Sleep deprivation effects

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. 

The principal disadvantages of barbiturates as hypnotics include the development of physical dependence, a relatively low therapeutic index (and the potential of poisoning, as in suicide), suppression of REM sleep, and possible hangover effects. As mentioned above, benzodiazepines (e.g., flurazepam or brotizolam) are hypnotics as effective as barbiturates and are much safer in terms of their therapeutic index, addiction potential, and REM sleep-deprivation effects. Thus benzodiazepines have displaced barbiturates as sedative hypnotics. 

Webb WB. A further analysis of age and sleep deprivation effects. Psychophysiology 1985 22 156-161. 

Baranski JV, Pigeau RA. Self-monitoring cognitive performance during sleep deprivation effects of modafmil, d-amphetamine and placebo. J Sleep Res 1997 6 84—91. 

Rodgers CD, Paterson DH, Cunningham DA, Noble EG, Pettigrew FP, Myles WS, Taylor AW. Sleep deprivation effects on work capacity, self-paced walking, contractile properties and perceived exertion. Sleep 1995 18 30-38. 

Dinges DF. Homeostatic and circadian regulation of wakefulness during jet lag and sleep deprivation effect of wake-promoting countermeasures. AFOSR Technical Report No. 31-08-2000. Arlington, VA Air Force Office of Scientific Research. 2000. 

Borbely AA, Baumann F, Brandeis D, Strauch I, Lehmann D. Sleep deprivation effect on sleep stages and EEG power density in man. Electroencephalogr Clin Neurophysiol 1981 51 483-495. 

Vgontzas AN, Mastorakos G, Bixler EO, Kales A, Gold PW, Chrousos GP (1999) Sleep deprivation effects on the activity of the hypothalamic-pituitary-adrenal and growth axes potential clinical implications. Clin Endocrinol 51 205-215... 

The effects of chronic sleep deprivation or cumulative minor sleep losses have been relatively under investigated. Little is known about the relationships among the size of the sleep deficit, its rate of accumulation, the amount and timing of optimum recovery sleep, and their effect on human performance and productivity. 

The functions of these different phases of sleep are not at all clear but chronic sleep deprivation does eventually lead to death. It seems to be the slow-wave component of sleep (SWS) that is vital and it is thought to serve a restorative purpose. This would be consistent with its greater occurrence during the early stages of the sleep cycle when hormone secretion supports anabolic metabolism. If subjects are wakened every time they enter a period of REM sleep (evidenced by the EEG) there appears to be no overt harmful effect on their behaviour. In fact, REM sleep deprivation has even been used, with some claims of success, as a treatment for minor depression. However, there is an unproven belief that REM sleep is important for memory consolidation. 

Gulyani, S. Mallick, B. N. (1993). Effect of rapid eye movement sleep deprivation on rat brain Na-K ATPase activity. J. Sleep Res. 2, 45-50. 

Mallick, B. N. Thakkar, M. (1992). Effect of REM sleep deprivation on molecular forms of acetylcholinesterase in rats. Neuroreport 3, 676-8. 

Hamdi A., Brock J., Ross K, Prasad C. (1993). Effects of rapid eye movement sleep deprivation on the properties of striatal dopaminergic system. Pharmacol. Biochem. Behav. 46, 863-6. 

Lai S., Thavundayil J., Nair N. P. et al. (1981). Effect of sleep deprivation on dopamine receptor function in normal subjects. J. Neural Transm. 50(1), 39-45. 

Lara-Lemus A., Drucker-Colin R., Mendez-Franco J., Palomero-Rivero M., Perez de la Mora M. (1998). Biochemical effects induced by REM sleep deprivation in naive and in D-amphetamine treated rats. Neurobiology 6(1), 13-22. 

Zwicker A., Calil H. (1986). The effects of REM sleep deprivation on striatal dopamine receptor sites. Pharmacol. Biochem. Behav. 24, 809-12. 

Figure 8.2 A comparison of the effects on standardized NREM sleep delta total integrated amplitude (TIA) produced by (A) MK-801, (B) 12 h total sleep deprivation (TSD), and (C) MK-801 + TSD shows that the delta increase produced by MK-801 persists across a 12 h period of sleep deprivation. MK-801 injected at the start of the dark period produced a large increase in TIA that returned to baseline levels by the second hour of the light period. TSD throughout the 12 h dark period produced a 28% increase in TIA in the subsequent light period. MK-801 followed by TSD for the remainder of the dark period produced a 60% increase in light period delta TIA that was significantly greater than the effect of MK-801 alone or TSD alone. This finding indicated that MK-801 increased the homeostatic drive for delta.

Figure 8.3 The similarity of the EEG effects of 12 h total sleep deprivation (TSD) and 0.5mg/kg MK-801. Standardized power density functions for the 12 h light period are shown for the frequency ranges most affected by the two treatments. Both TSD and MK-801 increased power in the 1-4 Hz frequency band during NREM sleep and the 10-20 Hz frequency band during REM sleep. (A) MK-801 vs. saline, NREM (B) MK-801 vs. saline, REM (C) 12 h TSD vs. control, NREM (D) 12 h TSD vs. control, REM.

Tobler, I. Borbely, A. A. (1982). Sleep regulation after reduction of brain serotonin effect of p-chlorophenylalanine combined with sleep deprivation in the rat. Sleep 5, 145-53. 

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