The process of neuroplasticity, also referred to as neural plasticity or brain plasticity, involves the brain changing in a way that is both adaptive and functional. It is characterized as the nervous system’s capacity to adjust its activity in response to internal or external stimuli by rearranging its connections, structure, or functions following wounds like a stroke or traumatic brain injury (TBI). This activity discusses neuroplasticity, its assessment, and management, as well as the interprofessional team’s role in enhancing patient care.
Introduction
The process of neuroplasticity, also referred to as neural plasticity or brain plasticity, involves the brain changing in a way that is both adaptive and functional. The ability of the nervous system to alter its activity in response to internal or external stimuli by reorganizing its connections, structure, or functions is a good definition. In terms of medicine, it refers to the process by which the brain adapts to trauma, such as a stroke or traumatic brain injury (TBI). These modifications may be advantageous (restoring function after injury), neutral (causing no change), or harmful (possibly leading to pathological effects).
You can divide neuroplasticity into two main mechanisms:
- The terms “neuronal regeneration” and “collateral sprouting” refer to processes like synaptic plasticity and neurogenesis.
- Equpotentiality, vicariation, and diaschisis are some examples of concepts related to functional reorganisation.
William James used the term “plasticity” for the first time in relation to the nervous system in 1890. However, Jerzy Konorski is credited with coining the phrase “neural plasticity” in 1948; Donald Hebb popularized it in 1949. Also Read Impact of Masculinity on Men’s Health
Issues of Concern
Plasticity following injury: Neuroplasticity is a complex process that is still being understood, but the idea can be used in the case of brain injury. Traditionally, neuroplasticity has been thought to have three phases or epochs.
- Initial 48 hours: Depending on how the injury occurred (such as a stroke or traumatic brain injury), there may be initial damage that progresses to cell death and the loss of specific cortical pathways linked to the lost neurons. The brain makes an effort to maintain function by using secondary neuronal networks.
- The subsequent weeks: During this time, support cells are recruited as the cortical pathways switch from inhibitory to excitatory states. During this time, new connections and synaptic plasticity are formed.
- Weeks to months later: The brain continues to reorganize itself around the damage through axonal sprouting.
Mechanisms of Neuroplasticity
Neuronal Regeneration
Synaptic plasticity: Synaptic plasticity is the capacity to alter the strength of neuronal connections over time in response to experience. The idea of long-term potentiation is the most effective way to explain this. Repetitive stimulation of presynaptic fibres produced strong responses from granule cells of postsynaptic neurons, which Bliss and Lomo first noticed in 1973 while researching the rabbit hippocampus. They called this long-term potentiation because the postsynaptic potential persisted for a lot longer than anticipated. According to theory, when a postsynaptic neuron is stimulated by a presynaptic neuron, the postsynaptic neuron responds by developing more neurotransmitter receptors, thereby lowering the threshold required to be stimulated.
According to the theory put forth by Konorski and Hebb, this eventually improves the synapses. Numerous factors, including but not limited to physical activity, the environment, task repetition, motivation, neuromodulators (like dopamine), and drugs and medications, can have a positive impact on synaptic plasticity. Neuromodulators have been shown to decline with ageing and neurodegenerative diseases, which may also lessen the capacity for synaptic plasticity. The evolving complexity of synaptic communication is now better accounted for in the theory of synaptic plasticity.
These consist of:
- Spike-timing-dependent plasticity (STDP): This theory explains how some synapses are strengthened and others are weakened by taking into account the timing of action potentials produced by presynaptic and postsynaptic neurons.
- Metaplasticity: This enlarges the idea to include networks and deals with the activity-dependent adjustments in synapses’ behavior.
- Mechanisms that sustain the synaptic network’s homeostasis over time are known as homeostatic plasticity.
- These ideas will become more concrete as research advances, elaborating on how synaptic plasticity affects learning and helps the brain regain function.
Functional Reorganization
Equipotentiality and vicariation: The idea behind equipotentiality is that if one side of the brain is damaged, the opposite side will be able to maintain the lost function. This idea dates at least to Galen and served as an explanation for why the brain appeared to be “twinned.” This “redundancy theory” persisted until illustrious researchers like Pierre Paul Broca showed that unilateral lesions to a region of the left side of the brain caused loss of speech despite the opposite side being intact. According to Broca, a child would have an easier time relearning certain skills than an adult would, such as speech. This idea evolved into equipotentiality, which states that if the damage occurred very early, the brain has the potential to recover.
This differs slightly from the concept of vicariation, which holds that certain brain regions can be reorganised to perform tasks for which they were not originally designed. After observing that some of his patients still retained some function despite having left hemisphere damage, Broca came up with this theory. In the strictest sense, vicariation occurs when one portion of the brain takes control of an additional, unrelated task. Advanced imaging methods have demonstrated that neither theory is entirely accurate.
Diaschisis: -Neuroplasticity
According to the theory of diaschisis, damage to one area of the brain could result in a loss of function in a different region due to a connected pathway. This theory was put forth by Constantin von Monakow in an effort to explain why some people lost particular abilities (like speech) but did not have a lesion in the region of the brain thought to be responsible for those abilities.
Diaschisis has evolved
over time and is now used to explain a variety of ideas related to the functional connections in the brain and what happens when damage is sustained. While Carrera and Tononi discuss these, the following is briefly explained:
- Diaschisis ‘at rest’: The traditional von Monakow type, such as ipsilateral thalamic hypoperfusion in MCA stroke.
- Diaschisis that is found when another area of the brain is activated is known as a functional diaschisis. An illustration of this is when lesions in the putamen cause the ipsilateral cerebellums to become hypoactive. When performing a functional task with their ipsilateral hand, despite the fact that they were not hypoactive at rest. When certain parts of the brain can be both hypoactive and hyperactive depending on the task. Dynamic diaschisis can also be used and has been used.
- Connectional diaschisis: When a portion of the brain is lost, information must be rerouted. Subcortical lesions can result in a decrease in the interhemispheric connectivity of the motor strips. As has been observed in rat models.
- A map known as a connectome can be created as a result of advanced imaging techniques. That have revealed the enormous complexity of connections between neurons. This map displays groups of densely connected nodes that are later connected by a small number of nodes (hubs). A hub can sustain much more severe damage than a non-hub node if it is damaged.
The idea and function of diaschisis will keep changing as we learn more about the functional connections in the brain.
Clinical Significance -Neuroplasticity
The process of structural and functional changes to the brain following an internal or external insult is known as neuroplasticity. And it encompasses a wide range of distinct processes. Diaschisis, synaptic plasticity, and functional reorganization are examples of distinct mechanisms the brain employs to repair damage and regain function. We will be able to create more specialized therapies to aid the brain in regaining function more quickly. And completely as research into the functional connections in the brain and what influences those connections continues.
Constraint-induced movement therapy (CIMT) is one of the most researched rehabilitation methods. The idea is that by limiting the functional limb, the affected limb engages in repetitive task practice. And behavioral shaping, which is used in stroke patients. Patients who receive this therapy have been shown to have increased activity in their contralateral premotor and secondary somatosensory cortex. Which has been linked to improved function using functional magnetic resonance imaging (fMRI) technology.
Improving Healthcare Team Results
The best outcomes for patients will be achieved by an interprofessional team approach. That involves neurologists, physiatrists, therapists, nurses, and other health professionals involved in patients receiving rehabilitation after neurological injury. However, there is little research evaluating this care approach. The best treatment options that take advantage of neuroplasticity can be found by an interprofessional team. For positive results, communication, shared decision-making, and collaboration are essential. An integrated care pathway and an evidence-based approach to planning and evaluating. All activities must be used in the interprofessional care given to the patient. While telerehabilitation is becoming more popular, more research is still needed to understand how it affects the brain and promotes recovery. This can assist in leveraging technology to use telemedicine as a component of an all-encompassing team approach to patient care.