We read the article by van Gaalen et al. 1 with great interest. These authors reviewed the frequency and main type of movement disorders found in each form of spinocerebellar ataxia (SCA). They also reported unusual movement disorders and noncerebellar manifestations, such as stiff-person syndrome, camptocormia, restless legs syndrome, and periodic limb movements during sleep. One of the key points highlighted by this review is the pattern of extracerebellar degeneration in SCA, supporting previous data describing substantia nigra, pons, pallidum, putamen, caudate nucleus, motor cortex, and thalamus involvement. 2 For instance, the presence of parkinsonism in SCA3 is consistent with nigrostriatal impairment, a finding demonstrated in an early study. 3 Recently, our group reported a case of akathisia in a patient with clinically-and molecularly-proven SCA3. 4 Akathisia is known to occur frequently in Parkinson's disease, and striatal dopaminergic dysfunction is postulated to be the pathophysiological etiology of this movement disorder. 5 Similarly, basal ganglia involvement, associated with dopaminergic dysfunction, is the most likely explanation for common movement disorders in SCA3 such as dystonia and bradykinesia. Given the pathophysiological mechanisms outlined, we performed a dopamine transporter (DAT) scan in vivo, using a tropane-derivative dopamine transporter type 1-99m technetium based ligand ([TC 99m ]-TRODAT-1), as the radioligand, to elucidate the underlying pathophysiology of the patient's akathisia. Our results revealed DAT density within normal control ranges, suggesting that akathisia may not be related to presynaptic dopaminergic dysfunction. 4 In line with these results, other pharmacologic studies have also implicated nondopaminergic pathways in the pathophysiology of akathisia. In conclusion, we believe that akathisia should be considered in the context of unusual SCArelated movement disorders, and that future studies will confirm akathisia-related pathophysiology. We also speculate that movement disorders in SCA are more complex than previously thought, involving degeneration in other brain regions.