			Home About us Contact

Gait Dysfunction (gait + dysfunction)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

Gait Dysfunction in Mild Cognitive Impairment Syndromes

JOURNAL OF AMERICAN GERIATRICS SOCIETY, Issue 7 2008
Joe Verghese MBBS
OBJECTIVES: To conduct a systematic clinical and quantitative assessment of gait in older adults with mild cognitive impairment (MCI) syndromes. DESIGN: Cross-sectional. SETTING: Einstein Aging Study, a community-based longitudinal aging study. PARTICIPANTS: Fifty-four individuals with amnestic MCI (a-MCI), 62 with nonamnestic-MCI (na-MCI), and 295 healthy controls identified from the Einstein Aging Study participants. MEASUREMENTS: Comparison of clinical and quantitative gait performance in subjects with MCI subtypes with that of cognitively normal older adults. RESULTS: Neurological gaits were more common in a-MCI (31.5%, P=.008) but not in na-MCI (19.4%, P=.55), than in controls (16.3%). Quantitative gait in multiple parameters was worse in both MCI subtypes than in controls. Factor analysis revealed three independent factors representing pace, rhythm, and variability. Subjects with a-MCI had worse rhythm and variability scores than those with na-MCI and controls. Subjects with na-MCI had worse performance on the pace domain than the other two groups. Subjects with MCI and gait abnormalities had higher disability scores than subjects with MCI without gait abnormalities. CONCLUSION: Gait dysfunction is common in older individuals with amnestic and nonamnestic subtypes of MCI. [source]

REM sleep behavior disorder is not linked to postural instability and gait dysfunction in Parkinson,

MOVEMENT DISORDERS, Issue 11 2010
David H. Benninger MD
Abstract To evaluate a potential association of REM-sleep behavior disorder (RBD) with gait and postural impairment in Parkinson's disease (PD). Gait difficulties and postural impairment are frequent in PD and are a major cause of disability. Animal studies indicate a key role of the pedunculopontine nucleus (PPN) in gait, postural control, and REM sleep, and also in the pathophysiology of RBD. In humans, such an association has not been investigated. Twenty-six patients with mild-to-moderate PD (13 with polysomnography confirmed and 13 with excluded RBD), and 20 age-matched healthy controls were prospectively investigated. Gait assessment on a treadmill, and static and dynamic posturography were performed. PD patients with RBD do not differ from those without RBD in gait and postural control. Greater severity of PD or prevalence of gait and postural disturbances in the presence of RBD were not found. RBD was not associated with any particular motor phenotype. We found no association of RBD with gait disturbances and postural impairment. Human gait and postural control and RBD appear to depend upon different neuronal circuits. © 2010 Movement Disorder Society [source]

Dopaminergic transplantation for parkinson's disease: Current status and future prospects,

ANNALS OF NEUROLOGY, Issue 5 2009
C. Warren Olanow MD, FRCPC
Cell-based therapies that involve transplantation into the striatum of dopaminergic cells have attracted considerable interest as possible treatments for Parkinson's disease (PD). However, all double-blind, sham-controlled, studies have failed to meet their primary endpoints, and transplantation of dopamine cells derived from the fetal mesencephalon is associated with a potentially disabling form of dyskinesia that persists even after withdrawal of levodopa (off-medication dyskinesia). In addition, disability in advanced patients primarily results from features such as gait dysfunction, freezing, falling, and dementia, which are likely due to nondopaminergic pathology. These features are not adequately controlled with dopaminergic therapies and are thus unlikely to respond to dopaminergic grafts. More recently, implanted dopamine neurons have been found to contain Lewy bodies, suggesting that they are dysfunctional and may have been affected by the PD pathological process. Collectively, these findings do not bode well for the short-term future of cell-based dopaminergic therapies in PD. Ann Neurol 2009;66:591,596 [source]