Short-latency afferent inhibition during selective finger movement

Abstract

During individual finger movement, two opposite phenomena occur at the level of the central nervous system that could affect other intrinsic hand muscle representations, unintentional co-activation, and surround inhibition (SI). At rest, excitability in the motor cortex (M1) is inhibited at about 20 ms after electric stimulation of a peripheral nerve [short-latency afferent inhibition (SAI)]. We sought to determine whether SAI changes during selective index finger movement. Effects were measured by the response to transcranial magnetic stimulation in two functionally distinct target muscles of the hand [abductor digiti minimi muscle (ADM), first dorsal interosseus muscle (FDI)]. An increase in SAI in the ADM during index finger movement compared to at rest could help explain the genesis of SI. Electrical stimulation was applied to either the little finger (homotopic for ADM, heterotopic for FDI) or the index finger (heterotopic for ADM, homotopic for FDI). During index finger movement, homotopic SAI was present only in the ADM, and the effect of peripheral stimulation was greater when there was less co-activation. Heterotopic SAI found at rest disappeared with movement. We conclude that during movement, homotopic SAI on the muscle in the surround of the intended movement may contribute to SI.

Modulation of Short-Latency Afferent Inhibition Depends on Digit and Task-Relevance

“…We and others have shown that SAI is reduced during both the onset of muscle activity [6], [8], [9] and during sustained muscle contraction [6], [7]. Specifically, we observed reductions in SAI as early as movement preparation between an auditory “warning” and “go” cue and these reductions are likely cortically or sub-cortically mediated [6].…”

“…Specifically, we observed reductions in SAI as early as movement preparation between an auditory “warning” and “go” cue and these reductions are likely cortically or sub-cortically mediated [6]. Previous work [8] has suggested that SAI may contribute to surround inhibition, particularly during EMG onset. However, a number of questions regarding the functional significance of SAI remain unexplored.…”

“…First, how is SAI modified when the muscle is involved versus uninvolved in the task? [8], [9]. Second, does the modulation of SAI depend on the specific digit (i.e., digit 2 versus digit 5)?…”

Short-latency afferent inhibition determined by the sensory afferent volley

“…In contrast, SAI evoked by digital nerve (DN) stimulation demonstrates a somatotopic distribution such that SAI is greater (i.e., more inhibition) and occurs at an earlier latency in muscles that are in closer proximity to the stimulating electrode (Classen et al 2000). SAI is modulated during specific phases of movement (Asmussen et al 2013(Asmussen et al , 2014Voller et al 2006), indicating its use in studying motor control. SAI is reduced and/or abolished in Alzheimer's disease (Di Lazzaro 2004) and Parkinson's disease (Sailer et al 2003(Sailer et al , 2007, particularly in those presenting with mild cognitive impairment (Yarnall et al 2013) or dementia (Celebi et al 2012), although opposite effects are also observed (Di Lazzaro et al 2004;Nardone et al 2005).…”

“…Revealing the relationship between the cortical representation of the somatosensory afferent volley and the magnitude of M1 output may have implications for motor control. Recent research has shown the importance of SAI in both allowing movement and preventing unwanted actions (Asmussen et al 2013(Asmussen et al , 2014Voller et al 2006). In individuals with Parkinson's disease, reduced SAI is associated with slower gait speed (Rochester et al 2012) but is unrelated to freezing of gait symptoms (Picillo et al 2015).…”