Plasticity is an intrinsic property of the human brain and represents evolution's invention to enable the nervous system to escape the restrictions of its own genome and thus adapt to environmental pressures, physiologic changes, and experiences. Dynamic shifts in the strength of preexisting connections across distributed neural networks, changes in task-related cortico-cortical and cortico-subcortical coherence and modifications of the mapping between behavior and neural activity take place in response to changes in afferent input or efferent demand. Such rapid, ongoing changes may be followed by the establishment of new connections through dendritic growth and arborization. However, they harbor the danger that the evolving pattern of neural activation may in itself lead to abnormal behavior. Plasticity is the mechanism for development and learning, as much as a cause of pathology. The challenge we face is to learn enough about the mechanisms of plasticity to modulate them to achieve the best behavioral outcome for a given subject.

Background Transcranial direct current stimulation (tDCS) is a neuromodulatory technique that delivers low-intensity, direct current to cortical areas facilitating or inhibiting spontaneous neuronal activity. In the past ten years, tDCS physiological mechanisms of action have been intensively investigated giving support for the investigation of its applications in clinical neuropsychiatry and rehabilitation. However, new methodological, ethical, and regulatory issues emerge when translating the findings of preclinical and phase I studies into phase II and III clinical studies. The aim of this comprehensive review is to discuss the key challenges of this process and possible methods to address them. Methods We convened a workgroup of researchers in the field to review, discuss and provide updates and key challenges of neuromodulation use for clinical research. Main Findings/Discussion We reviewed several basic and clinical studies in the field and identified potential limitations, taking into account the particularities of the technique. We review and discuss the findings into four topics: (i) mechanisms of action of tDCS, parameters of use and computer-based human brain modeling investigating electric current fields and magnitude induced by tDCS; (ii) methodological aspects related to the clinical research of tDCS as divided according to study phase (i.e., preclinical, phase I, phase II and phase III studies); (iii) ethical and regulatory concerns; (iv) future directions regarding novel approaches, novel devices, and future studies involving tDCS. Finally, we propose some alternative methods to facilitate clinical research on tDCS.

Human parietal cortex is implicated in a wide variety of sensory and cognitive functions, yet its precise organization remains unclear. Visual field maps provide a potential structural basis for descriptions of functional organization. Here, we detail the topography of a series of five maps of the contralateral visual hemifield within human posterior parietal cortex. These maps are located along the medial bank of the intraparietal sulcus (IPS) and are revealed by direct visual stimulation during functional magnetic resonance imaging, allowing these parietal regions to be routinely and reliably identified simultaneously with occipital visual areas. Two of these maps (IPS3 and IPS4) are novel, whereas two others (IPS1 and IPS2) have previously been revealed only by higher-order cognitive tasks. Area V7, a previously identified visual map, is observed to lie within posterior IPS and to share a foveal representation with IPS1. These parietal maps are reliably observed across scan sessions; however, their precise topography varies between individuals. The multimodal organization of posterior IPS mirrors this variability in visual topography, with complementary tactile activations found immediately adjacent to the visual maps both medially and laterally. These visual maps may provide a practical framework in which to characterize the functional organization of human IPS.

Growing evidence suggests that sensory deprivation is associated with dramatic crossmodal neuroplastic changes in the brain. In the case of visual and auditory deprivation, there is functional recruitment of brain areas normally associated with the sense that is lost by those sensory modalities that are spared. Furthermore, these changes seem to underlie adaptive and compensatory behaviours observed in both blind and deaf individuals. Although there are differences between these two populations due the very nature of the deprived sensory modality, there seem to be common principles regarding how the brain copes with sensory loss and the factors that influence how neuroplastic changes come about. Here, we discuss crossmodal neuroplasticity with regards to behavioural adaptation following sensory deprivation and highlight the possibility of maladaptive consequences within the context of rehabilitation.

The lateral-occipital tactile-visual area (LOtv) is activated when objects are recognized by vision or touch. We report here that the LOtv is also activated in sighted and blind humans who recognize objects by extracting shape information from visual-to-auditory sensory substitution soundscapes. Recognizing objects by their typical sounds or learning to associate specific soundscapes with specific objects do not activate this region. This suggests that LOtv is driven by the presence of shape information.

BackgroundThe loss of vision has been associated with enhanced performance in non-visual tasks such as tactile discrimination and sound localization. Current evidence suggests that these functional gains are linked to the recruitment of the occipital visual cortex for non-visual processing, but the neurophysiological mechanisms underlying these crossmodal changes remain uncertain. One possible explanation is that visual deprivation is associated with an unmasking of non-visual input into visual cortex.Methodology/Principal FindingsWe investigated the effect of sudden, complete and prolonged visual deprivation (five days) in normally sighted adult individuals while they were immersed in an intensive tactile training program. Following the five-day period, blindfolded subjects performed better on a Braille character discrimination task. In the blindfold group, serial fMRI scans revealed an increase in BOLD signal within the occipital cortex in response to tactile stimulation after five days of complete visual deprivation. This increase in signal was no longer present 24 hours after blindfold removal. Finally, reversible disruption of occipital cortex function on the fifth day (by repetitive transcranial magnetic stimulation; rTMS) impaired Braille character recognition ability in the blindfold group but not in non-blindfolded controls. This disruptive effect was no longer evident once the blindfold had been removed for 24 hours.Conclusions/SignificanceOverall, our findings suggest that sudden and complete visual deprivation in normally sighted individuals can lead to profound, but rapidly reversible, neuroplastic changes by which the occipital cortex becomes engaged in processing of non-visual information. The speed and dynamic nature of the observed changes suggests that normally inhibited or masked functions in the sighted are revealed by visual loss. The unmasking of pre-existing connections and shifts in connectivity represent rapid, early plastic changes, which presumably can lead, if sustained and reinforced, to slower developing, but more permanent structural changes, such as the establishment of new neural connections in the blind.

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Multisensory interactions occur early in time and