Progress in brain research
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In order to study cerebral activity related to preparation and execution of movement, evoked and induced brain electrical activities were compared to each other and to fMRI results in voluntary self-paced movements. Also, the event-related desynchronization and synchronization (ERD/ERS) were studied in complex movements with various degrees of cognitive load. The Bereitschaftspotential (BP) and alpha (8-12 Hz) and beta (16-24 Hz) ERD/ERS rhythms in self-paced simple movements were analyzed in 14 epilepsy surgery candidates. ⋯ Some sites were only active in the task with the increased demand on executive functions. In the temporal neocortex only, the oscillatory, but not the evoked, activity was recorded in the self-paced movement. The temporal appearance of changes of oscillatory activities in the self-paced movement task as well as in the cued movement task with an increased load of executive functions raises the interesting question of the role of this region in cognitive-movement information processing.
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In the early stages of Parkinson's disease (PD), impaired motor preparation has been related to a decrease in the latency of mu rhythm event-related desynchronisation (ERD) compared with control subjects, suggesting hypo activation of the contralateral, primary sensorimotor (PSM) cortex. Following movement, a decrease in amplitude of beta rhythm ERS was observed over the same region and thought to be related to impairment in cortical deactivation. By monitoring ERD/ERS, we aimed (i) to extend to advanced PD the observations made in less-advanced parkinsonism and (ii) to test the effect of acute L-Dopa, internal pallidal or subthalamic stimulation on these abnormalities. ⋯ Mu rhythm ERD latency and the beta ERS amplitude further decreased in advanced PD compared with early stages, suggesting greater impairment of cortical activation/deactivation as the disease progresses and a partial restoration in relation to clinical improvement under treatments. Consequently, it appears that L-Dopa and deep brain stimulation partially restored the normal patterns of cortical oscillatory activity in PD, possibly by decreasing the low frequency hyper synchronisation at rest. This mechanism could be involved at the basal ganglia level in the sensorimotor integration implicated in the movement control.
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The discovery of event-related desynchronization (ERD) and event-related synchronization (ERS) by Pfurtscheller paved the way for the development of brain-computer interfaces (BCIs). BCIs allow control of computers or external devices with the regulation of brain activity only. Two different research traditions produced two different types of BCIs: invasive BCIs, realized with implanted electrodes in brain tissue and noninvasive BCIs using electrophysiological recordings in humans such as electroencephalography (EEG) and magnetoencephalography (MEG) and metabolic changes such as functional magnetic resonance imaging (fMRI) and near infrared spectroscopy (NIRS). ⋯ Invasive multielectrode BCIs in otherwise healthy animals allowed execution of reaching, grasping, and force variations from spike patterns and extracellular field potentials. Whether invasive approaches allow superior brain control of motor responses compared to noninvasive BCI with intelligent peripheral devices and electrical muscle stimulation and EMG feedback remains to be demonstrated. The newly developed fMRI-BCIs and NIRS-BCIs offer promise for the learned regulation of emotional disorders and also disorders of small children (in the case of NIRS).
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The autonomic nervous system modulates cardiac electrophysiology and abnormalities of autonomic function are known to increase the risk of ventricular arrhythmias. The abnormal and unstable autonomic control of the cardiovascular system following spinal cord injury also is well known. ⋯ Therefore, spinal cord injury may alter cardiac electrophysiology and increase the risk for ventricular arrhythmias. In this chapter, we discuss how the autonomic changes associated with cord injury can influence cardiac electrophysiology and the susceptibility to ventricular arrhythmias.
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Transection of the spinal cord that interrupts the spinobulbospinal micturition reflex pathway, abolishes voluntary voiding and initially produces an areflexic bladder with complete urinary retention. However, depending upon the species, reflex bladder activity slowly recovers over the course of weeks or months. In chronic spinal animals, reflex mechanisms in the lumbosacral spinal cord are capable of duplicating many of the functions performed by reflex pathways in animals with an intact spinal cord and can induce bladder hyperreflexia. ⋯ Changes in electrophysiological or neurochemical properties of bladder afferent cells in the dorsal root ganglia and of spinal pathways could contribute to the emergence of the spinal micturition reflex, bladder hyperreflexia and changes in the pharmacologic responses of reflex pathways in the lumbosacral spinal cord after spinal cord injury. Urinary bladder hyperreflexia after spinal cord injury may reflect a change in the balance of neuroactive compounds in bladder reflex pathways. This review will detail: (1) changes in the neurochemical phenotype of bladder afferent neurons and of spinal neurons mediating micturition reflexes after spinal cord injury, with an emphasis on three neuroactive compounds, neuronal nitric oxide synthase (nNOS), galanin, and pituitary adenylate cyclase activating polypeptide (PACAP); (2) possible functional consequences on bladder reflexes of changes in spinal cord neurochemistry after spinal cord injury, and (3) the potential role of neurotrophic factors expressed in the urinary bladder or spinal cord after spinal cord injury in mediating these neurochemical changes.