Neuromuscular signals of postural imbalance in older adults

Impairment in mobility and balance is often regarded as the hallmark of physical frailty. Indeed, balance control is a complex process that requires the integration of sensory inputs and motor responses. Some prior studies have shown the existence of cortical potentials as a result of postural disturbance. These signals, consisting of a small positive peak (P1) and a large negative deflection (N1), have been thought to represent afferent somatosensory signals caused by the perturbation.
The objective of this study is to quantify the sensation of imbalance during postural perturbation in older individuals. In contrast to young people, we predicted that older persons would have slower and smaller signals of imbalance. Such features will be exacerbated by a secondary cognitive task. Ten young adults (YA) (four females; 21-28 years) and seven healthy old adults (OA) (two females; 65-70 years) were recruited. A 32-channel EEG system was used to obtain cortical potentials during the trial. EMG recordings were obtained from the principal muscles of the lower limb. We employed a modified lean-and-release paradigm, where participants stood on a sloped platform with a harness system and experienced a sudden forward fall.
The first experiment had two conditions, each of which had at least 25 falls. On one condition, they were asked to remain relaxed and let the harness catch them upon release. In another condition, they made a forward-step adjustment to regain balance. Catch trials were inserted to minimize anticipation, and there was an inter-trial delay of 3-10 seconds. A 2-way ANOVA (condition x group) was subsequently performed for latency and amplitude respectively. In a second experiment, the same old adults were subjected to the same setup with a postural correction, but with a concurrent cognitive task involved.
Prior to the release, they had to memorize a series of numbers that were displayed to them on the LCD monitor. Activity in the central cortical region of the older group showed, not only a significantly smaller N1 amplitude (YA = -35.22 uV, OA = -21.70 uV), but also a slower latency (p<0.05) (YA = 125.10 msec, OA = 148.05 msec). The lack of differences in N1 between the two conditions supports the idea that N1 predominantly carries sensory information. Muscle latency and peak in both groups were found to be between 80-105 msec range with no reliable group difference. Within the older participants, the presence of a secondary cognitive task increased the N1 latency further to 174.33 msec. This may suggest the detrimental effect of a secondary cognitive task that will affect sensory processing while facing a postural imbalance. The results support the hypothesis that older adults exhibit less effective neural processing of sensory signals when losing balance. This knowledge can be useful in clinical research to identify neurophysiological markers of balance ability in prefrail individuals.