A study on intracerebral EEG recording during

A study on intracerebral EEG recording during sleep documented a dissociation of regional EEG activities during a parasomnia episode, illustrating how the guanidine hydrochloride phenomenon of “local sleep” can be the substrate for clinical dissociated states [17]. In this study, a young adult male with refractory focal epilepsy had a CA recorded by vPSG and intracerebral EEG. The dissociated state underlying the CA episode consisted of local arousal of the motor and cingulate cortices that contrasted with simultaneous increased slow waves in the frontoparietal associative cortices. These findings were present before the onset of the CA episode and throughout the CA. Therefore, this carefully documented CA episode was not a global sleep phenomenon, but rather a phenomenon of coexisting and contrasting local states of sleep and wakefulness. A new clinical frontier for achieving a deeper understanding of NREM sleep parasomnias and other sleep disorders has been opened up by the use of high-density (256 electrode channels) sleep EEG monitoring during vPSG studies, developed by the Tononi group. In a recent study utilizing high-density sleep EEG in six healthy subjects [18], a total of 141 falling-asleep periods were analyzed to assess changes in slow-wave and spindle activity during this transitional state. The major finding was that the number and amplitude of slow waves followed two dissociated, intersecting courses during the wake-sleep transition: slow wave number increased slowly at the beginning and rapidly at the end of the falling-asleep period, whereas amplitude at first increased rapidly and then decreased linearly. Most slow waves occurring early in the transition to sleep had a large amplitude, a steep slope, and involved broad regions of the cortex. Most slow waves occurring later had a smaller amplitude and slope, and involved more circumscribed parts of the cortex. Spindles were initially sparse, fast, and involved few cortical regions, then became more numerous and slower, and involved more areas. The two types of slow waves identified in the wake-sleep transition had distinct cortical origins and distributions. The authors hypothesized that these two types of slow waves result from two distinct synchronization processes: (1) a subcortico-cortical, arousal system-dependent, process that predominates in the early phase and leads to “type I slow waves”, and (2) a “horizontal”, cortico-cortical synchronization process that predominates in the late phase and leads to “type II slow waves”. The authors concluded that the dissociation between these two slow-wave synchronization processes in time and (brain) space suggests that they could become pathologically disturbed with sleep disorders – including NREM sleep parasomnias that emerge from slow-wave sleep. Other promising future research areas that could lead to a deeper understanding of NREM sleep parasomnias include various brain imaging techniques (including SPECT, PET, transcranial magnetic stimulation), and familial, genetic, and molecular studies that should provide additional critical information on the neurobiological substrate of NREM sleep parasomnias [13].
Update on RBD The “RBD odyssey” [19] continues at an accelerated pace while covering ever-expanding territories of research. The literature on RBD has continued to grow exponentially, both in breadth and depth since the exponential growth of RBD publications was first quantified [20]. The most compelling research, conducted by numerous international investigators, concerns the strong associations of RBD with neurodegenerative disorders, especially the alpha-synucleinopathies, viz. Parkinson disease (PD) dementia with Lewy bodies (DLB), and Multiple System Atrophy (MSA) [21,22]. There are two perspectives for considering this strong association. First, RBD can be the first clinical manifestation of future alpha-synucleinopathy neurodegeneration. Data from our center and from the Barcelona group have recently documented 81% and 82% “conversion rates”, respectively, from idiopathic RBD (iRBD) to a parkinsonian disorder, with a mean interval of approximately 12–14 years from onset of iRBD to the clinical emergence of parkinsonism and/or dementia [23,24]. Second, RBD has a strong presence in established neurodegenerative disorders: 90–100% in MSA, approximately 75% in DLB, and up to nearly 50% in PD [21]. The pathogenesis for how RBD can emerge before, during or after the emergence of an alpha-synucleinopathy has been proposed [22].