Rapid eye movement (REM) sleep is the main sleep correlate of dreaming. Ponto-geniculo-occipital (PGO) waves are a signature of REM sleep. They represent the physiological mechanism of REM sleep that specifically limits the processing of external information. PGO waves look just like a message sent from the pons to the lateral geniculate nucleus of the visual thalamus, the occipital cortex, and other areas of the brain. The dedicated visual pathway of PGO waves can be interpreted by the brain as visual information, leading to the visual hallucinosis of dreams. PGO waves are considered to be both a reflection of REM sleep brain activity and causal to dreams due to their stimulation of the cortex. In this review, we summarize the role of PGO waves in potential neural circuits of two major theories, i.e., (1) dreams are generated by the activation of neural activity in the brainstem; (2) PGO waves signaling to the cortex. In addition, the potential physiological functions during REM sleep dreams, such as memory consolidation, unlearning, and brain development and plasticity and mood regulation, are discussed. It is hoped that our review will support and encourage research into the phenomenon of human PGO waves and their possible functions in dreaming.

Sleep – wake disturbances (SWDs) are one of the most common complaints following traumatic brain injury (TBI). The high prevalence and socioeconomic burden of SWDs post-TBI have only been recognized in the past decade. Common SWDs induced by TBI include excessive daytime sleepiness (EDS), hypersomnia, insomnia, obstructive sleep apnea (OSA), and circadian rhythm sleep disorders. Sleep disturbances can significantly compromise quality of life, strain interpersonal relationships, diminish work productivity, exacerbate other clinical conditions, and impede the rehabilitation process of TBI patients. Consequently, the prompt regulation and enhancement of sleep homeostasis in TBI patients is of paramount importance. Although studies have shown that abnormal neural network function, neuroendocrine changes, disturbance of sleep – wake regulators, and immune inflammatory responses related to brain structural damage induced by TBI are involved in the development of SWDs, the exact neuropathological mechanisms are still poorly understood. Therefore, we systematically review the current clinical and experimental studies on the characteristics and possible neural mechanisms of post-TBI SWDs. Elucidating the neural underpinnings of post-TBI SWDs holds the potential to diversify and enhance therapeutic approaches for these conditions. Such advancements could hasten the recuperation of TBI patients and ameliorate their overall quality of life. It is our aspiration that departments specializing in neurosurgery, rehabilitation, and neuropsychiatry will be able to recognize and address these conditions promptly, thereby facilitating the healing journey of affected individuals.

Background/Objectives: Sleep–wake states strongly influence seizure susceptibility, but the circuit mechanisms linking arousal regulation to seizure burden in chronic temporal lobe epilepsy (TLE) remain unclear. This study investigated whether hypothalamic orexin neurons regulate sleep architecture, spontaneous seizures, and epileptic network activity in a kainic acid (KA)-induced chronic TLE model in male mice. Methods: Continuous video-EEG/EMG recordings were used to quantify sleep–wake states, circadian seizure distribution, and seizure burden. Orexin neurons were bidirectionally manipulated in KA-treated Hcrt-Cre mice using Cre-dependent hM3Dq or hM4Di chemogenetic tools. Orexin receptor 1 signaling was pharmacologically blocked with SB334867. Power spectral density and phase–amplitude coupling analyses were performed across wakefulness, non-rapid eye movement sleep, and rapid eye movement sleep. Results: Spontaneous seizures occurred predominantly during wakefulness and non-rapid eye movement sleep, with no seizures observed during rapid eye movement sleep. Seizure occurrence was greater during the dark phase and remained higher during wakefulness after correction for state occupancy. Chemogenetic activation of orexin neurons increased wakefulness, reduced sleep, and increased seizure count and total seizure duration, whereas chemogenetic inhibition produced opposite effects. SB334867 promoted sleep and reduced seizure count and total seizure duration. Chronic KA mice showed state-dependent spectral remodeling and enhanced delta–high-gamma coupling, which was partially attenuated by SB334867 during non-rapid eye movement and rapid eye movement sleep. Conclusions: These findings suggest that orexin signaling is associated with sleep–wake regulation, abnormal network coupling, and seizure burden in chronic TLE. Modulating orexin signaling may represent a potential direction for future therapeutic investigation aimed at improving sleep disruption and reducing seizure burden.