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Reversed visual feedback during unimanual training increases transfer of skills to the opposite untrained hand and modulates plasticity in motor areas of the brain. However, it is unclear if unimanual training with reversed visual feedback also affects somatosensory areas. Here we manipulated visual input during unimanual training using left-right optical reversing spectacles and tested whether unimanual training with reversed vision modulates somatosensory cortical excitability to facilitate motor performance. Thirty participants practiced a unimanual ball-rotation task using the right hand with either left-right reversed vision (incongruent visual and somatosensory feedback) or direct vision (congruent feedback) of the moving hand. We estimated cortical excitability in primary somatosensory cortex (S1) before and after unimanual training by measuring somatosensory evoked potentials (SEPs). This was done by electrically stimulating the median nerve in the wrist while participants rested, and recording potentials over both hemispheres using electroencephalography. Performance of the ball-rotation task improved for both the right (trained) and left (untrained) hand after training across both direct and reversed vision conditions. Participants with direct vision of the right hand during training showed SEPs amplitudes increased bilaterally. In contrast, participants in the reversed visual condition showed attenuated SEPs following training. The results suggest that cortical suppression of S1 activity supports skilled motor performance after unimanual training with reversed vision, presumably by sensory gating of afferent signals from the movement. This finding provides insight into the mechanisms by which visual input interacts with the sensorimotor system and induces neuroplastic changes in S1 to support skilled motor performance.

Background Dual-site transcranial magnetic stimulation (ds-TMS) is a neurophysiological technique to measure functional connectivity between cortical areas. Objective/Hypothesis To date, no study has used ds-TMS to investigate short intra-hemispheric interactions between the somatosensory areas and primary motor cortex (M1). Methods We examined somatosensory-M1 interactions in the left hemisphere in six experiments using ds-TMS. In Experiment 1 (n = 16), the effects of different conditioning stimulus (CS) intensities on somatosensory-M1 interactions were measured with 1 and 2.5 ms inter-stimulus intervals (ISIs). In Experiment 2 (n = 16), the time-course of somatosensoy-M1 interactions was studied using supra-threshold CS intensity at 6 different ISIs. In Experiment 3 (n = 16), the time-course of short-interval cortical inhibition (SICI) and effects of different CS intensities on SICI were measured similar to Experiments 1 and 2. Experiment 4 (n = 13) examined the effects of active contraction on SICI and somatosensory-M1 inhibition. Experiments 5 and 6 (n = 10) examined the interactions between SAI with either 1 ms SICI or somatosensory-M1 inhibition. Results Experiments 1 and 2 revealed reduced MEP amplitudes when applying somatosensory CS 1 ms prior to M1 TS with 140 and 160% CS intensities. Experiment 3 demonstrated that SICI at 1 and 2.5 ms did not correlate with somatosensory-M1 inhibition. Experiment 4 found that SICI but not somatosensory-M1 inhibition was abolished with active contraction. The results of Experiments 5–6 showed SAI was disinhibited in presence of somatosensory-M1 while SAI was increased in presence of SICI. Conclusion Collectively, the results support the notion that the somatosensory areas inhibit the ipsilateral M1 at very short latencies.

The interconnection of the angular gyrus of right posterior parietal cortex (PPC) and the left motor cortex (LM1) is essential for goal-directed hand movements. Previous work with transcranial magnetic stimulation (TMS) showed that right PPC stimulation increases LM1 excitability, but right PPC followed by left PPC-LM1 stimulation (LPPC-LM1) inhibits LM1 corticospinal output compared with LPPC-LM1 alone. It is not clear if right PPC-mediated inhibition of LPPC-LM1 is due to inhibition of left PPC or to combined effects of right and left PPC stimulation on LM1 excitability. We used paired-pulse TMS to study the extent to which combined right and left PPC stimulation, targeting the angular gyri, influences LM1 excitability. We tested 16 healthy subjects in five paired-pulsed TMS experiments using MRI-guided neuronavigation to target the angular gyri within PPC. We tested the effects of different right angular gyrus (RAG) and LM1 stimulation intensities on the influence of RAG on LM1 and on influence of left angular gyrus (LAG) on LM1 (LAG-LM1). We then tested the effects of RAG and LAG stimulation on LM1 short-interval intracortical facilitation (SICF), short-interval intracortical inhibition (SICI), and long-interval intracortical inhibition (LICI). The results revealed that RAG facilitated LM1, inhibited SICF, and inhibited LAG-LM1. Combined RAG-LAG stimulation did not affect SICI but increased LICI. These experiments suggest that RAG-mediated inhibition of LAG-LM1 is related to inhibition of early indirect (I)-wave activity and enhancement of GABAB receptor-mediated inhibition in LM1. The influence of RAG on LM1 likely involves ipsilateral connections from LAG to LM1 and heterotopic connections from RAG to LM1.NEW & NOTEWORTHY Goal-directed hand movements rely on the right and left angular gyri (RAG and LAG) and motor cortex (M1), yet how these brain areas functionally interact is unclear. Here, we show that RAG stimulation facilitated right hand motor output from the left M1 but inhibited indirect (I)-waves in M1. Combined RAG and LAG stimulation increased GABAB, but not GABAA, receptor-mediated inhibition in left M1. These findings highlight unique brain interactions between the RAG and left M1.

Introduction Freezing of gait (FOG) is a complex symptom in Parkinson's disease (PD) that manifests during walking as limited forward progression despite the intention to walk. It is unclear if lower limb motor blocks (LLMB) that occur independently from FOG are related to overground FOG and the effects of dopaminergic medications. Methods Nineteen patients with PD were tested on two separate days in the dopaminergic medication “on” and “off” states. The patients completed a series of freezing-provoking tasks while videotaped. Raters assessed videos for FOG presence using Movement Disorders Society Unified Parkinson's Disease Rating Scale item 3.11 score greater than or equal to 1 and FOG severity using the standardized FOG score. Whilst seated in a virtual environment, patients and 20 healthy controls stepped in right-left sequence on foot pedals. Frequency and percent time in LLMB were assessed for accurate classification of FOG presence and correlation to the FOG score. Results Frequency and percent time spent in LLMB predicted the presence of FOG in both medication states. Percent time spent in LLMB correlated with FOG severity in both medication states. LLMB frequency predicted FOG severity in the “off” state only. Conclusions LLMB during bilateral stepping in a virtual environment predicted the presence and severity of FOG in PD in both “on” and “off” medication states. These findings support the use of this non-walking paradigm to detect and assess FOG in PD patients unable or unsafe to walk.

Classical schemes of basal ganglia organization posit that parkinsonian movement difficulties presenting after striatal dopamine depletion stem from the disproportionate firing rates of spiny projection neurons (SPNs) therein. There remains, however, a pressing need to elucidate striatal SPN firing in the context of the synchronized network oscillations that are abnormally exaggerated in cortical–basal ganglia circuits in parkinsonism. To address this, we recorded unit activities in the dorsal striatum of dopamine-intact and dopamine-depleted rats during two brain states, respectively defined by cortical slow-wave activity (SWA) and activation. Dopamine depletion escalated striatal net output but had contrasting effects on “direct pathway” SPNs (dSPNs) and “indirect pathway” SPNs (iSPNs); their firing rates became imbalanced, and they disparately engaged in network oscillations. Disturbed striatal activity dynamics relating to the slow (∼1 Hz) oscillations prevalent during SWA partly generalized to the exaggerated beta-frequency (15–30 Hz) oscillations arising during cortical activation. In both cases, SPNs exhibited higher incidences of phase-locked firing to ongoing cortical oscillations, and SPN ensembles showed higher levels of rhythmic correlated firing, after dopamine depletion. Importantly, in dopamine-depleted striatum, a widespread population of iSPNs, which often displayed excessive firing rates and aberrant phase-locked firing to cortical beta oscillations, preferentially and excessively synchronized their firing at beta frequencies. Conversely, dSPNs were neither hyperactive nor synchronized to a large extent during cortical activation. These data collectively demonstrate a cell type-selective entrainment of SPN firing to parkinsonian beta oscillations. We conclude that a population of overactive, excessively synchronized iSPNs could orchestrate these pathological rhythms in basal ganglia circuits. SIGNIFICANCE STATEMENT Chronic depletion of dopamine from the striatum, a part of the basal ganglia, causes some symptoms of Parkinson's disease. Here, we elucidate how dopamine depletion alters striatal neuron firing in vivo, with an emphasis on defining whether and how spiny projection neurons (SPNs) engage in the synchronized beta-frequency (15–30 Hz) oscillations that become pathologically exaggerated throughout basal ganglia circuits in parkinsonism. We discovered that a select population of so-called “indirect pathway” SPNs not only fire at abnormally high rates, but are also particularly prone to being recruited to exaggerated beta oscillations. Our results provide an important link between two complementary theories that explain the presentation of disease symptoms on the basis of changes in firing rate or firing synchronization/rhythmicity.

Measurements of somatosensory evoked potentials (SEPs), recorded using electroencephalography during different phases of movement, have been fundamental in understanding the neurophysiological changes related to motor control. SEP recordings have also been used to investigate adaptive plasticity changes in somatosensory processing related to active and observational motor learning tasks. Combining noninvasive brain stimulation with SEP recordings and intracranial SEP depth recordings, including recordings from deep brain stimulation electrodes, has been critical in identifying neural areas involved in specific temporal stages of somatosensory processing. Consequently, this fundamental information has furthered our understanding of the maladaptive plasticity changes related to pathophysiology of diseases characterized by abnormal movements, such as Parkinson's disease, dystonia, and functional movement disorders.

Voluntary movements are planned through the relative timing between submovements of movement sequences as part of the motor program. Different movement phases are characterized by specific amplitude modulation of cortical oscillations. The latter represent neurophysiological correlates of specific synchronization or desynchronization of different neuronal groups. In this Neuro Forum, we review recent evidence regarding the temporal relation between neurophysiological correlates of different phases of a repetitive motor task using electroencephalography and source localization using individualized MRI.

Early frontal somatosensory evoked potentials (SEPs) (i.e., N30) are known to be modulated by movement. Furthermore, individuals with prefrontal lesions have enhanced early frontal SEPs. However, it is currently unclear through what mechanism the prefrontal cortex may modulate early frontal SEPs. The current study investigated whether prefrontal modulatory effects on frontal SEPs may depend on the relevancy of somatosensory input for movement (i.e., interaction with motor areas). Two experiments were conducted to determine whether selective spatial attention alone (Experiment 1-Attend and Mentally Count) or when using attended somatosensory input in the preparation of finger sequences with the limb contralateral to somatosensory stimulation (Experiment 2-Attend for Movement Preparation) could modulate SEPs. In Experiment 1, SEPs elicited by median nerve (MN) stimulation at both wrists were measured in trials when individuals attended and mentally counted vibrotactile (VibT) input at either index finger. In Experiment 2, SEPs elicited by MN stimulation at the left wrist were measured in trials when individuals used attended VibT input at the left index finger to prepare finger sequences that were contralateral to MN stimulation. In both experiments, control conditions were performed where participants received passive VibT and MN stimulation. Results from Experiment 1 confirmed that selective spatial attention alone does not modulate frontal N30 peak amplitudes. However, Experiment 2 revealed that frontal N30 peak amplitudes were decreased (i.e., gated) when individuals used attended VibT input at the left index finger to prepare contralateral finger sequences. These results support a role of sensory gating of early frontal SEPs during finger sequence preparation of the limb contralateral to MN stimulation that may result from increased activity in prefrontal, motor preparatory areas, and basal ganglia.

Upper limb motor blocks (ULMB) (inability to initiate or sudden discontinue in voluntary movements) have been identified in both unimanual and bimanual tasks in individuals with Parkinson's disease (PD). In particular, ULMB have been observed during rhythmic bimanual coordination when switching between phase patterns which is required (e.g. between in-phase and anti-phase). While sensory-perceptual mechanisms have recently been suggested to be involved in lower limb freezing, there has been no consensus on the mechanism that evokes ULMB or whether motor blocks respond to dopamine replacement like other motor symptoms of PD. The current study investigated the occurrence of ULMB in PD participants without ('off') and with ('on') dopamine replacement using bimanual wrist flexion-extension with external auditory cues. In Experiment 1, coordination was performed in either in-phase (simultaneous flexion and extension) or anti-phase (asymmetrical flexion and extension between the limbs) in one of three sensory conditions: no vision, normal vision or augmented vision. Cycle frequency was increased within each trial across seven cycle frequencies (0.75-2 Hz). In Experiment 2, coordination was initiated in either phase pattern and participants were cued to make an intentional switch between phases in the middle of trials. Trials were performed at one of two cycle frequencies (1 or 2 Hz) and one of two sensory conditions: no vision or normal vision. Healthy age-matched control participants were also investigated in both experiments for the occurrence of motor blocks that were measured using automated detection from a computer algorithm. The results from Experiment 1 indicated that increasing cycle frequency resulted in more ULMB in individuals with PD during continuous coordinated movement, regardless of dopaminergic status, phase pattern or sensory condition. Experiment 2 also confirmed an increased occurrence of ULMB with increased cycle frequency. Furthermore, a large amount of ULMB were observed when initiating anti-phase coordination at 2 Hz, as well as after both externally-cued switches and in 'catch trials' with distracting auditory cues when no switch was required. Dopamine replacement was not found to influence the frequency of ULMB in either experiment. Therefore, ULMB likely result from non-hypodopaminergic impairments associated with PD. Specifically, ULMB may be caused by an inability to shift attentional control under increased cognitive demand that could be associated with hypoactivation in motor and prefrontal areas.

Switching between different coordinated movements has been shown to be slow, with delayed responses and even freezing deficits in individuals with Parkinson’s disease (PD). While it is well accepted that the dopaminergic system responds to dopamine replacement to ameliorate overall slowness (bradykinesia) and other motor symptoms of PD, it is unknown whether the dopaminergic system can influence overall coordination between limbs and if this may be impacted by the availability of sensory feedback. In the current study, PD and healthy age-matched control participants performed a rhythmic coordination task that required a cued voluntary switch between movement patterns (in-phase and anti-phase). PD participants performed the task first after overnight withdrawal (‘off’), and subsequently after administration (‘on’) of dopamine replacement. Coordinated movements were performed while paced by an auditory metronome in two sensory conditions: ‘no vision’ or ‘normal vision’. Measures of voluntary switch time and delayed responses revealed that PD ‘off’ required significantly more time than healthy participants to switch between movement patterns. Interestingly, PD ‘off’ demonstrated disrupted coordination, as revealed by mean (accuracy) and standard deviation (stability) of absolute error of relative phase. Dopamine replacement improved the time needed to switch and amount of delayed responses in PD participants, but had no influence on coordination itself. It is concluded that although modulation of the dopaminergic system improves the slowness during switching, coordination deficits may be the result of secondary impairments (possibly attention-related) that cannot be improved with dopamine replacement.

Introduction The posterior parietal cortices (PPCs) engage in motor processing during reach and grasp. Yet, the neural substrates behind their connections to the motor cortex (M1) are still unknown. It has been postulated that right PPC (rPPC) acts directly on left PPC (lPPC), which then acts on left M1 (lM1). Alternately, rPPC may act on lM1 circuits at the same time as lPPC. Here, we used triple-site transcranial magnetic stimulation (TMS) to test this hypothesis. Previous studies showed that rPPC or lPPC stimulation alone facilitates motor evoked potentials (MEPs), whereas rPPC and lPPC stimulation together inhibits the facilitated MEPs. To consider their interaction at M1, we tested two M1 circuits: short interval intracortical facilitation (SICF) and short interval intracortical inhibition (SICI). SICF is elicited by two suprathreshold pulses to M1 delivered in ∼ 1.5 ms intervals which facilitate M1 output. SICI inhibits M1 output and is elicited by a subthreshold conditioning stimulus delivered 1–6 ms prior to a suprathreshold pulse. We hypothesized that if rPPC and lPPC inhibit MEPs by acting on SICF or SICI in M1, a correlation would emerge. Methods 16 healthy adults participated (9 females, 22–64 years, 35.4 ± 14.6 years old). MRI-navigated TMS was delivered by 3 small coils over rPPC, lPPC and lM1. MEPs were recorded from the right first dorsal interosseous muscle. Exp 1 tested PPC-lM1 circuits and their interactions at several rPPC and lPPC stimuli intensities, including 90 and ∼ 108% RMT over lPPC and 30 to 130% RMT over rPPC. Exp 2 tested PPC-lM1 circuits and their interaction at different test MEP amplitudes of ∼ 0.2 mV, 1 mV, and 4 mV. Exp 3 tested the effect of rPPC on SICF. Exp 4 tested the effect of SICI on lPPC-lM1 and rPPC-lPPC-lM1 interactions. Results Exp 1: The interaction of rPPC and lPPC inhibited MEPs. This effect occurred when the rPPC was stimulated at 70% and 90% RMT, and the lPPC was stimulated at ∼ 108% RMT. rPPC-to-lM1 connectivity correlated with this interaction, whereas lPPC-to-lM1 connectivity did not. Exp 2: Compared to higher intensities, low intensity M1 stimulation at ∼ 0.2 mV showed facilitated rPPC-to-lM1 connectivity and increased the inhibitory effects of rPPC and lPPC interaction. Exp 3: rPPC inhibited SICF at 1.4 ± 0.1 ms, and this inhibition correlated with rPPC and lPPC inhibition. Exp 4: SICI abolished the facilitatory effect of lPPC-lM1 and the inhibitory effect of rPPC-to-lPPC-lM1 connection. SICI in the presence of lPPC-lM1 correlated with rPPC in the presence of lPPC-lM1. Conclusion We showed that the rPPC and lPPC inhibit the lM1, which is more prominent when tested at low M1 stimulation intensity. rPPC-to-lM1 connectivity correlated with this interaction. The effect of PPC on M1 may be mediated in part by cortical circuits SICF and SICI. We conclude that the effects of rPPC and lPPC likely interact at lM1.

Frontal N30 somatosensory evoked potentials (SEPs) represent early somatosensory input into non-primary motor areas. Importantly, modulations of frontal N30 SEPs can provide insight into the mechanisms involved in sensory processing for movement control. Enhancements of frontal N30 SEPs have been revealed during repetitive but not during the preparation of movements that are contralateral to median nerve (MN) stimulation (i.e. contralateral movements). Importantly, these enhancements during contralateral movements may be dependent on increased activity in several neural areas such as the primary motor cortex (M1), supplementary motor area (SMA) and basal ganglia (BG). Furthermore, research has also shown that patients with prefrontal lesions have enhanced early frontal SEPs (i.e. N28) at rest supporting a role of the prefrontal cortex in inhibitory modulation of early somatosensory input. The current study evaluated whether differential modulations of frontal N30 SEPs occurred during different time periods when individuals prepared and executed contralateral (right) finger sequences to attended vibrotactile (VibT) stimuli at the left index finger. SEPs were measured to median nerve (MN) stimuli elicited at the left wrist and MN stimuli were time-locked in four different periods relative to VibT onset (during pre-stimulus, early response preparation, late movement preparation and movement execution). Results revealed that frontal N30 SEPs were significantly enhanced when MN stimulation occurred in the late preparatory and/or early movement execution period (∼750 ms) after the attended VibT stimuli. This result supports that increases in frontal N30 amplitudes during contralateral movements are dependent on the complexity of preparing and executing finger sequences, which is associated with increased activity in several neural areas such as the non-primary motor areas, prefrontal cortex and BG. Furthermore, enhanced N30 SEPs during contralateral movement preparation and execution may be a necessary mechanism to decrease sensory gating to facilitate somatosensory processing in non-primary motor areas when there is a ‘noisy’ environment.

By hypothesis, awareness is involved in the modulation of feedback from semantics to the lexical level in the visual word recognition system. When subjects are aware of the fact that there are many related prime-target pairs in a semantic priming experiment, this knowledge is used to configure the system to feed activation back from semantics to the lexical level so as to facilitate processing. When subjects are unaware of this fact, the default set is maintained in which activation is not fed back from semantics to the lexical level so as to conserve limited resources. Qualitative differences in the pattern of data from two lexical decision experiments that employ masked priming are consistent with this hypothesis. Semantic context and stimulus quality interact when the prime is processed with awareness whereas these same two factors produce additive effects on RT when the prime is unlikely to have been processed with awareness. These experiments thus illustrate one way in which awareness (or lack thereof) affects the dynamics of visual word recognition.

Bradykinesia is a well-documented DOPA-responsive clinical feature of Parkinson’s disease (PD). While amplitude deficits (hypokinesia) are a key component of this slowness, it is important to consider how dopamine influences both the amplitude (hypokinesia) and frequency components of bradykinesia when a bimanually coordinated movement is required. Based on the notion that the basal ganglia are associated with sensory deficits, the influence of dopaminergic replacement on sensory feedback conditions during bimanual coordination was also evaluated. Bimanual movements were examined in PD and healthy comparisons in an unconstrained three-dimensional coordination task. PD were tested “off” (overnight withdrawal of dopaminergic treatment) and “on” (peak dose of dopaminergic treatment), while the healthy group was evaluated for practice effects across two sessions. Required cycle frequency (increased within each trial from 0.75 to 2 Hz), type of visual feedback (no vision, normal vision, and augmented vision), and coordination pattern (symmetrical in-phase and non-symmetrical anti-phase) were all manipulated. Overall, coordination (mean accuracy and standard deviation of relative phase) and amplitude deficits during bimanual coordination were confirmed in PD participants. In addition, significant correlations were identified between severity of motor symptoms as well as bradykinesia to greater coordination deficits (accuracy and stability) in PD “off” group. However, even though amplitude deficits (hypokinesia) improved with dopaminergic replacement, it did not improve bimanual coordination performance (accuracy or stability) in PD patients from “off” to “on.” Interestingly, while coordination performance in both groups suffered in the augmented vision condition, the amplitude of the more affected limb of PD was notably influenced. It can be concluded that DOPA-responsive hypokinesia contributes to, but is not directly responsible for bimanual coordination impairments in PD. It is likely that bimanual coordination deficits in PD are caused by the combination of dopaminergic system dysfunction as well as other neural impairments that may be DOPA-resistant or related to non-dopaminergic pathways.

Switching between different coordinated movements has been shown to be slow, with delayed responses and even freezing deficits in individuals with Parkinson's disease (PD). While it is well accepted that the dopaminergic system responds to dopamine replacement to ameliorate overall slowness (bradykinesia) and other motor symptoms of PD, it is unknown whether the dopaminergic system can influence overall coordination between limbs and if this may be impacted by the availability of sensory feedback. In the current study, PD and healthy age-matched control participants performed a rhythmic coordination task that required a cued voluntary switch between movement patterns (in-phase and anti-phase). PD participants performed the task first after overnight withdrawal ('off'), and subsequently after administration ('on') of dopamine replacement. Coordinated movements were performed while paced by an auditory metronome in two sensory conditions: 'no vision' or 'normal vision'. Measures of voluntary switch time and delayed responses revealed that PD 'off' required significantly more time than healthy participants to switch between movement patterns. Interestingly, PD 'off' demonstrated disrupted coordination, as revealed by mean (accuracy) and standard deviation (stability) of absolute error of relative phase. Dopamine replacement improved the time needed to switch and amount of delayed responses in PD participants, but had no influence on coordination itself. It is concluded that although modulation of the dopaminergic system improves the slowness during switching, coordination deficits may be the result of secondary impairments (possibly attention-related) that cannot be improved with dopamine replacement.

The Stroop effect typically refers to the fact that the time to identify the color of a visually presented word is affected by the relationship between the word and the color. When the (irrelevant) word is semantically related to the color (e.g., the wordgreen, presented in red) response time is slower than if the word is neutral or unrelated. One question that has been posed concerns whether semantics plays a role only when the task requires an explicit verbal response, or whether it also plays a role when the response is manual. Sharma and McKenna (1998) have reported that semantics plays a role only when the response is vocal. A reanalysis of their data shows that semantics also plays a role when manual responses are made.

Background There exists a lack of consensus regarding how cerebellar over-activity might influence tremor in Parkinson’s disease (PD). Specifically, it is unclear whether resting or postural tremor are differentially affected by cerebellar dysfunction. It is important to note that previous studies have only evaluated the influence of inhibitory stimulation on the lateral cerebellum, and have not considered the medial cerebellum. The aim of the current study was to compare the effects of a low-frequency rTMS protocol applied to the medial versus lateral cerebellum to localize the effects of cerebellar over-activity. Methods Fifty PD participants were randomly assigned to receive stimulation over the medial cerebellum (n = 20), lateral cerebellum (n = 20) or sham stimulation (n = 10). 900 pulses were delivered at 1Hz at 120 % resting motor threshold of the first dorsal interosseous muscle. Tremor was assessed quantitatively (before and after stimulation) using the Kinesia Homeview system which utilizes a wireless finger accelerometer to record tremor. Results The main finding was that resting tremor severity was reduced in tremor-dominant individuals, regardless of whether stimulation was applied over the medial (p = 0.024) or lateral (p = 0.033) cerebellum, but not in the sham group. Conclusion Given that the cerebellum is overactive in PD, the improvements in resting tremor following an inhibitory stimulation protocol suggest that over-activity in cerebellar nuclei may be involved in the generation of resting tremor in PD. Low-frequency rTMS over the medial or lateral cerebellum provides promise of an alternative treatment for tremor in PD, a symptom that is poorly responsive to dopaminergic replacement. Electronic supplementary material The online version of this article (doi:10.1186/s40673-016-0051-5) contains supplementary material, which is available to authorized users.