Abstract: Central post-stroke pain (CPSP), which is neuropathic pain associated with a brain lesion following a stroke, was first described by Dejerine and Roussy in 1906 in a thalamic infarct patient (Dejerine and Roussy, 1906; Watson and Sandroni, 2016). Since then, many studies have suggested that the pathophysiological mechanism underlying CPSP is activated by injury to the somatosensory nervous system (Watson and Sandroni, 2016). There are two major pathways within the somatosensory nervous system: the spinothalamic tract (STT), which is chiefly responsible for pain and touch sensations, and the medial lemniscus (ML) pathway, which is mainly involved in proprioception and tactile discrimination (Naidich et al., 2009). Many studies have suggested that STT injury is a major pathogenetic mechanism of CPSP, but a few studies have suggested that ML injury is related to the development of CPSP (Kim and Choi-Kwon, 1999; Seghier et al., 2005; Kim, 2007; Hong et al., 2010; Jang et al., 2017).