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At least 19 recordsLinked to original sources
PubMed2001

Amantadine increases gait steadiness in frontal gait disorder due to subcortical vascular encephalopathy: a double-blind randomized placebo-controlled trial based on quantitative gait analysis.

In a randomized, double-blind placebo-controlled trial, 40 patients diagnosed as subcortical vascular encephalopathy (SVE) were given a daily dose of 500 ml i.v. amantadine vs. placebo for 5 days. Both groups were treated with physiotherapy on a daily basis. Quantitative gait analyses were performed at days 1 and 6 to evaluate gait steadiness from cadence, length of heel-to-toe movements, variability of centre of gravity (COG) and double support time. Both placebo- and amantadine-receiving patient groups showed mild improvement in gait parameters after study, which failed to show the superiority of amantadine, when comparing drug-induced changes between both groups. However, analysing the treatment effects from day 0 to day 6 in both groups separately, statistically significant changes could be found in the amantadine group for cadence, length of heel-to-toe movements in single support phase as well as for variability in double support phase and double support time (two-tailed paired t-test, p < 0.05), whereas in the placebo group, a statistically significant effect could only be seen for double support time (p < 0.05). In this small pilot study, amantadine tends to improve gait steadiness as evaluated by cadence, length of heel-to-toe movements in single support phase, variability in double support phase and double support time, in patients with moderate frontal gait disorder due to SVE. Improvements in the placebo group can be interpreted as physiotherapy effect, which improved gait steadiness slightly, however, this was statistically significant only for double support time.

Amantadine↗
PubMed1998

Gait variability and basal ganglia disorders: stride-to-stride variations of gait cycle timing in Parkinson's disease and Huntington's disease.

The basal ganglia are thought to play an important role in regulating motor programs involved in gait and in the fluidity and sequencing of movement. We postulated that the ability to maintain a steady gait, with low stride-to-stride variability of gait cycle timing and its subphases, would be diminished with both Parkinson's disease (PD) and Huntington's disease (HD). To test this hypothesis, we obtained quantitative measures of stride-to-stride variability of gait cycle timing in subjects with PD (n = 15), HD (n = 20), and disease-free controls (n = 16). All measures of gait variability were significantly increased in PD and HD. In subjects with PD and HD, gait variability measures were two and three times that observed in control subjects, respectively. The degree of gait variability correlated with disease severity. In contrast, gait speed was significantly lower in PD, but not in HD, and average gait cycle duration and the time spent in many subphases of the gait cycle were similar in control subjects, HD subjects, and PD subjects. These findings are consistent with a differential control of gait variability, speed, and average gait cycle timing that may have implications for understanding the role of the basal ganglia in locomotor control and for quantitatively assessing gait in clinical settings.

Adult↗
PubMed2001

Enhancing the ability of gait analyses to differentiate between groups: scaling gait data to body size.

One goal of gait analysis is to distinguish clearly between a set of abnormal gait values measured from a patient referenced to a comparable population. However, the comparable population is often composed of individuals of various heights and weights, which increases inter-subject gait value variation which reduces the ability of a statistical test to identify a set of gait data outcomes with evaluative properties. Therefore, scaling gait data, based on subject leg length and mass, is commonly used to decrease the inter-subject variation but the efficacy of these methods is unknown. In this paper each of eight scaling strategies (none, ad hoc, dimensionless numbers, and five connected strategies based on similarity, dimensional analysis and muscle properties) were used to modify a set of gait data outcomes acquired from 10 individuals spanning a wide range of height (1.33-1.96 m) and mass (42.3-148.8 kg). These data were then examined to select that strategy and those scaling factors which maximally reduced inter-subject variation. The ad hoc, dimensionless numbers, and dynamic/mechanical/elastic (diameter of a limb (D) proportional to it's length (L) to the 1.5 power; time proportional to L(2) D(-1)) scaling strategies reduced the global inter-subject gait data outcome variation to 44% of its un-scaled value. Considering ten commonly reported gait data outcomes (temporal and spatial (stride time, stride length, progression velocity), kinematic (angles in the sagittal and frontal planes, angles in the transverse plane), external kinetic (ground reaction force and moment), and internal kinetic (joint force, moment, and power)) these three scaling strategies provided the largest number of minimum inter-subject variations (10, 10, and 9, respectively). Reduced inter-subject variation in gait data outcomes increases the ability of a statistical tool to detect a difference between a patient and a comparable group. With a statistically significant difference a clinician can then decide if this patient's gait pattern clinically deviates from that of the comparable group and an appropriate intervention warranted. The ad hoc, dimensionless numbers, and the dynamic/mechanical/elastic scaling strategies all reduce maximally the inter-subject variation in gait data outcomes.

Adolescent↗
PubMed1999

Gait pattern of severely disabled hemiparetic subjects on a new controlled gait trainer as compared to assisted treadmill walking with partial body weight support.

OBJECTIVES: To investigate to what extent and with how much therapeutic effort nonambulatory stroke patients could train a gait-like movement on a newly developed, machine-supported gait trainer. DESIGN: Open study comparing the movement on the gait trainer with assisted walking on the treadmill. SETTING: Motion analysis laboratory of a rehabilitation centre. SUBJECTS: Fourteen chronic, nonambulatory hemiparetic patients. INTERVENTION: Complex gait analysis while training on the gait trainer and while walking on the treadmill. MAIN OUTCOME MEASURES: Gait kinematics, kinesiological EMG of several lower limb muscles and the required assistance. RESULTS: Patients could train a gait-like movement on the gait trainer, characterized kinematically by a perfect symmetry, larger hip extension during stance, less knee flexion and less ankle plantar flexion during swing as compared to treadmill walking (p <0.01). The pattern and amount of activation of relevant weight-bearing muscles was comparable with an even larger activation of the M. biceps femoris on the gait trainer (p <0.01). The tibialis anterior muscle of the nonaffected side, however, was less activated during swing (p <0.01). Two therapists assisted walking on the treadmill while only one therapist was necessary to help with weight shifting on the new device. CONCLUSION: The newly developed gait trainer offered severely disabled hemiparetic subjects the possibility of training a gait-like, highly symmetrical movement with a favourable facilitation of relevant anti-gravity muscles. At the same time, the effort required of the therapists was reduced.

Adult↗
PubMed1989

[Clinical and physiological study of apraxia of gait and frozen gait].

A study of clinical features and an analysis of gait with floor reaction forces and EMG of leg flexors and extensors were made in patients with multiple cerebral infarction or patients with Parkinson's disease having frozen gait. A case with occlusion of the bilateral anterior cerebral arteries resulting in massive infarction of the infero-medial part of the frontal lobes was also studied as he showed a unique disorder characterized by apraxia of gait. Frozen gait is characterized by shuffling steps, broad-based stance, positive foot grasp, kinesia paradoxa and disturbance of postural reflexes. The vector angle which shows foot pressure in forward locomotion was decreased in patients with frozen gait. EMGs of lower leg muscles in frozen gait were grouping of potentials corresponding to the shuffle and reciprocity between flexors and extensors was preserved. The patient with infarction of the bilateral anterior cerebral arteries showed a peculiar disorder of gait which was characterized by an inability to initiate stepping. It is considered as "apraxia of gait" in a classical sense, which differs from frozen gait. Observation of this patient suggests that the infero-medical part of the frontal lobe plays an important role in the initiation of gait. Furthermore, common features of frozen gait in patients with Parkinson's disease and in patients with multiple cerebral infarction involving the frontal lobe suggest that the nigrostriatal structures and the frontal lobe are important in CNS mechanisms subserving smooth locomotion.

Aged↗
PubMed2002

Treadmill training with partial body weight support and an electromechanical gait trainer for restoration of gait in subacute stroke patients: a randomized crossover study.

BACKGROUND AND PURPOSE: The purpose of this study was to compare treadmill and electromechanical gait trainer therapy in subacute, nonambulatory stroke survivors. The gait trainer was designed to provide nonambulatory subjects the repetitive practice of a gait-like movement without overexerting therapists. METHODS: This was a randomized, controlled study with a crossover design following an A-B-A versus a B-A-B pattern. A consisted of 2 weeks of gait trainer therapy, and B consisted of 2 weeks of treadmill therapy. Thirty nonambulatory hemiparetic patients, 4 to 12 weeks after stroke, were randomly assigned to 1 of the 2 groups receiving locomotor therapy every workday for 15 to 20 minutes for 6 weeks. Weekly gait ability (functional ambulation category [FAC]), gait velocity, and the required physical assistance during both kinds of locomotor therapy were the primary outcome measures, and other motor functions (Rivermead motor assessment score) and ankle spasticity (modified Ashworth score) were the secondary outcome measures. Follow-up occurred 6 months later. RESULTS: The groups did not differ at study onset with respect to the clinical characteristics and effector variables. During treatment, the FAC, gait velocity, and Rivermead scores improved in both groups, and ankle spasticity did not change. Median FAC level was 4 (3 to 4) in group A compared with 3 (2 to 3) in group B at the end of treatment (P=0.018), but the difference at 6-month follow up was not significant. The therapeutic effort was less on the gait trainer, with 1 instead of 2 therapists assisting the patient at study onset. All but seven patients preferred the gait trainer. CONCLUSIONS: The newly developed gait trainer was at least as effective as treadmill therapy with partial body weight support while requiring less input from the therapist. Further studies are warranted.

Body Weight↗
PubMedDate not supplied

Development of an advanced mechanised gait trainer, controlling movement of the centre of mass, for restoring gait in non-ambulant subjects.

The study aimed at further development of a mechanised gait trainer which would allow non-ambulant people to practice a gait-like motion repeatedly. To simulate normal gait, discrete stance and swing phases, lasting 60% and 40% of the gait cycle respectively, and the control of the movement of the centre of mass were required. A complex gear system provided the gait-like movement of two foot plates with a ratio of 60% to 40% between the stance and swing phases. A controlled propulsion system adjusted its output according to patient's efforts. Two eccenters on the central gear controlled phase-adjusted the vertical and horizontal position of the centre of mass. The patterns of sagittal lower limb joint kinematics and of muscle activation of a normal subject were similar when using the mechanised trainer and when walking on a treadmill. A non-ambulatory hemiparetic subject required little help from one therapist on the gait trainer, while two therapists supported treadmill walking. Gait movements on the trainer were highly symmetrical, impact-free, and less spastic. The weight-bearing muscles were activated in a similar fashion during both conditions. The vertical displacement of the centre of mass was bi-instead of mono-phasic during each gait cycle on the new device. In conclusion, the gait trainer allowed wheelchair-bound subjects the repetitive practice of a gait-like movement without overstraining therapists.

Adult↗
PubMed1985

Afferent control of human stance and gait: evidence for blocking of group I afferents during gait.

The cerebral potentials (c.p.) evoked by electrical stimulation of the tibial nerve during stance and in the various phases of gait of normal subjects were compared with the c.p. and leg muscle e.m.g. responses evoked by perturbations of stance and gait. Over the whole step cycle of gait the c.p. evoked by an electrical stimulus were of smaller amplitude (3 microV and 9 microV, respectively) than that seen in the stance condition, and appeared with a longer latency (mean times to first positive peak: 63 and 43 ms, respectively). When the electrical stimulus was applied during stance after ischaemic blockade of group I afferents, the c.p. were similar to those evoked during gait. The c.p. evoked by perturbations were larger in amplitude than those produced by the electrical stimulus, but similar in latencies in both gait and stance (mean 26 microV and 40 microV; 65 ms and 42 ms, respectively) and configurations. The large gastrocnemius e.m.g. responses evoked by the stance and gait perturbations arose with a latency of 65 to 70 ms. Only in the stance condition was a smaller, shorter latency (40 ms) response seen. It is concluded that during gait the signals of group I afferents are blocked at both segmental and supraspinal levels which was tested by tibial nerve stimulation. It is suggested that the e.m.g. responses induced in the leg by gait perturbations are evoked by group II afferents and mediated via a spinal pathway. The c.p. evoked during gait most probably reflect the processing of this group II input by supraspinal motor centres for the coordination of widespread arm and trunk muscle activation, necessary to restablish body equilibrium.

Adult↗
PubMedDate not supplied

Idiopathic gait disorder among in-patients with acquired gait disorders admitted to a children's hospital.

Many children are admitted to hospital for treatment of an acquired gait disorder. Some gait disorders have a definite underlying physical cause and some are idiopathic. A literature review shows that there have been few attempts to estimate the incidence or prevalence of idiopathic gait disorder in children. The economic and social impact may be substantial with regard to therapy and investigations and school absence, respectively. This study attempted to estimate the incidence and impact of idiopathic gait disorder in a tertiary children's hospital. It evaluated prospectively all the children admitted with a gait disorder requiring physiotherapy treatment at Birmingham Children's Hospital, using a standardized pro-forma, during a 3-month period between March-June 1999. One hundred and three children (aged 2-16 years) were admitted with gait disorders (57 female and 46 male). Eight had an idiopathic gait disorder. All eight children exhibited significant functional impairment, pain and school absence. Idiopathic gait disorder accounted for 8% of children admitted to hospital with an acquired gait disorder and had an annual incidence of at least 2-4 per 100,000 children. The economic and social impact of these disorders is, therefore, substantial, especially with regard to diagnosis, investigations, treatment and school absence.

Adolescent↗
PubMed2001

An electromechanical gait trainer for restoration of gait in hemiparetic stroke patients: preliminary results.

Modern concepts of gait rehabilitation after stroke favor a task-specific repetitive approach. In practice, the required physical effort of the therapists limits the realization of this approach. Therefore, a mechanized gait trainer enabling nonambulatory patients to have the repetitive practice of a gait-like movement without overstraining therapists was constructed. This preliminary study investigated whether an additional 4-week daily therapy on the gait trainer could improve gait ability in 14 chronic wheelchair-bound hemiparetic subjects. The 4 weeks of physiotherapy and gait-trainer therapy resulted in a relevant improvement of gait ability in all subjects. Velocity, cadence, and stride length improved significantly (p < 0.01). The kinesiologic electromyogram of selected lower-limb muscles revealed a more physiologic pattern. The confounding influence of spontaneous recovery, the lack of a control group, and the double amount of therapy limit the clinical relevance of this study. Nevertheless, the gait trainer seems feasible as an adjunctive tool in gait rehabilitation after stroke; further studies are needed.

Adult↗
PubMed2001

[Gait disorders in Parkinson disease. Gait freezing and falls: therapeutic management].

GAIT ARRESTS: They affect the evolution of the disease. This freezing phenomenon which induces falls sometimes constitutes an initial sign. Like the gait initiation failure, freezing can be controlled by sensory stimulation, notably visual inputs, but also by more sustained attention. FALLS ARE MAINLY CONNECTED WITH BOTH POSTURAL INSTABILITY AND RIGIDITY: They are poorly influenced by dopaminergic therapies. The progressive decrease of step width represents a main factor in their occurrence. PRECOCITY OF GAIT DISORDERS IS UNUSUAL IN PARKINSON'S DISEASE: Other parkinsonian syndromes such as progressive supranuclear palsy, multiple system atrophy and vascular parkinsonian syndrome must then be evoked. Their association with a cognitive impairment and abnormal sphincter behaviour infers a diagnosis of normal pressure hydrocephalus. GAIT IMPROVES WITH L-DOPA THERAPY: Speed, step length and duration of the swing phase are increased without change of cadence. Progressive loss of L-dopa efficiency on gait and postural stability contrasts with the persistent effect on tremor, rigidity and bradykinesia; a functional abnormality of nondopaminergic systems can explain these symptoms. In the following stages, gait troubles increased by motor fluctuations and abnormal involuntary movements are less controlled by L-dopa therapy. PHYSICAL THERAPY PLAYS A MAJOR ROLE IN THERAPEUTIC MANAGEMENT: An individual or collective rehabilitation project must be established according to the stage of evolution; the exercises aim to protect postural control and coordination. Visual or sound rhythmic inputs can be employed in the case of gait initiation failure. THE EFFECTS OF FUNCTIONAL NEUROSURGERY ARE IN THE COURSE OF EVALUATION: Thermolesion and chronic electrical stimulation of deep brain structures have opposite effects on gait troubles. Bilateral thalamotomy or pallidotomy are sometimes a source of disequilibrium. Chronic thalamic stimulation does not induce either benefits or adverse effects. On the other hand, stimulation of the internal pallidum improves gait kinematic parameters; improved postural adjustments have also been reported. The effect of subthalamic nucleus stimulation is comparable to that of L-dopa, however the long-term effect remains to be evaluated.

Accidental Falls↗
PubMed2001

Microprocessor-based gait analysis system to retrain Trendelenburg gait.

A microprocessor-based gait analysis system is described that uses two electromyogram (EMG) amplifiers, two foot switches and an audio feedback device to allow the retraining of one type of improper gait, where the hip abductors (gluteus medius muscles) are weak on one side of the body, causing the opposite hip to drop during the swing phase of gait (Trendelenburg gait). As the abnormality is strictly on one side of the body in most people, the circuitry is minimised, as gait can be analysed by only comparing muscle activity in the affected gluteus medius muscle with that in the unaffected gluteus medius muscle, through the EMG. Two foot contact switches are used to help assess timing of the step cycle. If gait is different on the two sides of the body, an audio cue directs the patient to correct the abnormality by increasing activity on the affected side. The device is tested on five patients. Trendelenburg gait is reduced by an average of 29 degrees through the use of the device. The average stride length at the beginning of the study is 0.32 +/- 0.3 m. By the end of the study, the stride length is increased to 0.45 +/- 0.2 m for the entire group of five subjects. The speed of gait has increased from 1.6 +/- 0.4 kmh(-1) to 3.1 +/- 0.5km h(-1).

Adult↗
PubMed1999

Quantitative evaluation of gait pattern in patients with osteoarthrosis of the knee before and after total knee arthroplasty. Gait analysis using a pressure measuring system.

Using a pressure measuring system, we quantitatively evaluated gait pattern in patients with osteoarthrosis (OA) of the knee before and after total knee arthroplasty (TKA). In the OA group, the stance time was longer, and the average vertical component of the floor reaction force (AVF) was lower than the values in normal age-matched subjects. These gait parameters correlated with the clinical score. These results suggest that changes in the gait parameters reflect gait patterns that reduce load on the knee. The center of pressure (COP) under the foot was correlated with the axial alignment of the lower limb in the mid-stance phase. In the TKA group, the clinical scores and gait parameters were improved 12 months after surgery compared with the preoperative values. The COP in the mid-stance phase moved inward after the TKA. However, in patients examined more than 2 years after a TKA, stance time and AVF did not reach normal levels, despite the patients' good clinical scores. These findings indicate that the gait pattern before surgery continues although pain on walking is reduced early after a TKA. Gait evaluation with a simple pressure measuring system revealed the changes in gait that are difficult to define by subjective clinical assessment.

Aged↗
PubMedDate not supplied

Calcaneal gait in spastic diplegia after heel cord lengthening: a study with gait analysis.

Calcaneal gait or deformity can be a significant complication after heel cord lengthening. After heel cord lengthening, 20 children with spastic diplegia were evaluated by gait analysis to define calcaneal gait objectively and describe associated morbidity. Mean age was 5 years 2 months (range 2 years 7 months to 8 years 2 months), and mean length of follow-up was 5 years 8 months (range 1 years 1 month 11 year 3 months). Calcaneal gait was defined as dorsiflexion 1 SD beyond the mean in the sagittal plane for all phases of stance. Increased ankle dorsiflexion during mid-stance most accurately predicts calcaneal gait. Through gait analysis, a 30% (6 of 20) prevalence of calcaneal gait suggests that an increased incidence of calcaneal gait may be present after heel cord lengthening.

Cerebral Palsy↗
PubMed2001

[Gait disorders in Parkinson disease. Neuroanatomic and physiologic organization of gait].

GAIT IS A VOLUNTARY, AUTOMATIC AND REFLEX RHYTHMIC ACTIVITY: It is generated by a central pattern generator identified from animal models. This spinal gait generator (SGG) is controlled by various parts of the central nervous system: the descending tracts and locomotor regions of the brainstem, the cerebellum, the basal ganglia, the motor and parietal cortex and the hippocampus. Kinesthetic inputs which project to the SGG and the cerebellum, play an important role in the production of postural reflex responses; vestibular and visual inputs mainly control balance. GAIT MAINLY DEPENDS ON THE RELATIONSHIP BETWEEN POSTURE BALANCE AND MOVEMENT: As concerns posture each segment is under the control of both peripheral and central nervous systems and is used as a system of reference to organize movements of adjacent segments. Balance is maintained by sensory inputs which provide corrective mechanisms: anticipatory postural responses, reflex postural responses and voluntary responses. DIFFERENT DESCRIPTIVE PARAMETERS MAY BE PROPOSED: Analysis of kinematic (displacement, speed and acceleration of segments) and kinetic parameters during the four successive stages of gait (posture, initiation, rhythmic gait and return to the initial posture) provides an understanding of neurological gait disorders. In particular the relationship between the center of pressure and the center of gravity is used to analyze infraclinical gait abnormalities. NEW AND SOPHISTICATED INVESTIGATIONS METHODS ARE AVAILABLE: The optoelectronic system provides a tridimensional analysis of movement and can be combined with forceplate and electromyographic recordings. These methods constitute an interesting contribution to the clinical analysis of gait. CLASSIFICATION: This is established according to clinical data and the positionment of the lesion among the structures of the nervous system. The physiopathological approach is then specified taking into account the lesions of the muscular, skeletal and nervous structures.

Brain↗