The strength of the knees and ankles of a group of nursing home residents with a history of falls was compared to age-matched controls. Peak torque (PT) and power (POW) were recorded at two limb velocities (60 degrees/s and 120 degrees/s) on a Cybex II Isokinetic dynamometer for four muscle groups: knee extensors, knee flexors, ankle plantar flexors and ankle dorsiflexors. The PT and POW of fallers were significantly decreased for all four muscle groups in comparison to controls, with the ankles showing the greatest decrements. Although POW in fallers was significantly lower at the higher velocity in both joints, the decrease was most prominent in the ankles. Dorsiflexion POW production in fallers was the most affected of all the motions (7.5 times less than the control value). At the higher, more functional limb velocities, ankle weakness particularly involving the dorsiflexors appears to be an important factor underlying poor balance.
Balance training meaningfully improved all balance measures by restoring performance to a level analogous to an individual 3 to 10 years younger: LOB = -2.0 +/- 0.3 (adjusted paired differences, P < .005 ANOVA); SST = 7.0 +/- 1.2 sec; and FBOS = 9.0 +/- 2.0% of foot length (P < .05). Strengthening increased ISOK by 1.1 +/- 0.1 Nm kg-1 (P < .005). There was no interaction between balance and strength training. Significant gains persisted after 6 months of Tai Chi, although there was some decrement.
We compared neuropsychological findings in 28 longitudinally evaluated elderly subjects with their postmortem neuropathology, including senile plaque and neurofibrillary tangle counts from standardized sections. Nine of the subjects were not demented when evaluated just prior to their death. Numerous cortical senile plaques and other changes of Alzheimer's disease (AD) occurred in six of nine nondemented old-old subjects. Five of these six subjects had shown decline on yearly neuropsychological tests but their cognitive impairment was too mild to meet clinical criteria for dementia. Whereas cortical senile plaque count did not distinguish well between demented and nondemented subjects, every subject with numerous cortical neurofibrillary tangles was demented. The nondemented subjects with Alzheimer pathology may have had "preclinical" AD, or numerous cortical plaques may occur in some elderly subjects who would never develop clinical dementia.
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