Visual scanning area is abnormally enlarged in hereditary pure cerebellar ataxia.

The aim of paper was to investigate abnormalities in visual scanning using an eye-tracking device with patients with spinocerebellar ataxia type 6 (SCA6) and SCA31, pure cerebellar types of spinocerebellar degeneration. Nineteen SCA patients (12 patients with SCA6 and 7 patients with SCA31) and 19 normal subjects in total participated in the study. While the subjects viewed images of varying complexity for later recall, we compared the visual scanning parameters between SCA patients and normal subjects. SCA patients had lower image recall scores. The scanned area in SCA patients was consistently larger than that in normal subjects. The amplitude of saccades was slightly larger in SCA patients than that in normal subjects, although it did not statistically differ between the two groups and correlated significantly with the scanned area in most images in SCA patients. The instability ratio of fixation, reflecting gaze-evoked nystagmus and downbeat nystagmus, was higher in SCA patients than that in normal subjects. Since SCA patients showed low scores despite wide visual scanning, the scanned area is considered to be abnormally enlarged. The larger scanned area in SCA patients was supposed mainly to result from the slightly larger saccade amplitude. Additionally, SCA patients showed prominent fixation disturbances probably due to gaze-evoked nystagmus and downbeat nystagmus. Consequently, SCA patients suffer from recognizing various objects in daily life, probably due to the impaired saccade control and impaired fixation.

Roles of the cerebellum and basal ganglia in temporal integration: Insights from a synchronized tapping task.

OBJECTIVE: The aim of this study was to clarify the roles of the cerebellum and basal ganglia for temporal integration. METHODS: We studied 39 patients with spinocerebellar degeneration (SCD), comprising spinocerebellar atrophy 6 (SCA6), SCA31, Machado-Joseph disease (MJD, also called SCA3), and multiple system atrophy (MSA). Thirteen normal subjects participated as controls. Participants were instructed to tap on a button in synchrony with isochronous tones. We analyzed the inter-tap interval (ITI), synchronizing tapping error (STE), negative asynchrony, and proportion of delayed tapping as indicators of tapping performance. RESULTS: The ITI coefficient of variation was increased only in MSA patients. The standard variation of STE was larger in SCD patients than in normal subjects, especially for MSA. Negative asynchrony, which is a tendency to tap the button before the tones, was prominent in SCA6 and MSA patients, with possible basal ganglia involvement. SCA31 patients exhibited normal to supranormal performance in terms of the variability of STE, which was surprising. CONCLUSIONS: Cerebellar patients generally showed greater STE variability, except for SCA31. The pace of tapping was affected in patients with possible basal ganglia pathology. SIGNIFICANCE: Our results suggest that interaction between the cerebellum and the basal ganglia is essential for temporal processing. The cerebellum and basal ganglia and their interaction regulate synchronized tapping, resulting in distinct tapping pattern abnormalities among different SCD subtypes.

Cortical hemoglobin concentration changes underneath the coil after single-pulse transcranial magnetic stimulation: a near-infrared spectroscopy study.

Using near-infrared spectroscopy (NIRS) and multichannel probes, we studied hemoglobin (Hb) concentration changes when single-pulse transcranial magnetic stimulation (TMS) was applied over the left hemisphere primary motor cortex (M1). Seventeen measurement probes were centered over left M1. Subjects were studied in both active and relaxed conditions, with TMS intensity set at 100%, 120%, and 140% of the active motor threshold. The magnetic coils were placed so as to induce anteromedially directed currents in the brain. Hb concentration changes were more prominent at channels over M1 and posterior to it. Importantly, Hb concentration changes at M1 after TMS differed depending on whether the target muscle was in an active or relaxed condition. In the relaxed condition, Hb concentration increased up to 3-6 s after TMS, peaking at ∼6 s, and returned to the baseline. In the active condition, a smaller increase in Hb concentrations continued up to 3-6 s after TMS (early activation), followed by a decrease in Hb concentration from 9 to 12 s after TMS (delayed deactivation). Hb concentration changes in the active condition at higher stimulus intensities were more pronounced at locations posterior to M1 than at M1. We conclude that early activation occurs when M1 is activated transsynaptically. The relatively late deactivation may result from the prolonged inhibition of the cerebral cortex after activation. The posterior-dominant activation at higher intensities in the active condition may result from an additional activation of the sensory cortex due to afferent inputs from muscle contraction evoked by the TMS.

Effects of electromagnetic fields emitted from W-CDMA-like mobile phones on sleep in humans.

In this study, we investigated subjective and objective effects of mobile phones using a Wideband Code Division Multiple Access (W-CDMA)-like system on human sleep. Subjects were 19 volunteers. Real or sham electromagnetic field (EMF) exposures for 3 h were performed before their usual sleep time on 3 consecutive days. They were exposed to real EMF on the second or third experimental day in a double-blind design. Sleepiness and sleep insufficiency were evaluated the next morning. Polysomnograms were recorded for analyses of the sleep variables and power spectra of electroencephalograms (EEG). No significant differences were observed between the two conditions in subjective feelings. Sleep parameters including sleep stage percentages and EEG power spectra did not differ significantly between real and sham exposures. We conclude that continuous wave EMF exposure for 3 h from a W-CDMA-like system has no detectable effects on human sleep.

Temporal synchronization for in-phase and antiphase movements during bilateral finger- and foot-tapping tasks.

Appropriate motor performance, which must be precisely processed and timed to temporal and spatial requirements, can be studied using a synchronized tapping task. For gait rehabilitation, estimation of bilateral foot-tapping accuracy is important, as walking involves bilateral movements, usually antiphase, of the lower extremities. Rhythmic control of lower limb movements, such as gait, involves voluntary control and may also be automatically regulated by the central pattern generator. This study investigated the temporal synchronization of in-phase and antiphase movements using synchronized bilateral finger and foot-tapping tasks. Thirty healthy young adult volunteers were enrolled and instructed to tap the finger or foot button synchronously with the tones presented at fixed inter-stimulus intervals (ISIs). One of 10 different ISIs (250-4800 ms) was selected for each block, in which 110 tones were presented. Taps were performed by either unilateral or bilateral fingers or feet, either in-phase (to move bilateral fingers or ankles simultaneously) or antiphase (to move bilateral fingers or ankles alternately). The synchronization error (SE) and coefficient of variation (CV) of the inter-tap interval (ITI) were evaluated. In all trials with short ISIs, SEs were narrowly distributed, either clustered around 0 ms or with a slightly negative value. Although SE variability gradually increased with increasing ISI, the CV of ITI was significantly lower for antiphase movement than for unilateral or in-phase movement in the foot-tapping task, but not in the finger-tapping task. The preserved temporal synchronization for antiphase movement of the foot, but not finger tapping, may be due to the neural mechanisms underlying locomotion.

Small saccades restrict visual scanning area in Parkinson's disease.

The purpose of this study was to investigate abnormalities in visual scanning when Parkinson's disease patients view images of varying complexity. Eighteen nondemented Parkinson's disease patients and 18 normal subjects participated in the study. The ocular fixation position during viewing visual images was recorded using an eye-tracking device. The number of saccades, duration of fixation, amplitude of saccades, and scanned area in Parkinson's disease patients were compared with those in normal subjects. We also investigated whether the number of saccades, duration of fixation, or amplitude of saccades influenced the scanned area. While scanning images of varying complexity, Parkinson's disease patients made fewer saccades with smaller amplitude and longer fixation compared with normal subjects. As image complexity increased, the number of saccades and duration of fixation gradually approached those of normal subjects. Nevertheless, the scanned area in Parkinson's disease patients was consistently smaller than that in normal subjects. The scanned area significantly correlated with saccade amplitude in most images. Importantly, although Parkinson's disease patients cannot make frequent saccades when viewing simple figures, they can increase the saccade number and reduce their fixation duration when viewing more complex figures, making use of the abundant visual cues in such figures, suggesting the existence of ocular kinesie paradoxale. Nevertheless, both the saccade amplitude and the scanned area were consistently smaller than those of normal subjects for all levels of visual complexity. This indicates that small saccade amplitude is the main cause of impaired visual scanning in Parkinson's disease patients.

Time Distortion in Parkinsonism.

Although animal studies and studies on Parkinson's disease (PD) suggest that dopamine deficiency slows the pace of the internal clock, which is corrected by dopaminergic medication, timing deficits in parkinsonism remain to be characterized with diverse findings. Here we studied patients with PD and progressive supranuclear palsy (PSP), 3-4 h after drug intake, and normal age-matched subjects. We contrasted perceptual (temporal bisection, duration comparison) and motor timing tasks (time production/reproduction) in supra- and sub-second time domains, and automatic versus cognitive/short-term memory-related tasks. Subjects were allowed to count during supra-second production and reproduction tasks. In the time production task, linearly correlating the produced time with the instructed time showed that the "subjective sense" of 1 s is slightly longer in PD and shorter in PSP than in normals. This was superposed on a prominent trend of underestimation of longer (supra-second) durations, common to all groups, suggesting that the pace of the internal clock changed from fast to slow as time went by. In the time reproduction task, PD and, more prominently, PSP patients over-reproduced shorter durations and under-reproduced longer durations at extremes of the time range studied, with intermediate durations reproduced veridically, with a shallower slope of linear correlation between the presented and produced time. In the duration comparison task, PD patients overestimated the second presented duration relative to the first with shorter but not longer standard durations. In the bisection task, PD and PSP patients estimated the bisection point (BP50) between the two supra-second but not sub-second standards to be longer than normal subjects. Thus, perceptual timing tasks showed changes in opposite directions to motor timing tasks: underestimating shorter durations and overestimating longer durations. In PD, correlation of the mini-mental state examination score with supra-second BP50 and the slope of linear correlation in the reproduction task suggested involvement of short-term memory in these tasks. Dopamine deficiency didn't correlate significantly with timing performances, suggesting that the slowed clock hypothesis cannot explain the entire results. Timing performance in PD may be determined by complex interactions among time scales on the motor and sensory sides, and by their distortion in memory.

Influence of short-interval intracortical inhibition on short-interval intracortical facilitation in human primary motor cortex.

Using the paired-pulse paradigm, transcranial magnetic stimulation (TMS) has revealed much about the human primary motor cortex (M1). A preceding subthreshold conditioning stimulus (CS) inhibits the excitability of the motor cortex, which is named short-interval intracortical inhibition (SICI). In contrast, facilitation is observed when the first pulse (S1) is followed by a second one at threshold (S2), named short-interval intracortical facilitation (SICF). SICI and SICF have been considered to be mediated by different neural circuits within M1, but more recent studies reported relations between them. In this study, we performed triple-pulse stimulation consisting of CS-S1-S2 to further explore putative interactions between these two effects. Three intensities of CS (80-120% of active motor threshold: AMT) and two intensities of S2 (120 and 140% AMT) were combined. The SICF in the paired-pulse paradigm exhibited clear facilitatory peaks at ISIs of 1.5 and 3 ms. The second peak at 3 ms was significantly suppressed by triple-pulse stimulation using 120% AMT CS, although the first peak was almost unaffected. Our present results obtained using triple-pulse stimulation suggest that each peak of SICF is differently modulated by different intensities of CS. The suppression of the second peak might be ascribed to the findings in the paired-pulse paradigm that CS mediates SICI by inhibiting later I waves such as I3 waves and that the second peak of SICF is most probably related to I3 waves. We propose that CS might inhibit the second peak of SICF at the interneurons responsible for I3 waves.

Primary motor cortical metaplasticity induced by priming over the supplementary motor area.

Motor cortical plasticity induced by repetitive transcranial magnetic stimulation (rTMS) sometimes depends on the prior history of neuronal activity. These effects of preceding stimulation on subsequent rTMS-induced plasticity have been suggested to share a similar mechanism to that of metaplasticity, a homeostatic regulation of synaptic plasticity. To explore metaplasticity in humans, many investigations have used designs in which both priming and conditioning are applied over the primary motor cortex (M1), but the effects of priming stimulation over other motor-related cortical areas have not been well documented. Since the supplementary motor area (SMA) has anatomical and functional cortico-cortical connections with M1, here we studied the homeostatic effects of priming stimulation over the SMA on subsequent rTMS-induced plasticity of M1. For priming and subsequent conditioning, we employed a new rTMS protocol, quadripulse stimulation (QPS), which produces a broad range of motor cortical plasticity depending on the interval of the pulses within a burst. The plastic changes induced by QPS at various intervals were altered by priming stimulation over the SMA, which did not change motor-evoked potential sizes on its own but specifically modulated the excitatory I-wave circuits. The data support the view that the homeostatic changes are mediated via mechanisms of metaplasticity and highlight an important interplay between M1 and SMA regarding homeostatic plasticity in humans.

Effects of short-term W-CDMA mobile phone base station exposure on women with or without mobile phone related symptoms.

To investigate possible health effects of mobile phone use, we conducted a double-blind, cross-over provocation study to confirm whether subjects with mobile phone related symptoms (MPRS) are more susceptible than control subjects to the effect of electromagnetic fields (EMF) emitted from base stations. We sent questionnaires to 5,000 women and obtained 2,472 valid responses from possible candidates; from these, we recruited 11 subjects with MPRS and 43 controls. There were four EMF exposure conditions, each of which lasted 30 min: continuous, intermittent, and sham exposure with and without noise. Subjects were exposed to EMF of 2.14 GHz, 10 V/m (W-CDMA), in a shielded room to simulate whole-body exposure to EMF from base stations, although the exposure strength we used was higher than that commonly received from base stations. We measured several psychological and cognitive parameters pre- and post-exposure, and monitored autonomic functions. Subjects were asked to report on their perception of EMF and level of discomfort during the experiment. The MPRS group did not differ from the controls in their ability to detect exposure to EMF; nevertheless they consistently experienced more discomfort, regardless of whether or not they were actually exposed to EMF, and despite the lack of significant changes in their autonomic functions. Thus, the two groups did not differ in their responses to real or sham EMF exposure according to any psychological, cognitive or autonomic assessment. In conclusion, we found no evidence of any causal link between hypersensitivity symptoms and exposure to EMF from base stations.

Bidirectional long-term motor cortical plasticity and metaplasticity induced by quadripulse transcranial magnetic stimulation.

Repetitive transcranial magnetic stimulation (rTMS) has emerged as a promising tool to induce plastic changes that are thought in some cases to reflect N-methyl-d-aspartate-sensitive changes in synaptic efficacy. As in animal experiments, there is some evidence that the sign of rTMS-induced plasticity depends on the prior history of cortical activity, conforming to the Bienenstock-Cooper-Munro (BCM) theory. However, experiments exploring these plastic changes have only examined priming-induced effects on a limited number of rTMS protocols, often using designs in which the priming alone had a larger effect than the principle conditioning protocol. The aim of this study was to introduce a new rTMS protocol that gives a broad range of after-effects from suppression to facilitation and then test how each of these is affected by a priming protocol that on its own has no effect on motor cortical excitability, as indexed by motor-evoked potential (MEP). Repeated trains of four monophasic TMS pulses (quadripulse stimulation: QPS) separated by interstimulus intervals of 1.5-1250 ms produced a range of after-effects that were compatible with changes in synaptic plasticity. Thus, QPS at short intervals facilitated MEPs for more than 75 min, whereas QPS at long intervals suppressed MEPs for more than 75 min. Paired-pulse TMS experiments exploring intracortical inhibition and facilitation after QPS revealed effects on excitatory but not inhibitory circuits of the primary motor cortex. Finally, the effect of priming protocols on QPS-induced plasticity was consistent with a BCM-like model of priming that shifts the crossover point at which synaptic plasticity reverses from depression to potentiation. The broad range of after-effects produced by the new rTMS protocol opens up new possibilities for detailed examination of theories of metaplasticity in humans.

Short and long duration transcranial direct current stimulation (tDCS) over the human hand motor area.

The aim of the present paper is to study effects of short and long duration transcranial direct current stimulation (tDCS) on the human motor cortex. In eight normal volunteers, motor evoked potentials (MEPs) induced by transcranial magnetic stimulation (TMS) were recorded from the right first dorsal interosseous muscle, and tDCS was given with electrodes over the left primary motor cortex (M1) and the contralateral orbit. We performed two experiments: one for short duration tDCS (100 ms, 1, 3 or 5 mA) and the other for long duration tDCS (10 min, 1 mA). The stimulus onset asynchrony (SOA) between the onset of tDCS and TMS were 1-7 and 10-120 ms for the former experiment. In the latter experiment, TMS was given 0-20 min after the end of 10 min tDCS. We evaluated the effect of tDCS on the motor cortex by comparing MEPs conditioned by tDCS with control MEPs. Cathodal short duration tDCS significantly reduced the size of responses to motor cortical stimulation at SOAs of 1-7 ms when the intensity was equal to or greater than 3 mA. Anodal short duration tDCS significantly increased MEPs when the intensity was 3 mA, but the enhancement did not occur when using 5 mA conditioning stimulus. Moreover, both anodal and cathodal short duration tDCS decreased responses to TMS significantly at SOAs of 20-50 ms and enhanced them at an SOA of 90 ms. Long duration cathodal tDCS decreased MEPs at 0 and 5 min after the offset of tDCS and anodal long duration tDCS increased them at 1 and 15 min. We conclude that the effect at SOAs less than 10 ms is mainly caused by acute changes in resting membrane potential induced by tDCS. The effect at SOAs of 20-100 ms is considered to be a nonspecific effect of a startle-like response produced by activation of skin sensation at the scalp. The effect provoked by long duration tDCS may be short-term potentiation or depression like effects.

Does the Clock Tick Slower or Faster in Parkinson's Disease? - Insights Gained From the Synchronized Tapping Task.

The rhythm of the internal clock is considered to be determined by the basal ganglia, with some studies suggesting slower internal clock in Parkinson's disease (PD). However, patients may also show motor hastening when they walk (festination) or are engaged in repetitive tapping, indicating faster ticking of the internal clock. Is the internal clock slower or faster in PD? The purpose of this study was to answer this question, i.e., how fast and slow a rhythm they can synchronize with, especially with reference to the limit of sensorimotor synchronization or temporal integration, representing the threshold of slower pace they can entrain into their motor actions, which is known to lie between 2 and 3 s in normal subjects but not yet studied in PD. We employed a synchronized tapping task that required subjects to tap the key in synchrony with repetitive tones at fixed interstimulus intervals (ISI) between 200 and 4800 ms. Twenty normal subjects and sixteen PD patients were enrolled, who were classified into early and advanced PD groups by UPDRS-III (early: 15 or less, advanced: more than 15). The ISI at which the response changes from synchronizing with the tones to lagging behind them was considered to be the limit of temporal integration. Early PD patients responded ahead of the tones (negative asynchrony), which became more apparent with repeated tapping. This suggested "faster" ticking clock even in the presence of the pacing tones. In normal subjects, the limit of temporal integration was around 2-3 s: below this, subjects could synchronize with the tones, while above it they had difficulty in synchronization. In early PD patients, the limit of temporal integration was significantly longer than in normal subjects, pointing to their enhanced ability to synchronize also with slower paces of tones, but advanced PD patients had significantly shortened limits, suggesting that advanced patients lost this ability. In conclusion, the limit of temporal integration is initially longer but gets shorter as the disease progresses. It can be explained by the hastening of the internal clock at the earlier stages of PD, followed by the loss of temporal integration.

Effects of thirty-minute mobile phone exposure on saccades.

OBJECTIVE: To investigate whether exposure to pulsed high-frequency electromagnetic field (pulsed EMF) emitted by a mobile phone has short-term effects on saccade performances. METHODS: A double blind, counterbalanced crossover design was employed. In 10 normal subjects, we studied the performance of visually guided saccade (VGS), gap saccade (GAP), and memory guided saccade (MGS) tasks before and after exposure to EMF emitted by a mobile phone for thirty minutes or sham exposure. We also implemented a hand reaction time (RT) task in response to a visual signal. RESULTS: With the exception of VGS and MGS latencies, the parameters of VGS, GAP and MGS tasks were unchanged before and after real or sham EMF exposure. In addition, the latencies of VGS and MGS did not change differently after real and sham exposure. The hand RT shortened with the repetition of trials, but again this trend was of similar magnitude for real and sham exposures. CONCLUSIONS: Thirty minutes of mobile phone exposure has no significant short-term effect on saccade performances. SIGNIFICANCE: This is the first study to investigate saccade performance in relation to mobile phone exposure. No significant effect of mobile phone use was demonstrated on the performance of various saccade tasks, suggesting that the cortical processing for saccades and attention is not affected by exposure to EMF emitted by a mobile phone.

Differences in after-effect between monophasic and biphasic high-frequency rTMS of the human motor cortex.

OBJECTIVE: To study differences in the long-term after-effect between high-frequency, monophasic and biphasic repetitive transcranial magnetic stimulation (rTMS). METHODS: Ten hertz rTMS was delivered over the left primary motor cortex and motor evoked potentials (MEPs) were recorded from the right first dorsal interosseous muscle. To probe motor cortex excitability we recorded MEPs at several timings before, during and after several types of conditioning rTMSs. We also recorded F-waves to probe spinal excitability changes. Thousand pulses were given in total, with a train of 10 Hz, 100 pulses delivered every minute (ten trains for 10min). The intensity was fixed at 90% active motor threshold (AMT) or 90% resting motor threshold (RMT) for both monophasic and biphasic rTMS. In addition, we performed a monophasic rTMS experiment using a fixed intensity of 90% RMT for biphasic pulses. RESULTS: At 90% AMT, MEPs were enhanced for a few minutes after both monophasic and biphasic rTMS. On the other hand, at 90% RMT, a larger and longer enhancement of MEPs was evoked after monophasic rTMS than after biphasic rTMS. Monophasic rTMS at an intensity adjusted to biphasic 90% RMT elicited a great enhancement similar to that after monophasic rTMS at monophasic 90% RMT. Neither F-wave amplitude nor its occurrence rate was significantly altered by 90% RMT monophasic rTMS. CONCLUSIONS: These results suggest that enhancement after rTMS occurs at the motor cortex. Monophasic rTMS has a stronger after-effect on motor cortical excitability than biphasic rTMS. This is probably because monophasic pulses preferentially activate a relatively uniform population of neurons oriented in the same direction and their effects summate more readily than biphasic rTMS activating differently oriented neurons at slight different timings altogether. SIGNIFICANCE: The present results suggest that when using rTMS as a therapeutic tool or in research fields, the waveforms of magnetic pulses may affect the results profoundly.

Origin of facilitation in repetitive, 1.5ms interval, paired pulse transcranial magnetic stimulation (rPPS) of the human motor cortex.

OBJECTIVE: Repetitive paired-pulse TMS (rPPS) given at an interstimulus interval (ISI) of 1.5 ms has been reported to induce a lasting motor evoked potential (MEP) facilitation. This after-effect was considered to be a cortical event because F-waves were not affected by the same rPPS. To confirm its cortical facilitation, we compared the after-effects of rPPS on MEPs to single pulse TMS over the motor cortex (motor cortical MEPs) with those to brainstem stimulation (brainstem MEPs). METHODS: Subjects were 10 healthy volunteers. Suprathreshold paired-pulse TMS at an ISI of 1.5 ms was applied to the motor cortex for 30 min at a rate of 0.2 Hz. After intervention, we measured motor cortical MEPs for 30 min. We also studied brainstem MEPs in five subjects. RESULTS: Motor cortical MEPs were facilitated to about 190% of baseline (p<0.001) for 10 min post rPPS intervention and returned to the baseline at 10-15 min post intervention. Brainstem MEPs were not affected by the intervention. CONCLUSIONS: The facilitation of MEPs after rPPS at an interval of 1.5 ms occurs at the motor cortex. SIGNIFICANCE: rPPS at an interval of 1.5 ms is an effective method for increasing motor cortical excitability.

Median nerve somatosensory evoked potentials and their high-frequency oscillations in amyotrophic lateral sclerosis.

OBJECTIVE: To investigate sensory cortical changes in amyotrophic lateral sclerosis (ALS), we studied somatosensory evoked potentials (SEPs) and their high-frequency oscillation potentials. METHODS: Subjects were 15 healthy volunteers and 26 ALS patients. Median nerve SEPs were recorded and several peaks of oscillations were obtained by digitally filtering raw SEPs. The patients were sorted into three groups according to the level of weakness of abductor pollicis brevis muscle (APB): mild, moderate and severe. The latencies and amplitudes of main and oscillation components of SEP were compared among normal subjects and the three patient groups. RESULTS: The early cortical response was enlarged in the moderate weakness group, while it was attenuated in the severe weakness group. No differences were noted in the size ratios of oscillations to the main SEP component between the patients and normal subjects. The central sensory conduction time (CCT) and N20 duration were prolonged in spite of normal other latencies. CONCLUSIONS: The median nerve SEP amplitude changes are associated with motor disturbances in ALS. The cortical potential enhancement of SEPs with moderate weakness in ALS may reflect some compensatory function of the sensory cortex for motor disturbances. SIGNIFICANCE: The sensory cortical compensation for motor disturbances is shown in ALS, which must be important information for rehabilitation.

Quadro-pulse stimulation is more effective than paired-pulse stimulation for plasticity induction of the human motor cortex.

OBJECTIVE: Repetitive paired-pulse transcranial magnetic stimulation (TMS) at I-wave periodicity has been shown to induce a motor-evoked potential (MEP) facilitation. We hypothesized that a greater enhancement of motor cortical excitability is provoked by increasing the number of pulses per train beyond those by paired-pulse stimulation (PPS). METHODS: We explored motor cortical excitability changes induced by repetitive application of trains of four monophasic magnetic pulses (quadro-pulse stimulation: QPS) at 1.5-ms intervals, repeated every 5s over the motor cortex projecting to the hand muscles. The aftereffects of QPS were evaluated with MEPs to a single-pulse TMS, motor threshold (MT), and responses to brain-stem stimulation. These effects were compared to those after PPS. To evaluate the QPS safety, we also studied the spread of excitation and after discharge using surface electromyograms (EMGs) of hand and arm muscles. RESULTS: Sizes of MEPs from the hand muscle were enhanced for longer than 75min after QPS; they reverted to the baseline at 90min. Responses to brain-stem stimulation from the hand muscle and cortical MEPs from the forearm muscle were unchanged after QPS over the hand motor area. MT was unaffected by QPS. No spreads of excitation were detected after QPS. The appearance rate of after discharges during QPS was not different from that during sham stimulation. CONCLUSIONS: Results show that QPS can safely induce long-lasting, topographically specific enhancement of motor cortical excitability. SIGNIFICANCE: QPS is more effective than PPS for inducing motor cortical plasticity.

Vocal amusia in a professional tango singer due to a right superior temporal cortex infarction.

We describe the psychophysical features of vocal amusia in a professional tango singer caused by an infarction mainly involving the superior temporal cortex of the right hemisphere. The lesion also extended to the supramarginal gyrus, the posterior aspect of the postcentral gyrus and the posterior insula. She presented with impairment of musical perception that was especially pronounced in discriminating timbre and loudness but also in discriminating pitch, and a severely impaired ability to reproduce the pitch just presented. In contrast, language and motor disturbances were almost entirely absent. By comparing her pre- and post-stroke singing, we were able to show that her singing after the stroke lacked the fine control of the subtle stress and pitch changes that characterized her pre-stroke singing. Such impairment could not be explained by the impairment of pitch perception. The findings suggest that damage to the right temporoparietal cortex is enough to produce both perceptive and expressive deficits in music.

Effects of thirty-minute mobile phone use on visuo-motor reaction time.

OBJECTIVE: To investigate whether exposure to pulsed high-frequency electromagnetic field (pulsed EMF) emitted by a mobile phone has short-term effects on the visuo-motor choice reaction time (RT) and movement time (MT). METHODS: A double blind, counterbalanced crossover design was employed. In 16 normal subjects, we studied the performance of a visuo-motor precued choice reaction time task (PCRT) before and after exposure to EMF emitted by a mobile phone for 30 minutes or sham exposure. RESULTS: The RTs and MTs under different conditions of precue information were not affected by exposure to pulsed EMF emitted by a mobile phone or by sham phone use. CONCLUSIONS: Thirty minutes of mobile phone use has no significant short-term effect on the cortical visuo-motor processing as studied by the present PCRT task. SIGNIFICANCE: This is the first study to investigate visuo-motor behavior in relation to mobile phone exposure. No significant effect of mobile phone use was demonstrated on the performance of the visuo-motor reaction time task.