Stimulation of motor tracts in motor neuron disease.

The muscle responses evoked by cortical and cervical stimulation in 11 patients with motor neuron disease were studied. The muscle potential in the abductor pollicis brevis, evoked by median nerve stimulation and the somatosensory potential evoked by wrist stimulation were also studied. In eight of 11 patients there was absence or increased central delay of the responses evoked by cortical stimulation. In four patients muscle responses on cervical stimulation and muscle action potentials on median nerve stimulation were also altered, indicating peripheral abnormalities. Somatosensory responses evoked by wrist stimulation were normal. Electrophysiological techniques are helpful in estimating the site of motor involvement in motor neuron disease.     

Magnetic stimulation of the motor cortex in cervical spondylosis

We report a new technique of transcranial magnetic stimulation of the motor cortex to measure conduction within central motor pathways of 67 patients with cervical spondylosis or disk herniation. There were upper motor neuron signs in 34 patients (51%) and x-ray evidence of cervical cord compression in 44 (66%). Muscle action potentials (MAPs) to cortical stimulation were abnormal in 84% of patients with, and 22% of those without, radiologic signs of cervical cord compression. Median nerve somatosensory evoked potentials were altered in only 25% of patients. The frequency of MAP alterations correlated with upper motor neuron signs. In 5 (11%) of the 44 patients with x-ray evidence of cervical cord compression, subclinical cord compression was disclosed by cortical stimulation. In 10 patients restudied 3 months after surgical decompression, normalization of central motor conduction time did not occur, indicating permanent damage to the cervical cord.     

Electrical stimulation of the motor tracts in cervical spondylosis.

Motor action potentials evoked by percutaneous electrical stimulation of the scalp and of the cervical (or lumbar) vertebral region were recorded from the biceps, thenar and tibialis anterior muscles in 30 patients with cervical spondylosis. Twelve normal controls were matched for age and height. Abnormalities of central motor conduction (absence or increased central delay of cortical responses) for at least one muscle were observed in all (but one) the patients with myelopathy alone or combined with radiculopathy. An increase in latency of the responses evoked by cervical stimulation occurred in 40% of patients with radiculopathy or myelo-radiculopathy. Changes of motor conduction occurred even in the absence of abnormalities of somatosensory evoked potentials, while the opposite was never observed. Direct stimulation of the motor tracts may be of value in the functional assessment of the motor pathways in cervical spondylosis.     

Central motor and sensory conduction in X-linked recessive bulbospinal neuronopathy.

Central conduction was studied in 12 patients with X-linked recessive bulbospinal neuronopathy (XBSN) using percutaneous electrical cortical, cervical and lumbar stimulation and somatosensory evoked potentials (SEPs). The central motor conduction time from the motor cortex to the cervical and lumbar segments of the spinal cord was normal in XBSN. SEPs, however, were abnormal or central sensory conduction time was prolonged in patients with XBSN. These results are consistent with the clinicopathological findings of XBSN in which the primary sensory neurons are involved as well as the lower motor neurons in the CNS, whereas the upper motor neurons are well preserved.     

Stimulation of motor tracts in multiple sclerosis.

Percutaneous electrical stimulation of the motor cortex was used to evaluate corticospinal conduction to upper-limb motoneurons in 29 patients with multiple sclerosis. Central motor conduction abnormalities were correlated with clinical signs and somatosensory evoked potentials. Muscle responses to cortical stimulation were altered in 20 patients. The most common abnormality was increased central motor conduction time; in two cases the responses to cortical stimulation were absent. Abnormalities were also present in patients with no clinical evidence of corticomotoneuron deficit. Alterations of muscle responses and of somatosensory evoked potentials were usually correlated, but may appear independently. Both testing methods are useful in the study of patients with multiple sclerosis.     

Somatosensory evoked potentials from musculocutaneous nerve in the diagnosis of brachial plexus injuries

A technique for recording somatosensory evoked potentials using stimulation of musculocutaneous sensory nerve fibers proximal to the wrist has been used in 10 normal subjects and in 8 patients with traumatic lesions of proximal parts of the brachial plexus. The technique gave satisfactory evoked potentials in all normal subjects and provided useful information in patients with avulsion of the 5th and 6th cervical roots. The results were similar to those obtained by radial nerve stimulation. The results in 3 patients with upper trunk injuries and in 1 patient with avulsion of the 5th cervical root were unhelpful. In 2 patients with multiple cervical root avulsions the evoked potentials from cervical cord and contralateral scalp were absent and were attenuated at Erb's point. This is the first report where musculocutaneous nerve evoked potentials have been applied to a group of patients.     

Multimodality evoked potentials in motor neuron disease

We performed median and tibial nerve somatosensory evoked potentials (SEPs), pattern-shift visual evoked potentials (PSVEPs), and brain-stem auditory evoked potentials (BAEPs) on 27 patients with motor neuron disease (MND). Median and tibial nerve SEPs were abnormal in 8 (30%) of 27 and 3 (14%) of 21 patients tested, respectively. Central and peripheral abnormalities were recorded in the absence of spondylosis. As a group, patients with MND and no evidence of cervical spondylosis had normal conduction to Erb's point following median nerve stimulation, but conduction times beyond this point were prolonged. The PSVEPs and BAEPs were within normal limits in all patients, excluding abnormalities attributable to other disease, but the group P100 latency was significantly prolonged in the group with MND. The BAEPs were normal in the group with MND. This study provides neurophysiological evidence of sensory system involvement in MND.     

Cortical motor neuron excitability during cutaneous silent period

Objective: To investigate cortical motor neuron excitability during cutaneous silent period (CSP), motor evoked potentials (MEPs) from abductor pollicis brevis following transcranial magnetic stimulation (TCM) were recorded with and without a conditioning of ipsilateral painful digital nerve electric stimulation.Methods: MEPs following TCM were recorded with and without a conditioning stimulation at an interstimulus interval (ISI) from 0 ms to 100ms in 6 controls and four patients who had reduced pain sensation in unilateral upper limbs associated with cervical syringomyelia. In addition MEPs and evoked spinal cord potentials (ESCPs) from cervical epidural space following TCM with and without a conditioning stimulation were recorded in four patients with thoracic myelopathy.Results: MEP amplitude was clearly attenuated by a conditioning stimulation at an ISI from 40 ms to 80 ms in controls (statistically significant at 60 ms). In patients with cervical syringomyelia, MEP amplitude was attenuated by a conditioning stimulation in asymptomatic hands similarly in controls but that was unchanged by a conditioning stimulation in the symptomatic hand with reduced pain sensation. In patients with thoracic myelopathy MEP amplitude was attenuated by conditioning stimulation similarly in controls, but ESCP amplitude was unchanged.Conclusions: We demonstrated that noxious cutaneous nerve stimulation suppressed spinal motor neurons but cortical motor neuron excitability was unchanged during CSP. In clinical practice, measurement of MEP suppression after noxious cutaneous nerve stimulation may provide useful information in patients with damaged pain related nerve fibers.     

Electrophysiologic evaluation of spinal cord motor conduction

Spinal cord motor conduction was determined by stimulating with a monopolar needle at the C5 cord level and recording evoked motor potentials from the ipsilateral tibialis anterior muscle. Minimal F wave and direct motor latencies from the peroneal nerve were used to calculate peripheral conduction time. Mean velocity index (defined as the distance from C5 to L4 divided by central conduction time) of 15 normal subjects was 64.9 m/sec (SD 7.5). In 5 patients with multiple sclerosis the mean velocity index was 40.6 m/sec (SD 6.5), whereas in 3 patients with cervical myelopathies, due to extradural compression, the mean velocity index was 32.8 m/sec. A repeat study in one of the latter patients, 4 days after removal of a C5 disc, documented a marked improvement in cord conduction. In a patient with a thoracic and cervical syrinx, cervical cord stimulation on the clinically affected side failed to evoke a motor potential, whereas the unaffected side was normal. This method provides a simple and effective way to evaluate spinal cord motor conduction using routine electrodiagnostic equipment.     

Evoked potentials and contingent negative variation during treatment of multiple sclerosis with spinal cord stimulation.

Cervical somatosensory evoked potentials, brainstem evoked potentials, visual evoked potentials, and the cerebral contingent negative variation were recorded in patients with definite multiple sclerosis before, during, and after spinal cord stimulation. Improvements were seen in the cervical somatosensory and brainstem evoked potentials but neither the visual evoked potential nor the contingent negative variation changed in association with spinal cord stimulation. The results indicate that spinal cord stimulation acts at spinal and brainstem levels and that the clinical improvements seen in patients are caused by an action at these levels rather than by any cerebral arousal or motivational effect. The evoked potentials were not useful in predicting which patients were likely to respond to stimulation.     

Mechanism of prolonged central motor conduction time in compressive cervical myelopathy.

OBJECTIVE: To investigate the mechanism of prolonged central motor conduction time (CMCT) in compressive cervical myelopathy, we compared the calculated CMCT following transcranial magnetic stimulation (TCM) and evoked spinal cord potentials (ESCPs) following transcranial electric stimulation (TCE). METHOD: Motor evoked potentials following TCM were recorded from abductor digiti minimi and abductor hallucis brevis muscles in 16 patients with compressive cervical myelopathy. CMCT was calculated by subtracting peripheral conduction time using peripheral nerve stimulation from MEP latency. ESCPs following TCE were recorded intraoperatively from posterior epidural space. RESULTS: CMCT was prolonged and significant attenuation of the ESCP amplitude following TCE was observed in all patients with cervical myelopathy. In 8 of 16 patients CMCT was significantly prolonged but ESCPs were recorded at the C6-7 level with normal negative peak latency. CONCLUSIONS: Prolonged CMCT may occur with only a minor amount of conduction slowing in the corticospinal tract in compressive cervical myelopathy. Impaired temporal summation of multiple descending potentials following TCM produced delays of motor neuron firing that contribute to the mechanism of prolonged CMCT.     

Magnetic brain stimulation: central motor conduction studies in multiple sclerosis

Central motor conduction (CMC) was evaluated in 32 normal subjects and 83 patients with multiple sclerosis, and the findings were correlated with clinical signs and evoked potential data. CMC time was obtained from the latency difference in responses from the abductor muscle of the little finger to magnetic stimulation of the motor cortex and electrical stimulation at the C-7/T-1 interspace. Mean CMC time in normal subjects was 6.2 msec (SD 0.86 msec), and amplitudes of responses to cortical stimuli were at least 18% of those obtained with stimuli at the wrist. CMC was abnormal in 60 patients with multiple sclerosis (72%); this correlated well with brisk finger flexor jerks (p less than 0.005). CMC was abnormal in 79% of patients with weakness of the abductor muscle of the little finger and in 54% with a normal muscle. Neurological examination was normal in 7 arms with abnormal CMC. Visual evoked potentials were abnormal in 67%, somatosensory evoked potentials in 59%, and brainstem auditory evoked potentials in 39% of those tested. For each procedure more subjects had abnormal CMC and normal evoked potentials than the reverse. The technique is of value for demonstrating and documenting central motor pathway lesions in multiple sclerosis, especially when physical signs are equivocal.     

Neurophysiological evaluation of sensorimotor functions of the leg: comparison of evoked cortical potentials following electrical and mechanical stimulation,long-latency muscle responses,and transcranial magnetic stimulation

Summary Twenty-two patients with localized lesions of the central nervous system (unilateral cerebral ischaemia, cervical myelopathy, spinal tumour, familial spastic paraplegia) underwent neurophysiological evaluation of sensorimotor deficits of the leg. Functional methods using muscle stretch as stimulus, i.e. long-latency muscle responses and cortical potentials evoked by dorsiflection of the foot, were compared with transcranial magnetic stimulation and somatosensory evoked cortical potentials following electrical stimulation of the posterior tibial nerve. The functional neurophysiological methods yielded no diagnostic superiority with respect to the procedures using artificial (i.e. magnetic and electrical) stimulation. However, in most cases of missing compound motor action potentials following transcranial magnetic stimulation or missing electrically evoked cortical potentials, the long-latency muscle responses still allowed quantitative assessment of sensorimotor function.     

Impaired heteronymous somatosensory motor cortical inhibition in dystonia.

A typical pathophysiological abnormality in dystonia is cocontraction of antagonist muscles, with impaired reciprocal inhibitory mechanisms in the spinal cord. Recent experimental data have shown that inhibitory interactions between antagonist muscles have also a parallel control at the level of the sensorimotor cortex. The aim of this work was to study heteronymous effects of a median nerve stimulus on the corticospinal projections to forearm muscles in dystonia. We used the technique of antagonist cortical inhibition, which assesses the conditioning effect of median nerve afferent input on motor evoked potentials (MEPs) elicited by transcranial magnetic stimulation (TMS) in ipsilateral forearm extensor muscles at rest. Nine healthy subjects and 10 patients with torsion dystonia participated in the study. MEPs and somatosensory evoked potentials were normal in patients. In healthy subjects, median nerve stimulation at 15- to 18-msec intervals inhibited the test MEPs in forearm extensors. In dystonic patients, median nerve stimulation delivered at the same conditioning-test intervals elicited significantly less inhibition of the test MEP. On the whole, these data suggest an impaired sensory-motor integration in dystonia and, more specifically, the decreased antagonistic cortical inhibition could suggest that functional interactions between antagonist muscles are primarily impaired at the cortical level.     

Motor and somatosensory evoked potentials in asymptomatic spondylotic cord compression.

To assess whether electrophysiological tests are of use in differentiating between patients with asymptomatic cervical stenosis and patients with clinical evidence of myelopathy, we studied motor evoked potentials (MEPs) to magnetic brain stimulation and somatosensory evoked potentials (SEPs) in patients with asymptomatic cervical cord compression and compared the results to healthy age-matched controls. The MEPs were normal in 23 of 25 patients and SEPs in 22 of 23 patients. Thus, MEPs and SEPs are normal in most cases of asymptomatic cervical stenosis. As previous studies have shown MEPs, and to a lesser extent SEPs, to be sensitive in the detection of spondylotic myelopathy, our data indicate that MEP and SEP may be clinically useful for differentiating patients with cervical stenosis who have myelopathy from those who have not.     

Short latency somatosensory evoked potentials in patients with neurological lesions

Short latency somatosensory potentials following median nerve stimulation were recorded in patients grouped according to anatomic location of neurological lesion. Patients with cerebral lesions causing severe sensory deficit lacked a major positive wave of cortical origin that in normal subjects peaked at a mean latency of 20.5 ms. Patients with severe cervical spinal cord disease lacked all of the normal somatosensory response except for the earliest component attributed to peripheral nerve activity. Patients with brain-stem lesions showed delayed latencies of later waves and prolonged interwave latencies. However, auditory evoked potentials measured in the group with brain-stem lesions were more helpful in localization. Analysis of short latency somatosensory potentials can discriminate between peripheral nerve, spinal cord, brain-stem, and cerebral lesions. Further experience and refinement of technique of measurement should increase the value of this procedure.     

Direct cortical stimulation but not transcranial electrical stimulation motor evoked potentials detect brain ischemia during brain tumor resection

Motor evoked potentials (MEPs) elicited by both direct cortical stimulation (DCS) and transcranial electrical stimulation are used during brain tumor resection. Parallel use of direct cortical stimulation motor evoked potentials (DCS-MEPs) and transcranial electrical stimulation motor evoked potentials (TCeMEPs) has been practiced during brain tumor resection. We report that DCS-MEPs elicited by direct subdural grid stimulation, but not TCeMEPs, detected brain ischemia during brain tumor resection. Following resection of a brainstem high-grade glioma in a 21-year-old, the threshold of cortical motor-evoked-potentials (cMEPs) increased from 13 mA to 20 mA while amplitudes decreased. No changes were noted in transcranial motor evoked potentials (TCMEPs), somatosensory evoked potentials (SSEPs), auditory evoked potentials (AEPs), anesthetics, or hemodynamic parameters. Our case showed the loss of cMEPs and SSEPs, but not TCeMEPs. Permanent loss of DCS-MEPs and SSEPs was correlated with permanent left hemiplegia in our patient even when appropriate action was taken. Parallel use of DCS- and TCeMEPs with SSEPs improves sensitivity of intraoperative detection of motor impairment. DCS may be superior to TCeMEPs during brain tumor resection.     

Dissociation of somatosensory and motor evoked potentials in non-comatose patients after head injury.

OBJECTIVES: This study was performed to evaluate the clinical value of combined use of somatosensory evoked potentials (SEPs) and motor evoked potentials (MEPs) in patients with different brain lesions after head trauma. METHODS: A total of 64 patients with minor and moderate head injury were investigated by means of SEPs recorded over the parietal and frontal areas and MEPs following single-pulse transcranial magnetic stimulation (sTMS) and slow-rate repetitive transcranial magnetic stimulation (rTMS). RESULTS: In almost 50% of the patients, a dissociated impairment of somatosensory and motor evoked potentials was found. This dissociation was related to different distribution of SEP and MEP abnormalities in head injury subgroups. The higher threshold to sTMS and increased variability of the MEP amplitude during slow-rate rTMS were the most prominent features in patients with focal brain contusions, suggesting impairment of the cortical excitability. SEP abnormalities, as well as central conduction impairments, were more noticeable in patients with diffuse brain injury. CONCLUSIONS: A combined analysis of SEPs and MEPs may improve the assessment of cortical dysfunctions and central conduction abnormalities in non-comatose patients with head injury. A slow-rate rTMS may be considered as a complementary technique to the evaluation of the threshold in assessment of the excitability of the motor cortex in minor and moderate head injury.     

Somatosensory conduction times and peripheral, cervical and cortical evoked potentials in patients with cervical spondylosis.

Peripheral, cervical and cortical somatosensory evoked potentials after median or ulnar nerve stimulation were recorded in 21 patients with cervical spondylosis with radiculopathy or myelopathy. The test was normal when pain and paraesthesias were the only symptoms, while pathological in radiculopathy with objective neurological signs. The results varied in patients with cervical myelopathy.     

A comparison of somatosensory evoked and motor evoked potentials in stroke

Nineteen patients with radiologically confirmed stroke, and varying degrees of hemiparesis, were studied using somatosensory evoked potentials and the recently developed technique of transcutaneous motor cortex stimulation. The functional deficit caused by stroke was assessed at the time of evoked potential testing and again on follow-up 2 months after stroke. Stroke location and degree of recovery were compared with the evoked potentials elicited an average of 8 days after the acute event. The motor response was better (p less than 0.01) than somatosensory response at predicting an outcome in terms of functional recovery, both overall and when comparing patients with similar degrees of weakness. Normal somatosensory evoked potentials also predicted recovery but were not as sensitive as the motor evoked potentials (0.01 less than p less than 0.05). Motor evoked potentials in conjunction with clinical assessment may offer a means of more accurately predicting functional outcome following stroke than can be achieved with clinical assessment, with or without somatosensory evoked potentials. The additional finding that cortically evoked motor evoked potentials were delayed only by subcortical lesions is of interest and may extend the understanding of the pathophysiological mechanism of this response in humans.