Gait Hypokinesia Research Articles

Diagnosis of vascular parkinsonism: A new tool for gait hypokinesia occurring in older persons

IntroductionReliable diagnosis of vascular parkinsonism (VaP) in the presence of a gait hypokinesia is an issue that is encountered in geriatrics. The EVAMAR-AGEX study was focusing on the phenomenon of recurrent falls in older persons (OP) with this parkinsonian gait. The present study is focusing on the diagnosis of VaP-related parkinsonian gait by developing a diagnostic guidance model adapted to OP. MethodsData from baseline and the 2-year follow-up visit were used to carry out univariate analysis and calculation of odds ratios, allowing to identify relevant variables to include in the diagnostic guidance model. To evaluate the model, confusion matrices were created, evaluating true positive, false negative, false positive and true negative incidences, sensitivity and specificity, and negative and positive predictive values. Results79 patients included 58% male; average age 81.24 years. VaP diagnosis according to Zijlmans criteria occurred in 28%; neurodegenerative parkinsonian syndromes in 72%. A 4-criteria model was established to facilitate diagnostic: lack of prior hallucinations, lack of movement disorders tremor excluded, no cognitive fluctuations, and ≥75 years of age at diagnosis. In combination of 4/4 criteria, all of them were required to disclose a specificity of 91% in the diagnosis of VaP. In combination of 3/4, in case of negative test, a negative predictive value for VaP diagnosis of 0.97 was obtained. ConclusionThe challenge of our tool is both to be able to rule out what is probably not a VaP and to argue what makes a VaP diagnosis probable in OP.

Association Between Gait and Dysautonomia in Patients With De Novo Parkinson's Disease: Forward Gait Versus Backward Gait.

Studies on gait and autonomic dysfunction have been insufficient so far, particularly de novo Parkinson's disease (PD). The aim of this study was to identify the association between gait dynamics and autonomic dysfunction in patients with de novo PD. A total 38 patients with de novo PD were retrospectively included in this study. Details of patients' dysautonomia were assessed using the Scales for Outcomes in Parkinson's Disease-Autonomic Dysfunction (SCOPA-AUT). For assessment of gait, a computerized gait analysis was performed using the GAITRite system for forward gait and backward gait. High SCOPA-AUT score (PD-HSAS) group and low SCOPA-AUT score (PD-LSAS) group were identified according to their SCOPA-AUT scores. Nineteen (50%) patients with high SCOPA-AUT scores above median value (12.5) were assigned into the PD-HSAS group and others were assigned to the PD-LSAS group. Compared with the PD-LSAS group, the PD-HSAS group exhibited slower gait, shorter stride, decreased cadence, increased double support phase, decreased swing phase, and increased variability in swing time. Total SCOPA-AUT score showed significantly positive correlations with gait variability and instability but a negative correlation with gait hypokinesia. In subdomain analysis, urinary dysautonomia was highly associated with impairment of gait dynamics. All significant results were found to be more remarkable in backward gait than in forward gait. Our findings suggest that alteration in gait dynamics, especially backward gait, is highly associated with autonomic dysfunction in patients with de novo PD.

Characterization of idiopathic Parkinson’s disease subgroups using quantitative gait analysis and corresponding subregional striatal uptake visualized using 18F-FP-CIT positron emission tomography

BackgroundGait disturbance is one of the most common symptoms among patients with idiopathic Parkinson’s disease (IPD). Nevertheless, Parkinson’s disease subtype clustering according to gait characteristics has not been thoroughly investigated. Research questionThe aim of this study was to identify subgroups according to gait pattern among patients with IPD. MethodsThis study included 88 patients with IPD who underwent 18F-fluorinated-N-3-fluoropropyl-2-β-carboxymethoxy-3-β-4-iodophenyl-nortropane positron emission tomography (18F-FP-CIT PET) and three-dimensional gait analysis (3DGA) between January 1, 2014 and December 31, 2016. We performed cluster analysis using temporal-spatial gait variables (gait speed, stride length, cadence, and step width) and divided patients into four subgroups. The kinematic and kinetic gait variables in 3DGA were compared among the four subgroups. Furthermore, we compared the uptake patterns of striatum among the four subgroups using 18F-FP-CIT PET. ResultsThe patients were clustered into subgroups based on gait hypokinesia and cadence compensation. Group 1 had decreased stride length compensating with increased cadence. Group 2 had decreased stride length without cadence compensation and wider step width. Group 3 had relatively spared stride length with decreased cadence. Group 4 had spared stride length and cadence. The uptake of posterior putamen was significantly decreased in Group 3 compared with Group 4. SignificanceGait hypokinesia and cadence can help to classify gait patterns in IPD patients. Our subgroups may reflect the different gait patterns in IPD patients.

Maximum Step Length Test Performance in People With Parkinson Disease: A Cross-sectional Study.

The Maximum Step Length Test (MSLT), a measure of one's capacity to produce a large step, has been studied in older adults, but not in people with Parkinson disease (PD). We characterized performance and construct validity of the MSLT in PD. Forty participants (mean age: 65.12 ± 8.20 years; 45% female) with idiopathic PD completed the MSLT while "OFF" and "ON" anti-PD medication. Construct validity was investigated by examining relationships between MSLT and measures of motor performance. The following measures were collected: Mini-Balance Evaluation Systems Test (Mini-BESTest), Activities-specific Balance Confidence (ABC) scale, gait velocity, 6-minute walk test (6MWT), Movement Disorder Society-Unified Parkinson Disease Rating Scale subsection III (MDS-UPDRS III), and Timed Up and Go (TUG) test. A repeated-measures analysis of variance tested for main effects of medication and stepping direction and the interaction between the 2. Pearson or Spearman correlations were used to assess the relationships between MSLT and motor performance measures (α = 0.05). Regardless of medication status, participants stepped further in the forward direction compared with the backward and lateral directions (P < 0.001). Participants increased MSLT performance when ON-medication compared with OFF-medication (P = 0.004). Regardless of medication status, MSLT was moderately to strongly related to Mini-BESTest, TUG, and 6MWT. People with PD stepped furthest in the forward direction when performing the MSLT. Increased MSLT performance was observed in the ON-medication state compared with OFF-medication; however, the small increase may not be clinically meaningful. Given the relationships between the MSLT and the Mini-BESTest, 6MWT, and TUG, MSLT performance appears to be associated with balance and gait hypokinesia in people with PD.Video Abstract available for more insights from the authors (see Video, Supplemental Digital Content 1, http://links.lww.com/JNPT/A186).

Recuperation of slow walking in de novo Parkinson’s disease is more closely associated with increased cadence, rather than with expanded stride length

IntroductionGait characteristics in the early stages of Parkinson’s disease (PD) have been less investigated so far. Moreover, the levodopa effect on gait in early PD remains to be further elucidated. We prospectively designed the study to examine gait dynamics and effect of dopaminergic treatment in patients with de novo PD. MethodsSpatiotemporal parameters were measured in healthy controls and drug naïve patients with PD, using computerized analysis with GAITRite system during usual gait. In PD group, motor symptoms and gait parameters were examined in both drug naive and levodopa 100mg trial conditions. ResultsTwenty four de novo PD patients and 27 healthy controls (matched for age, sex, and height) were selected for the study. Compared with the controls, patients with de novo PD showed the decrease in stride length, in both Med-OFF and Med-ON conditions. Notably, drug naïve patients with PD demonstrated slow walking velocity, whereas those with levodopa administration exhibited the increase of cadence by shortening stride time, which resulted in the improvement of gait speed. In addition, the stride length (gait hypokinesia) correlated with postural instability and gait difficulty subscore, but not with tremor, rigidity, bradykinesia, or total motor score. ConclusionAs a compensatory mechanism of slow walking, we found that the increment in cadence (frequency) is more important than the increment in stride length (amplitude) in gait dynamics in de novo PD. Additionally, the results may indicate that gait hypokinesia in PD could be regarded as one of axial symptoms.

Does Nordic Walking restore the temporal organization of gait variability in Parkinson\u2019s disease?

BackgroundGait disorders of Parkinson’s disease (PD) are characterized by the breakdown of the temporal organization of stride duration variability that was tightly associated to dynamic instability in PD. Activating the upper body during walking, Nordic Walking (NW) may be used as an external cueing to improve spatiotemporal parameters of gait, such as stride length or gait variability, in PD. The aim of this study was to evaluate the beneficial effects of NW on temporal organization of gait variability and spatiotemporal gait variables in PD.MethodsFourteen mild to moderate PD participants and ten age-matched healthy subjects performed 2 × 12 min overground walking sessions (with and without pole in a randomized order) at a comfortable speed. Gait speed, cadence, step length and temporal organization (i.e. long-range autocorrelations; LRA) of stride duration variability were studied on 512 consecutive gait cycles using a unidimensional accelerometer placed on the malleola of the most affected side in PD patients and of the dominant side in healthy controls. The presence of LRA was determined using the Rescaled Range Analysis (Hurst exponent) and the Power Spectral Density (α exponent). To assess NW and disease influences on gait, paired t-tests, Z-score and a two-way (pathological condition x walking condition) ANOVA repeated measure were used.ResultsLeading to significant improvement of LRA, NW enhances step length and reduces gait cadence without any change in gait speed in PD. Interestingly, LRA and step length collected from the NW session are similar to that of the healthy population.ConclusionThis cross-sectional controlled study demonstrates that NW may constitute a powerful way to struggle against the randomness of PD gait and the typical gait hypokinesia. Involving a voluntary intersegmental coordination, such improvement could also be due to the upper body rhythmic movements acting as rhythmical external cue to bypass their defective basal ganglia circuitries.Ethics committee’s reference numberB403201318916Trial registrationNCT02419768

Treadmill training for patients with Parkinson's disease

Treadmill training is used in rehabilitation and is described as improving gait parameters of patients with Parkinson's disease. To assess the effectiveness of treadmill training in improving the gait of patients with Parkinson's disease and the acceptability and safety of this type of therapy. We searched the Cochrane Movement Disorders Group Specialised Register (see Review Group details for more information) (last searched September 2014), Cochrane Central Register of Controlled Trials (The Cochrane Library 2014, Issue 10), MEDLINE (1950 to September 2014), and EMBASE (1980 to September 2014). We also handsearched relevant conference proceedings, searched trials and research registers, and checked reference lists (last searched September 2014). We contacted trialists, experts and researchers in the field and manufacturers of commercial devices. We included randomised controlled trials comparing treadmill training with no treadmill training in patients with Parkinson's disease. Two review authors independently selected trials for inclusion, assessed trial quality and extracted data. We contacted the trialists for additional information. We analysed the results as mean differences (MDs) for continuous variables and relative risk differences (RD) for dichotomous variables. We included 18 trials (633 participants) in this update of this review. Treadmill training improved gait speed (MD = 0.09 m/s; 95% confidence interval (CI) 0.03 to 0.14; P = 0.001; I(2) = 24%; moderate quality of evidence), stride length (MD = 0.05 metres; 95% CI 0.01 to 0.09; P = 0.01; I(2) = 0%; low quality of evidence), but walking distance (MD = 48.9 metres; 95% CI -1.32 to 99.14; P = 0.06; I(2) = 91%; very low quality of evidence) and cadence did not improve (MD = 2.16 steps/minute; 95% CI -0.13 to 4.46; P = 0.07; I(2) = 28%; low quality of evidence) at the end of study. Treadmill training did not increase the risk of patients dropping out from intervention (RD = -0.02; 95% CI -0.06 to 0.02; P = 0.32; I(2) = 13%; moderate quality of evidence). Adverse events were not reported in included studies. This update of our systematic review provides evidence from eighteen trials with moderate to low risk of bias that the use of treadmill training in patients with PD may improve clinically relevant gait parameters such as gait speed and stride length (moderate and low quality of evidence, respectively). This apparent benefit for patients is, however, not supported by all secondary variables (e.g. cadence and walking distance). Comparing physiotherapy and treadmill training against other alternatives in the treatment of gait hypokinesia such as physiotherapy without treadmill training this type of therapy seems to be more beneficial in practice without increased risk. The gain seems small to moderate clinically relevant. However, the results must be interpreted with caution because it is not known how long these improvements may last and some studies used no intervention in the control group and underlie some risk of bias. Additionally the results were heterogenous and we found variations between the trials in patient characteristics, the duration and amount of training, and types of treadmill training applied.

Treadmill training for patients with Parkinson's disease.

Treadmill training is used in rehabilitation and is described as improving gait parameters of patients with Parkinson's disease. To assess the effectiveness of treadmill training in improving the gait of patients with Parkinson's disease and the acceptability and safety of this type of therapy. We searched the Cochrane Movement Disorders Group Specialised Register (see Review Group details for more information) (last searched September 2014), Cochrane Central Register of Controlled Trials (The Cochrane Library 2014, Issue 10), MEDLINE (1950 to September 2014), and EMBASE (1980 to September 2014). We also handsearched relevant conference proceedings, searched trials and research registers, and checked reference lists (last searched September 2014). We contacted trialists, experts and researchers in the field and manufacturers of commercial devices. We included randomised controlled trials comparing treadmill training with no treadmill training in patients with Parkinson's disease. Two review authors independently selected trials for inclusion, assessed trial quality and extracted data. We contacted the trialists for additional information. We analysed the results as mean differences (MDs) for continuous variables and relative risk differences (RD) for dichotomous variables. We included 18 trials (6 3 3 participants) in this update of this review. Treadmill training improved gait speed (MD = 0.09 m/s; 95% confidence interval (CI) 0.03 to 0.14; P = 0.001; I(2) = 24%; m oderate quality of evidence), stride length (MD = 0.05 metres; 95% CI 0.01 to 0.09; P = 0.01; I(2) = 0%; l ow quality of e vidence), but walking distance (MD = 48.9 metres; 95% CI -1.32 to 99.14; P = 0.06; I(2) = 91%; very low quality of evidence) and cadence did not improve (MD = 2.16 steps/minute; 95% CI -0.13 to 4.46; P = 0.07; I(2) = 28%; low quality of evidence) at the end of study. Treadmill training did not increase the risk of patients dropping out from intervention (RD = -0.02; 95% CI -0.06 to 0.02; P = 0.32; I(2) = 1 3%; m oderate quality of evidence). Adverse events were not reported in included studies. This update of our systematic review provides evidence from e ighteen trials with moderate to l ow risk of bias that the use of treadmill training in patients with PD may improve clinically relevant gait parameters such as gait speed and stride length (m oderate and low quality of evidence, respectively) . This apparent benefit for patients is, however, not supported by all secondary variables (e.g. cadence and walking distance ). Comparing physiotherapy and treadmill training against other alternatives in the treatment of gait hypokinesia such as physiotherapy without treadmill training this type of therapy seems to be more beneficial in practice without increased risk. The gain seems small to moderate clinically relevant . However, the results must be interpreted with caution because it is not known how long these improvements may last and some s tudies used no intervention in the control group and underlie some risk of bias . Additionally the results were heterogenous and we found variations between the trials in patient characteristics, the duration and amount of training, and types of treadmill training applied.

A case of ST elevation myocardial infarction precipitated by methylphenidate therapy for gait freeze

AbstractBackgroundParkinson's disease affects 1% of the population older than 60 years. Motor symptoms can be difficult to treat in end‐stage disease, leading to the use of therapies with less favourable adverse effect profiles.AimTo promote awareness of the risks associated with the off‐label use of methylphenidate for hypokinesia in Parkinson's disease patients with cardiovascular risk factors.Clinical detailsA 70‐year‐old Caucasian non‐smoking male presented to the hospital with chest pain and inferior ST segment elevation 2 months after commencing methylphenidate for gait hypokinesia. His past medical history was significant for end‐stage Parkinson's disease with associated psychosis, and ischaemic heart disease with previous myocardial infarction. Relevant therapies included levodopa, benserazide, amantadine, pramipexole, quetiapine, atorvastatin and perindopril.OutcomesThe patient received a drug eluting stent to the circumflex artery, followed by a staged percutaneous coronary intervention to the left anterior descending artery. Methylphenidate was discontinued on day 2 post myocardial infarction in light of published data indicating an increased risk of myocardial infarction with methylphenidate use. Methylphenidate is known to stimulate catecholamine release, thereby increasing the risk of ischaemic cardiovascular events by increasing myocardial oxygen demand.ConclusionThis is the first reported case to describe methylphenidate use in Parkinson's disease complicated by a myocardial infarction. This case, in conjunction with other published literature, suggests that the use of methylphenidate for this novel indication must be carefully considered for each individual, and avoided in those with cardiovascular risk factors or known ischaemic heart disease.

Gait and attentional performance in freezers under methylphenidate

BackgroundAttentional resources appear to be involved in the occurrence of FoG. The Parkgait study recently reported that methylphenidate reduces gait hypokinesia and freezing of gait (FoG) in advanced PD patients receiving STN-DBS in the off-dopaminergic drug condition. Methylphenidate is considered to improve attention. The primary objective of the present ancillary study was to determine whether methylphenidate reduced the interference between a cognitive task and gait in patients with FoG. The study's secondary objective was to compare attentional performance in methylphenidate-treated and placebo-treated patients. MethodsA total of 24 patients (from two centers) were included in the study. Patients were randomly assigned 1:1 to a three-month course of methylphenidate (1mg/kg/day) or placebo. Patients were assessed after an acute L-dopa challenge. The primary outcome criterion was the stride length ratio ((dual-task stride length minus free gait stride length)/free gait stride length). Trials with FoG episodes were excluded from the analysis. Secondary outcomes included changes in reaction times for computerized attention tasks and FoG severity. ResultsWhen comparing patients receiving methylphenidate with those receiving placebo, we did not observe any significant differences in the interaction between the dual task and gait or in attentional performance. ConclusionAs in the main Parkgait study, methylphenidate did not reduce gait hypokinesia in patients receiving dopaminergic treatment. Our present results suggest that the reduction in the number of FoG episodes previously observed in patients on methylphenidate was neither due to interaction between a dual-task and gait nor an increase in attentional performance.

Is reduced arm and leg swing in Parkinson's disease associated with rigidity or bradykinesia?

Background and purposeArm and leg swings during gait are reduced and asymmetric in Parkinson's disease (PD). Although rigidity and bradykinesia are interconnected with each other, and related with gait hypokinesia including arm and leg swing alteration, it remains uncertain which factor is more responsible for the decrease of arm and leg swings. The study aimed to uncover which factor between rigidity and bradykinesia is more associated with the reduction of arm and leg swings during gait. MethodsPatients with PD were selected and divided into a concordance group (21 patients) representing a match of both symptoms and a discordance group (nineteen patients) exhibiting a mismatch of pronounced rigidity and bradykinesia. Visual inspections of video clips for asymmetric features of gait and posture including arm swing, leg swing, shoulder position, external foot rotation were analyzed and accessed by two independent neurologists blindly. ResultsThe side of more pronounced rigidity was significantly and moderately related with the side of more decreased arm and leg swings (p<0.001, κ=0.592 in arm swing; p=0.011, κ=0.432 in leg swing, respectively), but the side of more dominant bradykinesia was associated with neither arm nor leg swing asymmetry (p=1, κ=0.014 in arm swing; p=1, κ=−0.036 in leg swing). In addition, asymmetric posturing including shoulder position and a laterally rotated foot showed no relationship with rigidity or bradykinesia. ConclusionThe reduction of arm and leg swings during gait in PD was associated with rigidity, but not with bradykinesia.

Auditory cueing of gait initiation in Parkinson’s disease patients with freezing of gait

ObjectiveImpaired gait initiation (GI) in patients with advanced Parkinson’s disease (PD) is a typical functional sign of akinesia. Failure to initiate the first step is frequently presented by patients with freezing of gait (FOG) and is often considered a sub-type of freezing. The literature on the effects of cueing of GI preparation and execution remains controversial. Our objective was to establish whether auditory cueing improves the preparation and/or execution of GI in PD patients with a history of FOG. MethodsWe recorded first-step preparation and execution in 30 PD patients with confirmed FOG under two randomised conditions: self-triggered (ST) gait and gait cued by a sound beep in off- and on-dopa conditions. Anticipatory postural adjustments (APAs) were evaluated by monitoring the trajectory of the centre of pressure. ResultsWe compared the patients with 30 patients without history of FOG and 30 healthy controls (HCs). l-Dopa only slightly improved the characteristics of APAs in freezers but was effective to improve gait hypokinesia. Auditory cueing was effective in improving step preparation in freezers, who showed adequate APAs more frequently. As seen with HCs and patients without FOG, patients released their APAs more quickly when auditory cueing was applied. However, cueing did not have a significant effect on step length. Clinically, auditory cueing also improved start hesitation in freezers. ConclusionsAuditory cueing improved step preparation but not step execution in PD patients. SignificanceA failure to link step preparation and execution during GI may explain the poor first-step execution seen in PD freezers.

Methylphenidate for gait hypokinesia and freezing in patients with Parkinson's disease undergoing subthalamic stimulation: a multicentre, parallel, randomised, placebo-controlled trial

Despite optimum medical management, many patients with Parkinson's disease are incapacitated by gait disorders including freezing of gait. We aimed to assess whether methylphenidate--through its combined action on dopamine and noradrenaline reuptake--would improve gait disorders and freezing of gate in patients with advanced Parkinson's disease without dementia who also received subthalamic nucleus stimulation. This multicentre, parallel, double-blind, placebo-controlled, randomised trial was done in 13 movement disorders departments in France between October, 2009, and December, 2011. Eligible patients were younger than 80 years and had Parkinson's disease, severe gait disorders, and freezing of gate despite optimised treatment of motor fluctuations with dopaminergic drugs and subthalamic stimulation. We randomly assigned patients (1:1 with a computer random-number generator in blocks of four) to receive methylphenidate (1 mg/kg per day) or placebo capsules for 90 days. Patients, their carers, study staff, investigators, and data analysts were masked to treatment allocation. To control for confounding effects of levodopa we assessed patients under standardised conditions with an acute levodopa challenge. Our primary outcome was a change in the number of steps during the stand-walk-sit (SWS) test without levodopa. We compared the respective mean numbers of steps at day 90 in the methylphenidate and placebo groups in a covariance analysis and adjusted for baseline differences. This trial is registered with ClinicalTrials.gov, number NCT00914095. We screened 81 patients and randomly assigned 35 to receive methylphenidate and 34 to receive placebo. 33 patients in the methylphenidate group and 32 patients in the placebo group completed the study. Efficacy outcomes were assessed in the patients who completed the study. Compared with patients in the placebo group (median 33 steps [IQR 26-45]), the patients in the methylphenidate group made fewer steps at 90 days (31 [26-42], F((1, 62))=6·1, p=0·017, adjusted size effect 0·61). Adverse events were analysed in all randomly assigned patients. There were significantly more adverse events in the methylphenidate group compared with placebo. Patients on methylphenidate had a significant increase in heart rate (mean 3·6 [SD 7·2] beats per min) and decrease in weight (mean 2·2 [SD 1·8] kg) compared with the placebo group. Methylphenidate improved gait hypokinesia and freezing in patients with advanced Parkinson's disease receiving subthalamic nucleus stimulation. Methylphenidate represents a therapeutic option in the treatment of gait disorders at the advanced stage of Parkinson's disease. The long term risk-benefit balance should be further studied. French Ministry of Health and Novartis Pharma.

Anxious, hypoactive phenotype combined with motor deficits in Gtf2ird1 null mouse model relevant to Williams syndrome

Williams–Beuren syndrome (WBS) is a rare genetic disorder caused by a hemizygous deletion of around 28 genes on the long arm of chromosome 7 (7q11.23), characterized by a unique spectrum of behavioral impairments, including mental retardation, deficits in visuospatial constructive cognition, hypersociability, anxiety and simple phobias. Physical characteristics include dysmorphic faces, short stature, oculomotor deficits, gross and fine coordination impairments, diminished control of balance and mild extrapyramidal signs as well as gait abnormalities resembling gait hypokinesia. Genes near the distal deletion breakpoint appear to contribute most to the WBS cognitive and behavioral profile and include the GTF family of transcription factors: GTF2I, GTF2IRD1, GTF2IRD2. We have previously shown that heterozygous deletions of GTF2IRD1 in humans and homozygous deletion in mice contributes to craniofacial abnormalities. Here we show an important role of this gene in motor coordination and anxiety ascertained from extensive behavioral mouse phenotyping. Gtf2ird1 null mice showed lower body weight, decreased spontaneous and circadian locomotor activity, diminished motor coordination and strength, gait abnormalities, increased anxiety and an elevated endocrinological response to stress. Gtf2ird1 heterozygous mice displayed lower body weight and decreased circadian activity, but only minor motor coordination and anxiety-related behavioral dysfunctions. Our study strongly supports a role for GTF2IRD1 in the motoric and anxiety-related abnormalities seen in Williams–Beuren syndrome, and suggests basal ganglia and potentially cerebellar abnormalities in Gtf2ird1 mice.

Examination of central gait control mechanisms in Parkinson's disease using movement‐related potentials

Gait disorders are common in people with Parkinson's disease. The pathophysiology of these disorders is not fully understood. Movement-related potentials reflect supplementary motor area activity associated with the preparation and execution of voluntary movement. Our aim was to investigate movement-related potentials associated with gait disturbances in patients with Parkinson's disease, as reflected by gait hypokinesia and initiation difficulties, in order to better understand the role of the basal ganglia in the pathogenesis of these conditions. Movement-related potentials were back-averaged from electroencephalography recordings performed on 11 participants with Parkinson's disease with no gait initiation difficulties, 9 participants with Parkinson's disease who suffered from gait initiation difficulties, 12 young healthy adults, and 8 healthy older adults. Participants took 3 steps forward, stepping off a force plate. Trigger signals from the force plate and electromyographic activity of the tibialis anterior muscle were used to identify gait initiation time. Participants' stride length was also measured using a 3-dimensional motion analysis system. Movement-related potentials showed significant group differences between the healthy young adults and the 2 Parkinson's disease groups as well as the Parkinson's disease group as a whole. No significant difference was found between the participants with Parkinson's disease and age-matched controls. A significant inverse relationship between movement-related potentials and stride length was found in patients with Parkinson's disease who did not experience gait initiation difficulties but not in those who did have this symptom. Gait-generated movement-related potentials appear to show electrical evidence of cortical disturbances correlated with stride length reduction in patients with Parkinson's disease without gait initiation difficulties.

Freezing of Gait and Activity Limitations in People With Parkinson's Disease

Tan DM, McGinley JL, Danoudis ME, Iansek R, Morris ME. Freezing of gait and activity limitations in people with Parkinson's disease. Objectives To investigate the relationships between freezing of gait (FOG) and activity limitations in ambulant people with Parkinson's disease (PD), and to explore the contribution of FOG and gait hypokinesia to activity limitations after adjusting for the effects of disease severity. Design Retrospective, cross-sectional design. Setting Participants were recruited from neurologists' clinics and the general public in metropolitan Melbourne, Australia. Participants Volunteers were screened for eligibility using the following inclusion criteria: diagnosis of idiopathic PD, modified Hoehn and Yahr stages 0 to IV, without dementia. Participants (N=210) were tested (mean age ± SD, 67.9±9.6y; mean PD duration ± SD, 6.7±5.6y; median Hoehn and Yahr stage=2.5). Interventions Not applicable. Main Outcome Measures FOG was measured using the FOG questionnaire. Gait hypokinesia was quantified using both the 6-meter walk test and the Timed Up and Go test. Activity limitation was measured using the modified Unified Parkinson's Disease Rating Scale activities of daily living (ADL) section and the Schwab and England ADL scale. Results Severity of gait freezing correlated significantly with the level of activity limitation (Spearman correlation coefficient, ρ=−.49 to .48; P<.001). A hierarchic regression model showed that disease severity explained 37.5% of the variance in Schwab and England ADL score ( P<.001). Gait hypokinesia and FOG severity scores explained an additional 9.1% of the variance in activity limitation ( R 2 change=.091; P<.001). Conclusions FOG severity and gait hypokinesia were associated with reduced levels of activity after adjusting for disease severity.

Les troubles de la marche dans la maladie de Parkinson : problématique clinique et physiopathologique

Gait disorders and axial symptoms are the main therapeutic challenges in advanced Parkinson's disease (PD). Gait disorders in PD are characterized by spatial and temporal dysfunction. Gait hypokinesia is the first to appear and is responsible for the decrease in velocity. A good sensitivity to the levodopa is well established. Morris et al. [Morris ME, Iansek R, Matyas TA, Summers JJ. Ability to modulate walking cadence remains intact in Parkinson's disease. J Neurol Neurosurg Psychiatry 1994a;57(12):1532-4; Morris ME, Iansek R, Matyas TA, Summers JJ. The pathogenesis of gait hypokinesia in Parkinson's disease. Brain 1994b;117(Pt. 5):1169-81; Morris ME, Iansek R, Matyas TA, Summers JJ. Stride length regulation in Parkinson's disease. Brain 1996;119:551-68] demonstrated that the ability to modulate walking cadence remains intact in PD, and could correspond to a compensatory mechanism. More advanced disease stages of the disease are characterized by abnormal temporal parameters (such as stride length variability, stride time variability and cadence elevation) which are unresponsive to levodopa therapy and may be correlated with the occurrence of falls and freezing of gait (FOG). Lastly, postural instability also results in falls and is poorly responsive to levodopa. A link between gait impairment and frontal disorders has recently been suggested. After a few years of evolution, paradoxical episodic phenomena are described: festination ("hastening gait" with rapid small, short steps) and FOG (involuntary and sudden cessation of gait). Both symptoms are often incapacitating for PD patients, because of their resultant loss of independence and their poor response to levodopa therapy. Kinematical studies of FOG revealed a decrease in velocity, stride length and an exponential increase in cadence, prior to a FOG episode. New approaches (functional MRI, wavelets...) should offer new perspectives concerning these disabling symptoms.

Abnormalities in the stride length-cadence relation in parkinsonian gait.

The purpose of this investigation was to clarify abnormalities in the stride length-cadence relation in gait hypokinesia in Parkinson's disease (PD). A second aim was to investigate the effect of levodopa medication on the foot-step pattern. In the first experiment, 20 subjects with idiopathic PD and 20 age-, sex-, and height-matched controls performed a series of 10 m walking trials at cadence rates ranging from 40 steps/min to 180 steps/min. Cadence rates were set by an electronic metronome, and gait patterns were measured by using a footswitch stride-analyzer system. By instructing subjects to concentrate on walking in time to the metronome beat, the baseline stride length could be monitored for a range of velocities with the compensatory effects of cadence removed. Linear-regression analysis revealed that the mean slope for the regression of stride length against cadence was not different from normal in PD, although there was a statistically significant difference in mean intercept between the PD group (0.25) and the control group (0.59); [t (19) = -4.76; p = 0.0001]. The second experiment evaluated the effects of levodopa on stride-length regulation in 10 subjects with idiopathic PD on average 45 min before and after the first morning dose was administered. There was a statistically significant increase in stride length for all cadence rates from premedication to postmedication phases and the maximal stride length was achieved at higher cadence rates after medication. The slope of the regression of stride length against cadence did not alter according to medication status, although the mean intercept was significantly lower before levodopa (-0.06) compared with after levodopa (0.27); [t (9) = -3.83; p = 0.004]. These results suggest that defective scaling of stride length underlies gait disturbance in PD.

Stride length regulation in Parkinson's disease. Normalization strategies and underlying mechanisms.

Results of our previous studies have shown that the slow, shuffling gait of Parkinson's disease patients is due to an inability to generate appropriate stride length and that cadence control is intact and is used as a compensatory mechanism. The reason for the reduced stride length is unclear, although deficient internal cue production or inadequate contribution to cortical motor set by the basal ganglia are two possible explanations. In this study we have examined the latter possibility by comparing the long-lasting effects of visual cues in improving stride length with that of attentional strategies. Computerized stride analysis was used to measure the spatial (distance) and temporal (timing) parameters of the walking pattern in a total of 54 subjects in three separate studies. In each study Parkinson's disease subjects were trained for 20 min by repeated 10 m walks set at control stride length (determined from control subjects matched for age, sex and height), using either visual floor markers or a mental picture of the appropriate stride size. Following training, the gait patterns were monitored (i) every 15 min for 2 h; (ii) whilst interspersing secondary tasks of increasing levels of complexity; (iii) covertly, when subjects were unaware that measurement was taking place. The results demonstrated that training with both visual cues and attentional strategies could maintain normal gait for the maximum recording time of 2 h. Secondary tasks reduced stride length towards baseline values as did covert monitoring. The findings confirm that the ability to generate a normal stepping pattern is not lost in Parkinson's disease and that gait hypokinesia reflects a difficulty in activating the motor control system. Normal stride length can be elicited in Parkinson's disease using attentional strategies and visual cues. Both strategies appear to share the same mechanism of focusing attention on the stride length. The effect of attention appears to require constant vigilance to prevent reverting to more automatic control mechanisms.

Ability to modulate walking cadence remains intact in Parkinson's disease.

Gait hypokinesia (slowness) is a characteristic feature of Parkinson's disease. It is not clear, however, whether the slowness is due to a problem in regulation of the timing of consecutive steps or the control of stride size. Examination of cadence control for slow to medium walking speeds has shown an increase in step frequency that was a compensation for reduced stride length. In this investigation the ability of Parkinsonian patients to modulate their cadence (steps per minute) at the fast walking speeds exhibited by age and height matched controls was examined. The findings indicated that cadence control remains unaffected throughout its entire range in Parkinson's disease and that gait hypokinesia is directly attributable to an inability to internally generate sufficiently large steps.