test. Circulation parameters were measured in one-minute-intervals during three periods of 7 minutes each, patients changing from rest to stress (standing up) to rest again. The pulse rate was measured during the fourth minute of each of the three periods. Success of treatment was achieved by reducing the cardiovascular disturbances during upright conditions. The amplitude was broadened, while the pulse rate went up only slightly. The level of flicker fusion rose, indicating heightened physical and mental shape. Side effects of disturbed orthostasis disappeared.
Adult↗
Psychomotor, physiological and cognitive effects of scopolamine and ephedrine in healthy man.
Three placebo-controlled double-blind studies in healthy volunteers were performed to reveal the psychophysiological effects of scopolamine, ephedrine and their combination. Single intravenous dose of scopolamine 6 micrograms/kg (scopolamine hydrobromide 7.4 micrograms/kg) impaired various psychomotor functions both subjectively and objectively. It caused sedation, impairment of coordinative and reactive skills, visual disturbances and impairment of shortterm memory. Oral scopolamine hydrobromide in single doses of 0.3 mg and 0.9 mg, or 0.9 mg b.d. for 3 days, had few effects. A slight impairment of shortterm memory and a decrease in the flicker fusion threshold were seen. The visual nearpoint and pupil diameter were increased and some subjects reported blurred vision and dizziness during treatment with scopolamine 0.9 mg b.d. Scopolamine showed clear cardiovascular effects in all studies: it decreased heart rate and systolic blood pressure. Ephedrine alone and in combination with scopolamine had no deleterious effects. On the contrary, it antagonized the scopolamine-induced impairment in the flicker fusion test and the decrease in blood pressure and heart rate. In sufficient doses scopolamine impairs various psychomotor and cognitive skills. An oral dose of scopolamine hydrobromide 0.9 mg on average has few effects, although they may be very striking in certain individuals. To avoid unwanted effects and diminution in performance by scopolamine, doses less than 0.9 mg should be used.
Blood Pressure↗
Effects of ketanserin and haloperidol on prepulse inhibition of the acoustic startle (eyeblink) response and the N1/P2 auditory evoked response in man.
Contraction of the orbicularis oculi muscle in response to a sudden loud sound (acoustic startle response) and the N1/P2 component of the auditory evoked potential are both attenuated when a brief low-intensity stimulus is presented 30-500 ms before the 'startle-eliciting' stimulus (prepulse inhibition). Here, we report the effects of the serotonin (5-HT)2 receptor antagonist ketanserin and the D2 dopamine receptor blocking antipsychotic drug haloperidol on these responses. Fifteen males (aged 18-35 years) participated in four sessions at 7-day intervals, in which they received ketanserin 20 mg, ketanserin 40 mg, haloperidol 3 mg and placebo, according to a balanced double-blind design. Electromyographic (EMG) responses of the orbicularis oculi muscle and N1/P2 auditory evoked potentials were recorded in a 20-min session, 3 h after ingestion of haloperidol or 1 h after ingestion of ketanserin. Subjects received 40 trials in which 1-kHz sounds were presented: (i) 40 ms, 115 dB ('pulse alone' trials), and (ii) 40 ms, 85 dB, followed after 120 ms by 40 ms, 115 dB ('prepulse/pulse' trials). Mean amplitudes of the EMG response and the N1/P2 potential were derived from the pulse-alone trials and, in each case, percentage prepulse inhibition was calculated. Serum prolactin was measured after each treatment, and autonomic (heart rate, blood pressure, salivation) and psychological (visual analogue self-ratings of mood and alertness, critical flicker fusion frequency) measures were taken before and after each treatment. Ketanserin 40 mg significantly reduced the amplitude of the EMG response and both doses of ketanserin significantly suppressed prepulse inhibition of the response; haloperidol had no effect on EMG response amplitude or prepulse inhibition. Neither drug affected N1/P2 amplitude or prepulse inhibition of this response. Ketanserin, but not haloperidol, reduced subjective alertness and critical flicker fusion frequency. Haloperidol, but not ketanserin, elevated serum prolactin level. These results confirm that prepulse inhibition of the startle response and of the N1/P2 complex have different pharmacological sensitivities. The ability of ketanserin to attenuate the startle response may reflect its sedative action, as other drugs with sedative properties have also been found to attenuate the startle response in man. The ability of ketanserin to suppress prepulse inhibition of the startle response is consistent with previous evidence for the involvement of 5-HTergic mechanisms in the regulation of prepulse inhibition in man.
Acoustic Stimulation↗
The effects of sulpiride on psychomotor performance and subjective tolerance.
In many European countries, the substituted benzamide sulpiride is used with antidepressant indication in the dosage range of 150-300 mg on an outpatient population. This raises the concern of possible impairments of psychomotor performance in this dosage range. To address this question, the psychometric effects of 300 mg of sulpiride in comparison with placebo in 12 healthy volunteers was evaluated in this study. In a randomised, double-blind, two-way, within-subjects (cross-over) design, visuomotor performance was assessed using time estimation, critical flicker fusion, and choice reaction time tasks at baseline and 4 h after oral administration of either 300 mg of sulpiride or placebo. In addition, self-ratings on subjective well-being were obtained. Results were evaluated using analysis of covariance (ANCOVA) with baseline levels as covariates. In healthy subjects, 300 mg of sulpiride caused no alteration in time estimation and choice reaction movement time, whereas critical flicker fusion frequency was lower and choice-reaction decision time were prolonged under medication. Self-rating scales showed no significant differences between sulpiride and placebo. Subjects were not able to tell whether they received placebo or sulpiride. This study indicates that sulpiride is subjectively well tolerated at a dosage of 300 mg. However, using psychometric methods, effects are demonstrable that can be interpreted as a reduction of excitatory arousal without causing the subjective experience of sedation. These results call for caution when prescribing the drug to outpatients.
Acoustic Stimulation↗
Evaluation of the alpha 2-adrenoceptor blocking properties of buspirone and ipsapirone in healthy subjects. Relationship with the plasma concentration of the common metabolite 1-(2-pyrimidinyl)-piperazine.
1. Because the 5-HT1A agonist anxiolytic azapirones have a common alpha 2-adrenoceptor antagonist metabolite, 1-(2-pyrimidinyl)-piperazine (1PP), we measured central and peripheral alpha 2-adrenoceptor dependent responses before and after intravenous administration of 0.15 mg clonidine when healthy subjects were taking buspirone (30 mg day-1 for 4 days and 10 mg on day 5), ipsapirone (15 mg day-1 for 4 days and 5 mg on day 5) or placebo. 2. Clonidine decreased blood pressure, heart rate, oral body temperature, salivary excretion, plasma noradrenaline, 3,4-dihydroxyphenylglycol (DHPG) concentrations, increased plasma growth hormone but did not modify plasma insulin and C-peptide concentrations. Treatments tended to modify only the effect of clonidine on growth hormone (P = 0.07). 3. The azapirones reduced clonidine induced prolongation of choice reaction time (P = 0.015) and tended to antagonise clonidine induced fall in critical flicker fusion frequency (P = 0.066). 4. Only buspirone reduced total reaction time and increased critical flicker fusion threshold measured 12 h after the evening dose and these effects were correlated with the residual plasma 1PP concentration which was higher on buspirone than on ipsapirone (2.76 micrograms l-1, 95% CI:1.3-4.22 vs 0.65 microgram l-1, 95% CI: 0.32-0.98, P = 0.006). 5. Mean AUC of the 1PP plasma concentrations after the last dose of treatments were 3.7 times greater with buspirone than with ipsapirone (P = 0.0011). The AUC ipsapirone/AUC 1PP ratio was 6.45 and the AUC buspirone/AUC 1PP ratio was 0.076.(ABSTRACT TRUNCATED AT 250 WORDS)
Adrenergic alpha-Antagonists↗
The effects of D- and L-fenfluramine (and their interactions with D-amphetamine) on psychomotor function and mood.
This study reports the results on psychomotor functioning of D- and L-fenfluramine alone, and in combination with D-amphetamine, in a placebo-controlled trial on 12 normal male volunteers, in order to investigate their CNS activity in humans. The major findings were that D-amphetamine increased alertness, L-fenfluramine increased unhappiness whilst D-fenfluramine decreased hunger and increased the critical flicker fusion threshold. D-Amphetamine in combination with D-fenfluramine increased the critical flicker fusion threshold and in combination with L-fenfluramine the alerting action was diminished. The differing actions of the fenfluramine isomers and their interactions with D-amphetamine suggest that D-fenfluramine is predominantly serotonergic in its activity, whereas L-fenfluramine may be causing dopamine blockade, reducing certain actions of amphetamine possibly mediated by dopamine receptors. The significance of these results in relationship to the psychopharmacology of serotonin, dopamine, and noradrenaline is discussed.
Adult↗
Effects of haloperidol and clozapine on prepulse inhibition of the acoustic startle response and the N1/P2 auditory evoked potential in man.
Contraction of the orbicularis oculi muscle in response to a sudden loud sound (acoustic startle response) and the N1/P2 component of the auditory evoked potential are both attenuated when a brief low-intensity stimulus is presented 30-500 ms before the 'startle-eliciting' stimulus (prepulse inhibition). Here, we report the effects of the 'conventional' antipsychotic drug haloperidol and the 'atypical' antipsychotic clozapine on these responses. Fifteen males (aged 19-54 years) participated in four sessions at 7-day intervals, in which they received clozapine 3 mg, clozapine 6 mg, haloperidol 3 mg and placebo, according to a balanced double-blind design. Electromyographic (EMG) responses of the orbicularis oculi muscle and N1/P2 auditory evoked potentials were recorded in a 20-min session, 3 h after treatment. Subjects received 40 trials in which 1-kHz sounds were presented: (i) 40 ms, 115 dB ('pulse alone' trials) and (ii) 40 ms, 85 dB, followed after 120 ms by 40 ms, 115 dB ('prepulse/pulse' trials). Mean amplitudes of the EMG response and the N1/P2 potential were derived from the pulse-alone trials and, in each case, percentage prepulse inhibition was calculated. Serum prolactin was measured after each treatment, and autonomic (heart rate, blood pressure, salivation) and psychological (visual analogue self-ratings of mood and alertness, critical flicker fusion frequency) measures were taken before and after each treatment. Clozapine 6 mg significantly reduced the amplitude of the EMG response without altering its inhibition by prepulses. Clozapine 6 mg did not affect the amplitude of the N1/P2 potential, but significantly attenuated prepulse inhibition of that response. Clozapine 3 mg and haloperidol had no significant effect on either response. Clozapine 3 mg and 6 mg, but not haloperidol, reduced subjective alertness and critical flicker fusion frequency. Clozapine 6 mg reduced salivation. Haloperidol, but not clozapine, elevated serum prolactin levels. These results confirm that prepulse inhibition of the startle response and of the N1/P2 complex have different pharmacological sensitivities. The abililty of clozapine to attenuate the startle response may reflect its sedative action. The basis of the abililty of clozapine to suppress prepulse inhibition of the N1/P2 potential remains uncertain.
Acoustic Stimulation↗
Psychomotor skills during subacute treatment with thioridazine and bromazepam, and their combined effects with alcohol.
Twenty paid healthy students volunteered for a doubleblind cross-over trial on the effects of two weeks' treatment with placebo, thioridazine and bromazepam on psychomotor skills. The doses used were thioridazine 10 mg t.i.d. during the first week and 20 mg t.i.d. during the second week, or 6 mg of bromazepam t.i.d. during two weeks choice reaction test, two co-ordination tests, a divided attention test, flicker fusion, and proprioception tests were used. The psychomotor skills were measured in the afternoon of the 7th and 14th day of each treatment, 30, 90 and 150 minutes after the second daily administration of the drug in combination with either an alcoholic or a placebo drink. There were no significant differences between the test weeks. Thioridazine alone resembled placebo and had no major combined effect with alcohol. Bromazepam impaired reactive and co-ordinative skills and attention deteriorated. The combination of bromazepam and alcohol potentiated the deterious effects of the single agents, and this effect was most remarkable at 30 minutes. The subjects also gave exaggerated responses in the proprioceptive tests. No significant alterations were recorded in the flicker fusion frequency after any treatment.
Adult↗
Technique for differentiating cortical hemispheric activity following exercise.
Peripheral Critical Flicker Fusion technology was explored as a basis for inferred differences between right and left cortical hemispheric activity following exercise. 18 subjects underwent three treatments presented in randomized order with 1-wk. intervals in between them. Conditions included a control, 30 min. of steady-state treadmill running, and 20 min. of treadmill running followed by progressively increasing speed until exhaustion intervened. Immediately following each treatment, subjects were given a test of peripheral critical flicker fusion as measured in both peripheral retinal fields. Differences between right and left peripheral retinal field perception were analyzed for the three conditions with a one-way analysis of variance using a repeated-measures design. A significant difference was found among the three treatments for peripheral CFF differences between right and left peripheral fields. A Newman-Keuls test demonstrated a significant shift in cortical activation toward the left hemisphere following the exhaustive exercise. The inferred shift in cortical activity inferred from peripheral CFF, occurs following exhaustive exercise. The left hemisphere was viewed as the dominant locus of cortical activation in that fatigue state.
Adult↗
The internship year: a study of sleep, mood states, and psychophysiologic parameters.
Previous reports have suggested that first-year graduate physicians have a high incidence of psychologic distress and may show cognitive impairment as a result of sleep deprivation. We periodically evaluated 27 interns during their training year to determine amount of sleep, mood states, reaction time, critical flicker fusion, and symptoms of depression. We found the incidence of major depression in our subjects (four of 27) to be lower than previously reported but higher than expected for that age group in the general population. Risk factors for depression during the internship year were history of major depression, female sex, and unmarried status. The only significant change in average mood state was that anger progressively increased during the year. Subjects slept an average of 5.95 hours per 24-hour day during the year. Correlational analysis indicated that, contrary to predictions, performance on reaction time and critical flicker fusion improved with less sleep. At the end of the year, subjects regarded the year as stressful but not more so than had been anticipated.
Adult↗