Noise-exposure at levels low enough to avoid a permanent threshold shift has been found to cause a massive, delayed degeneration of spiral ganglion neurons (SGNs) in mouse cochleae. Damage to the afferent innervation was initiated by a loss of synaptic ribbons, which is largely irreversible in mice. A similar delayed loss of SGNs has been found in guinea pig cochleae, but at a reduced level, suggesting a cross-species difference in SGN sensitivity to noise. Ribbon synapse damage occurs “silently” in that it does not affect hearing thresholds as conventionally measured, and the functional consequence of this damage is not clear. In the present study, we further explored the effect of noise on cochlear afferent innervation in guinea pigs by focusing on the dynamic changes in ribbon counts over time, and resultant changes in temporal processing. It was found that (1) contrary to reports in mice, the initial loss of ribbons largely recovered within a month after the noise exposure, although a significant amount of residual damage existed; (2) while the response threshold fully recovered in a month, the temporal processing continued to be deteriorated during this period.

The purpose of the study was to evaluate the capacity of an expanded set of force steadiness tasks to explain the variance in the time it takes young men and women to complete the grooved pegboard test. In a single experimental session, 30 participants (mean ± SD) (24.2 ± 4.0 yr; 15 women) performed the grooved pegboard test, two tests of hand speed, measurements of muscle strength, and a set of submaximal, steady contractions. The steadiness tasks involved single and double actions requiring isometric contractions in the directions of wrist extension, a pinch between the index finger and thumb, and index finger abduction. Time to complete the grooved pegboard test ranged from 41.5 to 67.5 s. The pegboard times (53.9 ± 6.2 s) were not correlated with any of the strength measurements or the reaction time test of hand speed. A stepwise, multiple-regression analysis indicated that much of the variance (R(2) = 0.70) in pegboard times could be explained by a model that comprised two predictor variables derived from the steadiness tasks: time to match the target during a rapid force-matching task and force steadiness (coefficient of variation for force) during a single-action task. Moreover, the pegboard times were significantly faster for women (51.7 ± 6.8 s) than men (56.1 ± 4.9 s). Participants with slower pegboard times seemed to place a greater emphasis on accuracy than speed as they had longer times to match the target during the rapid force-matching task and exhibited superior force steadiness during the single-action task.

Fatigue is one of the most common debilitating symptoms reported by persons with multiple sclerosis (MS). It reflects feelings of tiredness, lack of energy, low motivation, and difficulty in concentrating. It can be measured at a specific instant in time as a perception that arises from interoceptive networks involved in the regulation of homeostasis. Such ratings indicate the state level of fatigue and likely reflect an inability to correct deviations from a balanced homeostatic state. In contrast, the trait level of fatigue is quantified in terms of work capacity (fatigability), which can be either estimated (perceived fatigability) or measured (objective fatigability). Clinically, fatigue is most often quantified with questionnaires that require respondents to estimate their past capacity to perform several cognitive, physical, and psychosocial tasks. These retrospective estimates provide a measure of perceived fatigability. In contrast, the change in an outcome variable during the actual performance of a task provides an objective measure of fatigability. Perceived and objective fatigability do not assess the same underlying construct. Persons with MS who report elevated trait levels of fatigue exhibit deficits in interoceptive networks (insula and dorsal anterior cingulate cortex), including increased functional connectivity during challenging tasks. The state and trait levels of fatigue reported by an individual can be modulated by reward and pain pathways. Understanding the distinction between fatigue and fatigability is critical for the development of effective strategies to reduce the burden of the symptom for individuals with MS.