Sleep caffeine

The nucleophilicity of the nitrogen atom survives in many different functional groups, although its basicity may be lost. Reactions of non-basic, but nucleophilic urea nitrogens provide, for example, an easy entry to sleeping-pills (barbiturates) as well as to stimulants (caffeine). The nitrogen atoms of imidazoles and indole anions are also nucleophilic and the NH protons can be easily substituted. 

Glassification of Substance-Related Disorders. The DSM-IV classification system (1) divides substance-related disorders into two categories (/) substance use disorders, ie, abuse and dependence and (2) substance-induced disorders, intoxication, withdrawal, delirium, persisting dementia, persisting amnestic disorder, psychotic disorder, mood disorder, anxiety disorder, sexual dysfunction, and sleep disorder. The different classes of substances addressed herein are alcohol, amphetamines, caffeine, caimabis, cocaine, hallucinogens, inhalants, nicotine, opioids, phencyclidine, sedatives, hypnotics or anxiolytics, polysubstance, and others. On the basis of their significant socioeconomic impact, alcohol, nicotine, cocaine, and opioids have been selected for discussion herein. 

Caffeine is considered by pharmacologists to be a mild stimulant of the central nervous system. It has been shown to promote feelings of well being and increased abiUty to perform certain mental tasks efficiently. There are people who are oversensitive to the effects of caffeine overindulgence by these individuals, eg, intake of more than 600 mg caffeine/d, can bring unwanted effects such as anxiety, restlessness, sleeping difficulties, headache, or palpitations of the heart (54). 

In addition, adenosine is implicated in sleep regulation. During periods of extended wakefulness, extracellular adenosine levels rise as a result of metabolic activity in the brain, and this increase promotes sleepiness. During sleep, adenosine levels fall. Caffeine promotes wakefulness by blocking the interaction of extracellular adenosine with its neuronal receptors. ... 

ENHANCING SLEEP PATTERNS. To promote the effects of the sedative or hypnotic the nurse provides supportive care, such as back rubs, night lights or a darkened room, and a quiet atmosphere. The patient is discouraged from drinking beverages containing caffeine, such as coffee, tea, or cola drinks, which can contribute to wakefulness. 

Caffeine binds to adenosine receptors in the brain, preventing adenosine from inducing sleep or opening blood vessels. Caffeine also increases levels of dopamine, the neurotransmitter associated with pleasure. This is the chemical mechanism for addiction. The response to adenosine competition causes increased adrenaline flow. 

Legal nicotine, caffeine, alcohol, a number of sleeping tablets and tranquillizers. Illegal heroin, cocaine, crack, cannabis, amphetamine, crystal meth (methamphetamine). 

To reduce nocturia, patients should be instructed to stop drinking fluids several hours before going to bed, and then voiding before going to sleep. During the day, patients should avoid excessive caffeine intake, as this may cause urinary frequency. In addition, toilet mapping (knowing the location of toilets on the way to and from various destinations) may help reassure the patient that he can still continue with many of his routine daily activities. 

Rosenthal, L., Roehrs, T., Zwyghuizen-Doorenbos, A., Plath, D., et-al., Alerting effects of caffeine after normal and restricted sleep. Neuropsychopharmacology 4(2), 103-108, 1991. 

Penetar, D., McCann, U., Thorne, D. and Kamimori, G., Caffeine reversal of sleep deprivation effects on alertness and mood. Psychopharmacology 112(2-3), 359-365, 1993. 

Beaumont, M., Batejat, D., Coste, O. et al. (2005). Recovery after prolonged sleep deprivation residual effects of slow-release caffeine on recovery sleep, sleepiness and cognitive functions. Neuropsychobiology 51 (1), 16-27. 

De Valck, E. Cluydts, R. (2001). Slow-release caffeine as a countermeasure to driver sleepiness induced by partial sleep deprivation./. Sleep Res. 10 (3), 203-9. 

Rogers, P. J., Heatherley, S. V., Hayward, R. C. et al. (2005). Effects of caffeine and caffeine withdrawal on mood and cognitive performance degraded by sleep restriction. Psychopharmacology 179 (4), 742-52. 

Virus, R. M., Ticho, S., Pilditch, M. Radulovacki, M. (1990). A comparison of the effects of caffeine, 8-cyclopentyltheophylline, and alloxazine on sleep in rats. Possible roles of central nervous system adenosine receptors. Neuropsychopharmacology 3 (4), 243-9. 

Wesensten, N. J., Killgore, W. D. Balkin, T. J. (2005). Performance and alertness effects of caffeine, dextroamphetamine, and modafinil during sleep deprivation./. Sleep Res. 14 (3), 255-66. 

Yanik, G., Glaum, S. 8r Radulovacki, M. (1987). The dose-response effects of caffeine on sleep in rats. Brain Res. 403 (1), 177-80. 

Some CNS stimulants have an effect on the same systems that are involved in wakefulness, including glutamate-, NE-, DA-, 5-HT-, histamine-, hypocretin- and ACh-containing neurons. This group includes molecules such as cocaine, amphetamine, and nicotine. The sleep-promoting systems are concentrated in the medial part of the brainstem, dorsal reticular substance of the medulla, anterior hypothalamus, and basal forebrain (Jones 2005). Other stimulants, such as caffeine and theophylline, block some sleep-inducing mechanisms. Modafinil is also a CNS stimulant with an unknown mechanism of action. 

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