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.

Figure 1

Changes in interhemispheric interaction and inhibitory noninvasive brain stimulation (NIBS) therapy in patients with subcortical stroke. (a) Mechanisms underlying the changes in interhemispheric interaction after stroke. In healthy subjects, the interhemispheric interaction changes from an inhibitory to an excitatory influence on the active motor cortex around movement onset. In contrast, stroke patients with motor deficits do not show this release from interhemispheric inhibition for the movement of the paretic hand; rather, they exhibit a persistent inhibitory influence on the ipsilesional motor cortex [34]. These pathological effects contribute to the reduced performance of the paretic hand. (b) Inhibitory NIBS over the unaffected hemisphere. Inhibitory NIBS decreases the excitability of the contralesional motor cortex and reduces the interhemispheric inhibition from the contralesional to the ipsilesional motor cortex. The excitatory interhemispheric interaction from the contralesional to the ipsilesional motor cortex might be relatively strong because of a reduced inhibitory influence. The change in interhemispheric interaction after inhibitory NIBS increases the excitability of the ipsilesional motor cortex. Facilitation of the ipsilesional motor cortex improves the motor function of the paretic hand in patients with subcortical stroke [99, 115]. However, it remains to be determined whether the excitatory interhemispheric interaction itself actually changes after inhibitory NIBS.

Figure 2

Amputation alters the interhemispheric interactions through the corpus callosum and induces bilateral neural activity. After amputation, reorganization of the deafferented sensorimotor cortex (SM1) occurs due to the absence of an afferent input from the missing hand. This change leads to an imbalance between the hemispheres in patients with amputations. Moreover, experience-dependent changes in representation by overuse of the intact hand increase this imbalance between the hemispheres. The imbalance between the hemispheres alters the interhemispheric interactions through the corpus callosum. In particular, the reduced interhemispheric inhibition observed in patients with amputations induces the neural activation of both hemispheres due to the failed inhibition of the opposite hemisphere. When tactile stimulation is delivered to the stump of the amputated limb, the overflow of the afferent information induces the activation of the nondeafferented SM1. In addition to the sensory system, the motor overflow increases the activity of the deafferented SM1 during the movement of the intact hand.