Sleep disorders appear when sleep homeostasis can no longer be efficiently modulated by astrocytes. Astrocytes adjust the neuronal activity by releasing chemical neurotransmitters, through glial transmission. Sleep depravation manifests its consequences on cognition as well as daily performance diminish.

          Sleep mechanism

          Although astrocytes cannot be electrically stimulated, they have high levels of calcium and are activated by metabotropic receptors. Synaptic activation of astrocytes leads to signals determined by Ca 2+, in exchange to releasing a number of chemical neurotransmitters from these glial cells. The glial transmission process modulates the synaptic activity. (Jourdain 2007, Pasqual 2005). Astrocytes prevent adenosine extracellular accumulation that acts on A1 receptors (Pasqual 2005), and this intervenes in the homeostasis of sleep inducing cycle, followed by a long awaking period. (Porkka-Heiskanen 1997) This adenosine mechanism is not entirely understood (Heller 2006). These astrocytes that are dependant on adenosine accumulation adjust the synaptic transmission, and the glial path modulates the progressive changes in sleep homeostasis.

          The necessary sleep period increases after sleep deprivation, and compensatory it produces an increase in the recovering period (Franken 1991). Astrocytes can explain the homeostasis sleep control, because they diminish adenosine accumulation, which protects the nervous system. Adenosine levels are lowered by astrocytes in hippocampic synapses, and that is the reason why accumulation of sleep deprivation periods, with prolonged activity, can damage the cognitive function. (Yoo 2007).

          Previous studies (Stickgold 2001), have concluded that sleep pays an important role in memory consolidation, and sleep deprivation can lead to cognitive decline. Cerebral adjusting of sleep takes place in medulla oblongata, thalamus and hypothalamus.

          There are 4 sleep stages regarding the sleep’s deepness, and a stage of REM sleep with fast ocular moves, period when dreams occur. These stages have special types of cerebral waves that mark each stage.

          Sleep adjusting is possible through the circadian rhythm from medulla oblongata, through reticular matter, thalamus and hypothalamus.

          These 5 stages compose a cycle and they appear successively approximately 5 times, during 7-8 hours of sleep. When these cycles are not complete, sleep disorders appear, manifested either by difficulty in falling asleep, continuous sleep or awaking difficulties, as well as: apnea, the impossibility to relax one’s feet during sleep, nocturnal ambulatory automatisms (sleep-waking), bruxisms (teeth clenching), narcolepsy (falling asleep during the day no matter the place, without being able to control it). Sleep disorders can appear as a secondary symptom to other diseases, such as: epilepsy, anxiety and panic attacks, chronic fatigue or fibromyalgia, nightmares, night terrors.

          Throughout the years there have been performed many studies regarding sleep, EEG modifications in nocturnal sleep and its disorders, primary and secondary (Guilleman,1999, 2006; Sterman 1996; Cox 1975; Empson 1973; Feighner 1973; Flemenbaum 1974; Gibson 1983; McKenzie 1976; Magora 1965, 1967; Taylor 1991). Sleep studies are the basis for neurofeedback protocols regarding sleep disorders.

          In the 1970’s, Sterman’s studies regarding epilepsy and appropriate neurofeedback protocol noted an improvement of sleep quality, fact noted by others in their studies (Cortoos 2006). Sterman stimulated the frequencies from 12-15 Hz band, which he called SMR.

          Other devises proved to be efficient in improving sleep quality, such as: Alpha Stim and pROSHI.

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