During REM (rapid eye movement) sleep, mammals exhibit skeletal muscle twitches as well as disjunctive eye movements (Zhou and King 1997), under suppression of skeletal body movements due to the inhibition both of the alpha and gamma spinal cord neurons and of the 1a sensory afferents that carry proprioceptive information (Chase and Harper 1971; Blumberg et al. 2013a; Pompeiano 1967). As well, breathing becomes faster and irregular during REM sleep, and the heart rate and blood pressure increase to near waking levels. It is believed that the muscle twitches during sleep, including REM sleep, contribute to learning during development and adulthood (Blumberg et al. 2013ab). The result of conscious/motor learning is the establishment of a series of well-organized muscle contractions that can be put under volitional or automatic control to produce behavior (Hebb 1949; James 1890; Kimura 1993; Penfield and Roberts 1966; Sherrington 1906; Tehovnik, Hasabegović, Chen 2024; Vanderwolf 2007). Especially during development, the twitches could update the efference-copy signal at the cerebellar Purkinje neurons (Bell et al. 1997; De Zeeuw 2021; Loyola et al. 2019; Shadmehr 2020; Tehovnik et al. 2021; Wang et al. 2023) to accommodate oculo- and skeletomotor behaviors that develop at an accelerated rate, especially during the adolescent growth spurt (Blumberg et al. 2013b).
Measuring complex-spike transients with calcium imaging in the cerebellum has revealed that transient activity during REM sleep occurs twice following a muscle twitch, at 100 and 500 ms after a twitch (Canto, De Zeeuw et al. 2023). Given that the first 100-ms transient activation occurs during wakefulness and during slow-wave sleep, it is highly likely that this represents proprioceptive feedback even though the transmission of proprioception is under inhibition during sleep (Canto, De Zeeuw et al. 2023; Chase and Harper 1971; Blumberg et al. 2013a; Pompeiano 1967). Significantly, during sleep the magnitude of the transient activation is suppressed when compared to the waking state (see Fig. 1). The second peak at 500 ms could very well be related to that other characteristic of REM sleep, namely, dreaming (Hobson 2002). During wakefulness and slow-wave sleep, there is no second transient activation. Single unit recordings have revealed that complex-spike activity is most robust during REM sleep, as compared to periods of waking and slow-wave sleep (see Fig. 6 of Hobson and McCarley 1972). Also, complex-spike firing tends to precede an eye movement during REM sleep (based on recordings done from oculomotor lobule VI, see Fig. 5 of Hobson and McCarley 1972).
As REM sleep progresses, there are not only fragments of movement expressed (i.e., skeletal muscle twitches and disjunctive ocular movements) but also fragments of consciousness (i.e., dreaming, Hobson 2002; also see Senzai and Scanziani 2022), meaning that perhaps both movement and consciousness are being programmed simultaneously during REM sleep (Boyce et al. 2016; Louie and Wilson 2001). During slow-wave sleep, however, which is not associated with dreaming, only movements (anchored to sensations, e.g., place fields) are being programmed by performing the replay of learned activity under temporal compression (Wilson and McNaughton 1994), that is, not in real time as occurs for memory consolidation during REM sleep (Boyce et al. 2016; Louie and Wilson 2001).
Following a twitch during REM sleep, a proprioceptive signal is fed-back to the hippocampus, neocortex, and cerebellum (Canto, De Zeeuw et al. 2023; Khazipov et al. 2004; Mohns and Blumberg 2010; Tiriac et al. 2012), which could be used to modify synapses for learning (Hebb 1949; Kandel 2006; Peever and Fuller 2016). It is suggested that the twitches during REM sleep occur independently of the neocortex, since disconnecting the neocortex from the brainstem by a midbrain transection does not abolish the twitches (but the rapid eye movements are diminished by fixing the eyes in orbit, Villablanca 1966), but this says nothing about whether the twitches are linked to the dreams when neocortex is intact. It is curious that Parkinson’s patients with a 99% reduction of dopamine exhibit a neocortical EEG profile of slow-wave sleep, suggesting that they are in a perpetual slow-wave state of unconsciousness (Sacks 2012); such patients have arrested movements and arrested thinking/conscious flows with little evidence of new learning, a tendency that can last for decades (Sacks 1976, 2012).
Accordingly, it is suggested that both movement execution and consciousness are being programmed at the level of the hippocampus, neocortex, and cerebellum during REM sleep as part of the memory consolidation process that must occur simultaneously throughout the central nervous system.
Figure 1: During REM sleep, some 100 and 500 ms after a muscle twitch (of neck muscles) there is evidence of calcium-transient activity, which has been used to suggest an enhancement in the generation of complex spikes in the cerebellum of mice. Data are also included for periods of wakefulness for comparison. From figure 4 of Canto, De Zeeuw et al. (2023).
Since thinking IS (stands for) dreaming - you can separate dreaming in the mind's the awake state from dreaming in its sleeping state. Since mind self-organizes during sleep one might define the REM-state with its eye movement is a simulation of the minds waken habits of programming the memory. Otherwise is seems difficult to account for the eye movement.
However, this is merely speculations - and I think you have to ask your mind - and I am pretty certain your mind has no opinion of how human beings in general use their words ... So, this is a question that lacks of answer.
However, abnormal REM-state signals can be a diagnostic indicator of brain damage or other insufficiencies ...
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