Contents I. Introduction
Stroke occurs when the blood supply to the brain is reduced or blocked completely, which prevents brain tissue from getting oxygen and nutrients [1]. More than 795,000 people in the United States experience a stroke each year. It is the fifth leading cause of death and the leading cause of serious long-term disability [2]. Specifically, a stroke that occurs in the motor and somatosensory cortices will cause focal damage to the cortices and to their descending pathways [3]. This causes a variety of physical effects, including hemiparesis, loss of sensation in the extremities, abnormal muscle synergies, spasticity, and loss of fine motor skills. [4]. Most (80%) ischemic stroke survivors report movement impairment on the side of the body contralateral to the lesioned hemisphere [4]. As a result of the damage to the ipsilesional motor cortex or its descending pathway, i.e., the corticospinal tract (CST) [5], there is a maladaptive hyperexcitability in the cortico-reticulospinal tract (CRST) in the contralesional hemisphere [5], hyperexcitability in post stroke motor impairments, specifically in more severe individuals and particularly in the expression of abnormal muscle synergies in the paretic upper limb [6]. The medial CRST primarily originates from the dorsal premotor cortex (PMd) and travels through the pontine reticular formation [7]. Previous studies applying transcranial magnetic stimulation (TMS) to patients after stroke demonstrated that the medial CRST is responsive to the excitatory ipsilateral input from the PMd in the contralesional hemisphere [8], [9]. This finding makes the contralesional PMd a potential target for combating moderate-to-severe movement impairment.
