Synchronization of neuronal activity in the human primary motor cortex by transcranial magnetic stimulation: an EEG study.
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Using multichannel electroencephalography (EEG), we investigated temporal dynamics of the cortical response to transcranial magnetic stimulation (TMS). TMS was applied over the left primary motor cortex (M1) of healthy volunteers, intermixing single suprathreshold pulses with pairs of sub- and suprathreshold pulses and simultaneously recording EEG from 60 scalp electrodes. Averaging of EEG data time locked to the onset of TMS pulses yielded a waveform consisting of a positive peak (30 ms after the pulse P30), followed by two negative peaks [at 45 (N45) and 100 ms]. Peak-to-peak amplitude of the P30-N45 waveform was high, ranging from 12 to 70 microV; in most subjects, the N45 potential could be identified in single EEG traces. Spectral analysis revealed that single-pulse TMS induced a brief period of synchronized activity in the beta range (15-30 Hz) in the vicinity of the stimulation site; again, this oscillatory response was apparent not only in the EEG averages but also in single traces. Both the N45 and the oscillatory response were lower in amplitude in the 12-ms (but not 3-ms) paired-pulse trials, compared with the single-pulse trials. These findings are consistent with the possibility that TMS applied to M1 induces transient synchronization of spontaneous activity of cortical neurons within the 15- to 30-Hz frequency range. As such, they corroborate previous studies of cortical oscillations in the motor cortex and point to the potential of the combined TMS/EEG approach for further investigations of cortical rhythms in the human brain. (+info)
Primary lateral sclerosis: clinical, neurophysiological, and magnetic resonance findings.
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OBJECTIVE: To describe the clinical, neurophysiological, and MRI findings in 10 patients with primary lateral sclerosis (PLS). RESULTS: The course of the disease was very slowly progressive. Spasticity due to upper motor neuron dysfunction was the most prominent sign, but EMG showed slight lower motor neuron signs, such as a mixed pattern on maximal voluntary contraction and enlarged motor unit potentials. One patient had clinically mild lower motor neuron involvement. Central motor conduction times (CMCT) were more prolonged in PLS than is the case in ALS. Minor sensory signs were found on neurophysiological examination, comparable with those in ALS. In four patients serum creatine kinase activity was raised. On MRI cortical atrophy was seen, most pronounced in the precentral gyrus and expanding into the parietal-occipital region. CONCLUSIONS: PLS is a distinct clinical syndrome, part of the range of motor neuron diseases. Besides pronounced upper motor neuron symptoms, mild lower motor neuron symptoms can also be found, as well as (subclinical) sensory symptoms. PLS can be distinguished from ALS by its slow clinical course, a severely prolonged MEP, and a more extensive focal cortical atrophy. (+info)
Visual and motor evoked potentials in the course of multiple sclerosis.
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While evoked potentials are sensitive tools for diagnosing multiple sclerosis, little is known about their prognostic value and their role in determining the course of the disease. To validate the visual and motor evoked potentials (VEP and MEP) as measures for the course of multiple sclerosis, we examined prospectively 30 patients with relapsing-remitting or secondary progressive multiple sclerosis. The Expanded Disability Status Scale (EDSS), VEP and MEP were measured at entry and after 6, 12 and 24 months. The Spearman rank correlation was used for statistical analysis. Applying multiple regression in 15 randomized patients allowed derivation of a formula for predicting changes in EDSS score based on changes in MEP and VEP. Validation was done by comparing the predicted with the real changes in EDSS in the other 15 patients. The number of pathological VEP and MEP results correlated at all four measurement points with the EDSS (rho > or = 0.6, P < or = 0.01). When the latencies of VEP and MEP were combined using the sum of their Z scores, correlation with the EDSS was even more significant (rho > or = 0.6, P < 0.001). Changes over time of electrophysiological data and EDSS were also correlated (rho = 0.43, P < 0.05). Moreover, VEP and MEP at baseline correlated with the EDSS after 2 years (rho = 0.43,P = 0.03). Reliable prediction of the course of multiple sclerosis for individual patients is not possible from VEP and MEP data. However, we conclude that, for groups of patients with secondary progressive or relapsing-remitting multiple sclerosis the combined testing of VEP and MEP yields numerical data that allow objective estimation of the course and prognosis of the disease. (+info)
Cervical sprouting of corticospinal fibers after thoracic spinal cord injury accompanies shifts in evoked motor responses.
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The adult central nervous system (CNS) of higher vertebrates displays a limited ability for self repair after traumatic injuries, leading to lasting functional deficits [1]. Small injuries can result in transient impairments, but the mechanisms of recovery are poorly understood [2]. At the cortical level, rearrangements of the sensory and motor representation maps often parallel recovery [3,4]. In the sensory system, studies have shown that cortical and subcortical mechanisms contribute to map rearrangements [5,6], but for the motor system the situation is less clear. Here we show that large-scale structural changes in the spared rostral part of the spinal cord occur simultaneously with shifts of a hind-limb motor cortex representation after traumatic spinal-cord injury. By intracortical microstimulation, we defined a cortical area that consistently and exclusively yielded hind-limb muscle responses in normal adult rats. Four weeks after a bilateral transsection of the corticospinal tract (CST) in the lower thoracic spinal cord, we again stimulated this cortical field and found forelimb, whisker, and trunk responses, thus demonstrating reorganization of the cortical motor representation. Anterograde tracing of corticospinal fibers originating from this former hind-limb area revealed that sprouting greatly increased the normally small number of collaterals that lead into the cervical spinal cord rostral to the lesion. We conclude that the corticospinal motor system has greater potential to adapt structurally to lesions than was previously believed and hypothesize that this spontaneous growth response is the basis for the observed motor representation rearrangements and contributes to functional recovery after incomplete lesions. (+info)
Prevention of spinal cord injury with time-frequency analysis of evoked potentials: an experimental study.
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OBJECTIVES: To verify the applicability and validity of time-frequency analysis (TFA) of evoked potential (EP) signals in detecting the integrity of spinal cord function and preventing spinal cord injury. METHODS: The spinal cord was simulated during surgery in 20 mature rats by mechanically damaging the spinal cord. Cortical somatosensory evoked potential (CSEP), spinal somatosensory evoked potential (SSEP), cortical motor evoked potential (CMEP), and spinal cord evoked potential (SCEP) were used to monitor spinal cord function. Short time Fourier transform (STFT) was applied to the CSEP signal, and cone shaped distribution (CSD) was used as the TFA algorithm for SSEP, CMEP, and SCEP signals. The changes in the latency and amplitude of EP signals were measured in the time domain, and peak time, peak frequency, and peak power were measured in the time-frequency distribution (TFD). RESULTS: The TFDs of EPs were found to concentrate in a certain location under normal conditions. When injury occurred, the energy decreased in peak power, and there was a greater dispersion of energy across the time-frequency range. Strong relations were found between latency and peak time, and amplitude and peak power. However, the change in peak power after injury was significantly larger than the corresponding change in amplitude (p<0.001 by ANOVA). CONCLUSIONS: It was found that TFA of EPs provided an earlier and more sensitive indication of injury than time domain monitoring alone. It is suggested that TFA of EP signals should therefore be useful in preventing spinal cord injury during surgery. (+info)
Reduced excitability of the motor cortex in untreated patients with de novo idiopathic "grand mal" seizures.
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OBJECTIVES: Transcranial magnetic stimulation (TMS) was used to investigate motor cortex excitability, intracortical excitatory, and inhibitory pathways in 18 patients having experienced a first "grand mal" seizure within 48 hours of the electrophysiological test. All had normal brain MRI, and were free of any treatment, drug, or alcohol misuse. Results were compared with those of 35 age matched normal volunteers. METHODS: The following parameters of responses to TMS were measured: motor thresholds at rest and with voluntary contraction, amplitudes of responses, cortical silent periods, and responses to paired pulse stimulation with interstimulus intervals of 1 to 20 ms. RESULTS: In patients, there were significantly increased motor thresholds with normal amplitudes of motor evoked potentials (MEPs), suggesting decreased cortical excitability. Cortical silent periods were not significantly different from those of normal subjects. Paired TMS with short interstimulus intervals (1-5 ms) induced normal inhibition of test MEPs, suggesting preserved function of GABAergic intracortical inhibitory interneurons. On the contrary, the subsequent period of MEP facilitation found in normal subjects (ISIs of 6-20 ms) was markedly reduced in patients. This suggests the existence of abnormally prolonged intracortical inhibition or deficient intracortical excitation. In nine patients retested 2 to 4 weeks after the initial seizure, these abnormalities persisted, although to a lesser extent. CONCLUSION: The present findings together with abnormally high motor thresholds could represent protective mechanisms against the spread or recurrence of seizures. (+info)
Cortical excitability and sleep deprivation: a transcranial magnetic stimulation study.
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The objective was to assess the changes in cortical excitability after sleep deprivation in normal subjects. Sleep deprivation activates EEG epileptiform activity in an unknown way. Transcranial magnetic stimulation (TMS) can inform on the excitability of the primary motor cortex. Eight healthy subjects (four men and four women) were studied. Transcranial magnetic stimulation (single and paired) was performed by a focal coil over the primary motor cortex, at the "hot spot" for the right first dorsal interosseous muscle. The following motor evoked potential features were measured: (a) active and resting threshold to stimulation; (b) duration of the silent period; (c) amount of intracortical inhibition on paired TMS at the interstimulus intervals of 2 and 3 ms and amount of facilitation at interstimulus intervals of 14 and 16 ms. The whole TMS session was repeated after a sleep deprivation of at least 24 hours. After the sleep deprivation, the threshold to stimulation (in the active and resting muscle), as well as the silent period, did not change significantly. By contrast, the paired stimulus study showed a significant (p<0.05) reduction in both intracortical inhibition and facilitation. Thus, TMS showed that sleep deprivation is associated with changes in inhibition-facilitation balance in the primary motor cortex of normal subjects. These changes might have a link with the background factors of the "activating" effects of sleep deprivation. (+info)
Mechanisms of motor-evoked potential facilitation following prolonged dual peripheral and central stimulation in humans.
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1. Repetitive electrical peripheral nerve or muscle stimulation can induce a lasting increase in the excitability of the corticomotor projection. By pairing peripheral stimulation with transcranial magnetic brain stimulation it is possible to shorten the duration of stimulation needed to induce this effect. This ability to induce excitability changes in the motor cortex may be of significance for the rehabilitation of brain-injured patients. The mechanisms responsible for the increases in excitability have not been investigated thoroughly. 2. Using two paired transcranial magnetic stimuli protocols we investigated the excitability of intracortical inhibitory and excitatory systems before and following a period of repetitive dual muscle and brain stimulation. The dual stimulation consisted of motor point stimulation of first dorsal interosseous (FDI; 10 Hz trains of 1 ms square waves for 500 ms) delivered at one train every 10 s, paired with single transcranial magnetic stimulation given 25 ms after the onset of the train. 3. Following 30 min of dual stimulation, motor-evoked potentials (MEPs) were significantly increased in amplitude. During this period of MEP facilitation there was no significant difference in the level of intracortical inhibition. There was, however, a significant increase in the intracortical facilitation demonstrated with paired magnetic stimuli. The increase in facilitation was seen only at short interstimulus intervals (0.8-2.0 ms). These intervals comprised a peak in the time course of facilitation, which is thought to reflect I wave interaction within the motor cortex. 4. The relevance of this finding to the MEP facilitation seen following dual peripheral and central stimulation is discussed. (+info)