Transcranial magnetic stimulation (TMS) can produce effects not only at the site of stimulation but also at distant sites to which it projects. Here we examined the connection between supplementary motor area (SMA) and the hand area of the primary motor cortex (M1 Hand ) by testing whether prolonged repetitive TMS (rTMS) over the SMA can produce changes in excitability of the M1 Hand after the end of the stimulus train. We evaluated motor-evoked potentials (MEPs) and the cortical silent period (CSP) evoked by a single-pulse TMS, short-interval intracortical inhibition (SICI) and intracortical facilitation (ICF) produced by a paired-pulse TMS, and forearm flexor H reflexes before and after 750 pulses of 5 Hz rTMS over SMA at an intensity of 110% active motor threshold (AMT) for the first dorsal interosseous (FDI) muscle. The amplitude of MEPs recorded from the right FDI muscle at rest as well as during voluntary contraction increased for at least 10 min after the end of rTMS, although the duration of the CSP, SICI and ICF did not change. There was no effect on H reflexes in the flexor carpi radialis muscle, even though the amplitude of the MEP obtained from the same muscle increased after rTMS. The effects on MEPs depended on the intensity of rTMS and were spatially specific to the SMA proper. We suggest that 5 Hz rTMS over SMA can induce a short-lasting facilitation in excitability of the M1 Hand compatible with the anatomical connections between SMA and the M1 Hand . A series of studies from this laboratory and from other groups have shown that it is possible to distinguish the effects of transcranial magnetic stimulation (TMS) of primary motor cortex (M1) from those seen after stimulation over the presumed dorsal premotor cortex (PMd), some 1.5-2 cm anterior. Thus, single-pulse conditioning stimuli over PMd reduce the excitability of the primary motor cortex hand area (M1 Hand ) some 6 ms later (Civardi et al. 2001), whereas the same conditioning stimuli applied over M1 Hand have a maximum effect at 1-2 ms (Kujirai et al. 1993). Repetitive TMS (rTMS) of PMd at an intensity of 90% active motor threshold (AMT) can either increase (5 Hz rTMS; Rizzo et al. 2003) or decrease (1 Hz rTMS; Gerschlager et al. 2001) the excitability of M1 Hand for several minutes depending on the frequency of the conditioning rTMS, whilst the same stimulation applied directly over M1 Hand has no effect. Behavioural studies have also revealed differences between stimulation of PMd and M1. For example, single-pulse TMS over M1 can delay reaction times if it is given late in the reaction period between stimulus and response, whereas the pulse has to be applied early in the reaction period for effects to be seen after stimulation of PMd (Schluter et al. 1998;Day et al. 1989). Finally, functional imaging studies, which show the effects of TMS both at the site of stimulation and at connected sites at a distance, reveal that rTMS over M1 produces quite a different pattern of after-effects on rCBF than stimulation over PMd Lee et al. 2003). Ind...
Athletic training is known to induce neuroplastic alterations in specific somatosensory circuits, which are reflected by changes in somatosensory evoked potentials and event-related potentials. The aim of this study was to clarify whether specific athletic training also affects somatosensory Nogo potentials related to the inhibition of movements. The Nogo potentials were recorded at nine cortical electrode positions (Fz, Cz, Pz, F3, F4, C3, C4, P3 and P4) in 12 baseball players (baseball group) and in 12 athletes in sports, such as track and field events and swimming, that do not require response inhibition, such as batting for training or performance (sports group). The Nogo potentials and Go/Nogo reaction times (Go/Nogo RTs) were measured under a somatosensory Go/Nogo paradigm in which subjects were instructed to rapidly push a button in response to stimulus presentation. The Nogo potentials were obtained by subtracting the Go trial from the Nogo trial. The peak Nogo-N2 was significantly shorter in the baseball group than that in the sports group. In addition, the amplitude of Nogo-N2 in the frontal area was significantly larger in the baseball group than that in the sports group. There was a significant positive correlation between the latency of Nogo-N2 and Go/Nogo RT. Moreover, there were significant correlations between the Go/Nogo RT and both the amplitude of Nogo-N2 and Nogo-P3 (i.e., amplitude of the Nogo-potentials increases with shorter RT). Specific athletic training regimens may induce neuroplastic alterations in sensorimotor inhibitory processes.
Recent studies have reported that acute aerobic exercise modulates intracortical excitability in the primary motor cortex (M1). However, whether acute low-intensity aerobic exercise can also modulate M1 intracortical excitability, particularly intracortical excitatory circuits, remains unclear. In addition, no previous studies have investigated the effect of acute aerobic exercise on short-latency afferent inhibition (SAI). The aim of this study was to investigate whether acute low-intensity aerobic exercise modulates intracortical circuits in the M1 hand and leg areas. Intracortical excitability of M1 (Experiments 1, 2) and spinal excitability (Experiment 3) were measured before and after acute low-intensity aerobic exercise. In Experiment 3, skin temperature was also measured throughout the experiment. Transcranial magnetic stimulation was applied over the M1 non-exercised hand and exercised leg areas in Experiments 1, 2, respectively. Participants performed 30 min of low-intensity pedaling exercise or rested while sitting on the ergometer. Short- and long-interval intracortical inhibition (SICI and LICI), and SAI were measured to assess M1 inhibitory circuits. Intracortical facilitation (ICF) and short-interval intracortical facilitation (SICF) were measured to assess M1 excitatory circuits. We found that acute low-intensity aerobic exercise decreased SICI and SAI in the M1 hand and leg areas. After exercise, ICF in the M1 hand area was lower than in the control experiment, but was not significantly different to baseline. The single motor-evoked potential, resting motor threshold, LICI, SICF, and spinal excitability did not change following exercise. In conclusion, acute low-intensity pedaling modulates M1 intracortical circuits of both exercised and non-exercised areas, without affecting corticospinal and spinal excitability.
Athletic training is known to induce neuroplastic alterations in specific somatosensory circuits, which are reflected by changes in short-latency somatosensory-evoked potentials (SEPs). The aim of this study is to clarify whether specific training in athletes affects the long-latency SEPs related to information processing of stimulation. The long-latency SEPs P100 and N140 were recorded at midline cortical electrode positions (Fz, Cz, and Pz) in response to stimulation of the index finger of the dominant hand in fifteen baseball players (baseball group) and in fifteen athletes in sports such as swimming, track and field events, and soccer (sports group) that do not require fine somatosensory discrimination or motor control of the hand. The long-latency SEPs were measured under a passive condition (no response required) and a reaction time (RT) condition in which subjects were instructed to rapidly push a button in response to stimulus presentation. The peak P100 and peak N140 latencies and RT were significantly shorter in the baseball group than the sports group. Moreover, there were significant positive correlations between RT and both the peak P100 and the peak N140 latencies. Specific athletic training regimens that involve the hand may induce neuroplastic alterations in the cortical hand representation areas playing a vital role in rapid sensory processing and initiation of motor responses.
BackgroundWater immersion therapy is used to treat a variety of cardiovascular, respiratory, and orthopedic conditions. It can also benefit some neurological patients, although little is known about the effects of water immersion on neural activity, including somatosensory processing. To this end, we examined the effect of water immersion on short-latency somatosensory evoked potentials (SEPs) elicited by median nerve stimuli. Short-latency SEP recordings were obtained for ten healthy male volunteers at rest in or out of water at 30°C. Recordings were obtained from nine scalp electrodes according to the 10-20 system. The right median nerve at the wrist was electrically stimulated with the stimulus duration of 0.2 ms at 3 Hz. The intensity of the stimulus was fixed at approximately three times the sensory threshold.ResultsWater immersion significantly reduced the amplitudes of the short-latency SEP components P25 and P45 measured from electrodes over the parietal region and the P45 measured by central region.ConclusionsWater immersion reduced short-latency SEP components known to originate in several cortical areas. Attenuation of short-latency SEPs suggests that water immersion influences the cortical processing of somatosensory inputs. Modulation of cortical processing may contribute to the beneficial effects of aquatic therapy.Trial RegistrationUMIN-CTR (UMIN000006492)
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