FREEZING OF GAIT, BRADYKINESIA & PARKINSONS DISEASE

本子项目是利用由NIH/NCRR资助的中心赠款提供的资源的众多研究子项目之一。子项目和研究者（PI）可能已经从另一个NIH来源获得了主要资金，因此可以在其他CRISP条目中表示。列出的机构是中心的，不一定是研究者的机构。步态冻结（FOG）的病理生理学及其与其他帕金森症状的关系尚不清楚。为了深入了解这些运动障碍，我们评估了帕金森病（PD）中FOG和其他帕金森特征以及左旋多巴反应之间的关系。19例PD患者在“关闭”状态下，在服用抗帕金森药物12小时后，在“打开”状态下，在服用常规左旋多巴剂量后约1小时，对“关闭”状态下具有临床显著FOG进行评估。评估包括统一帕金森病评定量表（UPDRS）和130米的录像步行。三名观察员独立观看了录像带并对FOG频率进行了评分。通过将相关UPDRS项目分组分析帕金森病的特征。三个观察者之间的观察者间和类内信度通过Pearson和Friedman检验进行评估。Pearson相关系数用于评估FOG与其他帕金森病特征之间的关系。三位观察者之间有高度的一致性（R=0.7）。FOG频率与任何其他帕金森病特征的严重程度均不相关，仅与言语和写作严重程度指数相关。左旋多巴治疗显著降低了FOG频率。这种减少与震颤（R=0.80）和言语（R=0.62）指标的改善密切相关。未发现FOG对左旋多巴的反应与强直、运动迟缓或平衡指标的改善之间存在相关性。左旋多巴治疗可降低PD患者的FOG频率。FOG显然是PD的一种独立的运动症状，由一种发作性病理引起，不同于导致运动迟缓、僵硬或姿势不稳定的病理。正在进行的研究旨在了解PD中这种特征性步态障碍的机制。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The pathophysiology of freezing of gait (FOG) and its relationship to other Parkinsonian symptoms is unclear. To gain insight into these motor disturbances, we assessed the relationship between FOG and other Parkinsonian features in Parkinson's disease (PD) and the response to levodopa. 19 PD patients with clinically significant FOG at "off" state were assessed while in "off" state, 12 hours after taking their anti-Parkinsonian medications, and while in "on" state, about 1 hour after their regular morning levodopa dose. Assessments included the Unified Parkinson's disease Rating Scale (UPDRS) and a 130 meter, videotaped walk. Three observers independently viewed the videotapes and scored FOG frequency. Parkinsonian features were analyzed by grouping together related UPDRS items. Inter-observer and intra-class reliability between the three observers were evaluated by Pearson and Friedman tests. Pearson correlation coefficients were used to assess the relationships between FOG and other Parkinsonian features. There was a high level of agreement between the three observers (R=0.7). FOG frequency was not correlated with severity of any other Parkinsonian features at "off" and only with speech and writing severity indexes at "on". FOG frequency was significantly decreased by levodopa treatment. This decrement was strongly correlated with improvement of tremor (R=0.80) and speech (R=0.62) indexes. No correlation was found between the response of FOG to levodopa and improvement in rigidity, bradykinesia, or balance indexes. Levodopa treatment decreases FOG frequency in PD patients. FOG is apparently an independent motor symptom of PD, caused by a paroxysmal pathology that is different from that responsible for bradykinesia, rigidity or postural instability. Ongoing research is aimed at understanding the mechanism of this characteristic gait disorder in PD.