The durations of successive sleep cycles, defined according to NREM (stage 2) or REM onsets, were objected to trend analysis in three groups of normal subjects and in a group of elderly patients with chronic brain syndrome (CBS). NREM sleep cycles showed consistent curvilinear trends for all groups except that the trend in children was distinguished by a lengthy first NREM cycle. REM steep cycles showed quite similar curvilinear trends for the three normal age groups with the middle two cycles being longer than the first and fourth. In the CBS patients, REM sleep cycles did not show a significant trend across the night. Real-time cycles (i.e., with time awake included) manifested trends quite similar to those excluding waking. The trends in sleep cycle durations are normative characteristics of sleep which may not be apparent on a single night. A more constant cycle was found in the CBS elderly and may indicate brain pathology. Sleep cycle trends, along with such other temporal characteristics as the decline in stage 4, may provide clues to the metabolic processes which underlie the sleep EEG. They also provide a more exact basis for investigation of hypothesized biorhythm correlates of NREM-REM cycles.

Systematic Trends Across the Night in Human Sleep Cycles

Alcohol primarily interferes with the ability to form new long-term memories, leaving intact previously established long-term memories and the ability to keep new information active in memory for brief periods. As the amount of alcohol consumed increases, so does the magnitude of the memory impairments. Large amounts of alcohol, particularly if consumed rapidly, can produce partial (i.e., fragmentary) or complete (i.e., en bloc) blackouts, which are periods of memory loss for events that transpired while a person was drinking. Blackouts are much more common among social drinkers--including college drinkers--than was previously assumed, and have been found to encompass events ranging from conversations to intercourse. Mechanisms underlying alcohol-induced memory impairments include disruption of activity in the hippocampus, a brain region that plays a central role in the formation of new autobiographical memories.

/pdf/what-happened-alcohol-memory-blackouts-and-the-brain-vmavri49pm.pdf

What Happened? Alcohol, Memory Blackouts, and the Brain


Rationale Several studies suggest that cognitive deficits seen in late stages of alcoholism are related to executive function However, little is known about the acute effects of alcohol on cognitive executive functions 
Aims The present investigation examined the acute effects of a moderate alcohol dose on tests of planning and spatial working memory as well as on tests of spatial and pattern recognition The relationship between the acute alcohol effects on performance in these tasks and extreme drinking patterns were also studied 
Methods Alcohol (08 g/kg) or placebo was administered to 95 social drinkers In the planning task, alcohol decreased the number of solutions with the minimum moves Alcohol also decreased the thinking time before initiating a response, while it increased the subsequent thinking time in the same task Under alcohol, participants recognised fewer items in the spatial recognition task; however no effect of alcohol was found in a spatial working memory task and in a pattern recognition task Among the participants with moderate to heavy use of alcohol, those who were 'bingers' performed worse in the spatial working memory and in the pattern recognition task than 'non-bingers'; no interaction between treatment and drinking pattern was found 
Conclusion These data suggest that alcohol given acutely impairs executive-type cognitive functions and that binge drinking may be associated with impaired cognitive function in a working memory and a pattern recognition task

Acute alcohol effects on cognitive function in social drinkers: Their relationship to drinking habits.

Ethanol is a drug that is classified as a general CNS depressant. Long-term exposure can result in tolerance and physical dependence. Ethanol consumption can affect the pharmacologic and therapeutic actions of prescription drugs, over-the-counter drugs, and illicit drugs. Ethanol-drug interactions have been reported to be the most frequent cause of drug-related medical crises in the United States. Alcohol misuse has a pervasive and potentially detrimental effect on the body from its point of entry through the gastrointestinal tract, to related organs such as the liver and the pancreas. The liver is one of the organs most significantly damaged and physiologically deranged as a result of alcohol ingestion. The two most common hepatic complications of alcoholism are hepatitis and cirrhosis. Cirrhosis was the seventh most common cause of death in the United States in 1975. Alcohol abuse interacts with physiological and metabolic processes of digestion to contribute to nutrient deficiency. Alcohol abuse has been suggested as the most common cause of vitamin and trace element deficiency in adults in the United States. Alcohol-derived nutritional deficiencies result in suboptimal health and are contributory to such abnormalities as anemia, convulsions, small-bowel dysfunction, and overt disorders such as Wernicke's encephalopathy. Brain dysfunction has been estimated to be present in from 50% to 70% of detoxified alcoholics entering treatment. Abstracting and adaptive abilities of social drinkers who had consumed no alcohol for 24 hours at the time of testing were found to be negatively associated with the amount of alcohol normally consumed per drinking occasion. Alcohol consumption alters numerous functions of the endocrine system, and excessive consumption has been implicated in impotency and early onset of postmenopausal amenorrhea. Recent evidence suggests that alcoholism may be a multifactorial genetically influenced disorder. In addition to genetics, social and environmental influences play significant roles. There is an association between alcoholism and depression in both men and women. Alcoholics often have high levels of depression and alcohol itself can increase depression. A disproportionately high number of people with drinking problems commit suicide, and more than a third of suicides involve alcohol. A propensity for suicide is thought to be associated with certain alcohol-related conditions such as depression, anxiety, mood fluctuations, and deteriorated social integration. Alcoholism has been associated with a number of adverse effects on the cardiovascular system, including a specific cardiomyopathy, low mean cardiac output, and depressed myocardial contractility. The drinking of large amounts of alcohol is associated with significant increases in blood pressure. Noncardiac myopathy has also been related to alcohol consumption. Heavy drinking increases the risk of cancer developing in the tongue, mouth, oropharynx, hypopharynx, esophagus, larynx, and liver. In the United States, these sites represent 6.1% to 9.1% of all cancer in the white population and 11.3% to 12.5% in the black population. In the broadest scope, alcohol abuse appears to be a risk factor in adverse fetal outcome. Fetal alcohol syndrome (FAS) has been identified among some children of alcoholic women. Fetal alcohol syndrome is characterized by CNS dysfunction, growth deficiency, a specific cluster of facial abnormalities, and other malformations, particularly skeletal, urogenital, and cardiac. It has been suggested that FAS is one of the leading causes of birth defects associated with mental retardetion. Short of the full complement of defects that characterize FAS, heavy alcohol use by women has been associated with birth anomalies. These effects of alcohol are independent of likely confounding variables, including smoking. Decreased birth weight is frequently associated with increased neonatal risk and has been observed among the children of women who consume an average of 30 mL of absolute alcohol per day (two standard drinks). Teratogenesis has also been noted in studies using alcohol-consuming animal models in whom the human condition is mimicked. Laboratory experiments have found that alcohol significantly impairs performance on sensory-motor and cognitive tasks at blood alcohol levels as low as 40 mg/dL. Such acute alcohol effects may contribute to other health hazards that may require medical treatment. For example, one third of all traffic fatalities are alcohol related; a significant number of industrial accidents, drownings, burns, and falls have been attributed to drinking; and a relatively high involvement of alcohol has been reported in assault, rape, child abuse and neglect, child molestation, and family violence in general. ( JAMA 1981;246:648-666)

Health Hazards Associated With Alcohol Consumption

THE EXISTENCE of a temporal relationship between sleep and the migraine syndrome has long been reported in the literature. One of the best descriptions is by Bingl who stated, “Sometimes it (migraine) descends upon the patient like a bolt from the blue, when the latter goes to bed with a free head and in a general state of well-being in the evening, and wakes up in the morning with a bad headache.” Migraine can also occur during the middle of the patient’s nocturnal sleep period and frequently follows brief periods of diurnal sleep. Some attacks of nocturnal headache are reported to occur during dreams, and occasionally, the aura of attacks of classic migraine are incorporated into the content of a dream which precedes the arousal with the severe headache. In the late 1940s, Gans2#3 recognized this relationship between sleep and migraine and, by selectively depriving patients of nocturnal “deep sleep,” reported a decrease in both frequency and severity of the migraine attacks. He states: “As soon as he (the patient) showed the faintest sign of falling into deep sleep (unnatural body posture, sinking back of the head, or snoring) he was gently touched, whereupon he immediately returned to the superficial deep level.” The precise stages of sleep which were “rationed are not known due to the absence of electroencephalographic monitoring; however, this procedure may have had the effect of decreasing both stages 3 and 4 (slow-wave sleep) and rapid eye movement sleep (REM) .4 In view of this long-recognized clinical relationship between migraine and sleep, we felt it would be of considerable interest to investigate the nocturnal sleep patterns of patients who had the onset of migraine during nocturnal sleep and to determine if a relationship might exist between the headache attack and a stage of sleep.

The relationship of nocturnal headaches to sleep stage patterns

MEMORY loss caused by alcohol is a common occurrence. Most alcoholics report “blackouts” (amnesia) in connexion with drinking, and many nonalcoholics sometimes have trouble remembering events that occurred while they were intoxicated1. The cause of this is unknown. Some psychiatrists believe blackouts to be a functional disturbance, related to guilt or anxiety. Others believe they reflect a toxic effect of alcohol on the brain. There are few data to support either concept. Blackouts usually occur erratically; comparable amounts of alcohol do not always produce memory loss, and it has not been possible to predict when an intoxicated person will suffer amnesia. During the amnesic interval, the person may function reasonably well and perform complicated acts, suggesting that the amnesia is retrograde2. To confirm this, however, memory must be observed systematically during drinking periods followed by amnesia, which heretofore has not been done.

Loss of short term memory as a predictor of the alcoholic "blackout".

Twenty-four-hour polygraphic tracings from normal humans indicate that a pattern of alternating periods of the presence and absence of rapid eye movement, shown to exist for normal sleep, exist over all 24 hours of the daily period. This finding suggests that the so-called sleep-dream cycle of human sleep is not specific to sleep, but is a general activity pattern of the brain.

https://science.sciencemag.org/content/sci/164/3878/447.full.pdf

Encephalic Cycles during Sleep and Wakefulness in Humans: A 24-Hour Pattern

A moderate amount of alcohol produced a coma-like state in a 24-year-old man with narcolepsy. This response differed from a typical narcoleptic sleep attack. The patient could not be fully awakened for a several hour period and electrophysiological data obtained during the episode were uncharacteristic of narcolepsy, showing slow-wave sleep and absence of rapid eye movements. It is unknown whether this represents a common response of narcoleptics to alcohol.

Ekkehard Othmer

Papers

Loss of short term memory as a predictor of the alcoholic "blackout".

Encephalic Cycles during Sleep and Wakefulness in Humans: A 24-Hour Pattern

Alcohol and Narcolepsy