Sensory Deprivation: Arousal and Rapid Eye Movement Correlates of Some Effects

1964 ◽  
Vol 19 (2) ◽  
pp. 447-451 ◽  
Author(s):  
Ascanio M. Rossi ◽  
Allan Furhman ◽  
Philip Solomon
Keyword(s):  
Eye Movements ◽  
Eye Movement ◽  
Sensory Deprivation ◽  
Mental States ◽  
Rapid Eye Movement ◽  
Rapid Eye Movements ◽  
Retrospective Reports

Three Ss in sensory deprivation were continuously monitored by electroencephalographic (EEG) and electrooculographic (EOG) recordings. Retrospective reports of their mental states were given upon receipt of a signal. Ratings of report contents were compared with EEG determined levels of arousal and with the occurrence of rapid eye movements (REMs). Results indicate that the incidences of hallucinations and thought disorganization vary inversely with level of arousal, and hallucinations are not accompanied by REMs as occurs during dreaming.

Rapid Eye Movement during Sleep Considered as Nystagmus

1986 ◽  
Vol 63 (2) ◽  
pp. 595-598
Author(s):  
John Di Prete
Keyword(s):  
Eye Movements ◽  
Eye Movement ◽  
Motion Sickness ◽  
Paradoxical Sleep ◽  
Physiological Mechanism ◽  
Rapid Eye Movement ◽  
Supportive Evidence ◽  
Sleeping Position ◽  
Rapid Eye Movements ◽  
Spatial Sense

Based on supportive evidence, it is proposed in this paper that rapid eye movements during paradoxical sleep actually represent nystagmus, the latter due to the occurrence of conflicting perceptions of bodily position in space. During rapid eye movements in sleep, the brain's perception of bodily position in a dream is opposed to the sensory perception of the dreamer's sleeping position. The split in perception triggers nystagmus, a physiological mechanism known to accompany motion sickness and other waking forms of spatial sense distortion. Supportive evidence from studies on motion sickness, nystagmus, and sleep is presented. A number of experiments are suggested to lend validity to the hypothesis.

scholarly journals Regional low-frequency oscillations in human rapid-eye movement sleep

2018 ◽  
Author(s):  
Giulio Bernardi ◽  
Monica Betta ◽  
Emiliano Ricciardi ◽  
Pietro Pietrini ◽  
Giulio Tononi ◽  
...  
Keyword(s):  
Eye Movements ◽  
Eye Movement ◽  
Rem Sleep ◽  
Low Frequency ◽  
Nrem Sleep ◽  
Slow Waves ◽  
Gamma Activity ◽  
Rapid Eye Movement ◽  
Rapid Eye Movements ◽  
Low Frequency Oscillations

AbstractAlthough the EEG slow wave of sleep is typically considered to be a hallmark of Non Rapid Eye Movement (NREM) sleep, recent work in mice has shown that slow waves can also occur in REM sleep. Here we investigated the presence and cortical distribution of low-frequency (1-4 Hz) oscillations in human REM sleep by analyzing high-density EEG sleep recordings obtained in 28 healthy subjects. We identified two clusters of low-frequency oscillations with distinctive properties: 1) a fronto-central cluster characterized by ∼2.5-3.0 Hz, relatively large, notched delta waves (so-called ‘sawtooth waves’) that tended to occur in bursts, were associated with increased gamma activity and rapid eye movements, and upon source modeling, displayed an occipito-temporal and a fronto-central component; and 2) a medial occipital cluster characterized by more isolated, slower (<2 Hz) and smaller waves that were not associated with rapid eye movements, displayed a negative correlation with gamma activity and were also found in NREM sleep. Thus, low-frequency oscillations are an integral part of REM sleep in humans, and the two identified subtypes (sawtooth and medial-occipital slow waves) may reflect distinct generation mechanisms and functional roles. Sawtooth waves, which are exclusive to REM sleep, share many characteristics with ponto-geniculo-occipital (PGO) waves described in animals and may represent the human equivalent or a closely related event while medio-occipital slow waves appear similar to NREM sleep slow waves.

RAPID EYE MOVEMENTS AND RAPID EYE MOVEMENT PERIODS

1969 ◽  
Vol 6 (1) ◽  
pp. 45-48 ◽  
Author(s):  
JohnS. Antrobus ◽  
Judith S. Antrobus
Keyword(s):  
Eye Movements ◽  
Eye Movement ◽  
Rapid Eye Movement ◽  
Rapid Eye Movements

Human amygdala activation during rapid eye movements of rapid eye movement sleep: an intracranial study

2016 ◽  
Vol 25 (5) ◽  
pp. 576-582 ◽  
Author(s):  
María Corsi-Cabrera ◽  
Francisco Velasco ◽  
Yolanda del Río-Portilla ◽  
Jorge L. Armony ◽  
David Trejo-Martínez ◽  
...  
Keyword(s):  
Eye Movements ◽  
Eye Movement ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Rapid Eye Movements ◽  
Amygdala Activation

Quantitative Analysis of Abducens Neuron Discharge Dynamics During Saccadic and Slow Eye Movements

1999 ◽  
Vol 82 (5) ◽  
pp. 2612-2632 ◽  
Author(s):  
Pierre A. Sylvestre ◽  
Kathleen E. Cullen
Keyword(s):  
Eye Movements ◽  
Firing Rate ◽  
Eye Movement ◽  
Neuronal Activity ◽  
Smooth Pursuit ◽  
Slow Phase ◽  
Vestibular Nystagmus ◽  
Firing Rates ◽  
Rapid Eye Movements ◽  
Eye Velocity

The mechanics of the eyeball and its surrounding tissues, which together form the oculomotor plant, have been shown to be the same for smooth pursuit and saccadic eye movements. Hence it was postulated that similar signals would be carried by motoneurons during slow and rapid eye movements. In the present study, we directly addressed this proposal by determining which eye movement–based models best describe the discharge dynamics of primate abducens neurons during a variety of eye movement behaviors. We first characterized abducens neuron spike trains, as has been classically done, during fixation and sinusoidal smooth pursuit. We then systematically analyzed the discharge dynamics of abducens neurons during and following saccades, during step-ramp pursuit and during high velocity slow-phase vestibular nystagmus. We found that the commonly utilized first-order description of abducens neuron firing rates (FR = b + kE + rE˙, where FR is firing rate, E and E˙ are eye position and velocity, respectively, and b, k, and r are constants) provided an adequate model of neuronal activity during saccades, smooth pursuit, and slow phase vestibular nystagmus. However, the use of a second-order model, which included an exponentially decaying term or “slide” (FR = b + kE + rE˙ + uË − c[Formula: see text]), notably improved our ability to describe neuronal activity when the eye was moving and also enabled us to model abducens neuron discharges during the postsaccadic interval. We also found that, for a given model, a single set of parameters could not be used to describe neuronal firing rates during both slow and rapid eye movements. Specifically, the eye velocity and position coefficients ( r and k in the above models, respectively) consistently decreased as a function of the mean (and peak) eye velocity that was generated. In contrast, the bias ( b, firing rate when looking straight ahead) invariably increased with eye velocity. Although these trends are likely to reflect, in part, nonlinearities that are intrinsic to the extraocular muscles, we propose that these results can also be explained by considering the time-varying resistance to movement that is generated by the antagonist muscle. We conclude that to create realistic and meaningful models of the neural control of horizontal eye movements, it is essential to consider the activation of the antagonist, as well as agonist motoneuron pools.

Sleeping Pills and Dream Content

1974 ◽  
Vol 124 (583) ◽  
pp. 547-553 ◽  
Author(s):  
Hugh Firth
Keyword(s):  
Eye Movements ◽  
Eye Movement ◽  
Rem Sleep ◽  
Normal Values ◽  
Dream Content ◽  
Rapid Eye Movement ◽  
Sleeping Pills ◽  
Almost All ◽  
Natural Pattern

Almost all sleep-promoting drugs distort the natural pattern of sleep by suppressing rapid eye movement (REM) sleep, and cause a rebound to above-normal values on withdrawal which typically lasts about six weeks (Oswald, 1968, 1969). Furthermore, barbiturates reduce the number of eye movements per unit time in REM sleep (Oswald et al., 1963; Baekeland, 1967; Lester et al., 1968; Feinberg et al., 1969), with a rebound in eye movement (EM) profusion on withdrawal (Oswald, 1970). Non-barbiturate hypnotics do likewise, also with a rebound in EM profusion on withdrawal (Allen et al., 1968; Lewis, 1968).

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