¹²³I-β-CIT SPECT for Imaging Serotonin Transporters in Parkinson’s Disease

TO THE EDITOR:

We read with interest the article by Kim et al. published in the June 2003 issue (1), in which the authors reported on results of ¹²³I-β-2β-carbomethoxy-3β-(4-iodophenyl)tropane (β-CIT) SPECT studies performed on patients with Parkinson’s disease (PD) and a matched control group. SPECT scanning was repeated up to 24 h after radiotracer injection to determine the time dependency of midbrain serotonin transporter (SERT) and striatal dopamine transporter (DAT) binding. Kim et al. correlated the obtained SPECT data with clinical scores on severity of parkinsonian symptoms, including depression (the mentation, behavior, and mood subscale of the Unified Parkinson’s Disease Rating Scale; Hamilton Depression Scale). They found the specific midbrain uptake of the radiotracer to reach a peak at about 6 h after injection. No differences in midbrain SERT availability were detected between patients and controls, despite a significantly lower striatal DAT availability for the PD patients. In 7 depressed PD patients, the midbrain SERT data did not correlate with severity of depression (1).

From their results, the authors concluded that DAT and SERT are differentially affected in PD. We want to stress, however, that the authors neglected to discuss their findings in light of the results of a previous study of very similar design. Using the same radiotracer and imaging technique, our group studied cerebral SERT and DAT in patients with PD in 2001 (2). We reported on differential patterns of midbrain SERT and striatal DAT availability in this disorder (2), results that have now been confirmed by Kim et al. (1). In contrast to the results of Kim et al., however, we found the midbrain SERT availability to correlate with the severity of depression, expressed as the mentation, behavior, and mood subscale of the Unified Parkinson’s Disease Rating Scale (2). By comparing the methods used to detect SERT in both studies, we presume that the difference in results between the 2 studies was caused by different approaches to define the target brain regions or by different scanner characteristics. First, in our study, we defined the midbrain region after coregistering the SPECT data with the individual MRI data of the scanned subjects. In contrast, Kim et al. did not coregister the SPECT data with morphologic imaging data. Image coregistration, however, is an effective tool to overcome the lack of anatomic information in SPECT images. Previously, for instance, our group showed that diagnosis of PD improves by applying SPECT-MRI image coregistration rather than solely SPECT analysis (3). Second, optimized spatial resolution and scanner sensitivity seem indispensable for minimizing partial-volume effects while detecting SERT density in the relatively small midbrain region. In our study, we therefore used a brain-dedicated SPECT scanner (Ceraspect; DSI). In comparison with a triple-head scanner such as that used in the study by Kim et al. (the authors did not specify the scanner applied), the dedicated brain scanner provides not only higher spatial resolution but also count ratios that are closer to the true activity distribution, as reported recently by our group (4).

Apart from these methodologic drawbacks, the findings of the dynamic SPECT data analysis in the publication by Kim et al. (1) confirm the results of Brücke et al. that had already been published in 1993 (5). With respect to those results, we cannot distinguish the novelty in the results of Kim et al. Also, we regret that the authors again neglected to discuss their data in light of the cited literature.

Finally, from our point of view, the paper by Kim et al. (1) does not provide an up-to-date overview of current knowledge on SERT imaging using ¹²³I-β-CIT SPECT in neuropsychiatry. No studies on that issue were cited in their publication. Instead, the authors claimed that “…¹²³I-β-CIT…should be useful for studying serotonergic neuronal integrity in cerebral degenerative processes.” (1). To formulate this statement in such a presumptive form does not seem appropriate. Clearly, there is a list of disorders in which cerebral SERT has already been clinically investigated using ¹²³I-β-CIT and SPECT. A review of current knowledge in that field was published in 2002 by the University of Vienna group, which was among the first to apply this technique clinically (6). Recently, our group investigated cerebral SERT availability in patients with Wilson’s disease. In keeping with the results in PD patients, we found the degree of depression to correlate negatively with availability of brain SERT (7). Altogether, because of the extensive experience in ¹²³I-β-CIT SPECT imaging of SERT acquired by the brain-imaging community over the last few years, this method can undoubtedly be considered an established clinical research technique.