These findings are not surprising considering the teratogenic effects of alcohol to brain regions associated with motor functioning such as the cerebellum and basal ganglia. Animal research has found that cerebellar neurons are sensitive to alcohol-induced damage (Goodlett, Pearlman, & Lundahl, 1998; Hamre & West, 1993; Thomas, Goodlett, & West, 1998), and neuroimaging research has documented significant volume and size reductions in the cerebellum and caudate nucleus of the basal ganglia (Archibald et al., 2001) (for detail, see Lebel et al., this issue). The causes of motor impairment observed in individuals with FASD are not limited to brain dysfunction. In addition to central nervous system abnormalities, peripheral motor nerve damage is also evident. Children prenatally exposed to alcohol show increased motor delay variability (Simmons, et al., 2009) that is likely attributable to atypical muscle development (David & Subramaniam, 2005), reduced motor neurons (Bradley, Beaman, Moore, & Heaton, 1997; Heaton & Bradley, 1995), poor peripheral nerve myelination (Zoeller, Butnariu, Fletcher, & Riley, 1994), and slowed nerve conductivity (de los Angeles Avaria et al., 2004) that are associated with prenatal alcohol exposure.
