Background: The functional 6-[¹⁸F]FDOPA positron emission tomography (PET) can be a helpful tool in differentiating parkinsonism with dopaminergic deficiency from clinically similar differential diagnoses. Furthermore, in T2*/susceptibility-weighted imaging (SWI) magnetic resonance imaging (MRI) sequences the structural integrity of the Nigrosome 1 (N1) can be assessed by checking the presence of the swallow tail sign (STS). We therefore retrospectively compared the performance of the 6-[¹⁸F]FDOPA PET with the N1 detection in patients suspected with parkinsonian diseases. Forty-three consecutive patients (m: 23, f: 20, mean age: 63 ± 12 years) were included in the study. They underwent clinically indicated 6-[¹⁸F]FDOPA PET/MRI scans as part of their neurological evaluation of uncertain parkinsonian syndromes. Visual and semi-quantitative PET imaging results were statistically compared with visual N1 assessment on 3 T SWI. As the gold standard, we defined the clinical diagnosis at the last follow-up, which included idiopathic Parkinson syndrome (IPS; n = 18), atypical parkinsonian syndromes (APS; n = 9) and other neurological diseases without dopaminergic deficit (n = 16). Results: Thirty-five of 43 patients (81%, Kappa 0.611) had corresponding results in 6-[¹⁸F]FDOPA PET and SWI. Seven of the remaining 8 patients were correctly diagnosed by 6-[¹⁸F]FDOPA PET alone. Sensitivity, specificity and accuracy for 6-[¹⁸F]FDOPA and N1 imaging were 93%, 94%, 93% and 82%, 75%, 79%, respectively. Conclusions: 6-[¹⁸F]FDOPA PET and Nigrosome 1 evaluation had an overall good intermodality agreement. Diagnostic agreement was very good in cases of clinically suspected idiopathic Parkinson syndrome and fair in atypical parkinsonian syndromes, but poor in patients with non-parkinsonian disorders. 6-[¹⁸F]FDOPA PET showed higher sensitivity, specificity and accuracy in discriminating parkinsonian syndromes from non-parkinsonian disorders than the N1 evaluation. In summary, the additional benefit of N1 assessment in patients with APS or parkinsonism without dopaminergic deficit needs to be proven by prospective studies.