Early MRI studies of Parkinson’s disease used T2-weighted images to delineate the SN (22, 23), and researchers interpreted the hypointense region to result from iron in the SN pars reticulata (SNr) (24). However, Rutledge et al. (25) and Mänz et al. (26) have observed that the correlation between this hypointense region and the SN was imperfect. Since T2-weighted images do not accurately depict the SN, others have employed additional MR imaging techniques, including diffusion weighted imaging (4), inversion recovery imaging (27, 28), quantitative T1 mapping (3), and susceptibility weighted imaging (2).
Recently, Sasaki et al. (1, 7) used a T1-weighted fast spin echo sequence to visualize the SN and locus ceruleus. They referred to this technique as neuromelanin-sensitive MRI, arguing that the contrast results from neuromelanin as a byproduct of dopamine and noradrenalin metabolisms. They applied this technique to distinguish patients with schizophrenia and depression from healthy controls (1). They found increased signal intensity in the SN in patients with schizophrenia, which is consistent with elevated levels of dopamine, and reduced signal intensity in the locus ceruleus in patients with depression, which is consistent with dysfunction of the noradrenergic system. To image the SN in patients with Parkinson’s disease, Schwarz et al. (29) recently used a T1-weighted fast spin echo sequence with additional magnetization transfer contrast pulses. They found smaller regions of hyperintensity with reduced contrast in the SN in patients compared to controls, consistent with the loss of dopamine neurons in the SN pars compacta (SNc). Because neuromelanin is a byproduct of dopamine and noradrenalin synthesis, alterations to these catecholamines or loss of dopaminergic neurons could have an effect on images sensitive to neuromelanin.