The original conceptualization of REM sleep as paradoxical sleep was based on its EEG resembling wakefulness and its association with dreaming. Over time, the concept of paradox was expanded to include various associations with REM sleep, such as dream exclusivity, high recall, and pathophysiology. However, none of these associations are unique to REM sleep; they can also occur in other sleep states. Today, after more than fifty years of focused research, two aspects of REMS clearly retain paradoxical exclusivity. Despite the persistent contention that the EEG of human REMS consists of wake-like, low-voltage, non-synchronous electrical discharges, REMS is based on and defined by the intracranial electrical presence of 5-8 Hz. theta, which has always been the marker of REMS in other animals. The wake-like EEG used to define REMS on human polysomnography is secondary to a generalized absence of electrophysiological waveforms because the strong waves of intracranial theta do not propagate to scalp electrodes placed outside the skull. It is a persistent paradox that the theta frequency is restricted to a cyclical intracranial dynamic that does not extend beyond the lining of the brain. REMS has a persistent association with narratively long and salient dream reports. However, the extension of this finding to equate REMS with dreaming led to a foundational error in neuroscientific logic. Major theories and clinical approaches were built upon this belief despite clear evidence that dreaming is reported throughout sleep in definingly different physiologic and phenomenological forms. Few studies have addressed the differences between the dreams reported from the different stages of sleep so that today, the most paradoxical aspect of REMS dreaming may be how little the state has actually been studied. An assessment of the differences in dreaming between sleep stages could provide valuable insights into how dreaming relates to the underlying brain activity and physiological processes occurring during each stage. The brain waves and dreams of REMS persist as being paradoxically unique and different from waking and the other states of sleep consciousness.

The ventral subiculum regulates emotion, stress responses, and spatial and social cognition. In our previous studies, we have demonstrated anxiety- and depression-like symptoms, deficits in spatial and social cognition in ventral subicular lesioned (VSL) rats, and restoration of affective and cognitive behaviors following photoperiod manipulation (short photoperiod regime, SPR; 6:18 LD cycle). In the present study, we have studied the impact of VSL on sleep-wake behavioral patterns and the effect of SPR on sleep-wakefulness behavior. Adult male Wistar rats subjected to VSL demonstrated decreased wake duration and enhanced total sleep time due to increased non-rapid eye movement sleep (NREMS) and rapid eye movement sleep (REMS). Power spectral analysis indicated increased delta activity during NREMS and decreased sigma band power during all vigilance states. Light is one of the strongest entrainers of the circadian rhythm, and its manipulation may have various physiological and functional consequences. We investigated the effect of 21-day exposure to SPR on sleep-wakefulness (S-W) behavior in VSL rats. We observed that SPR exposure restored S-W behavior in VSL rats, resulting in an increase in wake duration and a significant increase in theta power during wake and REMS. This study highlights the crucial role of the ventral subiculum in maintaining normal sleep-wakefulness patterns and highlights the effectiveness of photoperiod manipulation as a non-pharmacological treatment for reversing sleep disturbances reported in mood and neuropsychiatric disorders like Alzheimer\'s disease, bipolar disorder, and major depressive disorder, which also involve alterations in circadian rhythm.

Sleep is an indispensable normal physiology of the human body fundamental for healthy functioning. It has been observed that Parkinson\'s disease (PD) not only exhibits motor symptoms, but also non-motor symptoms such as metabolic irregularities, altered olfaction, cardiovascular dysfunction, gastrointestinal complications and especially sleep disorders which is the focus of this review. A good understanding and knowledge of the different brain structures involved and how they function in the development of sleep disorders should be well comprehended in order to treat and alleviate these symptoms and enhance quality of life for PD patients. Therefore it is vital that the normal functioning of the body in relation to sleep is well understood before proceeding on to the pathophysiology of PD correlating to its symptoms. Suitable treatment can then be administered toward enhancing the quality of life of these patients, perhaps even discovering the cause for this disease.

Depression occurs frequently with sleep disturbance such as insomnia. Sleep in depression is associated with disinhibition of the rapid eye movement (REM) sleep. Despite the coincidence of the depression and sleep disturbance, neural substrate for depressive behaviors and sleep regulation remains unknown. Habenula is an epithalamic structure regulating the activities of monoaminergic neurons in the brain stem. Since the imaging studies showed blood flow increase in the habenula of depressive patients, hyperactivation of the habenula has been implicated in the pathophysiology of the depression. Recent electrophysiological studies reported a novel role of the habenular structure in regulation of REM sleep. In this article, we propose possible cellular mechanisms which could elicit the hyperactivation of the habenular neurons and a hypothesis that dysfunction in the habenular circuit causes the behavioral and sleep disturbance in depression. Analysis of the animals with hyperactivated habenula would open the door to understand roles of the habenula in the heterogeneous symptoms such as reduced motor behavior and altered REM sleep in depression.

Recently, we proposed a novel biophysical concept regarding on the appearance of brilliant lights during near death experiences (NDEs) (Bókkon and Salari, 2012). Specifically, perceiving brilliant light in NDEs has been proposed to arise due to the reperfusion that produces unregulated overproduction of free radicals and energetically excited molecules that can generate a transient enhancement of bioluminescent biophotons in different areas of the brain, including retinotopic visual areas. If this excess of bioluminescent photon emission exceeds a threshold in retinotopic visual areas, this can appear as (phosphene) lights because the brain interprets these intrinsic retinotopic bioluminescent photons as if they originated from the external physical world. Here, we review relevant literature that reported experimental studies (Imaizumi et al., 1984; Suzuki et al., 1985) that essentially support our previously published conception, i.e., that seeing lights in NDEs may be due to the transient enhancement of bioluminescent biophotons. Next, we briefly describe our biophysical visual representation model that may explain brilliant lights experienced during NDEs (by phosphenes as biophotons) and REM sleep associated dream-like intrinsic visual imageries through biophotons in NDEs. Finally, we link our biophysical visual representation notion to self-consciousness that may involve extremely low-energy quantum entanglements. This article is intended to introduce novel concepts for discussion and does not pretend to give the ultimate explanation for the currently unanswerable questions about matter, life and soul; their creation and their interrelationship.