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At least 19 recordsLinked to original sources
PubMed2002

Relative contributions of balance and voluntary leg-coordination deficits to cerebellar gait ataxia.

Different cerebellar regions participate in balance control and voluntary limb coordination, both of which might be important for normal bipedal walking. We wanted to determine the relative contributions of balance versus leg-coordination deficits to cerebellar gait ataxia in humans. We studied 20 subjects with cerebellar damage and 20 control subjects performing three tasks: a lateral weight-shifting task to measure balance, a visually guided stepping task to measure leg- coordination, and walking. We recorded three-dimensional joint position data during all tasks and center of pressure coordinates during weight-shifting. Each cerebellar subject was categorized as having no detectable deficits, a balance deficit only, a leg-placement deficit only, or both deficits. We then determined the walking abnormalities associated with each of these categories. Five of 10 measures of gait ataxia were abnormal in cerebellar subjects with a balance deficit, but only 1 was abnormal in cerebellar subjects with a leg-placement deficit. Furthermore, subjects with a balance deficit performed worse than subjects with a leg-placement deficit on 9 of the 10 gait measures. Finally, performance on the balance task, but not the leg-placement task, explained a significant proportion of the variance in walking speed for the entire cerebellar group. We conclude that balance deficits are more closely related to cerebellar gait ataxia than leg-placement deficits. Our findings are consistent with animal literature, which has suggested that cerebellar control of balance and gait are interrelated, and dissociable from cerebellar control of voluntary, visually guided limb movements.

Adult↗
PubMed2003

GDNF and IGF-I trophic factors delay hereditary Purkinje cell degeneration and the progression of gait ataxia.

Neurotrophic factors GDNF and/or IGF-I were chronically infused into shaker mutant rats to rescue cerebellar Purkinje neurons from adult-onset heredodegeneration. The natural expression of the shaker mutation is characterized by spatially restricted degeneration of Purkinje cells that occurs earlier and faster in an anterior vermal compartment and slightly later and more slowly in a posterior vermal compartment. Gait ataxia and whole body tremor develop concomitant with the degeneration of Purkinje neurons. The number and spatial distribution of surviving Purkinje neurons, identified by cell-specific calbindin immunoreactivity, were quantitatively analyzed in mid-sagittal sections and correlated with quantitative movement analysis of hindlimb gait patterns. Compared to the number of surviving Purkinje cells in age-matched, non-infused, or saline-infused control mutants, 4 weeks of infusion of GDNF or IGF-I rescued many anterior compartment Purkinje cells from early degeneration. However, 2 and 4 weeks after cessation of GDNF or IGF-I infusion, respectively, the number and spatial distribution of surviving Purkinje cells was comparable to that observed in age-matched controls. Eight weeks of infusion of trophic factors did not support the continued survival of most anterior compartment Purkinje cells and was partially, and probably only transiently, neuroprotective for some posterior compartment Purkinje cells. When GDNF and IGF-I were infused together for 4 weeks the number of surviving Purkinje cells was additively greater than with either factor alone. Behaviorally, 4 weeks of infusion of trophic factors delayed the development of gait ataxia. Infused GDNF appeared to preserve hip stability, whereas IGF-I stabilized step length. Tremor was attenuated with 8 weeks of infusion of GDNF or IGF-I. GDNF-infused animals showed low power tremor frequencies, whereas IGF-I infusion resulted in a single large power peak with decreased numbers of low-amplitude frequencies. Collectively these findings indicate that exogenous trophic factors can delay the onset of hereditary Purkinje cell degeneration and gait ataxia. Quite surprisingly, GDNF and IGF-I appeared to act on disparate populations of mutant Purkinje cells, whose differential survival affected different aspects of locomotion.

Animals↗
PubMed1996

Reversible cerebellar gait ataxia with postural tremor during episodes of high pyrexia.

We describe five patients presenting with high fever and isolated cerebellar gait ataxia. In all these patients, neurological examination revealed dysmetria, intention tremor and postural tremor during sustained posture, all restricted to the legs. Brain MRI was normal. In four of these patients, the recording of leg tremor during sustained postures showed a 3-Hz frequency. Cerebellar gait ataxia resolved within 3-10 days. We suggest that the ataxic gait was due to a reversible dysfunction of the spinocerebellar part of the anterior lobe.

Adult↗
PubMedDate not supplied

Vertigo and gait ataxia without usual signs of lateral medullary infarction: a clinical variant related to rostral-dorsolateral lesions.

Isolated vertigo and ataxia have not been reported as manifestations of lateral medullary infarction. The author describes 3 patients with lateral medullary infarction who presented with almost isolated vertigo and gait ataxia without usual signs/symptoms of lateral medullary infarction such as facial/hemibody sensory changes, dysphagia, hoarseness, hiccup, limb ataxia, and Horner sign. Brain MRI showed small infarcts selectively involving the most dorsolateral portion of the rostral medulla that corresponds to the vestibulocerebellar pathway. These patients illustrate that lateral medullary infarction may present as an isolated vertigo and gait ataxia. Clinicians should be aware of this clinical variant, because these patients may be misdiagnosed as having labyrinthine disorders.

Aged↗
PubMed1986

Gait ataxia as a presenting symptom of malignant epidural spinal cord compression.

A 68 year old man with prostatic carcinoma developed spinal cord compression. The sole presenting feature was painless gait ataxia indistinguishable from cerebellar ataxia. He was investigated for cerebellar disease but the correct diagnosis was made when he subsequently presented with paraplegia and classical signs of spinal cord compression. Surgical decompression failed to produce neurological recovery. We discuss the importance of recognizing this unusual presentation of spinal cord compression, its possible mechanism and evidence that it may be under-reported.

Adenocarcinoma↗
PubMed1982

Characteristics of gait ataxia in spinocerebellar degeneration assessed by means of simple quantitative method.

Cerebellar ataxic gait was compared with normals by a simple quantitative method. Strain gauges attached to the heel, the first and the fifth metatarsal areas of a shoe, were used and the gait was telemetrically recorded. A natural and one per second click sound-synchronized gait was analyzed. A contact sequence of the three areas of the sole, the stride time, the stance-phase time and the foot contact pattern were compared between patients and normals. All of these items disclosed different results in the two groups.

Adult↗
PubMed2006

Dynamic imbalance in gait ataxia. Characteristics of plantar pressure measurements.

The present study was designed to evaluate the interaction between disequilibrium and irregular stepping components of ataxic gait. For this purpose, we compared the walking patterns of patients with cerebellar dominant multiple system atrophy (MSAc, n = 8), spinocerebellar ataxia type 6 (SCA6, n = 4) and 16q-linked autosomal dominant cortical cerebellar atrophy (16q-linked ADCA, n = 6), and 6 normal subjects, by measuring toe and heel plantar pressures. In healthy subjects, the heel contacted the floor at step-in followed by an immediate shift of the center of pressure (COP) to the contacted leg. In ataxic gait, however, both the heel and toes simultaneously contacted the floor and the disappearance of the immediate shift of the COP was noted. These changes appeared to be nonspecific compensations for the instability. Examination of two parameters of ataxia-specific changes showed that prolongation of the double support period was associated with proportionate increase in the coefficients of variance of the plantar pressures and the step lengths on walking of patients with SCA6, but not those with MSAc and 16q-linked ADCA. Our results suggest that disequilibrium and irregularity are two separate and independent components of cerebellar ataxic gait.

Adult↗
PubMed1996

Neurological signs, aging, and the neurodegenerative syndromes.

OBJECTIVES: To identify the prevalence of neurological signs said to be associated with "normal" aging in subjects 75 years and older. To examine the association of these signs with age, stroke, the neurodegenerative diagnoses (dementia, cognitive impairment, gait ataxia, gait slowing, and parkinsonism), and systemic diseases. DESIGN: Subjects participated in a standardized clinical history, examination, neurological evaluation, and neuropsychological assessment battery. A linear regression model that allowed the simultaneous consideration of multiple parameters was used to assess the independent contribution of age and disease to the presence of the signs. Correlations between the signs and age in the subgroup free of neurological diagnoses were performed. SETTING: Community-based study in Sydney, Australia. PARTICIPANTS: A random sample of 647 community-dwelling subjects older than 75 years. MAIN OUTCOME MEASURES: Standardized neurological examination in 537 subjects. RESULTS: With the exception of impaired vibration sense (beta = .009, P < .01), loss of upward gaze (beta = .005, P < .01), and bradykinesia (beta = .005, P < .01), all signs were associated with the neurodegenerative syndromes and stroke. Analysis of the subgroup free of neurological diagnoses confirmed these findings. Apart from impaired vibration sense of the thumbs (r = 0.22, P < .01) and gait instability (r = 0.20, P < .05), no significant associations with age were identified. CONCLUSION: It is not aging to which many neurological signs should be attributed, but rather to the neurodegenerative syndromes that accompany aging.

Aged↗