Motor Control and Neural Plasticity through Interhemispheric Interactions

Abstract

The corpus callosum, which is the largest white matter structure in the human brain, connects the 2 cerebral hemispheres. It plays a crucial role in maintaining the independent processing of the hemispheres and in integrating information between both hemispheres. The functional integrity of interhemispheric interactions can be tested electrophysiologically in humans by using transcranial magnetic stimulation, electroencephalography, and functional magnetic resonance imaging. As a brain structural imaging, diffusion tensor imaging has revealed the microstructural connectivity underlying interhemispheric interactions. Sex, age, and motor training in addition to the size of the corpus callosum influence interhemispheric interactions. Several neurological disorders change hemispheric asymmetry directly by impairing the corpus callosum. Moreover, stroke lesions and unilateral peripheral impairments such as amputation alter interhemispheric interactions indirectly. Noninvasive brain stimulation changes the interhemispheric interactions between both motor cortices. Recently, these brain stimulation techniques were applied in the clinical rehabilitation of patients with stroke by ameliorating the deteriorated modulation of interhemispheric interactions. Here, we review the interhemispheric interactions and mechanisms underlying the pathogenesis of these interactions and propose rehabilitative approaches for appropriate cortical reorganization.

Prediction of Motor Recovery Using Quantitative Parameters of Motor Evoked Potential in Patients With Stroke

“…In stroke patients, neuronal excitability decreases, which leads to higher motor threshold in the affected side causing an imbalance of motor threshold [2026]. Furthermore, several studies postulated that the interhemispheric balance is disrupted in stroke patients and this caused suppression of ipsilesional cortical excitability by the contralesional hemisphere [272829]. Prashantha et al [26] described that disruption of the transcallosal interaction could be the possible mechanism causing an imbalance of rMT.…”

Efficacy of Transcranial Direct Current Stimulation as Support for Neurorehabilitation Therapy: A Meta-analysis of Available Studies

“…Bilateral montage is often used based on the assumption that the movements of the impaired limbs are often associated with a high level of transcallosal inhibition by the hemisphere not affected by the hemisphere being injured [10,20]; some studies conducted with multimodal imaging techniques and mapping, such as fMRIs and TMSs, confirmed the existence of this imbalance of the hemisphere not affected, also called a hemispheric competition model, particularly during the preparation and execution of upperlimb motor acts [21,22], some authors hypothesize that the amount of this imbalance in inter-hemispheric excitability may be positively correlated with the degree of severity of motor disability [10,6]. Lindenberg motor function in the stimulated group, stimulation with simultaneous rehabilitation treatment based on physiotherapy techniques and occupational therapy with compared to the control group; the effects are verifiable even after one week after the end of the treatment; it has also been hypothesized that the magnitude of the electrode may affect the adjacent premotory cortex as well as the anodic somatosensory cortex; similarly, cathodal stimulation may have a similar effect in adjacent structures [19].…”

Developing Synaesthesia

“…Emerging savant skills have also been reported in many other cases of central nervous system injury or disease later in life (Fay, 1987;Dorman, 1991;Miller et al, 1998Miller et al, , 2000Lythgoe et al, 2005;Tammet, 2006;Treffert, 2006Treffert, , 2009Snyder, 2009). As is known from studies of autistic savants, downregulation of the serotonergic system in one hemisphere may result in an upregulation of the serotonergic system in contralateral brain regions (DeLong, 1999;Takeuchi et al, 2012), which might explain the development of savant skill and synesthesia following brain injury (Treffert, 2009). A second hypothesis is that the elevation in serotonin and glutamate levels in the days or weeks after brain injury can trigger disinhibited feedback or a structural binding of features through serotonergic hyperactivity in sensory neurons or neurons in parietal cortex involved in mental imagery.…”