Canadian journal of psychology最新文献

The purpose of this study was (a) to determine if vision and kinesthesis contribute differentially to the coding of a specific two-dimensional pattern and (b) to identify the effect of repetition on the spatial representation of this pattern. The reproductions of a specific pattern presented visually were compared with those of a pattern presented kinesthetically. The results showed that vision and kinesthesis had contributed equally to the coding of the directional components of the pattern. However, there was dominance of visual information over kinesthetic information when coding the distance between the intersecting points of the pattern, especially at the beginning of the process. Generally speaking, the visual or kinesthetic repetition, or both, have increased favourably the precision with which a specific pattern was reproduced in distance and direction.

The brain is the sole organ of homeotherms that do not undergo cell division. We thus have to explain how certain aspects of psychological heredity (found in homozygotes twins raised in different surroundings) may persist for a whole life (psychological individuation). A definitive genetic programming during development (by neurogenesis) is unlikely due to the plasticity of the nervous system. That's why we have to consider the possibility of an iterative genetic programming. The internal mechanisms (synchronous) of paradoxical sleep (SP) are particularly adapted to such programming. This would activate an endogenous system of stimulation that would stimulate and stabilize receptors genetically programmed by DNA in some neuronal circuits. The excitation of these neurons during SP leads to oniric behaviours that could be experimentally revealed--the lists of these behaviours are specific to each individual and indirect data suggest a genetic component of this programming. Amongst the mechanisms allowing the iterative programming of SP, sleep is particularly important. Security--and hence the inhibition of the arousal system--is a sine qua non condition for genetic programming to take place. In that sense, sleep could very well be the guardian of dreaming. On the other hand, sleep seems to be necessary for the accumulation of energetic resources used by the cholinergic mechanisms of SP. The temporal modalities of SP (diachronic organization) are also discussed in relation to phylogenesis. Thus, the absence of SP in poikilotherms is explained by a continual neurogenesis in the adult. During ontogenesis in mammals, a stage of programming by neurogenesis (seismic sleep) precedes the appearance of SP so long as the programming system isn't functional. The presence, or absence, of rebound after SP deprivation is interpreted in terms of the existence, or non existence, of stress during SP suppression. An explanation is proposed to account for the absence of specific effects of SP deprivation in humans. In the same way somatic intraspecific variability is one of the conditions of evolution, it is proposed that one of the functions of SP is to maintain psychological variability in a given population.

It is estimated that up to 10% of the elderly population have clinically significant cognitive deficits. The neuronal pathologies that underlie the dementing disorders cause both cognitive dysfunction and disturbances in normal sleep/wake patterns. Here we report the changes in sleep/wake patterns seen with increasing severity of Alzheimer's disease, probably the most common dementing disorder. In addition, studies examining sleep/wake patterns in a number of other dementing disorders are reviewed.

A model for narcolepsy is developed on the basis of data obtained from brains collected at post mortem from three patients with narcolepsy. The concentration of dopamine, noradrenaline, and serotonin and their metabolites was measured in many brain regions. The number and affinity of the 3-H-spiperone and 3-H-prazocin binding sites was also measured in many of these regions to characterize the D-2 dopamine and alpha-1-noradrenergic receptors, respectively. Evidence for significantly increased serotonin levels and serotonin turnover was found in many brain regions. Noradrenaline turnover was increased in the frontal cortex. DOPAC/DA was significantly reduced in the striatum. The number of D-2 dopamine receptors, however, was markedly increased in this region. The number of alpha-1-noradrenergic receptors was significantly decreased in the frontal cortex and amygdala. Our neurochemical data demonstrating increased NA and 5-HT turnover suggest that locus coeruleus noradrenergic neurones and raphe serotonergic neurones are overactive in narcolepsy. Current evidence posits that increased activity in these neurones depresses the activity of cholinergic pedunculopontine (PP) REM sleep effector neurones. PP neurones project to and stimulate the dopaminergic substantia nigra compacta neurones. Decreased PP activity in narcolepsy, thus, could lead to pontine cholinergic supersensitivity and could also reduce the firing rates of dopaminergic neurones, as the low striatal ratio of DOPAC/DA suggests. An increase in the number of D-2 dopamine receptors in the striatum may result. The reason for the increased activity of the noradrenergic and serotonergic neurones remains to be determined, but immune inactivation of alpha-1-noradrenergic receptors may be the initiating event. Low alpha-1-noradrenergic receptor numbers may account for the chronic drowsiness of narcolepsy. The repeated entry into sleep, and into REM sleep in particular, may represent a homeostatic response to increase these receptor numbers and, thus, to increase alertness. Some therapeutic implications of this model are presented in the discussion.

This research examined the relationship between cortical activation, defined by electroencephalographic (EEG) measures, and the ability to recall dreams following awakenings from Stage 2 sleep. Period-analyzed EEG data from 40 subjects were examined for the preawakening, postawakening, and preawakening-to-postawakening time intervals. Recall differed from nonrecall at the postawakening and preawakening-to-postawakening periods on measures of muscle activity and time spent in the sigma (12-16 Hz) frequency band. There were no distinctions in recall ability on EEG hemispheric asymmetry measures. Generally, the findings do not support the hypothesis linking increased recall ability to increases in cortical activation prior to awakening. However, the recall groups depicted a different pattern of arousal in their transition from sleep to wakefulness.

Six narcoleptic patients were tested three times on the 13-min waking/7-min resisting sleep paradigm each time after a night of sleep in the laboratory. The three experiments were conducted after 10 days without any antinarcoleptic treatment or after 2 weeks of daily treatment with either methyl-phenidate or aniracetam. The results showed that patients had pronounced levels of diurnal sleepiness in all three experimental conditions with a midafternoon peak at around 1300-1500 hr and a nadir at around 1800 hr. Methyl-phenidate significantly reduced REM sleep and marginally reduced total sleep in comparison with the no-treatment and aniracetam conditions. REM sleep in the 7/13 paradigm appeared cyclically with a dominant periodicity of 80 min/cycle. The cycles tended to be synchronized across patients and were unrelated to the temporal structure of total sleep. The present results support the continuation of the REM oscillator during brief periods of waking, but suggest that the REM periodicity is unrelated to Kleitman's BRAC model of arousal.

It has recently been proposed that there is a vulnerable period of time following successful learning when paradoxical sleep (PS) is necessary for learning. This vulnerable time period has been called the PS window. In Experiment 1, the protein synthesis inhibitor anisomycin (ANI) was administered following shuttle avoidance training in the Sprauge-Dawley rat to coincide with the onset of an established PS window. Control groups received either saline or ANI either 3 hours before or 3 hours after the beginning of the PS window. Three hours after the injection, each group was retested. Then animals were immediately sacrificed, and whole brain biochemical analyses were done on levels of acetylcholine (ACh) and activity of acetylcholinesterase (AChE). Only the rats given ANI timed to coincide with the beginning of the PS window showed learning deficits. All ANI-treated groups had less ACh and AChE activity. In Experiment 2, the ACh antagonist scopolamine (SCOP) was injected at the same times as in Experiment 1, and each of these groups had a corresponding saline control group as before. Retesting was done 1 day later; once again, the only group to show learning deficits was the group receiving SCOP timed to coincide with the PS window. Results suggested that the transmitter ACh plays an important role in learning/memory processes at the PS window.

The purpose of this study was to test the potential relationship between REM sleep and information processing with inversion of the visual field. In the first experiment, four male subjects slept in the laboratory for two sessions of 6 consecutive nights: 2 adaptation nights, 2 nights of polysomnography, and 2 nights of dream collection. During the days preceding Nights 3, 4, 5, and 6 of each session, the subjects wore glasses which, during the second session, completely inverted (rotation of 180 degrees) their visual field. In a second experiment with four other male subjects, the order of conditions was reversed, and the experimental condition (visual inversion) was introduced a second time. When the data of the two experiments were combined, there was a significant (p less than .01) increase in the percentage of REM sleep from Nights 3 and 4 of the control condition to Nights 3 and 4 of the visual inversion condition, but there was no significant change in any of the other sleep stages. There was a significant decrease in horizontal (p less than .04) and vertical (p less than .005) REM density and in the density of vertical REM bursts (p less than .02). The increase in REM sleep supports the hypothesis that REM sleep contributes to information processing while the decrease in REM density suggests that this component of REM sleep may be involved in a homeostatic process of sensory input.

Fibrositis (fibromyalgia) patients were compared with normal controls in terms of electrophysiology (EEG), self-report indicants of awakening, quality of sleep, behaviourally signalled awakenings, and Symptom Check List 90R (SCL-90R) scores. The results differentiated fibrositis patients from normal controls in terms of SCL-90R scores, with fibrositis patients showing significantly more psychopathology. Fibrositis patients had more alpha EEG sleep and less REM and Stage 1 sleep. They were better able to recall their behaviourally signalled awakenings the following morning and reported qualitatively less satisfying sleep than the normal controls. The alpha EEG sleep anomaly may reflect a vigilant arousal state during nocturnal sleep and result in the daytime experience of unrefreshing sleep, psychologic distress, that re-enforces the perpetuation of the sleep-related symptoms.