Changes In Motor Cortical Excitability Research Articles

The behavioral and neural effects of parietal theta burst stimulation on the grasp network are stronger during a grasping task than at rest

Repetitive transcranial magnetic stimulation (TMS) is widely used in neuroscience and clinical settings to modulate human cortical activity. The effects of TMS on neural activity depend on the excitability of specific neural populations at the time of stimulation. Accordingly, the brain state at the time of stimulation may influence the persistent effects of repetitive TMS on distal brain activity and associated behaviors. We applied intermittent theta burst stimulation (iTBS) to a region in the posterior parietal cortex (PPC) associated with grasp control to evaluate the interaction between stimulation and brain state. Across two experiments, we demonstrate the immediate responses of motor cortex activity and motor performance to state-dependent parietal stimulation. We randomly assigned 72 healthy adult participants to one of three TMS intervention groups, followed by electrophysiological measures with TMS and behavioral measures. Participants in the first group received iTBS to PPC while performing a grasping task concurrently. Participants in the second group received iTBS to PPC while in a task-free, resting state. A third group of participants received iTBS to a parietal region outside the cortical grasping network while performing a grasping task concurrently. We compared changes in motor cortical excitability and motor performance in the three stimulation groups within an hour of each intervention. We found that parietal stimulation during a behavioral manipulation that activates the cortical grasping network increased downstream motor cortical excitability and improved motor performance relative to stimulation during rest. We conclude that constraining the brain state with a behavioral task during brain stimulation has the potential to optimize plasticity induction in cortical circuit mechanisms that mediate movement processes.

Methodological approach for assessing motor cortical excitability changes with single-pulse transcranial magnetic stimulation

Transcranial Magnetic Stimulation (TMS) serves as a crucial tool in evaluating motor cortex excitability by applying short magnetic pulses to the skull, inducing neuron depolarization in the cerebral cortex through electromagnetic induction. This technique leads to the activation of specific skeletal muscles recorded as Motor-Evoked Potentials (MEPs) through electromyography. Although various methodologies assess cortical excitability with TMS, measuring MEP amplitudes offers a straightforward approach, especially when comparing excitability states pre- and post-interventions designed to alter cortical excitability. Despite TMS's widespread use, the absence of a standardized procedure for such measurements in existing literature hinders the comparison of results across different studies. This paper proposes a standardized procedure for assessing changes in motor cortical excitability using single-pulse TMS pre- and post-intervention. The recommended approach utilizes an intensity equating to half of the MEP's maximum amplitude, thereby ensuring equal likelihood of amplitude increase or decrease, providing a consistent basis for future studies and facilitating meaningful comparisons of results.•A method for assessing changes in motor cortical excitability using single-pulse TMS before and after a specified intervention.•We recommend using an intensity equal to half of the MEP's maximum amplitude during evaluations to objectively assess motor cortical excitability changes post-intervention.

Sensory and motor cortical excitability changes induced by rTMS and sensory stimulation in stroke: A randomized clinical trial.

The ability to produce coordinated movement is dependent on dynamic interactions through transcallosal fibers between the two cerebral hemispheres of the brain. Although typically unilateral, stroke induces changes in functional and effective connectivity across hemispheres, which are related to sensorimotor impairment and stroke recovery. Previous studies have focused almost exclusively on interhemispheric interactions in the primary motor cortex (M1). To identify the presence of interhemispheric asymmetry (ASY) of somatosensory cortex (S1) excitability and to investigate whether S1 repetitive transcranial magnetic stimulation (rTMS) combined with sensory stimulation (SS) changes excitability in S1 and M1, as well as S1 ASY, in individuals with subacute stroke. A randomized clinical trial. Participants with a single episode of stroke, in the subacute phase, between 35 and 75 years old, were allocated, randomly and equally balanced, to four groups: rTMS/sham SS, sham rTMS/SS, rTMS/SS, and sham rTMS/Sham SS. Participants underwent 10 sessions of S1 rTMS of the lesioned hemisphere (10 Hz, 1,500 pulses) followed by SS. SS was applied to the paretic upper limb (UL) (active SS) or non-paretic UL (sham SS). TMS-induced motor evoked potentials (MEPs) of the paretic UL and somatosensory evoked potential (SSEP) of both ULs assessed M1 and S1 cortical excitability, respectively. The S1 ASY index was measured before and after intervention. Evaluator, participants and the statistician were blinded. Thirty-six participants divided equally into groups (nine participants per group). Seven patients were excluded from MEP analysis because of failure to produce consistent MEP. One participant was excluded in the SSEP analysis because no SSEP was detected. All somatosensory stimulation groups had decreased S1 ASY except for the sham rTMS/Sham SS group. When compared with baseline, M1 excitability increased only in the rTMS/SS group. S1 rTMS and SS alone or in combination changed S1 excitability and decreased ASY, but it was only their combination that increased M1 excitability. clinicaltrials.gov, identifier (NCT03329807).

Multi-modal investigation of transcranial ultrasound-induced neuroplasticity of the human motor cortex

IntroductionThere is currently a gap in accessibility to neuromodulation tools that can approximate the efficacy and spatial resolution of invasive methods. Low intensity transcranial focused ultrasound stimulation (TUS) is an emerging technology for non-invasive brain stimulation (NIBS) that can penetrate cortical and deep brain structures with more focal stimulation compared to existing NIBS modalities. Theta burst TUS (tbTUS, TUS delivered in a theta burst pattern) is a novel repetitive TUS protocol that can induce durable changes in motor cortex excitability, thereby holding promise as a novel neuromodulation tool with durable effects. ObjectiveThe aim of the present study was to elucidate the neurophysiologic effects of tbTUS motor cortical excitability, as well on local and global neural oscillations and network connectivity. MethodsAn 80-s train of active or sham tbTUS was delivered to the left motor cortex in 15 healthy subjects. Motor cortical excitability was investigated through transcranial magnetic stimulation (TMS)-elicited motor-evoked potentials (MEPs), short-interval intracortical inhibition (SICI), and intracortical facilitation (ICF) using paired-pulse TMS. Magnetoencephalography (MEG) recordings during resting state and an index finger abduction-adduction task were used to assess oscillatory brain responses and network connectivity. The correlations between the changes in neural oscillations and motor cortical excitability were also evaluated. ResultstbTUS to the motor cortex results in a sustained increase in MEP amplitude and decreased SICI, but no change in ICF. MEG spectral power analysis revealed TUS-mediated desynchronization in alpha and beta spectral power. Significant changes in alpha power were detected within the supplementary motor cortex (Right > Left) and changes in beta power within bilateral supplementary motor cortices, right basal ganglia and parietal regions. Coherence analysis revealed increased local connectivity in motor areas. MEP and SICI changes correlated with both local and inter-regional coherence. ConclusionThe findings from this study provide novel insights into the neurophysiologic basis of TUS-mediated neuroplasticity and point to the involvement of regions within the motor network in mediating this sustained response. Future studies may further characterize the durability of TUS-mediated neuroplasticity and its clinical applications as a neuromodulation strategy for neurological and psychiatric disorders.

"Tricking the Brain" Using Immersive Virtual Reality: Modifying the Self-Perception Over Embodied Avatar Influences Motor Cortical Excitability and Action Initiation.

To offer engaging neurorehabilitation training to neurologic patients, motor tasks are often visualized in virtual reality (VR). Recently introduced head-mounted displays (HMDs) allow to realistically mimic the body of the user from a first-person perspective (i.e., avatar) in a highly immersive VR environment. In this immersive environment, users may embody avatars with different body characteristics. Importantly, body characteristics impact how people perform actions. Therefore, alternating body perceptions using immersive VR may be a powerful tool to promote motor activity in neurologic patients. However, the ability of the brain to adapt motor commands based on a perceived modified reality has not yet been fully explored. To fill this gap, we “tricked the brain” using immersive VR and investigated if multisensory feedback modulating the physical properties of an embodied avatar influences motor brain networks and control. Ten healthy participants were immersed in a virtual environment using an HMD, where they saw an avatar from first-person perspective. We slowly transformed the surface of the avatar (i.e., the “skin material”) from human to stone. We enforced this visual change by repetitively touching the real arm of the participant and the arm of the avatar with a (virtual) hammer, while progressively replacing the sound of the hammer against skin with stone hitting sound via loudspeaker. We applied single-pulse transcranial magnetic simulation (TMS) to evaluate changes in motor cortical excitability associated with the illusion. Further, to investigate if the “stone illusion” affected motor control, participants performed a reaching task with the human and stone avatar. Questionnaires assessed the subjectively reported strength of embodiment and illusion. Our results show that participants experienced the “stone arm illusion.” Particularly, they rated their arm as heavier, colder, stiffer, and more insensitive when immersed with the stone than human avatar, without the illusion affecting their experienced feeling of body ownership. Further, the reported illusion strength was associated with enhanced motor cortical excitability and faster movement initiations, indicating that participants may have physically mirrored and compensated for the embodied body characteristics of the stone avatar. Together, immersive VR has the potential to influence motor brain networks by subtly modifying the perception of reality, opening new perspectives for the motor recovery of patients.

Motor Cortical Excitability Changes in Preparation to Concentric and Eccentric Movements

Specific neural mechanisms operate at corticospinal levels during eccentric and concentric contractions. Here, we investigated the difference in corticospinal excitability (CSE) when preparing these two types of contraction. In this study we enrolled 16 healthy participants. They were asked to perform an instructed-delay reaction time (RT) task involving a concentric or an eccentric contraction of the right first dorsal interosseus muscle, as a response to a proprioceptive cue (Go signal) presented 1 s after a warning signal. We tested CSE at different time points ranging from 300 ms before up to 40 ms after a Go signal. CSE increased 300–150 ms before the Go signal for both contractions. Interestingly, significant changes in CSE in the time interval around the Go signal (from −150 ms to +40 ms) were only revealed in eccentric contraction. We observed a significant decrease in excitability immediately before the Go cue (Pre_50) and a significant increase 40 ms after it (Post_40) with respect to the MEPs recorded at Pre_150. Finally, CSE in eccentric contraction was lower before the Go cue (Pre_50) and greater after it (Post_40) compared to the concentric contraction. A similar result was also found in NoMov paradigm, used to disentangle the effects induced by movement preparation from those induced by the movement preparation linked to the proprioceptive cue. We could conclude that different neural mechanisms observed during concentric and eccentric contractions are mirrored with a different time-specific modulation of CSE in the preparatory phase to the movement.

Reduced Occipital Cortex Excitability in Amyotrophic Lateral Sclerosis.

In addition to motor cortex involvement, sensory abnormalities have been demonstrated in amyotrophic lateral sclerosis (ALS), including structural and metabolic alterations in the occipital cortex. The aim of this study was to examine occipital excitability changes in ALS. Twenty-one patients with ALS and 16 healthy subjects were enrolled into the study. Phosphene experience and phosphene threshold were studied to assess occipital excitability. Cognitive function was evaluated in both groups by means of Montreal Cognitive Assessment and Addenbrooke's Cognitive Examination-Revised visuospatial score tests. Phosphene was experienced in 13 (81.3%) healthy subjects and 9 (42.9%) patients with ALS ( P = 0.04). The mean phosphene threshold was not significantly different between the two groups. No correlation existed between phosphene threshold and motor cortical excitability parameters, ALS Functional Rating Scale Revised, Montreal Cognitive Assessment, and Addenbrooke's Cognitive Examination-Revised scores. Visual cortex is affected, and the occipital excitability is reduced in ALS, without any relation to motor cortical excitability changes, providing another clue suggestive of sensory involvement in ALS.

The influence of an acute bout of moderate-intensity cycling exercise on sensorimotor integration.

Acute cycling exercise can modulate motor cortical circuitry in the non-exercised upper-limb. Within the primary motor cortex, measures of intracortical inhibition are reduced and intracortical facilitation is enhanced following acute exercise. Further, acute cycling exercise decreases interhemispheric inhibition between the motor cortices and lowers cerebellar-to-motor cortex inhibition. Yet, investigations into the effects of acute exercise on sensorimotor integration, referring to the transfer of incoming afferent information from the primary somatosensory cortex to motor cortex, are lacking. The current work addresses this gap in knowledge with two experimental sessions. In the first session, we tested the exercise-induced changes in somatosensory and motor excitability by assessing somatosensory (SEP) and motor evoked potentials (MEPs). In the second session, we explored the effects of acute cycling exercise on short- (SAI) and long-latency afferent inhibition (LAI), and afferent facilitation. In both experimental sessions, neurophysiological measures were obtained from the non-exercised upper-limb muscle, tested at two time points pre-exercise separated by a 25-min period of rest. Next, a 25-min bout of moderate-intensity lower-limb cycling was performed with measures assessed at two time points post-exercise. Acute lower-limb cycling increased LAI, without modulation of SAI or afferent facilitation. Further, there were no exercise-induced changes to SEP or MEP amplitudes. Together, these results suggest that acute exercise has unique effects on sensorimotor integration, which are not accompanied by concurrent changes in somatosensory or motor cortical excitability.

The After-Effect of Accelerated Intermittent Theta Burst Stimulation at Different Session Intervals.

ObjectiveThe study aims to investigate the after-effect of three sessions of intermittent theta-burst stimulation (iTBS) on motor cortical excitability. The iTBS was induced over the primary motor cortex (M1) at different time intervals.MethodsThe study has a crossover design. Sixteen participants were assigned to three groups and received different accelerated iTBS (aiTBS) protocols during each visit: (1) three continuous sessions with no interval (iTBS18000); (2) three iTBS sessions with 10-min intervals (iTBS600 × 3∗10); and (3) three iTBS sessions with 30-min intervals (iTBS600 × 3∗30). As washout period, each visit is separated by at least 7 days. We measured the motor cortical excitability changes and intracortical inhibition.ResultsA dose of 1,800 pulses of aiTBS per day is tolerable. The iTBS1800 led to a reduced cortical excitability; whereas iTBS600 × 3∗10 and iTBS600 × 3∗30 enhanced cortical excitability to a differential extent. After a total dose of 1,800 pulses, iTBS600 × 3∗30 exhibited the longer effect and highest percentage of individuals with enhanced cortical excitability.ConclusionThe results suggest that aiTBS protocols at different time intervals result in different motor cortical excitability after-effects.

A new parameter to discriminate amyotrophic lateral sclerosis patients from healthy participants by motor cortical excitability changes.

We sought a combination of abnormalities to define a more sensitive measure of cortical excitability in amyotrophic lateral sclerosis (ALS). The automatic threshold tracking method was employed to assess the resting motor threshold, intracortical facilitation (ICF), short-interval intracortical inhibition (SICI), and short-interval intracortical faciilitation (SICF) in patients and controls. SICF at interstimulus intervals (ISI) between 1 and 1.8 ms and 2 and 3 ms as well as average SICI and SICI at ISIs of 1 and 2.5 ms were significantly reduced in ALS. The SICI curve was altered, displaying a solitary peak. Discriminant analysis revealed that the combination of SICI 2.5 ms and the mean SICF between 1 and 1.8 ms ISIs was the most sensitive parameter to distinguish patients with ALS from healthy participants. Along with the reduced SICI and its altered shape, connectivity between motor cortical circuits is changed in ALS. Combination with SICF increases the diagnostic utility of SICI in ALS.

Effects of L-DOPA on quadripulse magnetic stimulation–induced long-term potentiation in older adults

Reduced cortical plasticity has been previously reported in older adult as compared with young adults. However, the effects of dopamine on this plasticity reduction remain unknown. Here, we assessed the effects of high-dose (200 mg) and medium-dose (100 mg) L-3,4-dihydroxyphenylalanine (L-DOPA) intake on the long-term potentiation (LTP)-like effect induced by quadripulse magnetic stimulation (QPS) in older adults (aged ∼65 years). The subjects were 32 (200 mg) and 20 (100 mg) healthy older adult volunteers. This study was designed as a double-blind, crossover and placebo-controlled trial on one dose of L-dopa. Two hours after taking L-DOPA or placebo-drug, QPS was applied over the motor cortex. Motor evoked potentials were recorded to evaluate the motor cortical excitability changes. We found that both doses of L-DOPA enhanced LTP after QPS in older adults as one group. We classified subjects into QPS responders and QPS nonresponders. Both L-DOPA doses produced significant LTP enhancement in QPS nonresponders, whereas either of doses did not produce significant LTP enhancement in QPS responders. Collectively, our findings suggest that the neural plasticity reductions observed in older adults could be partly improved by dopamine.

Somatosensory cortical excitability changes precede those in motor cortex during human motor learning.

Motor learning is associated with plasticity in both motor and somatosensory cortex. It is known from animal studies that tetanic stimulation to each of these areas individually induces long-term potentiation in its counterpart. In this context it is possible that changes in motor cortex contribute to somatosensory change and that changes in somatosensory cortex are involved in changes in motor areas of the brain. It is also possible that learning-related plasticity occurs in these areas independently. To better understand the relative contribution to human motor learning of motor cortical and somatosensory plasticity, we assessed the time course of changes in primary somatosensory and motor cortex excitability during motor skill learning. Learning was assessed using a force production task in which a target force profile varied from one trial to the next. The excitability of primary somatosensory cortex was measured using somatosensory evoked potentials in response to median nerve stimulation. The excitability of primary motor cortex was measured using motor evoked potentials elicited by single-pulse transcranial magnetic stimulation. These two measures were interleaved with blocks of motor learning trials. We found that the earliest changes in cortical excitability during learning occurred in somatosensory cortical responses, and these changes preceded changes in motor cortical excitability. Changes in somatosensory evoked potentials were correlated with behavioral measures of learning. Changes in motor evoked potentials were not. These findings indicate that plasticity in somatosensory cortex occurs as a part of the earliest stages of motor learning, before changes in motor cortex are observed.NEW & NOTEWORTHY We tracked somatosensory and motor cortical excitability during motor skill acquisition. Changes in both motor cortical and somatosensory excitability were observed during learning; however, the earliest changes were in somatosensory cortex, not motor cortex. Moreover, the earliest changes in somatosensory cortical excitability predict the extent of subsequent learning; those in motor cortex do not. This is consistent with the idea that plasticity in somatosensory cortex coincides with the earliest stages of human motor learning.

Changes of motor cortical excitability and response inhibition in patients with obsessive–compulsive disorder

Deficits in cortical inhibitory processes have been suggested as underlying pathophysiological mechanisms of obsessive–compulsive disorder (OCD). We examined whether patients with OCD have altered cortical excitability using paired-pulse transcranial magnetic stimulation (TMS). We also tested associations between TMS indices and OCD-related characteristics, including age of onset and response inhibition in the go/no-go paradigm, to examine whether altered cortical excitability contributes to symptom formation and behavioural inhibition deficit in patients with OCD. We assessed motor cortex excitability using paired-pulse TMS in 51 patients with OCD and 39 age-matched healthy controls. We also assessed clinical symptoms and response inhibition in the go/nogo task. All patients were undergoing treatment with serotonin reuptake inhibitors. We performed repeated-measures multivariate analysis of covariance to compare TMS indices between patients with OCD and controls. Compared to controls, patients with OCD showed a shorter cortical silent period and decreased intracortical facilitation. However, we found no significant difference between groups for resting motor threshold or short-interval intracortical inhibition. In the OCD group, the shortened cortical silent period was associated with a prompt reaction time in the go/no-go task and with early onset of OCD. We could not exclude the influence of medications on motor cortex excitability. These findings suggest abnormal cortical excitability in patients with OCD. The associations between cortical silent period and response inhibition and age of onset further indicate that altered cortical excitability may play an important role in the development of OCD.

A short bout of high-intensity exercise alters ipsilesional motor cortical excitability post-stroke

ABSTRACTBackground: Acute exercise can increase motor cortical excitability and enhance motor learning in healthy individuals, an effect known as exercise priming. Whether it has the same effects in people with stroke is unclear.Objectives: The objective of this study was to investigate whether a short, clinically-feasible high-intensity exercise protocol can increase motor cortical excitability in non-exercised muscles of chronic stroke survivors.Methods: Thirteen participants with chronic, unilateral stroke participated in two sessions, at least one week apart, in a crossover design. In each session, they underwent either high-intensity lower extremity exercise or quiet rest. Motor cortical excitability of the extensor carpi radialis muscles was measured bilaterally with transcranial magnetic stimulation before and immediately after either exercise or rest. Motor cortical excitability changes (post-exercise or rest measures normalized to pre-test measures) were compared between exercise vs. rest conditions.Results: All participants were able to reach the target high-intensity exercise level. Blood lactate levels increased significantly after exercise (p < .001, d = 2.85). Resting motor evoked potentials from the lesioned hemisphere increased after exercise (mean 1.66; 95% CI: 1.19, 2.13) compared to the rest condition (mean 1.23; 95% CI: 0.64, 1.82), p = .046, d = 2.76, but this was not the case for the non-lesioned hemisphere (p = .406, d = 0.25).Conclusions: High-intensity exercise can increase lesioned hemisphere motor cortical excitability in a non-exercised muscle post-stroke. Our short and clinically-advantageous exercise protocol shows promise as a potential priming method in stroke rehabilitation.

Do inter-individual variations in electric fields affect motor cortical excitability changes following anodal tDCS?

Do inter-individual variations in electric fields affect motor cortical excitability changes following anodal tDCS?

Altered modulation of motor cortical excitability by electrical stimulation over the cerebellum in chronic migraine

Previous structural neuroimaging studies suggest that patients with chronic migraine (CM) with and without medication overuse have abnormal structural changes within the cerebellum. In humans, cerebellum exerts a suppressive effect on the contralateral motor cortical response through a cerebello-thalamo-cortical pathway. We recruited 10 patients affected from CM without medication overuse and 10 heathy volunteers (HVs). After a conditioning single pulse high-voltage electrical stimulation delivered over the posterior surface of the mastoid processes, a TMS pulse was delivered over the contralateral motor cortex with 5, 7, 10, and 15 ms interstimulus interval (ISI) in random order. Motor cortical excitability changes were evaluated by amplitude changes of EMG responses from the FDI muscle to motor cortical stimulation. In HVs, suppression occurred at ISI of 5 ms and lasted few milliseconds. In CM patients, conditioning electric stimulation over the cerebellum did not reduce the size of MEPs to test TMS of the motor cortex at conditioning-test intervals of 5 ms. Here, we found neurophysiological evidence for dysfunctional cerebello-thalamo-cortical inhibitory pathway in CM. Whether these functional abnormalities are due to primary abnormal cerebellar inhibitory dysfunction or are secondary to a disrupted cerebellar-thalamic-cortical connectivity, remains to be determined.

Changes in motor cortical excitability in schizophrenia following transcranial direct current stimulation

Schizophrenia is a disorder associated with cortical inhibition deficits. Transcranial direct current stimulation (tDCS) induces changes in cortical excitability in healthy subjects and individuals with neuropsychiatric disorders depending on the stimulation parameters. Our aim was to investigate whether a previously published tDCS protocol associated with symptomatic improvement in schizophrenia would induce changes in motor cortical excitability, assessed by transcranial magnetic stimulation paradigms, i.e., short-interval intracortical inhibition (SICI) and intra-cortical facilitation (ICF). We assessed cortical excitability measurements in 48 subjects with schizophrenia before and after a single session of active tDCS (20 min, 2 mA, anode over left dorsolateral prefrontal cortex, cathode over left temporoparietal cortex) or sham. Those who received active tDCS had a significant increase of SICI in the left motor cortex compared to those who received sham stimulation (Cohen's d = 0.54, p = .019). No changes were observed for ICF. In addition, lower SICI was associated with higher age (β = −0.448, p < .01). Increase in intracortical inhibition may indicate a mechanism of action of tDCS in this population. Future studies should investigate whether this finding is a biomarker of treatment response for schizophrenia.

S153. Changes of triad-conditioning facilitation in various neurological disorders

Recently, we have reported a triad-conditioning transcranial magnetic stimulation technique (TMS). In this technique, the intercortical facilitation is induced by 40 Hz (interval 25 ms) triad-conditioning stimulation in healthy volunteers, which may reflect the intrinsic rhythm of the primary motor cortex (M1). We used this method to study some changes in M1 in various neurological disorders. Participants were 7 cortical myoclonus, 13 Parkinson’s disease (PD), 13 amyotrophic lateral sclerosis (ALS), 5 focal dystonia and 14 healthy volunteers. Three conditioning stimuli over the primary motor cortex at an intensity of 110% active motor threshold preceded the supra-threshold test TMS at various inter-stimulus intervals corresponding to 10–200 Hz. Amplitude of conditioned motor evoked potentials (MEPs) was compared with the unconditioned MEPs. The facilitation by 40 Hz (gamma rhythm) triad-conditioning TMS observed in healthy volunteers was absent in patients with cortical myoclonus and PD, and reduced in ALS. Normal facilitation was induced in focal dystonia. In cortical myoclonus, facilitation was induced by 25 Hz (beta rhythm) conditioning stimulation. In PD, suppression was induced by 20–33 Hz (beta rhythm) conditioning stimuli. The changes in the triad conditioning facilitation shown above may be explained as follows. In cortical myoclonus, beta rhythms (25 Hz) is probably more preferential than gamma rhythms (40 Hz) due to dysfunction of inhibitory interneurons. The suppression in PD may be explained by abnormal beta rhythm itself. The reduction of 40 Hz triad facilitation may be explained by output cell dysfunction without any rhythm changes in ALS. This technique should give some new additional information about the motor cortical excitability changes in humans.

Recovery of the 20 Hz Rebound to Tactile and Proprioceptive Stimulation after Stroke.

Sensorimotor integration is closely linked to changes in motor-cortical excitability, observable in the modulation of the 20 Hz rhythm. After somatosensory stimulation, the rhythm transiently increases as a rebound that reflects motor-cortex inhibition. Stroke-induced alterations in afferent input likely affect motor-cortex excitability and motor recovery. To study the role of somatosensory afferents in motor-cortex excitability after stroke, we employed magnetoencephalographic recordings (MEG) at 1–7 days, one month, and 12 months in 23 patients with stroke in the middle cerebral artery territory and 22 healthy controls. The modulation of the 20 Hz motor-cortical rhythm was evaluated to two different somatosensory stimuli, tactile stimulation, and passive movement of the index fingers. The rebound strengths to both stimuli were diminished in the acute phase compared to the controls and increased significantly during the first month after stroke. However, only the rebound amplitudes to tactile stimuli fully recovered within the follow-up period. The rebound strengths in the affected hemisphere to both stimuli correlated strongly with the clinical scores across the follow-up. The results show that changes in the 20 Hz rebound to both stimuli behave similarly and occur predominantly during the first month. The 20 Hz rebound is a potential marker for predicting motor recovery after stroke.

P344 Motor cortical excitability changes in early stage ALS patients using automatic threshold tracking method

Objectives to determine motor cortical excitability changes in early stage ALS patients. Methods Twenty-seven ALS patients were recruited the study. The mean age was 55.2 years and seven patients were female. Cortical excitability tests performed on the diagnostic stage of the disease. Investigated cortical excitability parameters were; resting motor threshold: (RMT), short interval intracortical inhibition (SICI), short interval intracortical facilitation (SICF) and intracortical facilitation (ICF). Results Mean RMT was 60.1 ± 2.2% MSO for ALS patients, 52.9 ± 3.1% for control group. There was not significant difference between two groups ( p > 0.05 ). Factor analysis of SICI resulted in two factors with eigenvalues more than 1. In the calculation of factor 1 (SICI1-2.5 ms) values, short ISI values have more weight than long ISI values. The opposite was true for factor 2. (SICI2.5-5 ms). Mean SICI1-2.5 msvalues were 11.3 ± 11.7 in ALS group and 74.3 ± 9.9 in control group ( p 0.05 ) while mean SICI2.5-5 ms were 10.6 ± 9.7 in ALS group and 67.8 ± 9.8 in control group ( p 0.05 ). Factor analysis of SICF and ICF resulted in two factor with eigenvalues more than 1. There were no significant difference between two groups any of these two factors both for SICF and ICF ( p > 0.05 ). Comment SICI values are significantly reduced in ALS patients at the early stage of the disease. Significance SICI analysis with automatic threshold tracking method may have potential role for diagnosis of ALS. Reliability and reproducibility of this test should be performed before using it as a diagnostic test.