Central Motor Pathways Research Articles

Central motor conduction time: Reproducibility and discomfort of different methods

Central motor conduction time, a useful measure for studying central motor pathways, is calculated by determining the difference between the latency of motor-evoked potentials and peripheral conduction time. The intraindividual trial-to-trial variability of central motor conduction time and the discomfort associated with three methods of measuring peripheral motor conduction time (F-wave latency, cervical magnetic stimulation, and cervical needle stimulation) were studied in 5 healthy subjects with the use of transcranial magnetic stimulation to elicit motor-evoked potentials. Central motor conduction time was calculated by using measurements, made on 3 separate days, from the same three muscles on each hand. A visual analog pain scale was used to determine the level of discomfort for each method. Intraindividual trial-to-trial variability of central motor conduction time was similar for all methods, with coefficients of variation of 13% for the F-wave latency, 15% for cervical magnetic stimulation, and 11% for cervical needle stimulation. The last method was significantly more painful than the other two methods; there was no significant difference in discomfort between the F-wave method and cervical magnetic stimulation. To assess peripheral motor conduction time, when determining central motor conduction time, either the F-wave method or cervical magnetic stimulation is preferable to cervical needle stimulation. © 1998 John Wiley & Sons, Inc. Muscle Nerve 21: 1445–1450, 1998

Central motor conduction time: reproducibility and discomfort of different methods.

Central motor conduction time, a useful measure for studying central motor pathways, is calculated by determining the difference between the latency of motor-evoked potentials and peripheral conduction time. The intraindividual trial-to-trial variability of central motor conduction time and the discomfort associated with three methods of measuring peripheral motor conduction time (F-wave latency, cervical magnetic stimulation, and cervical needle stimulation) were studied in 5 healthy subjects with the use of transcranial magnetic stimulation to elicit motor-evoked potentials. Central motor conduction time was calculated by using measurements, made on 3 separate days, from the same three muscles on each hand. A visual analog pain scale was used to determine the level of discomfort for each method. Intraindividual trial-to-trial variability of central motor conduction time was similar for all methods, with coefficients of variation of 13% for the F-wave latency, 15% for cervical magnetic stimulation, and 11% for cervical needle stimulation. The last method was significantly more painful than the other two methods; there was no significant difference in discomfort between the F-wave method and cervical magnetic stimulation. To assess peripheral motor conduction time, when determining central motor conduction time, either the F-wave method or cervical magnetic stimulation is preferable to cervical needle stimulation.

Electrophysiological features of central motor conduction in spinocerebellar atrophy type 1, type 2, and Machado-Joseph disease

OBJECTIVESTo characterise electrophysiologically the central motor conduction of spinocerebellar atrophy type 1 (SCA1), type 2 (SCA2), and Machado-Joseph disease (MJD).METHODSMotor evoked potentials (MEPs) triggered by transcranial magnetic stimulation (TMS) was...

Sonic / Vocal Motor Pathways in Catfishes: Comparisons with Other Teleosts

Among teleost fishes, representatives of several distantly related groups have sound-producing (sonic/vocal) muscles associated with the swimbladder or pectoral girdle/fin. Here, the diversity of vocal organs and central motor pathways in four families of catfish, order Siluriformes, is compared to that in families from two distantly related orders, the Scorpaeniformes and Batrachoidiformes. Several catfish families have two sonic mechanisms – a swimbladder vibration established by ‘drumming muscles’ that differ in origin and insertion between families, and a pectoral spine stridulatory apparatus. In ariids, mochokids and doradids, sonic swimbladder muscles originate at various cranial or postcranial elements and insert onto an ‘elastic spring’ that vibrates the swimbladder, while in pimelodids the muscles insert ventrally at the swimbladder. Sonic motoneurons are located along the midline, ventral to the fourth ventricle/central canal in doradids and mochokids but lateral to the medial longitudinal fasciculus in ariids; pimelodids have motoneurons in both locations. The axonal trajectory for the lateral motoneurons in pimelodids and ariids implies that they are a migrated, midline population of sonic motoneurons. Pectoral spine-associated motoneurons are located in the ventral motor column. Unlike catfishes, a diversity of sonic mechanisms in Scorpaeniformes is not associated with different positions for sonic motoneurons. Cottids (sculpin) lack a swimbladder but have sonic muscles that originate at the occipital cranium and insert at the pectoral girdle; sonic motoneurons are located within the ventral motor column. Some triglids have intrinsic swimbladder muscles, although ontogenetic data indicate a transient association with the pectoral girdle; sonic motoneurons are in the same location as in cottids. Among Batrachoidiformes, all known representatives have intrinsic swimbladder muscles that are never associated with the pectoral girdle and are innervated by midline sonic motoneurons. The results suggest two patterns of organization for sound-producing systems in teleost fishes: pectoral fin/girdle-associated muscles are innervated by sonic motoneurons positioned within the ventral motor column, adjacent to the ventral fasciculus; non-pectoral associated muscles are innervated by sonic motoneurons located on or close to the midline, adjacent to the medial longitudinal fasciculus.

Motor pathway analysis in HAM/TSP using magnetic stimulation and F-waves.

Tropical Spastic Paraparesis/HTLV-I Associated Myelopathy (HAM/TSP) is a chronic, progressive myelopathy endemic to the Caribbean. In HAM/TSP, peripheral motor pathways have been assessed using electromyography and nerve conduction studies; central motor pathways have been assessed to a limited extent using electrocortical stimulation. We used magnetic cortical stimulation (a painless alternative to electrocortical stimulation) and F-wave analysis to study conduction in the central and peripheral motor pathways in 18 HTLV-I seropositive, Jamaican TSP patients (ages 29-70 years; duration of symptoms 3-20 years) and 22 normal controls. Magnetic cortical stimulation was effected using a 9 cm diameter undamped MES10 coil. F-waves and M-responses were elicited by electrical stimulation of the ulnar nerve at the wrist, and deep peroneal stimulation at the knee. Stimulation and recording of response latencies in abductor digitii minimi (ADM) and tibialis anterior (TA) were carried out using a Cadwell Excel system. With cortical stimulation, response latencies (TMCTs) to ADM and TA were prolonged in the patients relative to controls. F-wave and M-response latencies were unaffected, suggesting no peripheral pathology. Latency (CMCT) between cortex and lumbar cord was significantly prolonged; that between cortex and C7/T1, also, but less markedly (P < 0.0005). Amplitudes of cortically evoked responses were significantly reduced only in the lower limbs (TA). CMCT increased as the disease progressed from mild to moderate, thereafter remaining largely unchanged. Meta-analysis of interlaboratory control data revealed no significant differences in TMCTs between our controls and others studied using similar techniques. The observations are consistent with pathology affecting mainly the thoracolumbar cord in HAM/TSP.

Applications de la stimulation magnétique corticale

In the last decade, a new electrophysiological tool has become available since the development of painless magnetic stimulators able to activate the primary motor cortex and the motor roots in conscious man. Therefore, it became possible to measure the conduction time within fast-conducting central motor pathways by substracting from the total latency of muscle responses elicited by cortical stimuli the conduction time in peripheral nerves. This technique proved sensitive enough to illustrate early abnormalities of central motor conduction in various neurological diseases such as multiple sclerosis, amyotrophic lateral sclerosis, cervical spondylotic myelopathy, degenerative ataxias or hereditary spastic paraplegias. When recorded early after stroke, motor evoked potentials are also a valuable tool to predict functional outcome. They can also illustrate subtle pathophysiological disturbances in diseases where there is no direct involvement of central motor pathways such as Parkinson's disease, dystonia or epilepsy. Magnetic cortical stimulation also offers unique opportunities to explore intracerebral inhibitory and excitatory circuits and mechanisms of brain plasticity. The recent development of rapid rate stimulators also enables functional studies of non-motor cerebral regions such as visual or frontal cortices. Moreover, rapid rate stimulation seems useful in the treatment of drug-resistant depression but the safety of this procedure, particularly with regard to the production of seizures or kindling, remains to be fully documented.

5-28-02 A new method for transcranial magnetic motor evoked potentials (TcMMEP) for the evaluation of central motor pathways (II. clinical applications)

5-28-02 A new method for transcranial magnetic motor evoked potentials (TcMMEP) for the evaluation of central motor pathways (II. clinical applications)

Electrophysiologic study of central motor pathways in ataxia-telangiectasia.

To date, corticospinal tract functional integrity in ataxia-telangiectasia has not been studied. Thorough evaluation of central motor pathways is also lacking in neuropathologic and clinical studies. Using electromagnetic stimulation, we assessed the integrity of the corticospinal tracts in eight patients with ataxia-telangiectasia. Cortical and peripheral compound motor action potentials were recorded from the abductor pollicis brevis muscle. Recordings of the shortest F-wave latency and of the compound motor action potential distal latency were made from the abductor pollicis brevis muscle after electrical stimulation of the median nerve at the wrist. A significant increase in central motor conduction time was observed in four patients, two of whom had clinical findings compatible with a pyramidal lesion. This study demonstrates involvement of the central motor pathways in ataxia-telangiectasia, which appears to be more frequent late in the course of the disease.

Changes of central motor pathway excitability in obstructive sleep apnea: A case report

Changes of central motor pathway excitability in obstructive sleep apnea: A case report

A review of recent applications of cross-correlation methodologies to human motor unit recording

This article reviews some recent applications of time and frequency domain cross-correlation techniques to human motor unit recording. These techniques may be used to examine the pre-synaptic mechanisms involved in control of motoneuron activity during on-going motor tasks in man without the need for imposed and artificial perturbations of the system. In this review we examine, through several examples, areas in which insights have been gained into the basic neurophysiological processes that bring about motoneuron firing in man and illustrate how these processes are affected by central nervous system pathology. We will demonstrate that synchronization and coherence may be revealed between human motor unit discharges and give examples that support the hypothesis that these phenomena are generated by activity in a focused common corticospinal input to spinal motoneurons. Disruption of central motor pathways due to diseases of the nervous system leads to pathophysiological alterations in the activity of these pre-synaptic motoneuron inputs that can be revealed by cross-correlation analysis of motor unit discharges. The significance of these studies and outstanding questions in this field are discussed

Influence of peripheral nerve stimulation on human motor cortical excitability in patients with ventrolateral thalamic lesion.

To determine the peripheral afferent pathways that influence the activities of the motor cortex by examining the effects of peripheral nerve stimulation on motor cortical excitability. We examined 12 healthy volunteers and 4 patients with localized brain lesions caused by cerebrovascular attack. Of the 4 patients, 1 patient had pontine infarction, including medial lemniscus, and severe sensory deficit and 3 had small localized lesions in the lateral part of the thalamus and neither sensory impairment nor abnormal N20 waves on somatosensory evoked potential recordings. Central motor tract excitability was examined by measuring a change in the motor evoked potential (MEP), using transcranial magnetic stimulation of the motor cortex after peripheral nerve stimulation at the wrist significantly increased MEP response in the controls at long conditioning-test intervals of 28 to 60 milliseconds, as well as at short intervals of 0 to 6 milliseconds. A late MEP potentiation was not observed on the affected side in all patients. The loss of late MEP potentiation in patients with pontine and thalamic lesions indicates that this potentiation is caused by the alternation of the motor cortical excitability. Furthermore, the results in the patients with thalamic lesions suggest that the lateral nuclei of the thalamus, other than the ventral posterolateral nucleus and probably including the ventrolateral nucleus, have an important function in the processing of peripheral sensory input for tuning motor cortical excitability.

An electrophysiological study of the mechanism of fatigue in multiple sclerosis.

Fatigue is a common and disabling symptom in multiple sclerosis but is poorly understood. We investigated 'physiological' fatigue in 21 patients with multiple sclerosis who complained of disabling fatigue by measuring the decline in strength during a 45 s maximal contraction of the adductor pollicis muscle. The results were compared with those from a control group of 19 healthy subjects. The strength of control subjects declined by approximately 20% during the contraction; twitch interpolation showed central drive remained almost maximal throughout, and therefore that the fatigue was peripheral in origin. Patients had normal baseline strength, but developed greater fatigue (approximately 45%), which was central in origin. In both cases, the decline in strength followed a roughly linear time course suggesting that the patients, like the normals, were trying to maintain a maximum voluntary effort. Evidence for frequency-dependent conduction block (FDCB) in the patients' central motor pathways was sought by measuring the EMG responses to single and paired transcranial magnetic stimuli. Fatigue had no effect on the latency or size of EMG responses to transcranial magnetic stimulation, suggesting that FDCB was unlikely to have occurred. This was supported by measurements of the maximum speed of voluntary muscle contraction; although the patients showed relatively slow speeds before exercise, the decline in speed after fatigue was no greater than in normal subjects. We conclude that excessive 'physiological' fatigue contributes to the symptom of fatigue in multiple sclerosis and is central in origin. However, since the degree of exercise-induced fatigue did not correlate with the baseline complaint of fatigue, other factors must also be operating to produce the full range of clinical symptoms. We found no conclusive evidence that central fatigue is related to increased dysfunction in the primary central motor pathways and no evidence that FDCB is the pathophysiological mechanism. We postulate that central fatigue in multiple sclerosis is due to impaired drive to the primary motor cortex and several lines of evidence strongly suggest that this is not due to a lack of motivation.

Focal subcortical reflex myoclonus. A clinical and neurophysiological study.

Patients with progressive myoclonus epilepsy or progressive myoclonus ataxia often show a focal myoclonus, both spontaneous and reflex to somatosensory stimuli. Myoclonus is time-locked to large ("giant") electroencephalographic potentials. Previous authors have classified it as a "cortical reflex myoclonus," with the assumption that it invariably arises from an abnormal corticifugal neuron discharge. To identify the myoclonus source, using various neurophysiological techniques, in 5 patients with progressive myoclonus epilepsy/ataxia. Extensive investigations were performed to ascertain the clinical diagnosis. Electrophysiologically, the main method was transcranial cortical stimulation and motor evoked potential measurement. The latency and amplitude of the spontaneous myoclonus and the premyoclonus cortical spike, the reflex myoclonus (C-reflex), and the giant somatosensory evoked potential were also analyzed. The behavior of giant somatosensory evoked potentials and C-reflexes were then studied on single, consecutive trials. Finally, the central motor pathway excitability and its changes attributable to a prior somatosensory input were determined. The motor evoked potential studies showed that the expected corticomuscular conduction time (23 milliseconds) of the myoclonic electromyographic potential was longer than that previously suspected. Considering this, the premyoclonus cortical spike and the giant somatosensory evoked potential were so close to the spontaneous/reflex jerks that they could not reflect a cortical myoclonus source. In 4 patients, the C-reflex latency (< 41.6 milliseconds) was shorter than that often reported in previous studies. The giant somatosensory evoked potential and the C-reflex showed no simple cause-effect link. Motor pathways were hyperexcitable only in response to somatosensory inputs. The data pointed to a cortical myoclonus origin only in the patient whose C-reflex had the longest latency (44 milliseconds). In the remaining patients, a subcortical source was far more likely. In this group of patients, cortical stimulation disclosed a new myoclonus variety, for which the term focal subcortical reflex myoclonus is proposed; it mimics cortical reflex myoclonus but has a shorter latency.

Towards a neurophysiological marker of amyotrophic lateral sclerosis as revealed by changes in cortical excitability: Distinguishing characteristics of amyotrophic lateral sclerosis by using cortical stimulation

Motor evoked potentials (MEPs) to magnetic trans cranial stimulation (TCS) were recorded in 47 patients with amyotrophic lateral sclerosis (ALS) in order to evaluate both excitability and conductivity changes relating to central motor pathways. The results were compared with those obtained from a control population of 43 subjects, 34 patients with definite multiple sclerosis (MS) and 15 patients with a rigid early form of Parkinson's disease (PD). The excitability threshold to TCS was higher in ALS patients for both upper and lower limbs compared with both controls and PD patients, but lower than that of MS patients. The Silent Period duration (SP (hand recordings): 80.1 ms, SD: 38.5) was significantly shorter in ALS patients than in all the other examined subjects ( P<0.001), nor did it increase proportionally to TCS intensity as with control subjects. The abnormal behavior of the SP appears to be specifically linked to the ALS disease, since it was neither observed in PD patients, nor in those with multiple sclerosis, who, on the contrary, displayed a prolonged mean duration of the SP (161.6 ms, SD 77 vs. 115.7 ms, SD 62 for the control group). Due to the neuronal loss of the largest neurons in ALS, MEP latency, amplitude, duration and the motor central conduction time (CCT) were in different proportion found abnormal. Our study shows how different neurological diseases with central motor involvement share broadly similar MEP abnormalities, but a different involvement of the silent period. We suggest that in ALS patients there may be abnormalities of motor cortical inhibitory mechanisms which are detected with the measurement of the SP. The distinctive `depression' of this parameter in the case of ALS could be a significant marker for diagnosing this disease.

Transcranial cortical stimulation in disorders of the central motor pathways

Motor evoked potentials (MEPs) were studied in 63 patients with disorders affecting central motor pathways. These were classified into five subgroups: motor neuron disease (16), multiple sclerosis (13), cerebral infarction (19), spinal cord lesions (10) and hereditary spastic paraplegia (5). Three patients with hysterical paraplegia were also studied. Results were compared to those obtained from 30 normal subjects. In normal subjects the mean central motor conduction time (CMCT) was 6.4 ms (range 3.4–8.1 ms, SD 1.0 ms) for abductor digiti minimi and 13.2 ms (range 9.7–17.0 ms, SD 2.3 ms) for tibialis anterior. Amplitude of the cortical MEPs was defined as a percentage of the size of the peripheral compound muscle action potential (CMAP) and ranged from 14 to 85%. Fifteen of 16 patients with motor neuron disease and all patients with cerebral infarction, multiple sclerosis (MS), spastic paraparesis and non-MS spinal lesions had abnormal studies including low amplitude, dispersed or absent responses and prolonged CMCTs. Patients with MS had markedly prolonged CMCTs. In three cases of hysterical weakness MEPs were within normal limits. MEPs are a useful method to detect pathology in the central motor pathways and may have a significant role in the diagnosis of disorders involving the upper motor neuron.

Central motor Pathway Evaluation using magnetic coil stimulation in hereditary motor and sensory neuropathy type I (HMSN type I, Charco-Marie-Tooth disease

Central Motor Conduction Time (CMCT) was investigated in 18 patients (5 m, 13 f; age range: 11–69 yrs) with clinical and electrophysiological features of HMSN type I, using Magnetic Coil (MC) stimulation. No one exhibited clinically pyramidal signs. Brain stimulation Motor Evoked Potential (MEPs), recorded monolaterally from the left abductor digiti minimi (ADM) and tibialis anterior (TA) muscles, were evoked in all patients from upper extremities and absent in 11.1% from lower limbs. Total Motor Conduction Time (TMCT), as well as Peripheral Motor Conduction Time estimated by either magnetic nerve root stimulation (mag-PMCT) or F-wave latency values (F-PMCT), were markedly delayed in all patients. Central Motor Conduction Time was calculated by subtracting both the latency of mag-PMCT (mag-CMCT) and F-PMCT (F-CMCT) from that one obtained by cortical stimulation. F-CMCT was abnormal in 22.2% from ADM muscles and in 33.3% from TA muscles. Furthermore, CMCT to both methods was not possible to evaluate in 5.6% from upper and lower extremities and following magnetic root stimulation in 11.1% from lower limbs. These findings prove lower motor neuron involvement, in agreement with electroneurographic data, and suggest a possible central motor pathways impairment, even in patients without any clinical evidence, but they cannot explain which is the underlying pathophysiological mechanism, a true motor neuron involvement or an abnormal spinal motor neuron excitability.

Magnetic stimulation of the motor cortex: Clinical applications

Transcranial magnetic cortical stimulation provides the clinical neurophysiologist with a method to examine alterations in the function of central motor pathways in diseases affecting the motor system. The technique has great research potential and has led to increased understanding of intracortical physiology, corticospinal tract function, motor system plasticity and motor control. Subclinical cerebral and spinal cord lesions may be demonstrated, and the technique has a potential role for quantification and monitoring of disease progression, and for early prognostication after stroke. Intraoperative monitoring of motor evoked potentials (MEP) is of value during spinal cord surgery, but due to attenuation of magnetic MEPs during anaesthesia, transcranial electrical stimulation is more appropriate for intraoperative recordings.

Transcranial magnetic stimulation in patients with cerebellar stroke.

Conduction time of the central motor pathways (CMCT) by transcranial magnetic stimulation (TMS) was performed within the first two weeks in 7 patients with isolated hemicerebellar lesions after stroke. Cerebellar infarcts were small (< 2 cm in diameter) in 5 patients and no brainstem structure was involved in CT studies. The threshold (3 cases) and CMCT (4 cases) were abnormal or asymmetric by stimulation of the motor cortex contralateral to the impaired hemicerebellum. The follow-up study in 2 patients revealed electrophysiological improvement closely related to clinical cerebellar recovery rate. CMCT was significantly longer by cortex stimulation contralateral to the impaired hemicerebellum than by ipsilateral stimulation. Prolonged CMCT was significantly correlated with the rated severity of cerebellar signs. Increased threshold may be due to depressed facilitating action of the deep cerebellar nuclei on contralateral motor cortex. Abnormal CMCT might result in reduced size and increased dispersion of the efferent volleys. Recovery of electrophysiological results could represent in part true potentially reversible functional deficit. Whichever the pathophysiological mechanisms involved, our results demonstrate that the cerebellum dysfunction plays a role in the abnormalities of CMCT elicited by TMS.

Double cortical stimulation in amyotrophic lateral sclerosis.

Transcranial double magnetic stimulation on the motor cortex was used to investigate central motor tract function in 16 patients with amyotrophic lateral sclerosis, five with spinal muscular atrophy, and 16 age matched normal controls. Surface EMG responses were recorded from the relaxed abductor pollicis brevis (APB) muscle. Responses to test stimuli were markedly attenuated by a subthreshold conditioning stimulus given at a condition-test (C-T) interval of 1-4 ms in normal controls and patients with spinal muscular atrophy, but attenuation was mild in patients with amyotrophic lateral sclerosis. In the normal controls this suppression was caused by activation of the intracortical inhibitory mechanism because responses to electrical test stimuli and the H wave were not suppressed by the same magnetic subthreshold conditioning stimulus. In amyotrophic lateral sclerosis the effect of the conditioning cortical stimulus on the H wave was also in the normal range. The intracortical inhibitory mechanism may be impaired in patients with amyotrophic lateral sclerosis.

P430 Frequency dependent conduction delay in the central motor pathways in multiple sclerosis

P430 Frequency dependent conduction delay in the central motor pathways in multiple sclerosis