Arch Ital Biol
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Electroencephalographic activity in the context of disorders of consciousness is a swiss knife like tool that can evaluate different aspects of cognitive residual function, detect consciousness and provide a mean to communicate with the outside world without using muscular channels. Standard recordings in the neurological department offer a first global view of the electrogenesis of a patient and can spot abnormal epileptiform activity and therefore guide treatment. Although visual patterns have a prognosis value, they are not sufficient to provide a diagnosis between vegetative state/unresponsive wakefulness syndrome (VS/UWS) and minimally conscious state (MCS) patients. ⋯ Future progress will require large databases of resting state-EEG and ERPs experiment of patients of different etiologies. This will allow the identification of specific patterns related to the diagnostic of consciousness. Standardized procedures in the use of BCIs will also be needed to find the most suited technique for each individual patient.
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'What' do we call consciousness? 'When' and 'Where' in the brain do conscious states occur, and 'How' conscious processing and conscious access to a given content work? In the present paper, we present a non-exhaustive overview of each of these 4 major issues, we provide the reader with a brief description of the major difficulties related to these issues, we highlight the current theoretical points of debate, and we advocate for the explanatory power of the "global workspace" model of consciousness (Baars 1989; Dehaene and Naccache 2001; Dehaene, Changeux et al. 2006) which can accommodate for a fairly large proportion of current experimental findings, and which can be used to reinterpret apparent contradictory findings within a single theoretical framework. Most notably, we emphasize the crucial importance to distinguish genuine neural signatures of conscious access from neural events correlated with consciousness but occurring either before ('upstream') or after ('downstream').
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In a recent series of experiments we recorded the electroencephalogram (EEG) response to a direct cortical stimulation in humans during wakefulness, NREM sleep, REM sleep and anesthesia by means of a combination of transcranial magnetic stimulation (TMS) and high-density EEG (hd-EEG). TMS/hd-EEG measurements showed that, while during wakefulness and REM sleep the brain is able to sustain long-range specific patterns of activation, during NREM sleep and Midazolam-induced anesthesia, when consciousness fades, this ability is lot: the thalamocortical system, despite being active and reactive, either breaks down in causally independent modules (producing a local slow wave), or it bursts into an explosive and non-specific response (producing a global EEG slow wave). We hypothesize that, like spontaneous sleep slow waves, the slow waves triggered by TMS during sleep and anaesthesia are due to bistability between upand down-states in thalamocortical circuits. ⋯ According to animal experiments and computer simulations, thalamocortical bistability may result from increased K-currents, from alterations of the balance between excitation and inhibition and from partial cortical de-afferentation. We hypothesize that these factor may play an important role in determining loss, and recovery, of consciousness also in brain-injured subjects. If this is the case, some types of brain lesions may impair information transmission, above and beyond the associated anatomical disconnection, by inducing bistability in portions of the thalamocortical system that are otherwise healthy.
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The neural networks controlling vital functions such as breathing are embedded in the brain, the neural and chemical environment of which changes with state, i.e., wakefulness, non-rapid eye movement (non-REM) sleep and REM sleep, and with commonly administered drugs such as anaesthetics, sedatives and ethanol. One particular output from the state-dependent chemical brain is the focus of attention in this paper; the motor output to the muscles of the tongue, specifically the actions of state-dependent modulators acting at the hypoglossal motor pool. Determining the mechanisms underlying the modulation of the hypoglossal motor output during sleep is relevant to understanding the spectrum of increased upper airway resistance, airflow limitation, hypoventilation and airway obstructions that occur during natural and drug-influenced sleep in humans. Understanding the mechanisms underlying upper airway dysfunction in sleep-disordered breathing is also important given the large and growing prevalence of obstructive sleep apnea syndrome which constitutes a major public health problem with serious clinical, social and economic consequences.
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Pedunculopontine tegmental nucleus (PPN) contributes to the control muscle tone by modulating the activities of pontomedullary reticulospinal systems during wakefulness and rapid eye movement (REM) sleep. The PPN receives GABAergic projection from the substantia nigra pars reticulata (SNr), an output nucleus of the basal ganglia. Here we examined how GABAergic SNr-PPN projection controls the activity of the pontomedullary reticulospinal tract that constitutes muscle tone inhibitory system. ⋯ These results suggest that GABAergic basal ganglia output controls postural muscle tone by modulating the activity of cholinergic PPN neurons which activate the muscle tone inhibitory system. The SNr-PPN projection may contribute to not only control of muscle tone during movements in wakefulness but also modulation of muscular atonia of REM sleep. Dysfunction of the SNr-PPN projection may therefore be involved in sleep disturbances in basal ganglia disorders.