Mateos Jose J, Lomeña Francisco, Parellada Eduard, Mireia Font, Fernandez-Egea Emili, Pavia Javier, Prats Alberto, Pons Francisca, Bernardo Miquel
Nuclear Medicine Department, Hospital Clínic of Barcelona, University of Barcelona, Barcelona, Spain.
Psychopharmacology (Berl). 2007 Apr;191(3):805-11. doi: 10.1007/s00213-006-0570-5. Epub 2006 Sep 22.
Drug induced parkinsonism (DIP) is directly related to dopamine D2 receptor blockade. However, there are many references describing parkinsonian signs (PS) in naive-patients. In our previous study, we observed lower DAT binding in a group of first-episode schizophrenic patients after short-term treatment with risperidone, compared with age-matched healthy controls.
To clarify if DAT decrease could be an illness trait, excluding the effect of antipsychotics on DAT availability, and to determine whether DAT availability before treatment with antipsychotics may predict subsequent development of PS.
A new series of 20 neuroleptic-naive schizophrenic patients and 15 healthy subjects was recruited. SPECT with [(123)I] FP-CIT (DaTSCAN(R)) was performed before starting antipsychotics and after 4 weeks of treatment. PS and psychopathological status were assessed by the Simpson-Angus (SAS), CGI and PANSS scales. Quantitative analyses of SPECTs were performed using ROIs placed in the caudate, putamen and occipital cortex.
Schizophrenic patients showed lower DAT binding compared with the healthy subjects at baseline (p<0.001) and after a 4-week-treatment period (p=0.001). Six out of eight schizophrenic patients of the DIP group were symptomatic for PS at baseline, in comparison to two out of 12 in the NoDIP group. Nonetheless, no differences were observed on DAT between DIP and NoDIP, neither at baseline (p=0.360) nor at endpoint (p=0.984). Finally, no differences between baseline-endpoint DAT binding were observed, neither in the DIP group (p=0.767) nor in the NoDIP group (p=0.093).
Our new series of first-episode naive-schizophrenic patients (1) points out DAT dysfunction as an illness trait due to the significantly lower DAT binding in schizophrenic patients in comparison to healthy subjects; (2) supports the results of other authors who describe PS in never-treated patients; (3) confirms that [(123)I] FP-CIT does not allow us to predict which patients will develop parkinsonism due to the lack of differences between DIP and NoDIP patients; and (4) confirms a null effect of antipsychotics on DAT due to the lack of differences in [(123)I] FP-CIT before and after a 4-week-treatment period.
药物性帕金森综合征（DIP）与多巴胺D2受体阻滞直接相关。然而，有许多参考文献描述了初治患者的帕金森氏征（PS）。在我们之前的研究中，我们观察到与年龄匹配的健康对照相比，一组首发精神分裂症患者在短期使用利培酮治疗后多巴胺转运体（DAT）结合降低。
排除抗精神病药物对DAT可用性的影响，阐明DAT降低是否可能是一种疾病特征，并确定抗精神病药物治疗前的DAT可用性是否可预测PS的后续发展。
招募了新的一组20例未使用过抗精神病药物的精神分裂症患者和15名健康受试者。在开始使用抗精神病药物之前和治疗4周后，使用[（123）I] FP-CIT（DaTSCAN®）进行单光子发射计算机断层扫描（SPECT）。通过辛普森-安格斯量表（SAS）、临床总体印象量表（CGI）和阳性和阴性症状量表（PANSS）评估PS和精神病理状态。使用置于尾状核、壳核和枕叶皮质的感兴趣区（ROI）对SPECT进行定量分析。
与健康受试者相比，精神分裂症患者在基线时（p<0.001）和治疗4周后（p=0.001）DAT结合较低。DIP组的8例精神分裂症患者中有6例在基线时出现PS症状，而无DIP组的12例中有2例。尽管如此，DIP组和无DIP组在DAT上均未观察到差异，无论是在基线时（p=0.360）还是在终点时（p=0.984）。最后，在DIP组（p=0.767）和无DIP组（p=0.093）中，均未观察到基线至终点DAT结合的差异。
我们新的一组首发未使用过抗精神病药物的精神分裂症患者（1）指出DAT功能障碍是一种疾病特征，因为与健康受试者相比，精神分裂症患者的DAT结合显著降低；（2）支持其他作者描述未治疗患者中PS的结果；（3）证实由于DIP组和无DIP组患者之间缺乏差异，[（123）I] FP-CIT无法让我们预测哪些患者会发生帕金森综合征；（4）由于在4周治疗期前后[（123）I] FP-CIT缺乏差异，证实抗精神病药物对DAT无影响。
