SLC6A5 and hereditary hyperekplexia: EFS has also been compared (Rusbridge, 2005) with startle disease/hyperekplexia, typically characterized by noise- or touch-evoked neonatal hypertonicity due to defects in inhibitory glycine receptor (GLRA1, GLRB; Shiang et al., 1993; Rees et al., 2002) or glycine transporter GlyT2 (SLC6A5) genes (Rees et al., 2006; Harvey et al., 2008).