Peripheral Conduction Time Research Articles

Voluntary contraction shortens peripheral conduction time in response to transcranial magnetic stimulation of the brain

We investigated the effects of voluntary contraction on peripheral conduction time in response to transcranial magnetic stimulation (TMS) of the brain in 10 normal subjects. We obtained surface recordings of compound muscle action potentials (CMAP) from the abductor digiti minimi muscle (ADM) and nerve action potentials (NAP) from the ulnar nerve, at rest and during contraction (10% of maximal voluntary contraction) in response to TMS delivered at 100% output using a coil shaped like a figure 8. The distance between the two recording electrodes was 10 cm. The distal latency in response to TMS was calculated by subtracting the NAP latency from the CMAP latency. Distal latency was also measured by recording ADM responses to supramaximal electrical stimulation (ES) 10 cm proximal to the recording electrode. TMS-induced distal latency was significantly shorter during voluntary contraction than at rest ( P < 0.00001). There was no significant difference between TMS-induced distal latency during contraction and ES-induced distal latency. TMS-induced distal latencies at rest and during contraction were correlated with the ES-induced distal latencies ( r 2 = 0.468, P = 0.028 and r 2 = 0.769, P = 0.0009, respectively). Our results showed that the peripheral conduction time in response to TMS was related to the activity of the target muscle and to the fastest conduction velocity of the target nerve. Voluntary contraction reduced the peripheral conduction time in response to TMS.

Effect of stimulus intensity and voluntary contraction on corticospinal potentials following transcranial magnetic stimulation

Following magnetic transcranial stimulation, motor-evoked potentials (MEPs) from the abductor digiti minimi muscle, and evoked spinal cord potentials (ESCPs) from the cervical epidural space were recorded simultaneously in 9 subjects in the awake and anesthetized condition. In the awake condition, during voluntary contraction, one (n = 5) or two (n = 4) components of the ESCPs were elicited at the threshold stimulus intensity of the MEPs. As the stimulus intensity increased, an early response (n = 7) and multiple late components were recorded. The first component at high stimulus output (average 80%) preceded the small potentials elicited at threshold stimulus intensity. The latency of each component of the ESCPs during voluntary contraction was the same as that during the resting condition. In addition, the enhancement of amplitude of the ESCPs during voluntary contraction was not significant compared with that recorded at rest. During general anesthesia with volatile anesthetics, the first component of the ESCPs could be elicited at high stimulus intensity, but later components were markedly attenuated. In paired transcranial magnetic stimulation, the amplitude of this first potential following the test stimulus completely recovered within the 2 ms interstimulus interval. From these results, we hypothesized that the first component was generated non-synaptically (D-wave), but later components were generated transsynaptically (I-waves). Compound muscle action potentials (CMAPs) and F-waves also were recorded following supramaximal ulnar nerve stimulation at the wrist. Peripheral conduction time, which included synaptic delay in spinal motor neurons, was measured as follows (latency of CMAPs + latency of F-wave +1)/2 (ms). The central motor conduction time (CMCT) was measured by subtracting the peripheral conduction time from the onset latency of the MEP at high stimulus intensity in the awake state. During voluntary contraction, the calculated CMCT (4.9 ± 1.0 ms) was the same as the onset latency of the second component of the ESCPs (I-wave, 4.3 ± 0.2 ms) recorded from the C6-C6/7 epidural space. These results suggest that transcranial magnetic stimulation generates I-waves preferentially when the stimulus intensity was set at just the threshold level of the MEPs during voluntary contraction in the awake condition. At high stimulus intensity, transcranial magnetic stimulation can elicit both D- and I-waves, but most spinal cells require I-wave activation to fire. Facilitatory effects of voluntary contraction on the muscle response following transcranial magnetic stimulation mainly originates at a spinal level.

Effect of stimulus intensity and voluntary contraction on corticospinal potentials following transcranial magnetic stimulation

Following magnetic transcranial stimulation, motor-evoked potentials (MEPs) from the abductor digiti minimi muscle, and evoked spinal cord potentials (ESCPs) from the cervical epidural space were recorded simultaneously in 9 subjects in the awake and anesthetized condition. In the awake condition, during voluntary contraction, one ( n = 5) or two ( n = 4) components of the ESCPs were elicited at the threshold stimulus intensity of the MEPs. As the stimulus intensity increased, an early response ( n = 7) and multiple late components were recorded. The first component at high stimulus output (average 80%) preceded the small potentials elicited at threshold stimulus intensity. The latency of each component of the ESCPs during voluntary contraction was the same as that during the resting condition. In addition, the enhancement of amplitude of the ESCPs during voluntary contraction was not significant compared with that recorded at rest. During general anesthesia with volatile anesthetics, the first component of the ESCPs could be elicited at high stimulus intensity, but later components were markedly attenuated. In paired transcranial magnetic stimulation, the amplitude of this first potential following the test stimulus completely recovered within the 2 ms interstimulus interval. From these results, we hypothesized that the first component was generated non-synaptically (D-wave), but later components were generated transsynaptically (I-waves). Compound muscle action potentials (CMAPs) and F-waves also were recorded following supramaximal ulnar nerve stimulation at the wrist. Peripheral conduction time, which included synaptic delay in spinal motor neurons, was measured as follows (latency of CMAPs + latency of F-wave +1)/2 (ms). The central motor conduction time (CMCT) was measured by subtracting the peripheral conduction time from the onset latency of the MEP at high stimulus intensity in the awake state. During voluntary contraction, the calculated CMCT (4.9 ± 1.0 ms) was the same as the onset latency of the second component of the ESCPs (I-wave, 4.3 ± 0.2 ms) recorded from the C6-C6/7 epidural space. These results suggest that transcranial magnetic stimulation generates I-waves preferentially when the stimulus intensity was set at just the threshold level of the MEPs during voluntary contraction in the awake condition. At high stimulus intensity, transcranial magnetic stimulation can elicit both D- and I-waves, but most spinal cells require I-wave activation to fire. Facilitatory effects of voluntary contraction on the muscle response following transcranial magnetic stimulation mainly originates at a spinal level.

Clinical usefulness of ulnar motor responses recording from first dorsal interosseous

Following magnetic transcranial stimulation, motor-evoked potentials (MEPs) from the abductor digiti minimi muscle, and evoked spinal cord potentials (ESCPs) from the cervical epidural space were recorded simultaneously in 9 subjects in the awake and anesthetized condition. In the awake condition, during voluntary contraction, one (n = 5) or two (n = 4) components of the ESCPs were elicited at the threshold stimulus intensity of the MEPs. As the stimulus intensity increased, an early response (n = 7) and multiple late components were recorded. The first component at high stimulus output (average 80%) preceded the small potentials elicited at threshold stimulus intensity. The latency of each component of the ESCPs during voluntary contraction was the same as that during the resting condition. In addition, the enhancement of amplitude of the ESCPs during voluntary contraction was not significant compared with that recorded at rest. During general anesthesia with volatile anesthetics, the first component of the ESCPs could be elicited at high stimulus intensity, but later components were markedly attenuated. In paired transcranial magnetic stimulation, the amplitude of this first potential following the test stimulus completely recovered within the 2 ms interstimulus interval. From these results, we hypothesized that the first component was generated non-synaptically (D-wave), but later components were generated transsynaptically (I-waves). Compound muscle action potentials (CMAPs) and F-waves also were recorded following supramaximal ulnar nerve stimulation at the wrist. Peripheral conduction time, which included synaptic delay in spinal motor neurons, was measured as follows (latency of CMAPs + latency of F-wave +1)/2 (ms). The central motor conduction time (CMCT) was measured by subtracting the peripheral conduction time from the onset latency of the MEP at high stimulus intensity in the awake state. During voluntary contraction, the calculated CMCT (4.9 ± 1.0 ms) was the same as the onset latency of the second component of the ESCPs (I-wave, 4.3 ± 0.2 ms) recorded from the C6-C6/7 epidural space. These results suggest that transcranial magnetic stimulation generates I-waves preferentially when the stimulus intensity was set at just the threshold level of the MEPs during voluntary contraction in the awake condition. At high stimulus intensity, transcranial magnetic stimulation can elicit both D- and I-waves, but most spinal cells require I-wave activation to fire. Facilitatory effects of voluntary contraction on the muscle response following transcranial magnetic stimulation mainly originates at a spinal level.

Vincristine therapy for children with acute lymphoblastic leukemia impairs conduction in the entire peripheral nerve

Somatosensory evoked potentials were measured prospectively in 38 children with acute lymphoblastic leukemia to evaluate the side effects of vincristine therapy on conduction of the peripheral nerves. Nineteen patients at standard risk received vincristine 12 mg/m 2 during induction therapy and 19 patients at intermediate or high risk received 6 mg/m 2 during induction therapy and an additional 6 mg/m 2 during delayed intensification therapy. These latencies were compared with those of 38 age-, height-, and sex-matched controls. A prolongation in the peripheral conduction time of the posterior tibial nerve was found in the standard risk patients after induction compared with that of the controls, and a delay was found not only from the ankle to the popliteal fossa, but also from the popliteal fossa to the spinal cord ( P < .01). The conduction times of the median nerve from the wrist to the plexus ( P < .01) and from the wrist to the spinal cord ( P < .01) were prolonged after delayed intensification therapy. There was a significant delay in the median and tibial nerve conduction between the intermediate and high risk patients and their controls after a total vincristine dose of 12 mg/m 2. These delays were found along the entire length of the nerves, especially in the proximal part of the tibial nerve ( P < .001).

The simple frequency response of human stretch reflexes in which either short‐ or long‐latency components predominate.

1. The stretch reflexes of the human abductor digiti minimi (ADM) and biceps brachii muscles were compared using small-amplitude sinusoidal stretching at 10-50 Hz and recording the surface EMG. The stimulus was applied either to the relevant proximal phalanx or to the biceps tendon while the muscle studied was contracting; the same amplitude was used for all frequencies (range 0.5-2 mm for ADM, 0.1-1 mm for biceps). 2. As the frequency increased, the response of ADM decreased while that of biceps increased. Neither muscle showed a minimum at 20-25 Hz, as previously found for wrist muscles and attributed to an interaction between short- and long-latency components of the reflex. 3. For both muscles, the phase of the response lagged behind the stimulus by an amount which increased approximately linearly with frequency, without the gross inflexion found for wrist muscles. Such linearity would be found for a system dominated by a fixed time delay; its value sets the slope. The slope for biceps was half that for ADM. The values of reflex delay calculated from the slope of the phase plots agreed reasonably with the absolute latencies of the responses evoked by tap or ramp stimulation. Part of the difference between the muscles was due to differences in peripheral conduction time, since ADM lies more distally. Most of it, however, was due to different reflexes being involved, with biceps being predominantly controlled by short-latency pathways and ADM by long-latency pathways. 4. For both muscles, the phase lag at any given frequency was less than that expected from the reflex latency, determined from the slope of the phase plot. Thus, sensory transduction and central transmission had produced a phase advance in the reflex. The 'neural phase advance' of biceps was appreciably larger than that of ADM, and more than would be expected from the behaviour of its spindle afferents. The excess is suggested to be due to the action of Renshaw inhibition, which ADM may lack. 5. The results were substantiated by recording from single motor units in biceps. Stretching at the present amplitudes had rather little effect on the overall rhythmic behaviour, as shown by interspike interval histograms. However, cycle histograms showed that the discharge was modulated reasonably sinusoidally by the stretching, whatever its frequency (i.e. the probability of the occurrence of a spike varied over the cycle). Cyclic changes were also found in autocorrelograms and amplitude spectra of the spike trains.(ABSTRACT TRUNCATED AT 400 WORDS)

Cervical magnetic stimulation in children and adolescents: normal values and evaluation of the proximal lesion of the peripheral motor nerve in cases with polyradiculoneuropathy

Cervical magnetic stimulation was used to establish the normal values of the peripheral motor nerve conduction of the upper extremity muscle in normal children and adolescents. Seven patients with peripheral neuropathy were also examined to evaluate a lesion in the proximal site of the peripheral motor nerve. In normal subjects, onset latencies and negative wave durations tended to increase with age. The developmental profile of the latency, corrected for arm length, revealed a significant decline until the age of about 5 years. In 4 cases with polyradiculoneuropathy, motor evoked potentials following cervical magnetic stimulation showed increased latencies, prolonged durations and polyphasic shapes. The time differences between latencies by magnetic stimulation and peripheral motor conduction times by F technique were significantly prolonged. Motor evoked potentials obtained in 3 cases of axonal degeneration, on the other hand, showed slightly increased latencies and normal durations. The time differences between latencies and peripheral motor concution times were the normal range. Thus, we consider that cervical magnetic stimulation is a useful method for study of peripheral motor conduction in children and adolescents, and in particular to evaluate the proximal lesion of the nerve in patients with polyradiculoneuropathy.

Cervical magnetic stimulation in children and adolescents: normal values and evaluation of the proximal lesion of the peripheral motor nerve in cases with polyradiculoneuropathy

Cervical magnetic stimulation was used to establish the normal values of the peripheral motor nerve conduction of the upper extremity muscle in normal children and adolescents. Seven patients with peripheral neuropathy were also examined to evaluate a lesion in the proximal site of the peripheral motor nerve. In normal subjects, onset latencies and negative wave durations tended to increase with age. The developmental profile of the latency, corrected for arm length, revealed a significant decline until the age of about 5 years. In 4 cases with polyradiculoneuropathy, motor evoked potentials following cervical magnetic stimulation showed increased latencies, prolonged durations and polyphasic shapes. The time differences between latencies by magnetic stimulation and peripheral motor conduction times by F technique were significantly prolonged. Motor evoked potentials obtained in 3 cases of axonal degeneration, on the other hand, showed slightly increased latencies and normal durations. The time differences between latencies and peripheral motor concution times were the normal range. Thus, we consider that cervical magnetic stimulation is a useful method for study of peripheral motor conduction in children and adolescents, and in particular to evaluate the proximal lesion of the nerve in patients with polyradiculoneuropathy.

Glutaric Aciduria Type 1: First Reported Cases in Three Saudi Patients

The clinical and biochemical findings in three patients with glutaric aciduria Type 1 (GAT1) are presented. They had a normal postnatal period of three to 14 months. They developed sudden and severe encephalopathy following an infection or trauma (patient 3) that gradually progressed to severe dystonia, choreoathetosis, spastic quadriplegia and mental retardation. Neuroradiologic studies of the brain revealed white matter disease and frontotemporal lobe hypoplasia. The urine findings by gas chromatography/mass spectrometry (GC)/(MS) were characteristic of GAT1. Since GAT1 is an organic acidemia without intermittent acidotic attacks, but primarily manifests with progressive encephalopathy, it is important to recognize the potential of its existence among handicapped children in chronic care facilities. The good clinical response in two of the patients urges early diagnosis in subsequent newborn siblings of the families with the disease. The diagnosis of three patients in less than two years indicates the need for neonatal screening for the recognition of this disease, among other treatable metabolic diseases, in Saudi Arabia.

Quantification of D- and I-wave effects evoked by transcranial magnetic brain stimulation on the tibialis anterior motoneuron pool in man.

Transcranial stimulation in man evokes multiple descending volleys in the spinal cord giving rise to multiple subpeaks in a peri-stimulus-time histogram (PSTH) obtained from a cross-correlation of motor unit discharges with transcranial stimuli. The first volley is termed the D wave, as it is assumed to be evoked by direct excitation of pyramidal tract neurons, whereas the subsequent I waves appear to be generated by indirect excitation of the pyramidal tract neurons via cortical interneurons. It was the aim of this study to obtain an estimate of the effect induced by multiple volleys evoked by transcranial magnetic stimulation on the entire motoneuron pool of the tibialis anterior in awake subjects. A considerable part of a particular motoneuron pool was investigated by sampling responses of a large number (at least 19) from each muscle investigated. In total, three tibialis anterior muscles from three normal volunteers were studied. From each of the 63 units included in this study, a PSTH to 100 transcranial magnetic stimuli and a PSTH to 100 electrical stimuli given to the peroneal nerve were compiled. From the motor unit response to the peripheral nerve stimulation, the latency of the single-unit H reflex peak was obtained. This yielded, the timing of the subpeaks in response to the magnetic stimulation relative to the timing of the H reflex of the same unit, thus eliminating the influence of the peripheral conduction time from the motoneuron to the recording electrode. It was found that 50 (79%) of the motor units exhibited at least two subpeaks in response to the cortical stimulus.(ABSTRACT TRUNCATED AT 250 WORDS)

Magnetic stimulation in the determination of lumbosacral motor radiculopathy

Magnetic stimulation was utilised to diagnose lumbosacral motor radiculopathy non-invasively. Magnetic coil stimulation estimated peripheral motor nerve conduction time (MNCT) which, used in combination with F response, allowed calculation of “motor root conduction time (MRCT),” response being recorded from abductor hallucis. Twenty-five normal controls and 26 patients with lumbar spondylosis were studied. The mean interside difference (left minus right) of MRCT in the control was +0.06 msec (range: −0.88 to +0.74 msec). On clinical and radiological grounds, patients with spondylosis were grouped into those with: (1) no lumbosacral root compression, (II) root compression without motor sign, and (III) root compression with motor deficit. All patients in group III and 36% of cases of group II had MRCT significantly prolonged on the affected side.

Periodic Limb Movement Disorder is Associated with Normal Motor Conduction Latencies When Studied by Central Magnetic Stimulation— Successful Use of a New Technique

This study prospectively tested the hypothesis that patients with periodic limb movement disorder (PLMD) have longer motor conduction latencies than normals. Six healthy adults, 13 patients with PLMD, and 8 patients with long-term multiple sclerosis (MS) had recordings of motor conduction latencies during wake and sleep. MS subjects were included only to show that we could detect prolongation of central conduction; nonMS subjects were used to test the hypothesis. Subjects had no other medical or sleep problems. A novel magnetic stimulator, the Cadwell MES-10, was discharged over the vertex and the C7 cervical spine. It triggered compound muscle action potentials that were recorded in the abductor digiti minimi in the hand. The conduction latencies were the total conduction time (TCT), measured vertex to hand, and the peripheral conduction time (PCT), measured C7 to hand. The difference was the central conduction time (CCT). Only TCT could be obtained during sleep. Supporting the use of TCT as an indirect measure of central conduction was that, in all waking subjects, TCT correlated with CCT (r = 0.91, p = 0.001) but not with PCT. Reliabilities during wake and sleep were 0.95 or higher for TCT and PCT measurements. Waking CCT was greater in MS subjects (13.77 milliseconds) than those without MS (9.21 milliseconds), p = 0.001. Sleeping TCT was much less impressive in distinguishing MS subjects [27.08 milliseconds in nonrapid eye movement (NREM) sleep; 28.64 milliseconds in rapid eye movement (REM) sleep] from nonMS subjects (24.45 milliseconds in NREM; 24.84 milliseconds for REM), p = 0.07 for NREM and p = 0.04 for REM.(ABSTRACT TRUNCATED AT 250 WORDS)

Do motor evoked potentials allow quantitative assessment of motor function in patients with spinal cord lesions?

Motor evoked potentials (MEP) were recorded in a total of 110 patients with tumorous (n = 39) and non-tumorous (n = 71) lesions of the cervical (n = 59), thoracic (n = 37) and thoracolumbar (n = 14) spinal cord. In all cases MEP were elicited by electrical stimulations, and in 50 of them also by magnetoelectric stimulation, of the motor cortex. The peripheral conduction time was determined by electrical stimulation of the lumbar nerve roots. It was the aim of this study to determine whether 1. MEP are sensitive for detection of lesions along the spinal cord and 2. whether they allow quantitative assessment of motor function. To achieve this goal, we compared potential and clinical findings of our patients, each divided into seven categories. Our results clearly showed the high sensitivity of MEP for semi-quantitative evaluation of motor function, as there were no false negative results in our series. Moreover, unilaterally accentuated motor deficits correlated significantly with changes in MEP, which were affected more strongly on the corresponding side (Student's t-test, alpha = 0.05). However, clinical and electrophysiological findings did not correlate in the quantitative evaluation of the motor status as established by variance analysis (F = 0.52). There was no difference in results with respect to the electrical and magnetoelectric stimulation technique. Our results lead to the following conclusions. MEP are sensitive for semi-quantitative evaluation of spinal motor function; however, MEP do not allow quantification of the clinical motor status.(ABSTRACT TRUNCATED AT 250 WORDS)

Normwerte und altersabhängige Veränderungen magnetoelektrisch evozierter Muskelsummenpotentiale

A number of 57 normal subjects was investigated using transcranial magnetic stimulation of the motor cortex and transcutaneous magnetic stimulation of the spinal nerve root in order to obtain normative data for central and peripheral motor latencies. Under standardized conditions (site of stimulation, stimulus intensity, degree of voluntary tonic background activation) muscle compound action potentials were recorded from different muscles of the upper and lower extremity: M. biceps brachii, M. extensor carpi radialis, M. interosseus dorsalis I, M. vastus medialis, M. tibialis anterior, and M. extensor digitorum brevis. Onset latency, peak to peak amplitude (% of maximal M-wave), duration and configuration of the muscle compound action potentials were evaluated (Fig. 1 and Tab. 1-6). Central and peripheral motor latencies were determined by stimulation over two different points of the neuraxis (cortex/cervical or lumbar nerve roots). Central motor latencies were calculated by subtracting the peripheral conduction time from the onset latency of the fastest cortically evoked muscle response. Not only the peripheral but also the central motor latencies were found to increase in higher ages (Tab. 6). This has to be taken into account when elderly patients are examined for diagnosis of disorders of the descending motor tracts.

The development of cortico-motoneuronal projections investigated using magnetic brain stimulation in the infant macaque.

1. The effects of magnetic brain stimulation on electromyographic (EMG) activity recorded from arm and hand muscles have been investigated in five infant and six adult macaque monkeys under ketamine sedation. 2. In the adults, brief, short-latency EMG responses could be readily evoked with magnetic stimuli of 40-50% of the maximum stimulator output (1.5 T). 3. In a cross-sectional study of five infant macaques, it was difficult to evoke EMG responses in young infants (less than 5 months old). Clear short-latency responses were first evoked in an animal 5.75 months old. This change was accompanied by an increase in the probability of occurrence of the responses. 4. In a longitudinal study of two infant monkeys over a period ranging from 2.5 to 14.5 months of age we found that clear short-latency responses were first evoked at 4 and at 5.5 months, respectively. In both animals there was a steady fall in response threshold which reached the adult range at 6.5 and 8 months, respectively. EMG responses in animals older than 8 months were indistinguishable from those in adults. 5. In the longitudinal study we also noted that the latency of EMG responses to magnetic brain stimulation declined with age. Since there were no comparable changes in the peripheral conduction time in these animals, we attribute this result to a decrease in central conduction time. 6. Parallel behavioural observations of the natural behaviour of the same animals within a colony indicated that mature precision movements of the fingers were not used until 5-6 months of age. 7. In two adult monkeys, the latency of EMG responses evoked in the extensor digitorum and first dorsal interosseous muscles by direct stimulation of the corticospinal tract, via electrodes implanted in the medullary pyramids, was found to be 0.7-1.7 ms shorter than that of responses evoked by magnetic stimuli. It is argued that at least the earliest component of these latter responses is conducted over the cortico-motoneuronal pathway. 8. The mechanisms likely to contribute to the late appearance of EMG responses to brain stimulation are discussed. One of these is probably the establishment of mature cortico-motoneuronal connections, which are not present at birth.

Peripheral and central delays in the cortical projections from human truncal muscles. Rapid central transmission of proprioceptive input from the hand but not the trunk.

In contrast to the cortical connections to and from the muscles of the hand, the transmission of an afferent volley from the intercostal muscles to the cerebral cortex takes approximately 10 ms longer than it takes a cortical motor volley to reach the muscle. This disparity in afferent and efferent cortical transmission times could be due to a slower peripheral conduction velocity of intercostal muscle afferents or a slower afferent conduction within the central nervous system. The present study derived peripheral and central conduction times for the truncal muscles from the onsets of the mechanically evoked intercostal and abdominal spinal reflexes and the onsets of the cortical sensory potentials. Mean latencies of the ipsilateral intercostal and abdominal reflexes (evoked and recorded in the mid-clavicular line) were 11.9 +/- 0.7 (SEM) ms and 13.7 +/- 0.9 ms, respectively; calculated peripheral conduction velocities were 69.4 +/- 4.1 m/s and 56.2 +/- 2.3 m/s (assuming equal velocities for the sensory and motor axons and an intraspinal delay of 1 ms). Central sensory conduction time (spinal cord to cortex) was calculated by subtracting the peripheral conduction times for the intercostal and abdominal afferents (5.5 +/- 0.3 ms and 6.4 +/- 0.4 ms) from the onsets of the cortical sensory potentials (19.4 +/- 0.8 ms and 25.3 +/- 12.3 ms); central sensory conduction times (14.2 +/- 1.7 ms and 18.6 +/- 2.3 ms) were 8-11 ms longer than central motor conduction times. These results demonstrate that peripheral conduction velocities of intercostal and abdominal afferents are not slow, and that, when compared with the extremities, there is a relatively long central conduction time for proprioceptive information from the trunk to the cerebral cortex.

Motor evoked potentials to magnetic stimulation: technical considerations and normative data from 50 subjects.

Magnetic stimulation of the brain and cervical and lumbar spinal roots was performed on 50 healthy volunteers. Compound muscle action potentials (CMAPs) were recorded from biceps brachii, abductor digiti minimi (ADM), rectus femoris and tibialis anterior (TA). We assessed central conduction times by subtraction of peripheral from central latencies and compared results using either spinal root stimulation or the F-wave method. Side-to-side differences of total conduction time, peripheral conduction time and central conduction time (CCT) were measured and the effect of clockwise vs counterclockwise stimulations on latencies and sizes of CMAPs is emphasized. Amplitudes and areas of CMAPs were expressed as a percentage of the peripheral M response for ADM and TA. There was a positive correlation between CCT to the lumbosacral region and height, but not between the cervical region and height. No correlation was observed between genders and central conduction times, amplitudes or areas of CMAPs.

Magnetic stimulation of motor cortex and nerve roots in children. Maturation of cortico-motoneuronal projections

Magnetoelectrical stimulation of motor cortex and peripheral nerve roots was used to establish the maturational profiles of central and peripheral nervous system conduction times in normal children in upper and lower extremity muscles. To obtain true central conduction times, not contaminated by variation due to different preinnervational levels, a protocol using stimulation under full muscular relaxation was used. With this protocol cler responses of the upper extremity could be obtained after the first year of life, whereas in the lower extremity they could not be obtained before the fourth year of life. The developmental profile of central conduction times to upper and lower extremity muscles showed an age-dependent acceleration with adult values not being reached before the age of about 10 years. In contrast, peripheral conduction times obtained after cervical or lumbar root stimulation to upper and lower extremities showed a much faster maturational profile, with adult values being reached at about the age of 3 years. The data are discussed in relation to the available literature on neuromorphological development and provide normative values for the understanding of normal development of motor control in children as well as for application of this technique in children with motor disturbances.

Motorisch evozierte Potentiale nach elektrischer und magnetoelektrischer Stimulation: Wertigkeit und Vergleich beider Methoden

Motor evoked potentials (MEP) were recorded in a total of 145 patients with supratentorial (N = 29), infratentorial (N = 25) and spinal (N=91) lesions affecting the descending pathways. In all cases potentials were evoked by electrical, in addition in 55 of them by electromagnetic stimulation of the motor cortex. The peripheral conduction time was determined in all patients by electrical stimulation of the cervical and lumbar nerve roots, respectively. This study was designed to compare both stimulation techniques (electrical vs. electromagnetic) regarding their significance in recording of potentials as well as in correlation of potentials with the motor status as established by clinical examination

Clinical use of the magnetic stimulator in the investigation of peripheral conduction time

The application of rapidly changing magnetic fields (magnetic stimulation) over the neck or lower back elicits EMG responses in the muscles of the arm or leg respectively. Such responses have stable onset latencies but their amplitudes vary depending on the position of the coil over the neck or lower back. Supramaximal responses could not be obtained. Comparison of onset latencies with estimates of peripheral conduction time using a conventional F-wave technique suggest that the site of excitation of the motor axons is about 1.3 msec conduction time distal to the cervical motoneurons and 3 msec distal to the lumbosacral motoneurons. Response configuration after paravertebral magnetic stimulation was similar to that of the standard electrically evoked M-wave in the small hand muscles but not in lower limb muscles. Responses in lower limb muscles after paravertebral magnetic stimulation may consist of additional F-wave and H-reflex components. The possible clinical role of paravertebral magnetic stimulation in the investigation of peripheral and central motor pathways is discussed in the light of these findings.