Lorberboym Mordechai, Treves Therese A, Melamed Eldad, Lampl Yair, Hellmann Mark, Djaldetti Ruth
Department of Nuclear Medicine Edith Wolfson Medical Center, Holon, Israel.
Mov Disord. 2006 Apr;21(4):510-4. doi: 10.1002/mds.20748.
Parkinsonism in patients taking neuroleptic medications might be induced by dopamine receptor blockade alone or by dopamine blockade with nigrostriatal dysfunction. The differentiation between Parkinson's disease (PD) and drug-induced parkinsonism (DIP) is difficult to assess on clinical grounds alone. In this study, we have evaluated the clinical characteristics and striatal binding of (123)I-FP-CIT (N-omega-fluoropropyl-2beta-carboxymethoxy-3beta-{4-iodophenyl}tropane) in patients who developed DIP. A total of 20 patients (mean age, 62 +/- 13 years) who developed parkinsonism while on neuroleptic agents and 10 age-matched controls were enrolled. [123]-FP-CIT single-photon emission computed tomography (SPECT) was performed in all subjects. Neurological assessment was performed with the Motor part of the Unified Parkinson's Disease Rating Scale. [123]-FP-CIT binding of the entire striatum, caudate, and putamen was calculated. Patients were divided into two subgroups according to SPECT results for comparison of clinical characteristics. There were 9 patients who had normal scans and 11 who showed significantly diminished striatal binding, suggesting degeneration of the nigrostriatal system. Subanalyses of abnormal scans revealed significantly diminished binding in the caudate (P < 0.001 for right and left caudate) and putamen (P = 0.002 and P < 0.05 for right and left putamen, respectively). There were no differences in clinical features between patients with normal and abnormal scans. Symptoms included asymmetric tremor, bradykinesia, and rigidity in both groups. Freezing gait was present in two patients with normal scans. These results indicate that DIP is clinically indistinguishable from PD. Brain imaging with FP-CIT helps to determine whether DIP is entirely drug-induced or an exacerbation of subclinical PD.
服用抗精神病药物的患者出现帕金森综合征可能仅由多巴胺受体阻断引起,也可能由多巴胺阻断伴黑质纹状体功能障碍引起。仅根据临床依据很难区分帕金森病(PD)和药物性帕金森综合征(DIP)。在本研究中,我们评估了发生DIP的患者的临床特征以及(123)I-FP-CIT(N-ω-氟丙基-2β-羧甲氧基-3β-{4-碘苯基}托烷)的纹状体结合情况。共纳入了20例在服用抗精神病药物期间出现帕金森综合征的患者(平均年龄62±13岁)以及10例年龄匹配的对照。所有受试者均进行了[123]-FP-CIT单光子发射计算机断层扫描(SPECT)。使用统一帕金森病评定量表的运动部分进行神经学评估。计算了整个纹状体、尾状核和壳核的[123]-FP-CIT结合情况。根据SPECT结果将患者分为两个亚组以比较临床特征。有9例患者扫描结果正常,11例显示纹状体结合明显减少,提示黑质纹状体系统退变。对异常扫描的亚分析显示尾状核结合明显减少(右侧和左侧尾状核P<0.001),壳核结合也明显减少(右侧壳核P = 0.002,左侧壳核P<0.05)。扫描结果正常和异常的患者临床特征无差异。两组症状均包括不对称震颤、运动迟缓及强直。两名扫描结果正常的患者存在冻结步态。这些结果表明DIP在临床上与PD无法区分。使用FP-CIT进行脑成像有助于确定DIP是完全由药物引起还是亚临床PD的加重。