Recent research suggests that long-interval intracortical inhibition (LICI) is followed by a transitory period of late cortical disinhibition (LCD) that can even lead to a net increase in cortical excitability. The relationship between LICI/LCD and voluntary drive remains poorly understood. Our study aims at investigating the influence of index abduction on LICI and LCD in an actively engaged muscle and a neighboring muscle, while varying the intensity of the conditioning stimulus (CS). Motor-evoked potentials (MEPs) were recorded from the first dorsal interosseus (FDI) and abductor digiti minimi (ADM) muscles in 13 subjects. Paired-pulses were delivered with 10 different interstimulus intervals (ranging from 60 to 290 ms). Whatever the condition (relaxed or active FDI), the test stimulus was set to evoke an MEP of 1mV. The time course of conditioned MEP amplitude was compared for relaxed and active conditions when the CS intensity was set to (i) 130% of the rest motor threshold (RMT) or (ii) to evoke the same size of MEP under both conditions. LICI lasted longer (i.e. disinhibition occurred later) at rest than during abduction when evoked either by similar or matched conditioning stimuli. No post-LICI facilitation was observed at rest - even when the CS intensity was set to 160% RMT. In contrast, long-interval intracortical facilitation (LICF) was observed in the quiescent ADM when FDI was active. LICF may then be associated with voluntary activity albeit with lack of topographic specificity.

The objective of the present study was to investigate the time course of long-interval intracortical inhibition (LICI) and late cortical disinhibition (LCD) as a function of the motor task (index abduction, thumb-index precision grip). Motor-evoked potentials were recorded from the first dorsal interosseus (FDI) muscle of the dominant limb in 13 healthy subjects. We used paired-pulse transcranial magnetic stimulation (TMS) paradigms in which a test pulse was preceded by a suprathreshold priming pulse (130% of the resting motor threshold) with varying interstimulus intervals (ISIs). In each task, double pulses were delivered with ISIs ranging from 30% of the corresponding silent period (SP; ~ 45 ms) to 220% of the SP (~ 330 ms). In both tasks, we found that LICI was followed by LCD (namely a period of increased cortical excitability lasting until ~ 200% of the SP). The time-dependent modulation of LICI and LCD differed in the two tasks; LICI was shorter (i.e. disinhibition occurred earlier) and LCD was more intense during precision grip than during index abduction. Long-interval intracortical inhibition disappeared well before the end of the SP in the precision grip task, suggesting that the mechanisms underlying these two inhibitory phenomena are distinct. Our data suggest that disinhibition might reflect adaptation of neural circuit excitability to the functional requirements of the motor task.

These results provide insight into post-stroke changes in contralesional PPC-M1 connectivity.

No abstract