A delta wave is a high amplitude brain wave with a frequency of oscillation between 0–4 hertz. Delta waves, like other brain waves, are recorded with an electroencephalogram[1] (EEG) and are usually associated with the deepest stages of sleep (3 and 4 NREM), also known as slow-wave sleep (SWS), and aid in characterizing the depth of sleep.
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"Delta waves" were first described in the early 1900s by W. Grey Walter, who improved upon Dr. Hans Berger's electroencephalograph machine (EEG) to detect alpha and delta waves.
Delta waves, like all brain waves, are detected by electroencephalography (EEG). Delta waves were originally defined as having a frequency between 1-4 hertz, although more recent classifications put the boundaries at between 0.5 and 2 hertz. They are the slowest, but highest amplitude brainwaves. 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.[2] During N3 SWS, delta waves account for 20% or more of the EEG record during this stage.[3] 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.[4]
Females have been shown to have more delta wave activity, and this is true across most mammal species. This discrepancy does not become apparent until early adulthood (in the 30's or 40's, in humans), with men showing greater age-related reductions in delta wave activity than their female counterparts.[5] It has been suggested that this discrepancy may be due to larger skull size in males, but this theory has been refuted by intracranial data from female cats, which still show more delta activity.
Delta waves can arise either in the thalamus or in the cortex. When associated with the thalamus, they likely arise in coordination with the reticular formation.[6][7] In the cortex, the suprachiasmatic nuclei has 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.[8] Delta waves have been shown to be mediated in part by T-type calcium channels.[9] During delta wave sleep, neurons are globally inhibited by gamma-aminobutyric acid (GABA).[10]
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 from the pituitary. Like growth hormone, the secretion of prolactin - which is closely related to growth hormone (GH) - is also regulated by the pituitary. Thyroid stimulating hormone (TSH) activity is decreased in response to delta-wave signaling.[11]
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 wave forms 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.[12] 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.[13] 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.[14] 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 common seen in older adults, and incidences also increase with age.[15]
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.[16]
Temporal low-voltage irregular delta wave activity has been commonly detected in patients with ischemic brain diseases. In addition, small ischemic lesions have been shown to be closely correlated with TLID, and are indicative of early-stage cerebrovasular damage.[17]
Parasomnias 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 activity) compared to total time spent in stages 2, 3, and 4 sleep relative to healthy controls. Hypersynchronous Delta Activity (HSD) are continuous, high-voltage (> 150 uV) delta waves seen in sleep EEGs.[18] Parasomnias which occur deep in NREM sleep also include sleep terrors and confusional arousals.
Total sleep deprivation has been shown to increase delta wave activity during sleep recovery,[19] and has also been shown to increase hypersynchronous delta activity (HSD).[18]
Sleep disturbances, as well as dementia, are common features of Parkinson's disease, and patients with PD show disrupted brain wave activity. The drug rotigotine, developed for PD, has been shown to increase delta power and slow-wave sleep in those with Parkinson's disease. Interestingly, delta-wave inducing peptide injected into the substantia nigra of the rat model has been shown to increase parkinsonian symptoms.[20]
People suffering 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), schizophrenics 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.[21] 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.[22]
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.[23] Low-voltage irregular delta waves (TLID) have also been found in the left temporal lobe of diabetic patients, at a rate of 56% (compared to 14% in healthy controls).[24][25]
Patients suffering from 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.[26]
Alcohol has been shown to decrease slow wave sleep and 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.[27]
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.[28] 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.[29]
Other disorders frequently associated with disrupted delta-wave activity include:
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. Delta waves and delta wave activity are marked by an 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 the formation of declarative and explicit memory formation. [10]
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.
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.[36]
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