Delta wave

Last updated

A delta wave, recorded in a one-second sample of an EEG (electroencephalograph). This particular wave has a frequency of around 1 Hz. Eeg delta.svg
A delta wave, recorded in a one-second sample of an EEG (electroencephalograph). This particular wave has a frequency of around 1 Hz.

Delta waves are high amplitude neural oscillations with a frequency between 0.5 and 4 hertz. Delta waves, like other brain waves, can be recorded with electroencephalography [1] (EEG) and are usually associated with the deep stage 3 of NREM sleep, also known as slow-wave sleep (SWS), and aid in characterizing the depth of sleep. Suppression of delta waves leads to inability of body rejuvenation, brain revitalization and poor sleep. [2]

Contents

This is a screenshot of a patient during Slow Wave Sleep (stage 3). The high amplitude EEG is highlighted in red. This screenshot represents a 30-second epoch (30 seconds of data). Sleep EEG Stage 4.jpg
This is a screenshot of a patient during Slow Wave Sleep (stage 3). The high amplitude EEG is highlighted in red. This screenshot represents a 30-second epoch (30 seconds of data).

Background and history

"Delta waves" were first described in the 1930s by W. Grey Walter, who improved upon Hans Berger's electroencephalograph machine (EEG) to detect alpha and delta waves. Delta waves can be quantified using quantitative electroencephalography.

Classification and features

Delta waves, like all brain waves, can be detected by electroencephalography (EEG). Delta waves were originally defined as having a frequency between 1 and 4 Hz, although more recent classifications put the boundaries at between 0.5 and 2 Hz. They are the slowest and highest amplitude classically described brainwaves, although recent studies have described slower (<0.1 Hz) oscillations [3] Delta waves begin to appear in stage 3 sleep, but by stage 4 nearly all spectral activity is dominated by delta waves. Stage 3 sleep is defined as having less than 50% delta wave activity, while stage 4 sleep has more than 50% delta wave activity. These stages have recently been combined and are now collectively referred to as stage N3 slow-wave sleep. [4] During N3 SWS, delta waves account for 20% or more of the EEG record during this stage. [5] Delta waves occur in all mammals, and potentially all animals as well.

Delta waves are often associated with another EEG phenomenon, the K-complex. K-Complexes have been shown to immediately precede delta waves in slow wave sleep. [6]

Delta waves have also been classified according to the location of the activity into frontal (FIRDA), temporal (TIRDA), and occipital (OIRDA) intermittent delta activity. [7]

Neurophysiology

Sex differences

Females have been shown to have more delta wave activity, and this is true across most mammal species [ citation needed ]. This discrepancy does not become apparent until early adulthood (in the 30s or 40s in humans), with males showing greater age-related reductions in delta wave activity than females. [8]

Brain localization and biochemistry

Delta waves can arise either in the thalamus or in the cortex. When associated with the thalamus, they are thought to arise in coordination with the reticular formation. [9] [10] In the cortex, the suprachiasmatic nuclei have been shown to regulate delta waves, as lesions to this area have been shown to cause disruptions in delta wave activity. In addition, delta waves show a lateralization, with right hemisphere dominance during sleep. [11] Delta waves have been shown to be mediated in part by T-type calcium channels. [12] During delta wave sleep, neurons are globally inhibited by gamma-aminobutyric acid (GABA). [13]

Delta activity stimulates the release of several hormones, including growth hormone releasing hormone GHRH and prolactin (PRL). GHRH is released from the hypothalamus, which in turn stimulates release of growth hormone (GH) from the pituitary. The secretion of (PRL), which is closely related to (GH), is also regulated by the pituitary. The release of thyroid stimulating hormone (TSH), is decreased in response to delta-wave signaling. [14]

Development

Infants have been shown to spend a great deal of time in slow-wave sleep, and thus have more delta wave activity. In fact, delta-waves are the predominant waveforms of infants. Analysis of the waking EEG of a newborn infant indicates that delta wave activity is predominant in that age, and still appears in a waking EEG of five-year-olds. [15] Delta wave activity during slow-wave sleep declines during adolescence, with a drop of around 25% reported between the ages of 11 and 14 years. [16] Delta waves have been shown to decrease across the lifespan, with most of the decline seen in the mid-forties. By the age of about 75, stage four sleep and delta waves may be entirely absent. [17] In addition to a decrease in the incidence of delta waves during slow-wave sleep in the elderly, the incidence of temporal delta wave activity is commonly seen in older adults, and incidences also increase with age. [18]

Disruptions and disorders

Regional delta wave activity not associated with NREM sleep was first described by W. Grey Walter, who studied cerebral hemisphere tumors. Disruptions in delta wave activity and slow wave sleep are seen in a wide array of disorders. In some cases there may be increases or decreases in delta wave activity, while others may manifest as disruptions in delta wave activity, such as alpha waves presenting in the EEG spectrum. Delta wave disruptions may present as a result of physiological damage, changes in nutrient metabolism, chemical alteration, or may also be idiopathic. Disruptions in delta activity is seen in adults during states of intoxication or delirium and in those diagnosed with various neurological disorders such as dementia or schizophrenia. [19]

Temporal low-voltage irregular delta wave

Temporal low-voltage irregular delta wave activity has been commonly detected in patients with ischemic brain diseases, particularly in association with small ischemic lesions and is seen to be indicative of early-stage cerebrovascular damage. [20]

Parasomnias

Parasomnias, a category of sleep disorders, are often associated with disruptions in slow wave sleep. Sleep walking and sleep talking most often occur during periods of high delta wave activity. Sleep walkers have also been shown to have more hypersynchronous delta activity (HSD) compared to total time spent in stages 2, 3, and 4 sleep relative to healthy controls. HSD refers to the presence of continuous, high-voltage (> 150 µV) delta waves seen in sleep EEGs. [21] Parasomnias which occur deep in NREM sleep also include sleep terrors and confusional arousals.

Sleep deprivation

Total sleep deprivation has been shown to increase delta wave activity during sleep recovery, [22] and has also been shown to increase hypersynchronous delta activity. [21]

Parkinson's disease

Sleep disturbances, as well as dementia, are common features of Parkinson's disease, and patients with this disease show disrupted brain wave activity. The drug Rotigotine, developed for the treatment of Parkinson's disease, has been shown to increase delta power and slow-wave sleep.

Schizophrenia

People with schizophrenia have shown disrupted EEG patterns, and there is a close association of reduced delta waves during deep sleep and negative symptoms associated with schizophrenia. During slow wave sleep (stages 3 and 4), people with schizophrenia have been shown to have reduced delta wave activity, although delta waves have also been shown to be increased during waking hours in more severe forms of schizophrenia. [23] A recent study has shown that the right frontal and central delta wave dominance, seen in healthy individuals, is absent in patients with schizophrenia. In addition, the negative correlation between delta wave activity and age is also not observed in those with schizophrenia. [24]

Diabetes and insulin resistance

Disruptions in slow wave (delta) sleep have been shown to increase risk for development of Type II diabetes, potentially due to disruptions in the growth hormone secreted by the pituitary. In addition, hypoglycemia occurring during sleep may also disrupt delta-wave activity. [25] Low-voltage irregular delta waves, have also been found in the left temporal lobe of diabetic patients, at a rate of 56% (compared to 14% in healthy controls). [26] [27]

Fibromyalgia

Patients with fibromyalgia often report unrefreshing sleep. A study conducted in 1975 by Moldovsky et al. showed that the delta wave activity of these patients in stages 3 and 4 sleep were often interrupted by alpha waves. They later showed that depriving the body of delta wave sleep activity also induced musculoskeletal pain and fatigue. [28]

Alcoholism

Alcoholism has been shown to produce sleep with less slow wave sleep and less delta power, while increasing stage 1 and REM incidence in both men and women. In long-term alcohol abuse, the influences of alcohol on sleep architecture and reductions in delta activity have been shown to persist even after long periods of abstinence. [29]

Temporal lobe epilepsy

Slow waves, including delta waves, are associated with seizure-like activity within the brain. W. Grey Walter was the first person to use delta waves from an EEG to locate brain tumors and lesions causing temporal lobe epilepsy. [30] Neurofeedback has been suggested as a treatment for temporal lobe epilepsy, and theoretically acts to reduce inappropriate delta wave intrusion, although there has been limited clinical research in this area. [31]

Other disorders

Other disorders frequently associated with disrupted delta-wave activity include:

Consciousness and dreaming

Initially, dreaming was thought to only occur in rapid eye movement sleep, though it is now known that dreaming may also occur during slow-wave sleep.[ citation needed ] Delta waves and delta wave activity are marked, in most people, by an apparently unconscious state, and the loss of physical awareness as well as the "iteration of information".

Delta wave activity has also been purported to aid in declarative and explicit memory formation. [13]

Pharmacology

While most drugs that affect sleep do so by stimulating sleep onset, or disrupting REM sleep, a number of chemicals and drugs have been shown to alter delta wave activity.

Effects of diet

Diets very low in carbohydrates, such as a ketogenic diet, have been shown to increase the amount of delta activity and slow wave sleep in healthy individuals. [41]

See also

Brain waves

Related Research Articles

Physiological psychology is a subdivision of behavioral neuroscience that studies the neural mechanisms of perception and behavior through direct manipulation of the brains of nonhuman animal subjects in controlled experiments. This field of psychology takes an empirical and practical approach when studying the brain and human behavior. Most scientists in this field believe that the mind is a phenomenon that stems from the nervous system. By studying and gaining knowledge about the mechanisms of the nervous system, physiological psychologists can uncover many truths about human behavior. Unlike other subdivisions within biological psychology, the main focus of psychological research is the development of theories that describe brain-behavior relationships.

Non-rapid eye movement sleep (NREM), also known as quiescent sleep, is, collectively, sleep stages 1–3, previously known as stages 1–4. Rapid eye movement sleep (REM) is not included. There are distinct electroencephalographic and other characteristics seen in each stage. Unlike REM sleep, there is usually little or no eye movement during these stages. Dreaming occurs during both sleep states, and muscles are not paralyzed as in REM sleep. People who do not go through the sleeping stages properly get stuck in NREM sleep, and because muscles are not paralyzed a person may be able to sleepwalk. According to studies, the mental activity that takes place during NREM sleep is believed to be thought-like, whereas REM sleep includes hallucinatory and bizarre content. NREM sleep is characteristic of dreamer-initiated friendliness, compared to REM sleep where it's more aggressive, implying that NREM is in charge of simulating friendly interactions. The mental activity that occurs in NREM and REM sleep is a result of two different mind generators, which also explains the difference in mental activity. In addition, there is a parasympathetic dominance during NREM. The reported differences between the REM and NREM activity are believed to arise from differences in the memory stages that occur during the two types of sleep.

Sexsomnia, also known as sleep sex, is a distinct form of parasomnia, or an abnormal activity that occurs while an individual is asleep. Sexsomnia is characterized by an individual engaging in sexual acts while in non-rapid eye movement (NREM) sleep. Sexual behaviors that result from sexsomnia are not to be mistaken with normal nocturnal sexual behaviors, which do not occur during NREM sleep. Sexual behaviors that are viewed as normal during sleep and are accompanied by extensive research and documentation include nocturnal emissions, nocturnal erections, and sleep orgasms.

A gamma wave or gamma rhythm is a pattern of neural oscillation in humans with a frequency between 25 and 140 Hz, the 40 Hz point being of particular interest. Gamma rhythms are correlated with large-scale brain network activity and cognitive phenomena such as working memory, attention, and perceptual grouping, and can be increased in amplitude via meditation or neurostimulation. Altered gamma activity has been observed in many mood and cognitive disorders such as Alzheimer's disease, epilepsy, and schizophrenia. Elevated gamma activity has also been observed in moments preceding death.

<span class="mw-page-title-main">K-complex</span>

A K-complex is a waveform that may be seen on an electroencephalogram (EEG). It occurs during stage 2 NREM sleep. It is the "largest event in healthy human EEG". They are more frequent in the first sleep cycles.

Sleep spindles are bursts of neural oscillatory activity that are generated by interplay of the thalamic reticular nucleus (TRN) and other thalamic nuclei during stage 2 NREM sleep in a frequency range of ~11 to 16 Hz with a duration of 0.5 seconds or greater. After generation as an interaction of the TRN neurons and thalamocortical cells, spindles are sustained and relayed to the cortex by thalamo-thalamic and thalamo-cortical feedback loops regulated by both GABAergic and NMDA-receptor mediated glutamatergic neurotransmission. Sleep spindles have been reported for all tested mammalian species. Considering animals in which sleep-spindles were studied extensively, they appear to have a conserved main frequency of roughly 9–16 Hz. Only in humans, rats and dogs is a difference in the intrinsic frequency of frontal and posterior spindles confirmed, however.

Alpha waves, or the alpha rhythm, are neural oscillations in the frequency range of 8–12 Hz likely originating from the synchronous and coherent electrical activity of thalamic pacemaker cells in humans. Historically, they are also called "Berger's waves" after Hans Berger, who first described them when he invented the EEG in 1924.

<span class="mw-page-title-main">Slow-wave sleep</span> Period of sleep in humans and other animals

Slow-wave sleep (SWS), often referred to as deep sleep, consists of stage three of non-rapid eye movement sleep. It usually lasts between 70 and 90 minutes and takes place during the first hours of the night. Initially, SWS consisted of both Stage 3, which has 20–50 percent delta wave activity, and Stage 4, which has more than 50 percent delta wave activity.

<span class="mw-page-title-main">Neural oscillation</span> Brainwaves, repetitive patterns of neural activity in the central nervous system

Neural oscillations, or brainwaves, are rhythmic or repetitive patterns of neural activity in the central nervous system. Neural tissue can generate oscillatory activity in many ways, driven either by mechanisms within individual neurons or by interactions between neurons. In individual neurons, oscillations can appear either as oscillations in membrane potential or as rhythmic patterns of action potentials, which then produce oscillatory activation of post-synaptic neurons. At the level of neural ensembles, synchronized activity of large numbers of neurons can give rise to macroscopic oscillations, which can be observed in an electroencephalogram. Oscillatory activity in groups of neurons generally arises from feedback connections between the neurons that result in the synchronization of their firing patterns. The interaction between neurons can give rise to oscillations at a different frequency than the firing frequency of individual neurons. A well-known example of macroscopic neural oscillations is alpha activity.

<span class="mw-page-title-main">Mu wave</span> Electrical activity in the part of the brain controlling voluntary movement

The sensorimotor mu rhythm, also known as mu wave, comb or wicket rhythms or arciform rhythms, are synchronized patterns of electrical activity involving large numbers of neurons, probably of the pyramidal type, in the part of the brain that controls voluntary movement. These patterns as measured by electroencephalography (EEG), magnetoencephalography (MEG), or electrocorticography (ECoG), repeat at a frequency of 7.5–12.5 Hz, and are most prominent when the body is physically at rest. Unlike the alpha wave, which occurs at a similar frequency over the resting visual cortex at the back of the scalp, the mu rhythm is found over the motor cortex, in a band approximately from ear to ear. People suppress mu rhythms when they perform motor actions or, with practice, when they visualize performing motor actions. This suppression is called desynchronization of the wave because EEG wave forms are caused by large numbers of neurons firing in synchrony. The mu rhythm is even suppressed when one observes another person performing a motor action or an abstract motion with biological characteristics. Researchers such as V. S. Ramachandran and colleagues have suggested that this is a sign that the mirror neuron system is involved in mu rhythm suppression, although others disagree.

Recurrent thalamo-cortical resonance is an observed phenomenon of oscillatory neural activity between the thalamus and various cortical regions of the brain. It is proposed by Rodolfo Llinas and others as a theory for the integration of sensory information into the whole of perception in the brain. Thalamocortical oscillation is proposed to be a mechanism of synchronization between different cortical regions of the brain, a process known as temporal binding. This is possible through the existence of thalamocortical networks, groupings of thalamic and cortical cells that exhibit oscillatory properties.

<span class="mw-page-title-main">Spike-and-wave</span>

Spike-and-wave is a pattern of the electroencephalogram (EEG) typically observed during epileptic seizures. A spike-and-wave discharge is a regular, symmetrical, generalized EEG pattern seen particularly during absence epilepsy, also known as ‘petit mal’ epilepsy. The basic mechanisms underlying these patterns are complex and involve part of the cerebral cortex, the thalamocortical network, and intrinsic neuronal mechanisms.

Ponto-geniculo-occipital waves or PGO waves are distinctive wave forms of propagating activity between three key brain regions: the pons, lateral geniculate nucleus, and occipital lobe; specifically, they are phasic field potentials. These waves can be recorded from any of these three structures during and immediately before REM sleep. The waves begin as electrical pulses from the pons, then move to the lateral geniculate nucleus residing in the thalamus, and end in the primary visual cortex of the occipital lobe. The appearances of these waves are most prominent in the period right before REM sleep, albeit they have been recorded during wakefulness as well. They are theorized to be intricately involved with eye movement of both wake and sleep cycles in many different animals.

<span class="mw-page-title-main">Electroencephalography</span> Electrophysiological monitoring method to record electrical activity of the brain

Electroencephalography (EEG) is a method to record an electrogram of the spontaneous electrical activity of the brain. The biosignals detected by EEG have been shown to represent the postsynaptic potentials of pyramidal neurons in the neocortex and allocortex. It is typically non-invasive, with the EEG electrodes placed along the scalp using the International 10–20 system, or variations of it. Electrocorticography, involving surgical placement of electrodes, is sometimes called "intracranial EEG". Clinical interpretation of EEG recordings is most often performed by visual inspection of the tracing or quantitative EEG analysis.

Sleep onset is the transition from wakefulness into sleep. Sleep onset usually transmits into non-rapid eye movement sleep but under certain circumstances it is possible to transit from wakefulness directly into rapid eye movement sleep.

<span class="mw-page-title-main">Sleep and memory</span> Relationship between sleep and memory

The relationship between sleep and memory has been studied since at least the early 19th century. Memory, the cognitive process of storing and retrieving past experiences, learning and recognition, is a product of brain plasticity, the structural changes within synapses that create associations between stimuli. Stimuli are encoded within milliseconds; however, the long-term maintenance of memories can take additional minutes, days, or even years to fully consolidate and become a stable memory that is accessible. Therefore, the formation of a specific memory occurs rapidly, but the evolution of a memory is often an ongoing process.

EEG microstates are transient, patterned, quasi-stable states or patterns of an electroencephalogram. These tend to last anywhere from milliseconds to seconds and are hypothesized to be the most basic instantiations of human neurological tasks, and are thus nicknamed "the atoms of thought". Microstate estimation and analysis was originally done using alpha band activity, though broader bandwidth EEG bands are now typically used. The quasi-stability of microstates means that the "global [EEG] topography is fixed, but strength might vary and polarity invert."

<span class="mw-page-title-main">Brain activity and meditation</span>

Meditation and its effect on brain activity and the central nervous system became a focus of collaborative research in neuroscience, psychology and neurobiology during the latter half of the 20th century. Research on meditation sought to define and characterize various practices. The effects of meditation on the brain can be broken up into two categories: state changes and trait changes, respectively alterations in brain activities during the act of meditating and changes that are the outcome of long-term practice.

<span class="mw-page-title-main">Neuroscience of sleep</span> Study of the neuroscientific and physiological basis of the nature of sleep

The neuroscience of sleep is the study of the neuroscientific and physiological basis of the nature of sleep and its functions. Traditionally, sleep has been studied as part of psychology and medicine. The study of sleep from a neuroscience perspective grew to prominence with advances in technology and the proliferation of neuroscience research from the second half of the twentieth century.

Sharp waves and ripples (SWRs) are oscillatory patterns produced by extremely synchronised activity of neurons in the mammalian hippocampus and neighbouring regions which occur spontaneously in idle waking states or during NREM sleep. They can be observed with a variety of imaging methods, such as EEG. They are composed of large amplitude sharp waves in local field potential and produced by tens of thousands of neurons firing together within 30–100 ms window. They are some of the most synchronous oscillations patterns in the brain, making them susceptible to pathological patterns such as epilepsy.They have been extensively characterised and described by György Buzsáki and have been shown to be involved in memory consolidation in NREM sleep and the replay of memories acquired during wakefulness.

References

  1. ↑ Walker, Peter (1999). Chambers dictionary of science and technology . Edinburgh: Chambers. p.  312. ISBN   0-550-14110-3.
  2. ↑ Abhang, Priyanka A; Gawali, Bharti W.; Mehrotra, Suresh C. (2016). Introduction to EEG- and Speech-Based Emotion Recognition. Academic Press. pp. 51–79. ISBN   9780128044902.
  3. ↑ Hiltunen T1, Kantola J, Abou Elseoud A, Lepola P, Suominen K, Starck T, Nikkinen J, Remes J, Tervonen O, Palva S, Kiviniemi V, Palva JM. (2014). "Infra-slow EEG fluctuations are correlated with resting-state network dynamics in fMRI". [Article]. The Journal of Neuroscience, 34(2): 356–362.
  4. ↑ "Glossary. A resource from the Division of Sleep Medicine at Harvard Medical School, Produced in partnership with WGBH Educational Foundation". Harvard University. 2008. Retrieved 2009-03-11. "The 1968 categorization of the combined Sleep Stages 3–4 was reclassified in 2007 as Stage N3."
  5. ↑ Iber C, Ancoli-Israel S, Chesson A, and Quan SF for the American Academy of Sleep Medicine. The AASM Manual for the Scoring of Sleep and Associated Events: Rules, Terminology and Technical Specifications, 1st ed.: Westchester, Illinois: American Academy of Sleep Medicine, 2007.
  6. ↑ De Gennaro, L., Ferrara, M., & Bertini, M. (2000). "The spontaneous K-complex during stage 2 sleep: is it the 'forerunner' of delta waves?" [Article]. Neuroscience Letters, 291(1), 41–43.
  7. ↑ Brigo F (2011). "Intermittent rhythmic delta activity patterns". Epilepsy & Behavior (Review). 20 (2): 254–6. doi:10.1016/j.yebeh.2010.11.009. PMID   21276757. S2CID   11689350.
  8. ↑ Ehlers, C. L., and D. J. Kupfer. (1997). "Sleep: Do Young Adult Men and Women Age Differently?". J Sleep Res. 6 (3): 211–15. doi:10.1046/j.1365-2869.1997.00041.x. PMID   9358400. S2CID   33542993.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  9. ↑ Gross, Richard E. (1992). Psychology: the science of mind and behaviour. London: Hodder & Stoughton. pp. 112–113. ISBN   0-340-56136-X.
  10. ↑ Maquet, P., Degueldre, C., Delfiore, G., Aerts, J., Peters, J. M., Luxen, A., et al. (1997). Functional neuroanatomy of human slow wave sleep. Journal of Neuroscience, 17(8), 2807-2812.
  11. ↑ Mistlberger, R. E., Bergmann, B. M., & Rechtschaffen, A. (1987). RELATIONSHIPS AMONG WAKE EPISODE LENGTHS, CONTIGUOUS SLEEP EPISODE LENGTHS, AND ELECTROENCEPHALOGRAPHIC DELTA WAVES IN RATS WITH SUPRACHIASMATIC NUCLEI LESIONS. [Article]. Sleep, 10(1), 12-24.
  12. ↑ Lee, J., Kim, D., Shin, H. Lack of delta waves and sleep disturbances during non-rapid eye movement sleep in mice lacking a1g-subunit of T-type calcium channels. PNAS;101(52): 18195-18199.
  13. 1 2 Hobson, J., & Pace-Schott, E. (2002). The Cognitive Neuroscience of Sleep: Neuronal Systems, Consciousness and Learning. Nature Reviews Neuroscience, 3(9), 679-693.
  14. ↑ Brandenberger, G. (2003). The Ulradien Rhythm of Sleep: Diverse Relations with Pituitary and Adrenal Hormones. Revue Neurologique, 159(11), S5-S10.
  15. ↑ Taylor, Eric; Rutter, Michael (2002). Child and adolescent psychiatry . Oxford: Blackwell Science. p.  162. ISBN   0-632-05361-5.
  16. ↑ "Brain Wave Changes in Adolescence Signal Reorganization of the Brain". ScienceDaily. 8 December 2006. Retrieved 24 March 2008.
  17. ↑ Colrain, I. M., Crowley, K. E., Nicholas, C. L., Afifi, L., Baker, F. C., Padilla, M., et al. (2010). Sleep evoked delta frequency responses show a linear decline in amplitude across the adult lifespan. [Article]. Neurobiology of Aging, 31(5), 874-883.
  18. ↑ Inui, Koji, Eishi Motomura, Hiroyuki Kaige, and Sen Nomura. "Temporal Slow Waves and Cerebrovascular Diseases - Inui - 2008 - Psychiatry and Clinical Neurosciences." Psychiatry and Clinical Neurosciences 55.5 (2001): 525–31. Wiley Online Library. Web. 29 November 2010.
  19. ↑ Hales, Robert E.; Yudofsky, Stuart C. (2007). The American Psychiatric Publishing Textbook of Neuropsychiatry and Behavioral Neurosciences, Fifth Edition (American Psychiatric Press Textbook of Neuropsychiatry). American Psychiatric Publishing, Inc. ISBN   978-1-58562-239-9.
  20. ↑ Inui, Koji, Hozumi Kawamoto, Masahiko Kawakita, Kazuhisa Wako, Hiromichi Nakashima, Masanori Kamihara, and Junichi Nomura. "Temporal Delta Wave and Ischemic Lesions on MRI." Psychiatry and Clinical Neurosciences 48.4 (1994): 891–98. Print.
  21. 1 2 Pilon M; Zadra A; Joncas S et al. Hypersynchronous delta waves and somnambulism: brain topography and effect of sleep deprivation. SLEEP 2006;29(1): 77–84.
  22. ↑ Feinberg, I., T. Baker, R. Leder, and J. D. March. "Response of Delta (0-3 Hz) EEG and Eye Movement Density to a Night with 100 Minutes of Sleep." Sleep 11.5 (1988): 473–87. Print.
  23. ↑ Alfimova, M. V., & Uvarova, L. G. (2007). Changes in the EEG spectral power during perception of neutral and emotionally salient words in schizophrenic patients, their relatives and healthy individuals from general population. [Article]. Zhurnal Vysshei Nervnoi Deyatelnosti Imeni I P Pavlova, 57(4), 426-436.
  24. ↑ Sekimoto, M., et al., Cortical regional differences of delta waves during all-night sleep in schizophrenia, Schizophr. Res. (2010), doi : 10.1016/j.schres.2010.11.003
  25. ↑ Abdelkarim, T. H., Westin, T., Romaker, A., & Girish, M. (2002). Presence of delta waves in REM sleep during polysomnography as a sign of acute hypoglycemic encephalopathy. [Meeting Abstract]. Sleep, 25, 531.
  26. ↑ Appearance of Parkinsonian Syndrome after Administration of Delta Sleep-inducing Peptide into the Rat Substantia Nigra." Biull Eksp Biol Med. 109.2 (1990): 119–21. Print.
  27. ↑ Inui, K., H. Sannan, H. Ota, Y. Uji, S. Nomura, H. Kaige, I. Kitayama, and J. Nomura. "EEG Findings in Diabetic Patients with and without Retinopathy." Acta Neurologica Scandinavica 97.2 (1998): 107–09. Print.
  28. ↑ Nezu, Arthur M. ., Christine Maguth. Nezu, Pamela A. . Geller, and Irving B. . Weiner. Handbook of Psychology. New York: Wiley, 2003. Print.
  29. ↑ Colrain, I. M., S. Turlington, and F. C. Baker. "Impact of Alcoholism on Sleep Architecture and EEG Power Spectra in Men and Women." Sleep. 32.10 (2009): 1341–352. Print.
  30. ↑ Walter WG. The location of cerebral tumors by electroencephalography. Lancet 1936;2: 305–8.
  31. ↑ "Biofeedback for Epileptic Seizures; EEG Neurofeedback for Epilepsy". Epilepsyhealth.com. Retrieved 14 February 2011.
  32. ↑ EEG-defined subtypes of children with attention-deficit/hyperactivity disorder. Adam R Clarke, Robert J Barry, Rory McCarthy, Mark Selikowitz. Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology. 1 November 2001 (volume 112 issue 11 Pages 2098-2105)
  33. ↑ Lopes, M.C., Guilleminault, C., Rosa, A., Passarelli, C., Roizenblatt, S., Tufik, S. Delta sleep instability in children with chronic arthritis. Brazilian Journal of Medical and Biological Research. 2008;41(10): 938–43.
  34. ↑ Bagai, Kanika; Peltier, Amanda C.; Malow, Beth A.; Diedrich, André; Shibao, Cyndya A.; Black, Bonnie K.; Paranjape, Sachin Y.; Orozco, Carlos; Biaggioni, Italo; Robertson, David; Raj, Satish R. (15 May 2016). "Objective Sleep Assessments in Patients with Postural Tachycardia Syndrome using Overnight Polysomnograms". Journal of Clinical Sleep Medicine. 12 (5): 727–733. doi:10.5664/jcsm.5806. ISSN   1550-9389. PMC   4865560 . PMID   26951415.
  35. ↑ Hakim, Alan; De Wandele, Inge; O'Callaghan, Chris; Pocinki, Alan; Rowe, Peter (10 February 2017). "Chronic fatigue in Ehlers-Danlos syndrome-Hypermobile type". American Journal of Medical Genetics Part C: Seminars in Medical Genetics. 175 (1): 175–180. doi: 10.1002/ajmg.c.31542 . ISSN   1552-4868. PMID   28186393.
  36. ↑ Lands, William. "Alcohol, Slow Wave Sleep, and the Somatotropic Axis." Alcohol 18.2 (1999): 109–22.
  37. ↑ Davenne, D. M. "Enhancement of Quiet Sleep in Rabbit Neonates by Muramyl Dipeptide." Am J Physiol. 253.4 (1987): 646–54. Print.
  38. ↑ Foldvary-Schaefer, N., I. De Leon Sanchez, M. Karafa, D. Dinner, and H. H. Morris. "Gabapentin Increases Slow-wave Sleep in Normal Adults." Epilepsia 43.12 (2002): 1493–497. Print.
  39. 1 2 D'haenen, H. A. H., Johan A. Den Boer, and Paul Willner. Biological Psychiatry. Chichester: Wiley, 2002. Print.
  40. ↑ Kara J. Pavone, Oluwaseun Akeju, Aaron L. Sampson, Kelly Ling, Patrick L. Purdon, Emery N. Brown. Nitrous oxide-induced slow and delta oscillations" Journal of Clinical Neurophysiology, Jan. 2016
  41. ↑ Afaghi, A., O'Connor, H., & Chow, C. (2008). Acute Effects of the Very Low Carbohydrate Diet on Sleep Indices. Nutritional Neuroscience, 11(4), 146-154.
This page is based on this Wikipedia article
Text is available under the CC BY-SA 4.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.