The effect of gender and time-of-day on time perception and mental workload

Two experiments are reported which investigated how subject gender and time-of-day influenced the estimation of duration and the perception of task-related mental workload. In the first experiment, 24 subjects performed a filled time-estimation task in a constant blacked-out, noise-reduced environment at 0800h, 1200h, 1600h, and 2000h, respectively. In the second experiment, 12 different subjects performed an unfilled time estimation task in similar conditions at 0900h, 1400h, and 1900h. At the termination of all experimental sessions, participants completed the NASA Task Load Index workload assessment questionnaire as a measure of perceived mental workload. Results indicated that physiological response, reflected in body temperature change, followed an expected pattern of sequential increase with time-of-day. However, estimates of duration and the perception of mental workload showed no significant effects for time-of-day. In each of the experiments there were significant differences in time estimation and mental workload response contingent on the gender of the participant. These results are interpreted in light of the previous positive findings for circadian fluctuation in performance efficiency and the equivocal findings of a gender difference in time estimation. A unifying account of these collective results is given based on gender by time-of-day interactional effects. An earlier version of this paper was presented at the 32nd Annual Meeting of the Human Factors Society, Anaheim, CA, October, 1988.     

Relationship between religion-related factors and obsessive compulsive disorder

This exploratory study sought to determine whether selected religion-related factors differentiated between 86 patients with obsessive compulsive disorder (OCD), 73 patients with panic disorder, and 292 patients with other psychiatric (non-anxiety) disorders. A standard history questionnaire was used to obtain information from patients concerning religion of origin, involvement in religious activities, religious conflict, and perceived religiousness of parents. It was found that the percentage of patients who reported experiencing religious conflict was significantly higher for the OCD group than for the other two groups. Other findings suggested associations between Catholicism and OCD and between Protestantism and panic disorder, but further research is needed to clarify these relationships. This article is based on a paper presented at the 98th annual convention of the American Psychological Association, Boston, August 1990.     

Is anorexia nervosa a neuropsychological disease?

Evidence for central nervous system, and more particularly cortical, etiology of anorexia nervosa is reviewed. Topics covered are neuropsychiatric comorbidity, inheritance patterns, the neurobiology of body-image disturbance and of the eating function, perinatal and alcoholic insult to the brain, neurochemical and neuroelectric disturbance, anatomic and metabolic brain imaging, and neuropsychological impairment. It is concluded that there is indeed an important neuropsychological etiological dimension to anorexia nervosa. The profile most frequently associated with anorexia nervosa is right posterior hypometabolism, followed by right anterior hypermetabolism, both associated with right-sided abnormal electroencephalogram spiking. It is also proposed that bulimia consists of a positive neurological subtype and that restricting anorexia represents a negative neurological subtype. Priorities for further research into anorexia nervosa are specified to include twin adoption studies, brain electrical topography studies, postmortem histological studies, and experimentally inspired neuropsychological studies.     

Memory deficits in Alzheimer's patients: A comprehensive review

Despite considerable experimental work on Alzheimer's disease (AD), the underlying cognitive mechanisms as well as the precise localization of neuropathological changes critical for memory loss remains undefined. A review of the neuropsychological literature on long-term memory deficits in AD patients suggests that AD patients display (a) a pervasive deficit of explicit memory, (b) a partial deficiency of implicit memory for verbal and visuoperceptual material (as measured by repetition priming procedures), and (c) a substantial sparing of implicit memory for visuomotor skills. The explicit memory loss is likely a result of encoding as well as consolidation difficulties. A faulty lexical-semantic knowledge structure appears responsible for deficient repetition priming effects. Since neuropathological changes diffusely affect the brain of AD patients, establishing a clear relationship between localization of cerebral lesions and memory deficits is particularly difficult. Nevertheless, data suggest that extensive involvement of the hippocampal-amygdala complex plays a major role in explicit memory loss. Damage to associative cortical areas likely is involved in repetition priming deficits. The relative integrity of primary motor and sensory cortical areas and of the basal ganglia likely subsume, by contrast, the normal learning of visuomotor skills.     

Heart rate--QT relationships during baroreceptor stimulation with diminished autonomic influence on the ventricles. Ventricular autonomic tone and QT interval.

The shortening of the QT interval of the electrocardiogram coincident with acceleration of heart rate and vice versa has been accepted for many years as evidence that the action potential duration and hence QT are necessarily dependent on heart rate. Exceptions to this rule have been attributed to the intervention of counteracting autonomic effects. In order to test this assumption, 26 conscious dogs divided into three groups were tested during baroreceptor stimulation by a bolus injection of phenylephrine. Seventeen dogs had been used in earlier studies in which they had undergone an experimental anterior myocardial infarction with apparent full recovery. A group of those dogs underwent beta-adrenergic blockade by intravenous atenolol 30 min prior to the baroreceptor activation. To test the intactness of the baroreceptor responses in the previously infarcted dogs, a third group of nine dogs that had had no prior myocardial infarction was included. All dogs were adapted to the laboratory environment and were not sedated during experiments. Simultaneous recordings of RR, QT interval, and phasic arterial pressure were made in all dogs before and during baroreceptor stimulation. In the normal group, and the previously infarcted group that received no atenolol, baroreceptor stimulation elicited a small (8/msec), but significant prolongation of the QT associated with a nearly 50% reduction in heart rate. The QT interval of the atenolol-treated dogs, although significantly more prolonged before stimulation, remained unchanged during the reflex. The data indicate that withdrawal of ventricular sympathetic tone may prolong the QT interval, thereby confirming the role of sympathetic innervation in the control of QT.(ABSTRACT TRUNCATED AT 250 WORDS)     

Cocaine-induced brainstem seizures and behavior.

A variety of abnormal sensory/motor behaviors associated with electrical discharges recorded from the bilateral brainstem were induced in adult WKY rats by mechanical (electrode implants) and DC electrical current stimulations and by acute and chronic administration of cocaine. The electrode implant implicated one side or the other of the reticular system of the brainstem but subjects were not incapacitated by the stimulations. Cocaine (40 mg/kg) was injected subcutaneously for an acute experiment and subsequent 20 mg/kg doses twice daily for 3 days in a chronic study. Cocaine generated more abnormal behaviors in the brainstem perturbation group, especially the electrically perturbated subjects. The abnormal behaviors were yawning, retrocollis, hyperactivity, hypersensitivity, "beating drum" behavior, squealing, head bobbing, circling, sniffing, abnormal posturing, and facial twitching. Shifts in the power frequency spectra of the discharge patterns were noted between quiet and pacing behavioral states. Hypersensitivity to various auditory, tactile, and visual stimulation was present and shifts in the brainstem ambient power spectral frequency occurred in response to tactile stimulation. These findings suggest that the brainstem generates and propagates pathological discharges that can be elicited by mechanical and DC electrical perturbation. Cocaine was found to activate the discharge system and thus induce abnormal behaviors that are generated at the discharge site and at distant sites to which the discharge propagates. Cognitive functions may also be involved since dopaminergic and serotonergic cellular elements at the brainstem level are also implicated.     

The legal consensus about foregoing life-sustaining treatment: its status and its prospects

The legal consensus that has evolved through adjudication and legislation since the Karen Quinlan case in 1976 is founded on the premise that there is a bright line between passive euthanasia and active euthanasia. Indeed, the term passive euthanasia is often eschewed in favor of less emotionally-laden terminology such as "forgoing life-sustaining treatment" or "terminating life support" so as to further sever any possible connection with active euthanasia. Legal approval has been bestowed upon passive euthanasia under certain circumstances while active euthanasia is routinely condemned. This consensus was put to a test in 1990 when the United States Supreme Court ruled on the Cruzan case. However, the Court's narrow decision did not upset the consensus, and in the most significant appellate decisions handed down by state courts since Cruzan, there has been a reaffirmation--and possibly even an extension--of the consensus. Two other threats to the legal consensus about forgoing life-sustaining treatment have begun to manifest themselves: the increasing pressure for mercy killing and "futility" cases. Both of these challenge the fundamental premises on which the consensus is grounded.