Spinal cord-evoked potentials and muscle responses evoked by transcranial magnetic stimulation in 10 awake human subjects.
(1/997)
Transcranial magnetic stimulation (TCMS) causes leg muscle contractions, but the neural structures in the brain that are activated by TCMS and their relationship to these leg muscle responses are not clearly understood. To elucidate this, we concomitantly recorded leg muscle responses and thoracic spinal cord-evoked potentials (SCEPs) after TCMS for the first time in 10 awake, neurologically intact human subjects. In this report we provide evidence of direct and indirect activation of corticospinal neurons after TCMS. In three subjects, SCEP threshold (T) stimulus intensities recruited both the D wave (direct activation of corticospinal neurons) and the first I wave (I1, indirect activation of corticospinal neurons). In one subject, the D, I1, and I2 waves were recruited simultaneously, and in another subject, the I1 and I2 waves were recruited simultaneously. In the remaining five subjects, only the I1 wave was recruited first. More waves were recruited as the stimulus intensity increased. The presence of D and I waves in all subjects at low stimulus intensities verified that TCMS directly and indirectly activated corticospinal neurons supplying the lower extremities. Leg muscle responses were usually contingent on the SCEP containing at least four waves (D, I1, I2, and I3). (+info)
A clinical study of motor evoked potentials using a triple stimulation technique.
(2/997)
Amplitudes of motor evoked potentials (MEPs) are usually much smaller than those of motor responses to maximal peripheral nerve stimulation, and show marked variation between normal subjects and from one stimulus to another. Consequently, amplitude measurements have low sensitivity to detect central motor conduction failures due to the broad range of normal values. Since these characteristics are mostly due to varying desynchronization of the descending action potentials, causing different degrees of phase cancellation, we applied the recently developed triple stimulation technique (TST) to study corticospinal conduction to 489 abductor digiti minimi muscles of 271 unselected patients referred for possible corticospinal dysfunction. The TST allows resynchronization of the MEP, and thereby a quantification of the proportion of motor units activated by the transcranial stimulus. TST results were compared with those of conventional MEPs. In 212 of 489 sides, abnormal TST responses suggested conduction failure of various degrees. By contrast, conventional MEPs detected conduction failures in only 77 of 489 sides. The TST was therefore 2.75 times more sensitive than conventional MEPs in disclosing corticospinal conduction failures. When the results of the TST and conventional MEPs were combined, 225 sides were abnormal: 145 sides showed central conduction failure, 13 sides central conduction slowing and 67 sides both conduction failure and slowing. It is concluded that the TST is a valuable addition to the study of MEPs, since it improves detection and gives quantitative information on central conduction failure, an abnormality which appears to be much more frequent than conduction slowing. This new technique will be useful in following the natural course and the benefit of treatments in disorders affecting central motor conduction. (+info)
Corticospinal excitability modulation to hand muscles during movement imagery.
(3/997)
Motor evoked potentials (MEPs) to magnetic transcranial stimulation (TCS) were recorded from right abductor digiti minimi (ADM) and first dorsal interosseous (FDI) muscles, sharing the same peripheral innervation but engaged in two different motor demands. In seven healthy and trained subjects, the latencies, amplitudes and variability of MEPs were investigated under the following, randomly intermingled, conditions: full muscular and mental relaxation; mental simulation of selective index finger or little finger abduction; mental non-motor activity (arithmetical calculation); and real motor task (little and index finger abduction). The whole procedure was performed by continuous audiovisual monitoring of electromyographic 'silence' in the tested muscles. The maximal facilitatory effects (= latency shortening and amplitude increase) on MEPs were induced by the real motor task. An amplitude potentiation of MEPs in both tested muscles was present during non-motor mental activity, in comparison to basal values. A further amplitude potentiation, without latency shifts, was confined to the muscle acting as 'prime mover' for the mentally simulated movement, according to the motor program dispatched but not executed by the subject. Similar results were also found in the F-wave, showing that mental simulation affects spinal motoneuronal excitability as well, although -- due to the lack of MEP and F-wave latency shift -- the main effect takes place at cortical level. The study shows that movement imagery can focus specific facilitation on the prime-mover muscle for the mentally simulated movement. This is mainly evident on FDI muscle, which controls fingers (i.e. the index) with highly corticalized motor representation. (+info)
Axon guidance of outgrowing corticospinal fibres in the rat.
(4/997)
This review is concerned with the development of the rat corticospinal tract (CST). The CST is a long descending central pathway, restricted to mammals, which is involved both in motor and sensory control. The rat CST is a very useful model in experimental research on the development of fibre systems in mammals because of its postnatal outgrowth throughout the spinal cord as well as its experimental accessibility. Hence mechanisms underlying axon outgrowth and subsequent target cell finding can be studied relatively easily. In this respect the corticospinal tract forms an important example and model system for the better understanding of central nervous system development in general. (+info)
Brief theta-burst stimulation induces a transcription-dependent late phase of LTP requiring cAMP in area CA1 of the mouse hippocampus.
(5/997)
Memory storage in the mammalian brain can be divided into a short-term phase that is independent of new protein synthesis and a long-term phase that requires synthesis of new RNA and proteins. A cellular model for these two phases has emerged from studies of long-term potentiation (LTP) in the three major excitatory synaptic pathways in the hippocampus. One especially effective protocol for inducing robust and persistent LTP is "theta-burst" stimulation, which is designed to mimic the firing patterns of hippocampal neurons recorded during exploratory behavior in intact awake animals. Unlike LTP induced by non-theta tetanization regimens, little is known about the biochemical mechanisms underlying theta-burst LTP in the hippocampus. In the present study, we examined theta-burst LTP in the Schaffer collateral pathway. We found that 3 sec of theta-burst stimulation induced a robust and persistent potentiation (theta L-LTP) in mouse hippocampal slices. This theta L-LTP was dependent on NMDA receptor activation. The initial or early phase of theta-LTP did not require either protein or RNA synthesis and was independent of cAMP-dependent protein kinase (PKA) activation. In contrast, the late phase of theta-LTP required synthesis of proteins and RNA and was blocked by inhibitors of PKA. Prior induction of theta-LTP also occluded the potentiation elicited by chemical activation of PKA. Our results show that, like non-theta LTP, theta-induced LTP in area CA1 of the mouse hippocampus also involves transcription, translation, and PKA and suggest that cAMP-mediated gene transcription may be a common mechanism responsible for the late phases of LTP induced by both theta and non-theta patterns of stimulation. (+info)
Reactive oxygen species mediate activity-dependent neuron-glia signaling in output fibers of the hippocampus.
(6/997)
Nonsynaptic signaling is becoming increasingly appreciated in studies of activity-dependent changes in the nervous system. We investigated the types of neuronal activity that elicit nonsynaptic communication between neurons and glial cells in hippocampal output fibers. High-frequency, but not low-frequency, action potential firing in myelinated CA1 axons of the hippocampus resulted in increased phosphorylation of the oligodendrocyte-specific protein myelin basic protein (MBP). This change was blocked by tetrodotoxin, indicating that axonally generated action potentials were necessary to regulate the phosphorylation state of MBP. Furthermore, scavengers of the reactive oxygen species superoxide and hydrogen peroxide and nitric oxide synthase inhibitors prevented activation of this neuron-glia signaling pathway. These results indicate that, during periods of increased neuronal activity in area CA1 of the hippocampus, reactive oxygen and nitrogen species are generated, which diffuse to neighboring oligodendrocytes and result in post-translational modifications of MBP, a key structural protein in myelin. Thus, in addition to their well-known capacity for activity-dependent neuron-neuron signaling, hippocampal pyramidal neurons possess a mechanism for activity-dependent neuron-glia signaling. (+info)
Inosine stimulates extensive axon collateral growth in the rat corticospinal tract after injury.
(7/997)
The purine nucleoside inosine has been shown to induce axon outgrowth from primary neurons in culture through a direct intracellular mechanism. For this study, we investigated the effects of inosine in vivo by examining whether it would stimulate axon growth after a unilateral transection of the corticospinal tract. Inosine applied with a minipump to the rat sensorimotor cortex stimulated intact pyramidal cells to undergo extensive sprouting of their axons into the denervated spinal cord white matter and adjacent neuropil. Axon growth was visualized by anterograde tracing with biotinylated dextran amine and by immunohistochemistry with antibodies to GAP-43. Thus, inosine, a naturally occurring metabolite without known side effects, might help to restore essential circuitry after injury to the central nervous system. (+info)
MR-revealed myelination in the cerebral corticospinal tract as a marker for Pelizaeus-Merzbacher's disease with proteolipid protein gene duplication.
(8/997)
BACKGROUND AND PURPOSE: Pelizaeus-Merzbacher's disease (PMD) is caused by mutations in the proteolipid protein (PLP) gene. Recent studies have shown that an increased PLP dosage, resulting from total duplication of the PLP gene, invariably causes the classic form of PMD. The purpose of this study was to compare the MR findings of PMD attributable to PLP duplication with those of PMD arising from a missense mutation. METHODS: Seven patients with PMD, three with a PLP missense mutation in either exon 2 or 5 (patients 1-3), and four with PLP duplication (patient 4 having larger PLP duplication than patients 5-7) were clinically classified as having either the classic or connatal form of PMD. Cerebral MR images were obtained to analyze the presence of myelination and T1 and T2 shortening in the deep gray matter. Multiple MR studies were performed in six of the seven patients to analyze longitudinal changes. RESULTS: Four patients (patients 1-4) were classified as having connatal PMD, whereas the other three (patients 5-7) were classified as having classic PMD. Myelination in the cerebral corticospinal tract, optic radiation, and corpus callosum was observed in three cases of classic PMD with PLP duplication. In patient 4, myelination extended to the internal capsule, corona radiata, and centrum semiovale over a 3-year period. No myelination was observed in three PMD cases with a PLP point mutation. T2 shortening in the deep gray matter was recognized in all patients with PMD. CONCLUSION: The presence of myelination in the cerebral corticospinal tract with diffuse white matter hypomyelination on MR images could be a marker for PMD with PLP duplication. It is suggested that progression of myelination may be present in connatal PMD with large PLP duplication. (+info)