Slow eye movement

Arch. Gen. Psychiat., 1966, 14, 238-248) shows the frequency of these three ego states or states of consciousness with respect to psychophysiological criteria. The psychophysiological criteria are arranged on the horizontal axis in the order in which transition into sleep ordinarily takes place. You can see that the intact ego state is associated with alpha and REM or alpha and SEM (slow eye movement), the destructuralized ego state mainly with restructuralized ego state mainly with... 

Sylvestre, PA. and Cullen, K.E. 1999. Quantitative analysis of abducens neuron discharge dynamics during saccadic and slow eye movements. /. Neurophysiol, 82 (5) 2612-2632. 

Rapid eye movement sleep. Sleep stage characterized by rapid movements of the eyes and asynchronous EEG activity in the theta-frequency (5-10Hz) range. Counterpart is slow wave sleep, characterized by other electrophysiological (synchronized low frequency l-2Hz, large amplitude EEG and neuronal sharp wave-ripple oscillations) and endocrine (growth hormone surge) activities. 

As we relax in preparation for and pass into sleep, the active desynchronised awake EEG characterised by the low-amplitude (5-10 pV) high-frequency (10-30 Hz) beta waves becomes progressively more synchronised giving larger (20-30 pV) and slower (8-12 Hz) alpha waves, and then even slower (1-4 Hz) and bigger (30-150 pV) delta waves. This so-called slow-wave sleep is interrupted at intervals of some 1-2h by the break-up and desynchronisation of the EEG into an awake-like pattern. Since this is accompanied by rapid eye movements, even though sleep persists and can be deeper, the phase is known as rapid eye movement, REM or paradoxical, sleep. It is a time when dreaming occurs and when memory may be secured. 

Figure 22.4 Idealised EEG-like patterns in sleep and waking. When we are awake and aroused the EEG is desynchronised (a). As we become drowsy and pass into sleep the EEG waves become more synchronised with 8-12 Hz alpha waves (b), sleep spindles then appear (c) before the EEG becomes even more synchronised with slow (about 1-2 Hz) high-voltage waves characteristic of deep slow-wave sleep (SWS). About every 90 min this pattern is disrupted and the EEG becomes more like that in arousal (d) except that the subject remains asleep. This phase of sleep is also characterised by rolling, rapid eye movements, the so-called REM sleep. SWS is consequently also known as non-REM sleep. These tracings have been drawn to show the main features of the different EEG phases of sleep and as such are much simpler than those that are actually recorded...

Slow-wave sleep Rapid eye movement (REM) sleep... 

Lavia Fantini M., Gagnon J., Petit D. et al. (2003). Slowing of electroencephalogram in rapid eye movement sleep behavior disorder. Ann. Neurol. 53, 774-80. 

The patient experiences anxiety, apathy, bradyphrenia (slowness of thought processes), confusional state, dementia, depression, hallucinosis/psychosis (typically drug-induced), and sleep disorders (excessive daytime sleepiness, insomnia, obstructive sleep apnea, and rapid eye movement sleep behavior disorder). 

Blister agents were developed for military purposes and are intended to inflict casualties (delayed following exposure), restrict terrain access, and slow troop movement. They affect the eyes and lungs and blister the skin. Mustard was the primary blister agent used in World War I. It was recognized by its distinctive odor. Modern... 

Blister agents were developed to inflict casualties, restrict terrain access, and slow troop movement. They affect the eyes and lungs and blister the skin. Mustard was... 

AD subjects have a higher prevalence of sleep disturbances than normal elderly, including sleep fragmentation, advancement of the sleep-wake cycle, and decreased amounts of slow wave and rapid-eye movement (REM) sleep (Prinz et al., 1982 Reynolds et al., 1988 Bliwise et al., 1989). Sleep-wake cycle disruption in AD has been associated with a greater burden of neuropsychiatric disturbances (Rebok et al., 1991 Ancoli-Israel et al., 1994), particularly apathy and delusions (Kaufer et al., 2001). Several studies have observed a relationship between the degree of intellectual impairment and REM sleep abnormalities (Prinz et al., 1982 Vitiello et al., 1984 Moe et al., 1995), underscoring the role of REM sleep in memory consolidation (Wilson McNaughton, 1994). 

Based on standardized scoring procedures (Rechtschaffen and Kales 1968), the entire sleep period is internally characterized as either rapid eye movement (REM) sleep or non-REM sleep, the latter including stages 1, 2, 3, and 4. Furthermore, stages 3 and 4 form the so-called slow-wave sleep (SWS). In this section, we describe the sleep stage characteristics of depression. 

Another controversial but exciting area of research is the potential role of serotonin in sleep. 5-Hydroxytryptamine may trigger slow-wave sleep (non-REM sleep), whereas the muscarinic AChR and NE are involved in REM sleep (rapid-eye-movement sleep, paradoxical sleep, dream sleep). In addition to the aminergic regulation of sleep, recent research has identified several other presumed sleep factors delta-sleep-inducing peptide, sleep-promoting substance, interleukin-1, and muramyl peptides. 

Barbiturates are referred to as sedative-hypnotics. These drugs will induce sleep which can lead to even deeper sedation (hypnosis) and can cause a fatal depression of the RAS affecting the respiratory system. The sleep which is encountered does not have the normal cycles of slow wave and rapid eye movement activity, so it is not always restful. However, these agents prove to be useful in anesthesia for both short and longer durations of time. Many of you may have been given thiopental prior to wisdom tooth extraction. Thiopental "wears off quickly and so the actual anesthetic for the time of the extraction is usually nitrous oxide. 

The reason that we didn t guess that this region would be selectively underperfused in REM sleep is that the EEG shows no evidence of the implied deterioration. Why don t we suddenly see slowing in the frontal EEG in REM Maybe such slowing is really there because it has been seen at sleep onset by Alex Borbely s group in Zurich. We should go back and look for it. To do so we would need to filter out the eye movement potentials that can be picked up by the frontal EEG leads, and we would need to use more sensitive tasks of relative inactivation, such as those used by psychologists like Richard Davidson in his studies of frontal cortex EEG activation asymmetry. It could well be that not only is the frontal... 

Figure i. Records taken from a cat chronically prepared with electrodes to record the eye movements (EOG), the electroencephalogram from both sides of the skull (EEG), and the activity of the neck muscles (NMG). The animal was kept in an air-conditioned, sound-attenuated room supplied with a oneway mirror for observation. The records were taken while the animal was awake and active (top left), awake and resting (top right—note alpha waves), just dropped off to sleep (middle left —note "spindles"), in deeper sleep (middle right—note slow waves in EEG) in still sounder sleep (bottom left—note very slow waves), and in paradoxical sleep (bottom right—arousal pattern in EEG). (Note eye movements in awake animal and in paradoxical sleep). Note also reduced electrical muscle activity in paradoxical sleep. Calibrations vertical line at top middle = 100 microvolts (or o.oooi volt), horizontal line = l second. Original from author s laboratory. 

Overdose occurs when a drug is consumed in a dose that is greater than the body can handle. Symptoms of an overdose include intense tiredness, confusion, irritability, and fever or a low body temperature. The person may experience shortness of breath, sleepiness or difficulty getting to sleep, and weakness. Other signs of overdose are slurred speech, a slow heartbeat, and uncommon eye movements. 

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