The Book: Neuroscience-Based Rehabilitation for Stroke Patients | InTechOpen, Published on: 2017-05-10. Authors: Takayuki Kodama and Hideki Nakano
Chapter 9: Neuroscience-Based Rehabilitation for Stroke Patients
Abstract
Hitherto, physical therapy for rehabilitating patients with cerebral dysfunction has focused on acquiring and improving compensatory strategies by using the remaining functions; it has been presumed that once neural functions have been lost, they cannot be restored. However, neuroscience-based animal research and neuroimaging research since the 1980s have demonstrated that recovery arises from plastic changes in the central nervous system and reconstruction of neural networks; this research is ushering in a new age of neuroscience-based rehabilitation as a treatment for cerebral dysfunction (such as stroke). In this paper, in regard to mental practices using motor imagery and kinaesthetic illusion, we summarize basic discoveries and theories relating to motor function therapy based on neuroscientific theory; in particular, we outline a novel rehabilitation method using kinaesthetic illusion induced by vibrational stimulus, which the authors are currently attempting in stroke patients.
1. Introduction
Conventional physical therapy (PT) for the rehabilitation of patients with brain dysfunction focuses on the acquisition of function through alternative means by using and improving the patients’ existing functions, and it is based on the assumption that once a neutral function is lost, it can never be recovered [1]. However, animal neuroscience studies [2–4] that were conducted after the 1980s and neuroimaging studies [5, 6] have shown that recovery can occur as a result of plastic changes in the nervous system or reorganization of the neural network, and rehabilitation (neuroscience-based rehabilitation, NBR) after cerebral dysfunction (e.g. stroke) has reached a new era in treatment. These observations suggest that the plasticity that is observed in patients is related to the characteristic that the more the patient receives therapy in specific parts of their body, the more that the brain areas that control these parts will be functionally as well as anatomically extended.
Functional recovery originally referred to a patient’s recovery from limitations in their behavior, movements, and/or activity [7]. Therefore, the purpose of NBR is not only to induce the reorganization of brain functions through neural plasticity mechanisms but also recover comprehensive bodily motor functions and brain functions for autonomous and active social behavior. What type of treatment strategy is required so that patients feel positively engaged by it, gradually understand its effects, and work toward a goal? Previous studies have revealed important factors in the effects of NBR treatment, such as the amount of therapy [8, 9], rehabilitation implementation environment [10], and performance of neurocognitive rehabilitation [11] through mental practice techniques, such as motor imagery (MI) [12]. Among these factors, treatments involving MI are strongly recommended because MI contributes to the reorganization of neural functions. MI, which is an approach that is based on neuroscientific data and the motor learning theory, is defined as the capacity to internally mimic physical movements without any associated motor output [13]. The cognitive process that occurs during the imagination of movements involves various components, such as mutual understandings between oneself and others (environment), observations of movements, mental manipulations of objects, and psychological time and movement planning. Instead of repeating simple physical movements to receive feedback on outcome in the actual therapy, the practice of voluntary and skill-requiring movements that are geared toward task completion induces the functional recovery [14]. Thus, an important element of the patients’ engagement in the therapy is that it occurs in an active and top-down fashion through the use of MI. However, because MI has a task-specific nature, cognitive functions and memories of motor experiences that equip the patients to perform the task are required. Patients with neurofunctional states that make motor execution (ME) difficulty may suffer not only from impairments in motor-related brain areas but also from modifications in their intracerebral body representations (e.g. somatoparaphrenia) [15, 16]. In such cases, the exploitation of kinaesthetic illusions [17–20], which can be induced in the brain by extraneous stimuli, such as vibratory stimulations, becomes important for inputting appropriate motor-sensory information into the brain in a passive and bottom-up fashion. Therefore, the implementation of a mental practice to determine the criteria for adequate treatment according to the states of the patient’s cognitive functions and motor functions is important in order to select and implement the best therapy. Thus, this paper summarizes the basic understanding and theories of mental practices that use MI or kinaesthetic illusion and discusses, in particular, research results concerning kinaesthetic illusions that are induced by vibratory stimulations, which we are currently attempting on stroke patients.
2. What is neuroscience-based rehabilitation?
NBR involves a series of processes that are selected for the intervention according to the current brain function theories that have been revealed by neuroscience and other similar studies and verification of its outcomes. For example, the selection of a NBR strategy for a stroke patient requires a combination of deep clinical reasoning, the experience of the therapist, and a vast understanding of the evidence obtained by studies from wide-ranging academic fields on the factors that support recovery mechanisms and produce particular outcomes. First, the neural basis of brain cell reorganization will be presented.
2.1. Neural basis of brain cell reorganization
The current understanding of neural reorganization after dysfunction is not that the neurons themselves recover after their axons are damaged but rather that damaged functional networks recover due to several processes that induce the recovery of motor and cognitive functions. Cajal [1], who was a proponent of neuron theory, stated that the central nervous system (brain and spinal cord) of adult mammals would not recover once it is damaged. However, studies that have been conducted since the 1980s and that have shown that alterations in the peripheral nervous system, such as denervation and amputation, change somatic sensations and the representations of body parts while they are in motion have revealed that the brain has plasticity. In 1998, Eriksson et al. [21] reported the new formation of neurons in the central nervous system of human beings. These findings raised the question of whether the plastic changes and functional reorganization that occur in subjects with cranial nerve disorders originate from an ischemic state, such as a cerebrovascular disturbance. The underlying mechanisms of the plasticity that occurs after a cortical deficit are thought to involve (i) the redundancy of neuronal connections in the central nervous system, (ii) morphological changes in the neurons, and (iii) changes in synaptic information transmission [22]. If neurons are damaged, astrocytes begin to divide due to the activity of microglia. These glial cells then reinforce the areas that have been damaged by brain lesions and release neurotrophic factors, such as nerve growth factor, to promote neuronal sprouting (it takes around two weeks for synapses to grow after nerve damage [23]). The sprouted neurons are then connected to an existing neural network, which forms a new network. In other words, if neurons are damaged, new neurons begin to reorganize themselves in order to compensate for it. Adequate NBR stimulates the neural network with the neurofunction that is most similar to the predamaged functional state of the neural network, even though the new network is not located in the damaged region. If strong inputs enter the network multiple times, the synaptic connections will be reinforced. However, plasticity will not be induced in synapses with little information (input specificity), and the synapses will be excluded from the network formation [24, 25].
These findings have been confirmed by several famous studies. Nudo et al. [8] caused artificial cerebral infarcts in monkeys in the region of the primary motor cortex (M1) that corresponds to fingers and then forced the monkeys to use fingers with motor deficits. Thus, they reported that the brain region that previously controlled the shoulders and elbows prior to the therapy then controlled the fingers and more distal body parts (Figure 1). Merzenich et al. [26] surgically sutured the fingers of monkeys and then compared the pre- and post-surgical somatotopies of Brodmann area (BA) 3b, which corresponds to the sensorimotor area (SMA). Microelectrodes were used to record the responses in BA3b to finger stimuli. The third and fourth fingers were then surgically sutured, and the responses were recorded again a month later. Thus, the boundary between the third and fourth fingers became unclear. In addition, the results of a study that was conducted in human beings suggested that the plasticity of brain cells depends on sensory input. The results of a magnetoencephalography study that compared the somatotopies of the first and fifth fingers of string players to normal controls showed that a broader cerebral cortical area was activated for string players compared to the controls [6].
These findings suggest that the size of the intracerebral somatotopic representation, which is vital to ME, is determined by the degree of use of the region. If you try to induce plasticity in specific parts of the bodies of stroke patients, as mentioned above, the induction of neural plasticity in a pathway that allows highly efficient information processing by repeating movements in a pattern like the normal pattern should be possible, provided the patient has retained their motor functions to a certain degree. However, if a patient has the functional level of almost not able to perform movement or is only able to perform the movement in an abnormal pattern, the stimulation of the plasticity for the formation of a neural network that is required to be able to regain normal motor function may not be possible. Ward et al. [27] chronologically examined the relationships between motor function recovery scores and task-related brain activities for approximately 12 months after the onset of stroke with functional magnetic resonance imaging. They found a negative correlation between motor function recovery scores and a decline in the hyperactivity of brain areas in the damaged and undamaged hemispheres (M1, premotor cortex; PMC, supplementary motor cortex; SMC, cerebellum). These findings suggest that a better recovery of motor function is associated with better connectivity between the functional systems of multiple brain regions and that a continuous and long-term approach is required to study the changes in the morphologies and networks of neurons. Thus, a qualitative and continuous approach [28] is required in studies of the recovery of the entire neural system (e.g. transcortical network, M1-PMC neural network [29]) in order to be able to perform movement rather than merely establishing quantitative interventions of movement. Thus, next, we will discuss the current understanding of what is required in interventions for stroke patients.[…]
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