Sleep is a critical and ubiquitous neural and physiological behavior in the animal kingdom. Long-term sleep loss results in death, and acute sleep loss on the order of 24-72 hours results in significant cognitive degradation. While it is generally accepted that sleep is critical for normal brain function, there is as yet no agreement upon function of sleep. It is also the case that disturbances of sleep are a hallmark of most, if not all, neurological diseases and that disturbances of sleep itself can contribute to morbidity from obesity to depression and anxiety. Thus, to gain an improved understanding of the potentially synergistic effects of sleep pathology and neuropathology, it is critical to improve our knowledge of the changes in brain network function that accompany both normal and pathological sleep.
Clinically, human sleep and sleep pathology are defined based upon scalp recorded electrical potentials (electroencephalography, EEG), which have provided seminal information on changes of brain electrophysiology associated with pathologies that adversely affect, or are pathologies of, sleep. However, no single method can examine all aspects of the neural control of sleep or its disruption in pathology. Early studies of normal sleep network activity utilizing positron emission tomography (PET) imaging provided fundamental information on the global network changes associated with specific stages of sleep, much of which has been confirmed recently using functional magnetic resonance imaging (fMRI). Studies employing simultaneous EEG/fMRI have extended these findings to explore specific electrical signatures of sleep, such as sleep spindles. This technique has also contributed new information on the reconfiguration of functional brain networks during normal human sleep using graph theoretical approaches, showing that shifts in these networks are a hallmark of different sleep stages. Studies using EEG and transcranial magnetic stimulation (TMS) have provided new information on the propagation of slow waves in deep sleep, and mechanisms by which sensory information entering the brain during deep sleep is prevented from reaching higher cortical levels. These studies have been extended recently by use of electrocorticography (ECoG), showing that sleep is not solely a global change in functional brain activity, but can also occur locally. These findings may provide a mechanism for the cognitive dysfunction seen in sleep deprivation, where local brain regions may “sleep” even during behavioral wake.
Thus, modern sleep medicine requires a multi-modal approach to the investigation of brain changes occurring in response to or as causative mechanisms of sleep-related neuropathology. In this issue electromagnetic (EEG, magnetoencephalography (MEG), and ECoG), functional imaging (PET,(fMRI), anatomical (morphometry and diffusion imaging (DTI, DWI, DTT)) imaging and network modeling approaches will be utilized to study sleep across the lifespan and to examine changes associated with pathologies of sleep.
Sleep is a critical and ubiquitous neural and physiological behavior in the animal kingdom. Long-term sleep loss results in death, and acute sleep loss on the order of 24-72 hours results in significant cognitive degradation. While it is generally accepted that sleep is critical for normal brain function, there is as yet no agreement upon function of sleep. It is also the case that disturbances of sleep are a hallmark of most, if not all, neurological diseases and that disturbances of sleep itself can contribute to morbidity from obesity to depression and anxiety. Thus, to gain an improved understanding of the potentially synergistic effects of sleep pathology and neuropathology, it is critical to improve our knowledge of the changes in brain network function that accompany both normal and pathological sleep.
Clinically, human sleep and sleep pathology are defined based upon scalp recorded electrical potentials (electroencephalography, EEG), which have provided seminal information on changes of brain electrophysiology associated with pathologies that adversely affect, or are pathologies of, sleep. However, no single method can examine all aspects of the neural control of sleep or its disruption in pathology. Early studies of normal sleep network activity utilizing positron emission tomography (PET) imaging provided fundamental information on the global network changes associated with specific stages of sleep, much of which has been confirmed recently using functional magnetic resonance imaging (fMRI). Studies employing simultaneous EEG/fMRI have extended these findings to explore specific electrical signatures of sleep, such as sleep spindles. This technique has also contributed new information on the reconfiguration of functional brain networks during normal human sleep using graph theoretical approaches, showing that shifts in these networks are a hallmark of different sleep stages. Studies using EEG and transcranial magnetic stimulation (TMS) have provided new information on the propagation of slow waves in deep sleep, and mechanisms by which sensory information entering the brain during deep sleep is prevented from reaching higher cortical levels. These studies have been extended recently by use of electrocorticography (ECoG), showing that sleep is not solely a global change in functional brain activity, but can also occur locally. These findings may provide a mechanism for the cognitive dysfunction seen in sleep deprivation, where local brain regions may “sleep” even during behavioral wake.
Thus, modern sleep medicine requires a multi-modal approach to the investigation of brain changes occurring in response to or as causative mechanisms of sleep-related neuropathology. In this issue electromagnetic (EEG, magnetoencephalography (MEG), and ECoG), functional imaging (PET,(fMRI), anatomical (morphometry and diffusion imaging (DTI, DWI, DTT)) imaging and network modeling approaches will be utilized to study sleep across the lifespan and to examine changes associated with pathologies of sleep.
