FREEZING OF GAIT, BRADYKINESIA & PARKINSONS DISEASE

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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.