Hiroshi Yonemura

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.

A correlation between magnetic resonance imaging and electrophysiological findings in cervical spondylotic myelopathy.

Study Design. Correlation between compressed spinal cords on magnetic resonance imaging (MRI) and electrophysiological findings in cervical spondylotic myelopathy patients. Objective. To clarify the correlation between spinal-cord-evoked potentials and MRI measurements of compressed spinal cords in patients with cervical spondylotic myelopathy. Summary of Background Data. Compression of the spinal cord does not always cause clinical symptoms and it is difficult to infer the degree of dysfunction of the spinal cord from MRI findings. Methods. Seventeen patients with cervical spondylotic myelopathy were examined with MRI and spinal-cord-evoked potentials before surgery. Using abnormality in spinal-cord-evoked potentials as indicators of spinal cord morphology, spinal-cord transverse area and compression ratios (central and 1/4-lateral) were measured on T1-weighted axial imaging. The correlations between these dimensions and electrophysiological findings were investigated. Results. The mean preoperative transverse area of the spinal cord was 47.13 mm2.The mean preoperative central compression ratio of the spinal cord was 34.4%. The mean preoperative 1/4-lateral compression ratio of the spinal cord was 27.5%. A correlation (Spearman r=0.65, P < 0.01) was observed between the 1/4-lateral compression ratio of the spinal cord and the amplitude ratio of spinal-cord-evoked potentials after electric stimulation of the brain (Br(E)-SCEPs). Conclusions. The preoperative 1/4-lateral compression ratio of the spinal cord was found to reflect the degree of dysfunction of the corticospinal tracts.

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.

A new rabbit model for the study on cervical compressive myelopathy.

Development process and pathology of myelopathy due to chronic spinal cord compression have not been fully elucidated. This study was conducted in order to establish an experimental model which can efficiently produce myelopathy and be useful in the studies on myelopathy due to chronic spinal cord compression. Under electrophysiological monitoring of the spinal cord, anterior compression was produced on C5 using a plastic screw. Two weeks later, a plastic plate was inserted under the C5 arch. For the subsequent 10 months on average, walking pattern and MR images were periodically monitored. Before the sacrifice, electro‐physiological test was performed and then histopathological examination was done. Palsy appeared at 5 months on average after the addition of posterior compression. Mean compression ratio of the spinal cord calculated on MR images was 34%. All animals with compression showed a high intramedullary signal intensity, and the mean contrast‐to‐noise ratio (CNR) in the compressed area was 49%. Electrophysiological test showed a significant decrease in the amplitude of spinal cord evoked potentials (SCEPs) at the given compression level. Histology showed flattening of the anterior horn, disappearance and necrosis of anterior horn cells in the gray matter; and demyelination and axonal degeneration in the white matter. The antero‐posterior compression produces the condition of spinal canal stenosis. Repeated antero‐posterior compression to the spinal cord is important in establishing myelopathy. The present animal model was evaluated to be useful in the studies on myelopathy.

Differential recording of upper and lower cervical N13 responses and their contribution to scalp recorded responses in median nerve somatosensory evoked potentials

To distinguish the different origins of cervical N13 potentials in median nerve somatosensory evoked potentials (SSEPs), cervical N13 potentials were recorded by two different montages. The abnormal patterns of the SSEPs were compared to the abnormal evoked spinal cord responses (ESCPs) recorded from posterior epidural space in 13 patients with various cervical lesions. SSEPs from the posterior cervical surface were recorded from the mid-cervical level with anterior neck reference (Cv5-AN) and from the upper cervical level with inion reference (Cv2-IN). Scalp responses were recorded from the parietal region contralateral to the stimulating side with non-cephalic reference (shoulder contralateral to stimulating side). ESCPs were recorded from the posterior epidural space using catheter electrodes or needle electrodes inserted into the ligamentum flavum. Lower cervical N13 (LC-N13) recorded from the Cv5-AN montage showed similar latency to upper cervical N13 (UC-N13) recorded from the Cv2-IN montage. The latency of the early part of the P13-P14 complex in the scalp montage was similar to that of the UC-N13 and the negative peak latency of the ESCPs recorded at the C2-3 level. Attenuation of the LC-N13 and relatively preserved UC-N13 and P13-P14 were characteristic in patients with cervical syringomyelia and compression cervical myelopathy at the mid-cervical levels. Attenuation of the UC-N13 with normal LC-N13 was characteristic in patients with cervical spondylotic myelopathy who showed conduction blockade of the ESCPs at the C3-4 level. In a patient with schwannoma at the C1-2 level, conduction blockade of the ESCPs was observed at the C1-2 level. P13 was normal but P14 was prolonged. UC-N13 and P13 latencies were similar to the negative peak latency of the ESCPs at the C2-3 level. We demonstrated that two different cervical N13 potentials can be recorded by two different montages and they represent different behavior in various spinal cord lesions. In addition, at least the early part of the P13-P14 complex originates in the upper cervical region. To distinguish two different cervical N13, it is useful to detect not only the cervical pathology but also the symptomatic cervical cord compression level in patients with cervical myelopathy.

Does cortical motor neuron excitability change in peripheral nerve injury

OBJECTIVE To investigate changes in cortical motor neuron excitability after peripheral nerve injury, evoked spinal cord potentials (ESCPs) following hemispheric transcranial magnetic stimulation (TMS) were recorded in awake patients with unilateral brachial plexus injury. METHODS ESCPs following hemispheric TMS were recorded in 6 patients with unilateral complete type brachial plexus injury. Studies were performed within 6 months from the time of injury. ESCPs were recorded from posterior epidural space using catheter electrodes. Hemispheric TMS was applied on the motor cortex using a figure-of-8 coil. The threshold of ESCPs following hemispheric TMS was measured. The number, latency, and amplitude of ESCPs following high stimulus hemispheric TMS were measured and compared. RESULTS No significant change was observed in the threshold of ESCPs following TMS contra-lateral to the injured upper limb compared to that following TMS contra-lateral to the intact upper limb. Several ESCP components were recorded following high stimulus hemispheric TMS. No significant changes were observed in comparison with number, latency and amplitude of ESCPs following high stimulus TMS contra-lateral to the injured upper limb and those following TMS contra-lateral to the intact upper limb. CONCLUSIONS From a study of ESCPs following single TMS, no evidence was obtained that cortical motor neuron excitability changes in patients with traumatic unilateral brachial plexus injury at relatively early stages. We investigated the changes of cortical motor neuron excitability in patients with brachial plexus injury from the ESCPs following TMS. In single TMS, our data gave no evidence for cortical excitability changes at relatively early stages.

Spatial distribution of corticospinal potentials following transcranial electric and magnetic stimulation in human spinal cord

To investigate the spatial distribution of the human corticospinal tract in the spinal cord, evoked spinal cord potentials (ESCPs) following transcranial electrical and magnetic stimulation were recorded simultaneously from both the anterior and posterior epidural space in five anesthetized patients. One ESCP component following transcranial electrical stimulation (D-wave) and at least two ESCP components (initially D-wave and later I-wave) following transcranial magnetic stimulation were recorded in all subjects. The negative peak latency of all the potentials recorded from the posterior epidural space was the same as that recorded anteriorly. The amplitude ratio of the ESCP following electrical stimulation (posterior/anterior) was 1.10+/-0.12, while that of ESCPs following magnetic stimulation was 1.08+/-0.12 (N1) and 1.15+/-0.16 (N2). These results suggest that lateral corticospinal tract descending dorsolateral fasciculus in the spinal cord is main corticospinal pathway and spatial distribution of D and I-waves are similar in the human cervical cord.

Reconstruction of shoulder and elbow function using multiple muscle transfers for cervical spondylotic amyotrophy.

Study Design. This was a retrospective study of 8 patients with cervical spondylotic amyotrophy who underwent multiple muscle transfers. Objective. The purpose of this study was to evaluate results of multiple muscle transfers about the shoulder and elbow in patients with cervical spondylotic amyotrophy. Summary of Background Data. Cervical spondylotic amyotrophy is characterized by severe muscle atrophy of the shoulder girdle and elbow. Even after cervical spine surgery, many patients have poor shoulder and elbow function. Methods. Multiple muscle transfer procedures including the transfer of trapezius, pectoralis major, latissimus dorsi muscles, and the Steindler procedure for reconstruction of shoulder and elbow function were performed in 8 patients with cervical spondylotic amyotrophy. Patients were evaluated at a mean of 18.2 months (range, 5–75 mo). Results. All 8 patients obtained satisfactory functional recovery with improvement of active range of motion without any systemic and local complications within 3 to 6 months postoperatively. Patients at the last follow-up had obtained a mean of 91° of shoulder abduction, 111° of shoulder flexion, 23° of external rotation and 110° of elbow flexion. Disability scores (Japanese version) of the arm, shoulder, and hand improved by a mean of 28 points. Conclusion. Multiple muscle transfers can improve shoulder and elbow function in cervical spondylotic amyotrophy, in cases of not only poor outcome after cervical surgery, but also in advanced paralysis. It is a useful set of procedures even in old patients, and provides definitive functional improvement of shoulder and elbow function from 3 to 6 months. Level of Evidence: 4

Compound Muscle Action Potentials Under Dynamic Stress in Lumbar Spinal Canal Stenosis

Intermittent claudication is one of the characteristic symptoms in lumbar spinal canal stenosis. We recorded compound muscle action potentials (CMAPs) from the extensor digiti brevi (EDB) and the abductor hallucis (AH) before and after dynamic stress elicited by cauda equina electrical stimulation or transcranial magnetic stimulation. In 12 cases of 25 patients, the amplitudes of the CMAPs from the EDB or the AH elicited by cauda equina electrical stimulation decreased transiently, and recovered to the status of the control gradually within 5 min. In four cases of six patients, the amplitudes of the CMAPs elicited by transcranial magnetic stimulation decreased temporarily, and recovered to the status of the control within six minutes. It was suggested that a rapidly reversible physiological block by ischemia on the chronic injured cauda equina was the cause of the neurogenic intermittent claudication.