Hideaki Fujimoto

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.

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.

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.

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.