Gait and Balance Dysfunction: A Model of the Interaction of Age and Disease

Neuroscientist - Tập 7 Số 2 - Trang 178-183 - 2001
Leslie Wolfson1
1Department of Neurology, University of Connecticut School of Medicine, Farmington, Connecticut,

Tóm tắt

This article reviews age-associated changes in gait, balance, and sensorimotor function and contrasts them to the changes that occur as a result of disease. Strength peaks in the mid-20s but declines only modestly until the fifth decade, after which there is rapid decline. All aspects of sensory function diminish with age, resulting in modest sensory changes in older patients. Gait speed is stable until the seventh decade and thereafter slows modestly. Age-related changes in the balance of older persons result in an effective response that meets routine needs but may be ineffective under demanding circumstances capable of producing response. Thus, these modest age-related decrements may be an element in the increased incidence of falls in older people. The loss of function caused by disease is of greater magnitude as well as being superimposed on that caused by age and thus may lead to a failure of mobility. Neurologic diseases that impair sensorimotor function compromise mobility in a manner consistent with the deficits that they produce. In mobility dysfunction caused by white matter lesions, the gait/balance abnormalities may not have unique clinical features, making diagnosis difficult. We used quantitative MRI to study the brains of older subjects with mobility impairment. The volume of white matter lesions in mobility-impaired subjects was double that of controls and was unrelated to increasing age, suggesting that white matter lesions are a disease-related rather than an age-related occurrence. We also used stance perturbation evoked potentials to demonstrate delayed conduction in some mobility-impaired older subjects. Prolonged sensory conduction may contribute to maladaptive balance and thus may be useful for diagnosis. Contemporary imaging and neurophysiology thus provides insight into the pathophysiology of mobility impairment and allows for more accurate diagnosis.

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Tài liệu tham khảo

Bernheimer H, 1973, Clinical, morphological and neurochemical correlations. J Neurol Sci, 20, 415

10.1093/ptj/64.7.1067

Bruner A, 1971, Otolarygological Supplement, 282, 1

Buchthal F, 1975, Peripheral neuropathy, 442

10.1007/BF01249444

Carter A., 1979, Clinical geriatrics, 292

10.1212/WNL.29.1.38

10.1016/S1388-2457(99)00195-9

10.1212/WNL.54.6.1277

Imms FJ, 1979, Age Ageing, 8, 261, 10.1093/ageing/8.4.261

10.1093/geronj/49.6.M258

Klawans HL Jr, 1971, Dis Nerv Syst, 32, 274

10.1093/geronj/32.4.411

10.1001/archneur.1989.00520480034016

McGeer E., 1976, Alzheimer’s disease, senile dementia and related disorders, 427

10.1001/archneur.1977.00500130053010

10.1093/geronj/24.2.169

10.1007/BF00687009

10.1001/archneur.1994.00540180051013

Peterka RJ, 1990, J Vestib Res, 1, 49, 10.3233/VES-1990-1106

10.3109/00016487309121501

Schaumberg H, 1983, The neurology of aging, 111

10.1007/BF01182672

Skinner HB, 1984, Clin Orthop, 208

Welford A., 1980, Handbook of mental health and aging, 192

10.1111/j.1532-5415.1986.tb07256.x

10.1212/WNL.42.11.2069

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Neuroscientist

Tập 7 Số 2

178-183

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