China
Africa
Explore chapters and articles related to this topic
Embedding Ethics in Neural Engineering
Published in Evelyn Brister, Robert Frodeman, A Guide to Field Philosophy, 2020
For example, we ran an early focus group that looked at BCI-controlled exoskeletons, BCI-controlled prosthetics, and the possibility of reanimation of limbs through BCI control. Shortly afterwards, a site visit team encouraged the Center to eliminate the focus on the first two possibilities, given competing work at different institutions. A different site visit team pushed the leadership to better define the Center’s “product,” which led to a move toward “design principles for bidirectional BCI” as opposed to specific devices. In recent years, the focus has shifted to “engineered neural plasticity” as a goal, with different fundamental research groups defined and brought on board. Not all of these changes were drastic, of course, but responding to the pressures to shift in different directions, because of the recommendations of the funders, required flexibility and willingness to adapt on the fly. A project that uses the “old” Center language—e.g., a study looking at how BCI is depicted in the media, as a way to assess how prospective neural device users are likely to think about BCI when they consider entering a research study—might appear out of place within a year due to a shift from “BCI” to “neural devices” more generally (e.g., to capture the spinal stimulation work done by a PI working with human subjects).
Brain Stimulation Therapies
Published in Bahman Zohuri, Patrick J. McDaniel, Electrical Brain Stimulation for the Treatment of Neurological Disorders, 2019
Bahman Zohuri, Patrick J. McDaniel
Neuronal plasticity is the synaptic reorganization induced by the changes in the environment, due to the training or disease.3,9 TMS can be used to study neuronal plasticity; however, such studies are rare because of the complexity of study paradigms. The most widely applied paradigm for the investigation of neuronal plasticity includes some steps: firstly, TMS-induced movement direction is measured; then the subject is taught to perform a simple motor task in its direction opposite to TMS-induced movement.
Post-traumatic cognitive dysfunction
Published in Hemanshu Prabhakar, Charu Mahajan, Indu Kapoor, Essentials of Anesthesia for Neurotrauma, 2018
Ashima Nehra, Manju Mohanty, Shivani Sharma
The survivors of TBI often have residual deficits in physical functioning that are visible and well accepted by the patients and family. But the cognitive and psychological deficits often remain unrecognized, hence, they significantly impact the quality of life and return to premorbid level of functioning. Therefore, it is essential to develop efficacious programs for prevention and intervention. In recent years neuropsychological rehabilitation has gained importance as a method that has proven to be efficacious.49 It not only addresses the issue of cognitive deficits, but also focus on emotional and behavioral consequences. The role of neuronal plasticity is well recognized and allows the neurons in the brain to compensate for injury and adapt to their environment. Zangwill described three processes of rehabilitation; restoration, substitution, and compensation. Restoration refers to the process of restoring lost or impaired functions; substitution refers to replacing impaired functions by alternate functional strategies; while compensation requires using external sources that help to overcome limitations to a certain extent.50
Nitric oxide pathway as a plausible therapeutic target in autism spectrum disorders
Published in Expert Opinion on Therapeutic Targets, 2022
Rishab Mehta, Anurag Kuhad, Ranjana Bhandari
Autism is termed as a heterogeneous disorder as it is caused by a complex interplay of genetic, epigenetic, and environmental factors. However the pathogenesis of the disease is not understood well but genetic aberrations are known to be responsible in approximately 10% of the cases [6,7]. Genetic mutations and alterations are known to affect the development of neurons and thus affect neuronal plasticity. Genetic expressions can also be modified by environmental toxins through epigenetic mechanisms including methylation of DNA, histone protein changes, and change in expressions of noncoding RNA’s [8]. Environmental factors such as vitamin D deficiency, zinc deficiency, herbicides, and pesticide exposure, altered gut flora, and so on, are all found to be associated with the development of this spectrum of disorders by various scientific studies. Dysregulation of gut microflora has been proven to play a role in altering intestinal permeability, mucosal immune function, and intestinal motility and sensitivity. Low-grade inflammatory response and activation of cell-mediated immunity (CMI) leads to increase in oxidative and nitrosative stress causing damage to lipids, DNA, proteins, and mitochondria [9–13]. However, none of these factors yield autism rather they play a part in the interplay of cascades of pathways leading to the pathogenesis of autism. The nitric oxide pathway is believed to be involved in ASD-related behavioral and cognition deficit in preclinical studies. So, this pathway needs to be explored more in the paradigm of ASD.
The use of motor learning and neural plasticity in rehabilitation for ataxic hemiparesis: A case report
Published in Physiotherapy Theory and Practice, 2020
Ellen O. Crum, Mathew J. Baltz, David A. Krause
Neural plasticity is the adaptive capacity of neurons to alter their structure and function in response to a variety of internal and external stimuli (Kleim and Jones, 2008). The principles of neural plasticity (Table 1) are believed to be the basis for learning in the intact brain as well as relearning in the damaged brain (Kleim and Jones, 2008). The constructs of motor learning are also important in promoting carryover to practice of novel functional activities. Fundamental to motor learning is the amount of practice as well as the type and timing of feedback received during practice (Krakauer, 2006). Feedback about errors and ordering of activity to promote learning are components of patient interactions that need to be considered by the physical therapist (Winstein et al., 2014). Interventions that promote normal function rather than compensation should be utilized. The purpose of this case report is to describe an intervention program based on the principles of motor learning and neural plasticity for a patient with ataxic hemiparesis.
Of worms and men
Published in Journal of Neurogenetics, 2020
It may be instructive to consider whether some of the central topics in the studies of the human brain have relevance in the context of C. elegans. One prominent issue is the nature of consciousness. There are numerous definitions of what consciousness means but they are generally of the form: the state of being aware of one’s surroundings and self. The responses of C. elegans to external stimuli have been extensively studied and have been shown to elicit responses that are appropriate to the stimulus (Bargmann, 2006). So, in this sense a C. elegans is certainly conscious. Indeed, I would argue that an autonomously driven car is also conscious. Rather like the concept of vitalism, which has fallen into disuse because of current knowledge of cell physiology, consciousness may not be a useful concept for understanding the function of the nervous system of C. elegans. A concept derived from studies of higher nervous systems that is better defined is neural plasticity. At a gross level this is commonly seen as the ability of victims to eventually recover lost faculties following a stroke that kills off areas of the brain; however, it is likely that neural plasticity is a manifestation of the basic process of learning (Sweatt, 2016). There are well defined instances of neuronal plasticity during the development of the C. elegans nervous system and the detailed mechanisms are beginning to be understood at the molecular level (Jin & Qi, 2018), suggesting that this organism may have much to offer in the search for an understanding of this basic mechanism of cognition.