Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Sunday, May 26, 2024

Exploring the Role of Neuroplasticity in Stroke Rehabilitation: Mechanisms, Interventions and Clinical Implications

Nothing here tells us EXACTLY HOW TO MAKE NEUROPLASTICITY REPEATABLE!

You don't know why and how one neuron gives up its function to take on a neighbor's function. Without that knowledge neuroplasticity will never be repeatable on demand.

 

 

 Exploring the Role of Neuroplasticity in Stroke Rehabilitation: Mechanisms, Interventions and Clinical Implications

Dr. Sandeep Dey1, Dr. Aayush Arya2, Arya J Raut3, Shreyas Katta4, Prashant Sharma5 1,2MBBS Graduate, Anna Medical College and Research Centre, University of Technology, Mauritius 3,4,5Medical Student, Anna Medical College and Research Centre, University of Technology, Mauritius 
 

ABSTRACT 

 
 Neuroplasticity, the brain's remarkable ability to reorganize and adapt throughout life, has emerged as a central focus in neuroscience research. This abstract delves into the mechanisms underlying neuroplasticity and its profound implications for learning, memory, rehabilitation, and neurological disorders. At the cellular level, neuroplasticity involves synaptic plasticity, where the strength and efficacy of connections between neurons can be modified through activity-dependent processes such as long-term potentiation (LTP) and long-term depression (LTD). Molecular mechanisms, including changes in neurotransmitter release, receptor expression, and intracellular signaling pathways, mediate these synaptic changes. Beyond synaptic plasticity, structural plasticity encompasses alterations in neuronal morphology, including dendritic branching, spine density, and axonal sprouting. These structural changes facilitate the formation of new neural circuits and underlie learning and memory processes. Neuroplasticity is not limited to developmental stages but persists throughout life, with experience and environmental factors continuously shaping the brain's structure and function. Experience-dependent plasticity is evident in various contexts, from skill acquisition to recovery from brain injuries. Understanding neuroplasticity has profound implications for education, as it highlights the importance of enriched environments and active learning strategies in promoting cognitive development. Additionally, neuroplasticity forms the basis for rehabilitative interventions following brain damage, with therapies focusing on promoting adaptive neural rewiring and functional recovery. Moreover, dysregulation of neuroplasticity is implicated in numerous neurological and psychiatric disorders, including Alzheimer's disease, stroke, and depression. Elucidating the mechanisms underlying aberrant plasticity holds promise for developing targeted interventions to treat these conditions. In conclusion, neuroplasticity represents a fundamental property of the nervous system, allowing for adaptation and optimization in response to environmental demands. Continued research into the mechanisms governing neuroplasticity promises to unveil new therapeutic avenues and deepen our understanding of brain function and dysfunction.

INTRODUCTION

Neuroplasticity can be defined as the ability of the nervous system to respond to intrinsic or extrinsic stimuli by reorganizing its structure, function, and connections. Neural plastic changes are associated with development and learning. They occur throughout the lifespan and may be enhanced following injury . They are influenced by experience and the context in which that experience occurs. The major drivers of neuroplastic change are meaningful behavior. Evidence of neural plastic changes can be observed at various levels, e.g., cellular/synaptic changes, changes in the structure and function of brain regions and networks, and changes in behavior such as improved skill and adaptability. Strong scientific evidence demonstrates that the brain has remarkable capacity for plasticity and reorganisation, yet exploiting this knowledge to enhance clinical outcomes is in its infancy.After a brain injury, such as stroke, the person is challenged to sense, move, communicate, and engage in daily activities with the brain and body that are impacted by the stroke. Immediate and long-term effects of stroke include impairment in sensation, movement, cognition, psychological and emotional functions, and reduced independence and quality of life. There may be evidence of improvement and some regaining of lost skill. A trajectory of spontaneous and supported recovery over the days, weeks, and months after stroke has been described . Yet rehabilitation outcomes are currently suboptimal and variable , and evidence supporting novel or more effective treatments is limited. Neural plastic changes occur following brain injury, such as stroke. The changes may occur in the days, weeks, months, and years following stroke . They may be adaptive or maladaptive. For example, a person can learn nonuse of the limb or develop dystonic postures following sensory loss. However, we have yet to harness this window of opportunity for ongoing recovery both short- and long-term after stroke. The continuum of recovery after stroke presents opportunities for targeted rehabilitation to harness and enhance these mechanisms of neural plasticity for improved outcomes. Neuralplastic changes are experience and learning dependent. Learning is the process of acquiring a relatively lasting change in knowledge and skills. Learning cannot be measured directly, and assessment may address different criterion indicators of learning. The potential exists for the phenomenon of neural plasticity to be shaped by the experiences that occur following stroke and to be positively impacted by rehabilitation. The question is how can we build on and shape this experience and drive positive plasticity to achieve better outcomes for stroke survivors? Neurorehabilitation may be defined as “facilitation of adaptive learning”. Stroke rehabilitation founded on neuroscience is now recognised for its capacity to achieve more restorative outcomes. Experience and learning-dependent plasticity are core to this change . There are different conditions under which that plasticity may be enhanced, facilitated, and/or consolidated. These different conditions likely impact the type of neuroplasticity facilitated and behavioral outcomes observed. An advanced understanding of these will help guide the development of neuroscience-based interventions. The aim of our scoping review was (i) to search the evidence available in relation to the three core concepts of neural plasticity, stroke recovery, and learning; (ii) to identify how these concepts are linked to each other; and (iii) to identify and discuss the themes/topics that best characterise the intersection of these three concepts, in order to better inform the neuroscience basis of stroke rehabilitation and stroke recovery. In relation to neural plasticity, we were interested in the identification of evidence of neuroplastic changes, e.g., at cellular and neural network levels. This included evidence such as synaptic changes, brain networks, and functional connectivity. We anticipated this literature would be primarily found in neuroscience and neuroimaging type journals. For the concept of stroke recovery, we were interested in outcomes related to impairment, performance, participation, and quality of life, at different times in the recovery trajectory and in relation to rehabilitation. The concept of learning focused on the process of change and included domains such as experience, different types of learning, attention and cognition, adaptation, environment, motivation, and goal. Investigation of the links and intersection between these concepts has the potential to reveal the following: 1. the type of learning experience that can enhance neural plasticity; 2. the evidence that links neural plasticity and improved outcomes for stroke survivors; and 3. how the different learning experiences linked with neural plasticity might influence/contribute to better stroke outcomes. In achieving our aim, we sought to develop and use a methodology that would enable a broad and comprehensive scoping of the current literature. This included identification of key topics represented in the literature that relate to the three core concepts and an approach that permits searching and identification of related terms that may be used by authors. This was important to maximise the likelihood that a broad range of terms that are likely to have similar or overlapping meaning was able to be searched and accessed. Stroke continues to be a significant public health concern, ranking as the second-leading cause of mortality and the third-leading cause of mortality and disability combined, as measured by disability-adjusted life-years (DALYs) lost on facilitating functional recovery through compensatory strategies to alleviate the consequences of impairments rather than addressing their underlying causes. However, a growing realisation within the scientific and medical communities has underscored the extraordinary transformative potential embedded within neuroplasticity. This recognition has prompted a paradigm shift in stroke rehabilitation, emphasising the harnessing of neuroplasticity to facilitate functional recovery and promote substantial and enduring improvements in long-term outcomes for stroke survivors. This review aims to assess the role of neuroplasticity in facilitating stroke recovery and identify the challenges and limitations associated with its implementation. A comprehensive literature search was conducted to identify relevant studies, which were meticulously evaluated to determine the potential solutions for effectively harnessing neuroplasticity. The results indicate that neuroplasticity holds significant promise in stroke rehabilitation; however, individual variability in response to interventions, timing and duration of interventions and sociocultural and clinical factors pose challenges. Tailoring interventions to individual patient characteristics is crucial for optimising the impact of neuroplasticity. Despite challenges and limitations, the transformative potential of neuroplasticity in stroke rehabilitation is undeniable. The abstract concludes by emphasising the importance of a comprehensive understanding of individual variability, optimising intervention timing and duration and considering sociocultural and clinical factors. Future research and clinical practice should prioritise personalised interventions and interdisciplinary collaborations to fully exploit the vast potential of neuroplasticity in stroke recovery. Recent advances in functional imaging of human brain activity in stroke patients, (positron emission to- mographic (PET) and fMRI), reveal that cortical hemisphere contralateral to the infarction lesion plays an important role in this recovery process. There is also clinical evidence showing that the post ischemic reorganization occurring in somatosensory system of the contralesional (intact) hemisphere plays an important role for compensation for impaired functions. The underlying mechanism of this compensation occurring in the intact hemisphere is important for optimizing the functional recovery of human stroke patients. The brain, including the motor system, learns by repetition and training. Many basic mechanisms, however, are still poorly understood, and rehabilitative training is largely evidence based medicine. Nevertheless there are no generally accepted guidelines and no definite recommendations concerning the timing, kind and intensity of stroke rehabilitation. Stroke recovery is a complex process that probably occurs through a combination of restoration, substitution and compensation of functions. That is why it has been also difficult to translate results from rehabilitative studies in animals to recommendations for rehabilitative schedules in human stroke patients. A majority of clinical studies has been conducted in chronic stroke patients (>6months after the stroke) as recruitment of these patients was easier and baseline performance had stabilized These circumstances lead to functional outcome measurements probably gained largely from compensatory techniques to improve skills for daily living. The time courses of motor recovery differ among animal and human studies: While recovery in rodent models reaches the maximum around 4 weeks after stroke, human stroke survivors complete most of their recovery within 3 months. NIRS could be used to predict the potential for clinical improvement in chronic stroke patients. It is also the first to demonstrate the complementary nature of neurophysiological and imaging techniques with NIRS in the prediction of functional potential and clinical outcomes. These findings have implications for clinical decision-making. Evaluation of brain function, using a combination of neurophysiological measures and imaging, can inform the setting of therapeutic effectiveness and the selection of patients for particular rehabilitation programs. This may lead to the conceptualization of re-habilitation strategies that are designed to maximally enhance rehabilitation through tailoring to individual patient deficits. Rehabilitation strategies may now be designed and optimized by employing methods to synchronize functional training of brain regions undergoing neural plasticity. However, a larger sample size, longer duration of training, or a restricted inclusion of stroke location and volume may be needed to demonstrate a difference between individually tailored rehabilitation programs and generic rehabilitation programs in efficacy in producing behavioral changes. Therapeutic approaches which directly stimulate the peripheral nerve system or central nerve system electrically or by magnetic pulses may enhance neuroplasticity during post-stroke rehabilitation. Several studies showed that an increase of the excitability in the stroke-affected ipsilesional M1 by electrical devices resulted in improved motor outcome. The mechanisms of action of these techniques are under investigation but might involve changes in synaptic activity, gene expression and increases in neurotransmitter, receptor and neurotrophin levels or even enhanced fiber sprouting. A study of patients with stroke who had reached a plateau in motor recovery found that the volume of primary sensorimotor cortex activation in the ipsilesional hemisphere during affected hand movement was related to the level of behavioral recovery Mechanisms of Neuroplasticity in Stroke Recovery Review of cellular and molecular mechanisms underlying neuroplasticity post-stroke. Post-stroke, neuroplasticity mechanisms involve cellular and molecular changes to adapt and repair damaged brain tissue. Neurons undergo structural modifications, synaptic connections adjust, and neurogenesis may occur. Glial cells play supportive roles in neuroplasticity, aiding in tissue remodeling and neuronal survival. Molecular signaling pathways, including neurotrophic factors and neurotransmitters, orchestrate these processes. Additionally, inflammation and immune responses influence neuroplasticity post-stroke. Understanding these mechanisms is crucial for developing targeted therapies to enhance recovery and functional outcomes in stroke patients.
 
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