Iranzo et al. found that the δ and θ powers of the RBD group were increased and the α and β powers were reduced compared with the HC group. Maria Livia et al. studied patients with RBD during wakefulness and found that the θ power in the frontal, temporal, and occipital regions was significantly enhanced and the β-power in the occipital region was significantly reduced. In the REM sleep phase, only the β-power of the occipital region was decreased, suggesting that cortical activation of the occipital region was impaired. Raffaele et al. confirmed EEG instability during REM sleep in RBD patients, while the mean EEG power was not significantly affected . The results of this study show that compared with the HC group, the α power in the RBD group during REM sleep was significantly enhanced, inconsistent with the above results. This may be because this study focuses on the analysis data obtained during the REM phase, especially during abnormal behavior and selects more dream-related behaviors. The EEG signal from the average reference lead, used to obtain a more stable EEG signal, shows a significant difference in alpha power. It indicates that the cerebral cortical function of RBD patients has changed in REM sleep, especially during the period of dreaming. Figure 2 shows that the slow-wave frequency band (δ, θ) to α power ratio are significantly specific and there may be no significant change in the δ and θ band powers of the RBD group, while the α-band is significantly enhanced, indicating cerebral cortical function during RBD. The change is only related to the α band, but not to other neural bands, including the characteristic θ band.
John Peever et al. pointed out that REM sleep neuropathic disorders are the basis of RBD disease physiology. They state that in patients with RBD the dorsal nucleus-ventral giant cell reticular nucleus (SLD-GiV) pathway in the dorsal ganglion cannot inhibit spinal motor neurons, allowing them to accept the excitatory projection of the motor cortex, thereby producing motor behavior during REM sleep. McKenna et al. also suggested that during the REM phase, the lower dorsal side of the RBM sleep neuron was degenerated by the nucleus-ventral medial medulla (Sub-VMM), preventing it from inhibiting motor neurons, leading to REM sleep achalasia, resulting in excessive muscle activity and exercise-like behavior .
V-PSG monitoring can be used to observe the achalasia of the mandibular or tibialis anterior muscles of RBD patients. The cerebral cortical function changes in RBD may be similar to skeletal muscle achalasia, both of which are involved in RBD neuropathic disorders. Increased alpha power suggests the hyperactivity of the cerebral cortex, which is similar to what is seen during skeletal muscle activity. The α-rhythm is the main brain wave of EEG in the resting state during wakefulness. The increased α power indicates that the RBD group cannot enter the inhibited state like the HC group. Although the frequency band with dominant EEG power during the REM phase is still the θ band, the increase in α power may suggest that the cerebral cortex is over-inhibited and hyperactive.
Figure 3 shows that in the REM phase, descending SLD neurons activate gamma-aminobutyric acid (GABA) and glycinergic neurons in the GiV nucleus, continue to descend, and project to spinal skeletal motor neurons, resulting in REM muscle relaxation. Another group of ascending SLD neurons activates the thalamic cortical neurons, which in turn activate the cortex. In normal REM sleep, the SLD-GiV pathway inhibits spinal motor neurons and motor neurons block projections from the motor cortex. In RBD patients, the SLD-GiV pathway has degenerated, resulting in the loss of inhibition of motor neurons, which in turn allows motor neurons to project from the motor cortex .
Of course, the physiological mechanism of RBD is also related to the locus coeruleus, dorsal sulcus, substantia nigra, and lateral hypothalamus [11-13]. Neuronal degeneration leads to neurotransmitter disorders, such as GABA- and glycine-mediated loss of motor neuron inhibition [14-17].
This study found that during RBD, the cerebral cortex may be more active than during healthy REM sleep. Therefore, the degeneration of the SLD-GiV pathway causes it to attenuate spinal motor neurons activation in the descending pathway, and it is speculated that there may be another upstream pathway, which is also mediated by neurotransmitters, that also weakens the inhibition of this upward pathway. The cerebral cortex excitability is increased. The amygdala is the main nucleus that deals with negative emotions such as anger [18, 19]. In view of the fact that most dreams have violent content, it may weaken the inhibition of related nuclei in the amygdala. These nuclei are related to violent emotions, leading to excessive cerebral cortical activity and increased violent dreams.
Excessive cerebral cortical activity is another important phenomenon of RBD, in addition to muscle achalasia. Moderately inhibiting the cerebral cortex may be of great significance in the treatment of RBD. Li SX and other studies have shown that taking moderate doses of clonazepam can improve the dreams of RBD patients and reduce their dream-related behaviors such as speech and physical activity, but the patient’s persistent and temporal myoelectric activity increases . Therefore, clonazepam can effectively treat patients with RBD, an effect that may be closely related to the inhibition of cerebral cortex hyperactivity.