Brain Spikes During Rem Sleep: Understanding Eeg Readings

Electroencephalography (EEG) is a non-invasive technique used to measure brain activity through the scalp. It is used to detect brain activity during sleep and can be used to distinguish between the different stages of sleep. During REM sleep, the EEG reading is quite the opposite of what is seen in deep sleep, with low amplitude events at a high frequency. This is because of asynchronous firing activity in the brain, and REM sleep is sometimes also called paradoxical sleep.

During REM sleep, the brain acts as if it is awake, with cerebral neurons firing with the same overall intensity as in wakefulness. This is in contrast to the slow delta waves pattern of NREM deep sleep. An important element of this contrast is the 3–10 Hz theta rhythm in the hippocampus and 40–60 Hz gamma waves in the cortex.

REM sleep is characterised by low muscle tone and an abundance of the neurotransmitter acetylcholine

REM sleep is generated and maintained by the interaction of various neurotransmitter systems in the brainstem, forebrain, and hypothalamus. The subcoeruleus nucleus (SubC) or sublaterodorsal nucleus is a core region that is active during REM sleep. It is hypothesised that glutamatergic SubC neurons regulate REM sleep and its defining features, such as muscle paralysis and cortical activation.

During REM sleep, acetylcholine activates spinally projecting SubC neurons. These cholinergic inputs into the SubC neurons mediate muscle atonia by enhancing glutamate-driven postsynaptic excitation and facilitating presynaptic glutamate release. These results demonstrate that acetylcholine not only acts to directly entrain the core of the REM sleep circuitry but also modulates the glutamatergic mechanisms that underlie REM sleep muscle control.

REM sleep is also characterised by muscle atonia or paralysis. This is initiated when glutamatergic SubC cells activate neurons in the ventral medial medulla, which causes the release of GABA and glycine onto skeletal motoneurons. Both GABA and glycine inhibition of motoneurons are required for producing REM sleep muscle paralysis. However, acetylcholine also appears to suppress respiratory motoneuron activity during natural REM sleep.

During REM sleep, the brain acts similarly to when awake, with neurons firing at the same intensity

During REM sleep, the brain exhibits fast, low-amplitude, desynchronised neural oscillation (brainwaves) that resemble the pattern seen during wakefulness. This is in contrast to the slow delta waves observed during NREM deep sleep. The cortical and thalamic neurons in the REM sleeping brain are more depolarised (fire more readily) than in NREM deep sleep.

The EEG reading of a person in REM sleep shows a lot of low-amplitude events at a high frequency. This is the opposite of what is seen in deep sleep, where large-amplitude events occur at a low frequency. The brain in REM sleep has an asynchronous firing pattern, which is more similar to the brain activity of a person who is awake.

REM sleep is also characterised by an abundance of the neurotransmitter acetylcholine, combined with an almost complete absence of monoamine neurotransmitters such as histamine, serotonin, and norepinephrine. The absence of norepinephrine means that experiences of REM sleep are not transferred to permanent memory.

During REM sleep, the brain consumes an equal or greater amount of energy compared to when awake. This is in contrast to NREM sleep, where energy consumption is 11-40% lower.

The brainstem is thought to be responsible for electrical and chemical activity during REM sleep

REM sleep is characterised by a constellation of events, including:

• Low-amplitude synchronisation of fast oscillations in the cortical EEG (also called activated EEG).
• Very low muscle tone (atonia) in the EMG. The atonia is particularly strong in antigravity muscles, while the diaphragm and extra-ocular muscles retain substantial tone.
• Singlets and clusters of REMs in the EOG.

Two other physiological signs that can be used to identify REM sleep in non-human primates, rats, and cats are:

• Theta rhythm in the hippocampal EEG.
• Spiky field potentials in the pons (P-waves), lateral geniculate nucleus, and occipital cortex (called ponto-geniculo-occipital (PGO) spikes).

The brainstem is also associated with phasic REM sleep, which occurs episodically and includes rapid eye movements, muscle twitches, and autonomous instability.

REM sleep is also known as paradoxical sleep due to its similarities to wakefulness

REM sleep is also known as paradoxical sleep because of its similarities to wakefulness. While the body is paralysed during REM sleep, the brain acts as if it is somewhat awake, with cerebral neurons firing with the same overall intensity as in wakefulness.

Electroencephalography (EEG) readings during REM sleep reveal fast, low-amplitude, desynchronized neural oscillation (brainwaves) that resemble the pattern seen during wakefulness. This is in contrast to the slow delta waves pattern of NREM deep sleep. An important element of this contrast is the 3–10 Hz theta rhythm in the hippocampus and 40–60 Hz gamma waves in the cortex; patterns of EEG activity similar to these rhythms are also observed during wakefulness.

The cortical and thalamic neurons in the waking and REM sleeping brain are more depolarized (fire more readily) than in the NREM deep sleeping brain. Human theta wave activity predominates during REM sleep in both the hippocampus and the cortex.

During REM sleep, electrical connectivity among different parts of the brain manifests differently than during wakefulness. Frontal and posterior areas are less coherent in most frequencies, a fact which has been cited in relation to the chaotic experience of dreaming. However, the posterior areas are more coherent with each other; as are the right and left hemispheres of the brain, especially during lucid dreams.

Brain energy use in REM sleep, as measured by oxygen and glucose metabolism, equals or exceeds energy use in waking. The rate in non-REM sleep is 11–40% lower.

The core body and brain temperatures increase during REM sleep, and skin temperature decreases to its lowest values. Organisms in REM sleep suspend central homeostasis, allowing large fluctuations in respiration, thermoregulation, and circulation which do not occur in any other modes of sleeping or waking.

The transition to REM sleep brings marked physical changes, beginning with electrical bursts called "ponto-geniculo-occipital waves" (PGO waves) originating in the brain stem. These waves occur in clusters about every 6 seconds for 1–2 minutes during the transition from deep to paradoxical sleep. They exhibit their highest amplitude upon moving into the visual cortex and are a cause of the "rapid eye movements" in paradoxical sleep.

The monoamine neurotransmitters norepinephrine, serotonin, and histamine are completely unavailable during REM sleep. Injections of acetylcholinesterase inhibitor, which effectively increases available acetylcholine, have been found to induce paradoxical sleep in humans and other animals already in slow-wave sleep.

REM sleep is physiologically different from the other phases of sleep, which are collectively referred to as non-REM sleep (NREM sleep, NREMS, synchronized sleep).

Dreaming is more likely to occur during REM sleep

REM sleep, or rapid eye movement sleep, is a unique phase of sleep in humans and other mammals, during which the eyes move rapidly, and the body experiences muscle atonia, or loss of muscle control. This phase of sleep is characterised by brain activity that is similar to that of a waking brain. In fact, the brain in REM sleep has a pattern of activity that is more similar to a person who is awake than asleep! Because of this asynchronous firing activity, REM sleep is sometimes also called paradoxical sleep.

During REM sleep, the brain exhibits fast, low-amplitude, desynchronised neural oscillations (brain waves) that resemble the pattern seen during wakefulness. This is in contrast to the slow delta waves pattern of non-REM deep sleep. The cortical and thalamic neurons in the waking and REM sleeping brain are more depolarised (fire more readily) than in non-REM deep sleep. Human theta wave activity predominates during REM sleep in both the hippocampus and the cortex.

The transition to REM sleep brings about marked physical changes, beginning with electrical bursts called ponto-geniculo-occipital waves (PGO waves) originating in the brain stem. The body abruptly loses muscle tone, a state known as REM atonia.

REM sleep is also associated with dreaming. Waking up sleepers during a REM phase is a common experimental method for obtaining dream reports; 80% of neurotypical people can give some kind of dream report under these circumstances. Sleepers awakened from REM tend to give longer, more narrative descriptions of the dreams they were experiencing, and to estimate the duration of their dreams as longer. Lucid dreams are reported far more often in REM sleep.

During a typical night's sleep, humans usually experience about four or five periods of REM sleep; they are shorter at the beginning of the night and longer toward the end. The relative amount of REM sleep varies considerably with age. A newborn baby spends more than 80% of total sleep time in REM. REM sleep typically occupies 20–25% of total sleep in adult humans: about 90–120 minutes of a night's sleep. The first REM episode occurs about 70 minutes after falling asleep. Cycles of about 90 minutes each follow, with each cycle including a larger proportion of REM sleep.

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