Gait dynamics in Parkinson’s disease: relationship to Parkinsonian features, falls and response to levodopa Joanna D. Schaafsma a , Nir Giladi a , Yacov Balash a , Anna L. Bartels a , Tanya Gurevich a , Jeffrey M. Hausdorff a,b, * a Movement Disorders Unit, Department of Neurology, Tel Aviv Sourasky Medical Center, and Sackler School of Medicine, Tel Aviv University, 6 Weizmann Street, Tel Aviv 64239, Israel b Gerontology Division, Beth Israel Deaconess Medical Center and Division on Aging, Harvard Medical School, 330 Brookline Avenue, Boston, MA 02215, USA Received 26 September 2002; received in revised form 28 January 2003; accepted 13 March 2003 Abstract Objectives: Patients with Parkinson’s disease (PD) have an increased risk of falling that has yet to be fully explained. To better understand the gait disturbance in PD and the factors that contribute to falls, we quantitatively evaluated: (1) the relationship between gait variability (a marker of fall risk in other populations), fall history, and other parkinsonian features, and (2) the effects of levodopa on these relationships. Methods: The average stride time and stride-to-stride variability were measured using force-sensitive insoles during comfortable walking. Fall frequency, motor control, function, and mental health were measured using the Unified Parkinson’s Disease Rating Scale (UPDRS), the Mini-Mental State Exam (MMSE), and the timed motor tests of the Core Assessment Program for Intracerebral Transplantations (CAPIT) in 32 subjects with idiopathic PD, in an ‘‘off’’ (unmedicated) state and again in an ‘‘on’’ (medicated) state. Results: Average stride time was not associated with any UPDRS or CAPIT measure and was similar in fallers and non-fallers in ‘‘off’’ and ‘‘on’’states ( p > 0.27). Stride time variability was significantly associated with fall frequency as well as with total scores on the CAPIT and the UPDRS, ADL abilities, and motor function. Stride time variability and falls were not related to tremor, rigidity or bradykinesia in the ‘‘off’’ state. 41% of subjects reported one or more falls. Stride time variability was 8.8 F 7.9% in fallers and 4.2 F 1.3% in non-fallers ( p < 0.009). Stride time variability significantly improved in response to levodopa, both in fallers and non-fallers, but remained increased in fallers (vs. non-fallers). Conclusions: The patho-physiology responsible for impaired stride-to-stride regulation of gait timing is apparently independent of other cardinal features of PD, i.e., tremor, rigidity, or bradykinesia, but is responsive to levodopa. Stride-to-stride variability is especially impaired among PD subjects with a history of falls, suggesting, for the first time, the possibility of exaggerated impairment of internal clock function in PD fallers. D 2003 Elsevier Science B.V. All rights reserved. Keywords: Gait; Dynamics; Falls; Parkinson’s disease; Levodopa 1. Introduction One of the hallmarks of Parkinson’s disease (PD) is its effect on gait. Patients with PD often walk with a reduced gait speed, shorter stride length, stooped posture, and reduced arm swing [1–5]. Control of cadence (more specif- ically, the average step rate) is generally intact, but some patients may increase the stepping frequency to compensate for a reduced stride length [6]. Gait disturbances may also include gait instability and arrhythmicity, as manifest by increased stride-to-stride variability in walking [7,8]. Gait disturbances and instability may predispose to falls in PD. Many subjects with PD have a high risk of falling, even compared to age-matched controls. In a community- based sample of 63 patients with PD, Ashburn et al. [9] found that 40% had experienced one or more falls in the previous 12 months. In a 6-month, prospective study, Bloem at al. [10] observed that 51% of PD subjects with moder- ately advanced disease fell at least once while only 15% of age-matched control subjects fell. Gray and Hildebrand [11] observed that 59% of PD subjects fell during a 3-month 0022-510X/03/$ - see front matter D 2003 Elsevier Science B.V. All rights reserved. doi:10.1016/S0022-510X(03)00104-7 * Corresponding author. C/O Movement Disorders Unit, Tel Aviv Sourasky Medical Center, 6 Weizmann Street, Tel Aviv 64239, Israel. Tel.: +972-3-697-3081; fax: +972-3-697-4911. E-mail address: jhausdor@caregroup.harvard.edu (J.M. Hausdorff). www.elsevier.com/locate/jns Journal of the Neurological Sciences 212 (2003) 47 – 53