Amplitude Of Spinal Cord Evoked Potentials Research Articles

Significant correlation between corticospinal tract conduction block and prolongation of central motor conduction time in compressive cervical myelopathy

We examined the relationship between the CMCT and features of spinal cord evoked potentials (SCEPs) among 25 patients with compressive cervical myelopathy to elucidate the mechanism underlying the prolonged central motor conduction time (CMCT) in patients with compressive cervical myelopathy. CMCT values were calculated by measuring motor evoked potentials from the abductor digiti minimi muscles (ADMs) and abductor hallucis muscles (AHs) following transcranial magnetic stimulation and peripheral conduction times determined in the ulnar and tibial nerves. SCEPs following transcranial electrical stimulation were recorded intraoperatively from C2-3, C6-7 and T11-12. The shorter/longer CMCTs between the patients' right and left ADMs and AHs were 9.5 ± 3.2/11.5 ± 3.8 and 16.2 ± 2.8/18.8 ± 3.3 ms, respectively (mean ± SD). The percentage ratio of the amplitude of the D-wave at C6-7 or T11-12 to that at C2-3 was 19.4 ± 14.2 or 3.2 ± 3.1%, respectively. The CMCT value was significantly correlated with the attenuation of SCEP amplitude, but not with SCEP latency both at C6-7 and T11-12, suggesting that CMCT prolongation is primarily due to corticospinal conduction block rather than conduction delay. Spinal motor neurons might need more time to fire in patients with compressive cervical myelopathy when corticospinal potentials, but not conduction, are attenuated, thereby resulting in prolonged CMCT.

Corticospinal tract conduction block results in the prolongation of central motor conduction time in compressive cervical myelopathy

Objective The objective of this study was to analyze corticospinal function in patients with compressive cervical myelopathy and to elucidate the mechanism underlying its prolonged central motor conduction time (CMCT). Methods Motor evoked potentials following transcranial magnetic stimulation (TMS) and peripheral conduction time in the ulnar and tibial nerves following electrical stimulation were measured from the abductor digiti minimi (ADM) and abductor hallucis (AH) muscles in 24 patients with compressive cervical myelopathy and used to calculate CMCT. Spinal cord evoked potentials (SCEPs) following transcranial electric stimulation were recorded intraoperatively from the C2-3 to C6-7 intervertebral levels. Correlations between prolonged CMCT and SCEP values were then estimated. Results The shorter/longer CMCT between the patients' right and left ADM and AH were 8.5±2.9/11.5±3.3 and 16.2±3.1/18.4±3.3 ms, respectively (mean±SD). The SCEPs amplitude at C6-7, compared to C2-3, was 25.7±21.0%. The attenuation of SCEP amplitude, but not latency, at C6-7 correlated significantly with CMCT prolongation. Conclusions Our data support the view that CMCT prolongation is primarily due to corticospinal conduction block, rather than conduction delay. Significance Insight was provided into the mechanism of corticospinal dysfunction in compressive cervical myelopathy.

An L-type calcium channel blocker, nimodipine influences trauma induced spinal cord conduction and axonal injury in the rat.

The influence of the potent L-type Ca[2+] channel antagonist Nimodipine on spinal cord evoked potentials (SCEP) and axonal injury following trauma to the spinal cord was examined in a rat model. Spinal cord injury (SCI) was produced by an incision into the right dorsal horn of the T10-11 segments under urethane anaesthesia (1.5 g/kg, i.p.). SCEPs were recorded by epidural electrodes placed over the T9 (rostral) and T12 (caudal) segments after stimulation of the right tibial and sural nerves. SCI induced a pronounced decrease of the SCEP negative amplitude in the rostral (T9) recordings immediately after trauma. Axonal injury seen as degradation of myelin basic protein (MBP) immunostaining and myelin vesiculation at the ultrastructural level was most pronounced at 5 h. Continuous administration of Nimodipine (2 microg/kg/min, i.v.) from 30 min prior to injury until sacrifice markedly attenuated the changes in SCEP amplitude and latency. Axonal damage, loss of MBP, and myelin vesiculation were much less evident in the nimodipine treated traumatised rats. These observations suggest that Ca[2+] channels play an important role in the trauma induced alterations in SCEP and axonal injury, and indicate a therapeutic value of Ca[2+] blockers in SCI.

Spinal cord evoked potentials and edema in the pathophysiology of rat spinal cord injury. Involvement of nitric oxide.

The possibility that nitric oxide is somehow involved in the early bioelectrical disturbances following spinal cord injury in relation to the later pathophysiology of the spinal cord was examined in a rat model of spinal cord trauma. A focal trauma to the rat spinal cord was produced by an incision of the right dorsal horn of the T 10-11 segments under urethane anaesthesia. The spinal cord evoked potentials (SCEP) were recorded using epidural electrodes placed over the T9 and T12 segments of the cord following supramaximal stimulation of the right tibial and sural nerves in the hind leg. Trauma to the spinal cord significantly attenuated the SCEP amplitude (about 60%) immediately after injury which persisted up to 1 h. However, a significant increase in SCEP latency was seen at the end of 5 h after trauma. These spinal cord segments exhibited profound upregulation of neuronal nitric oxide synthase (NOS) immunoreactivity, and the development of edema and cell injury. Pretreatment with a serotonin synthesis inhibitor drug p-chlorophenylalanine (p-CPA) or an anxiolytic drug diazepam significantly attenuated the decrease in SCEP amplitude, upregulation of NOS, edema and cell injury. On the other hand, no significant reduction in SCEP amplitude, NOS immunolabelling, edema or cell changes were seen after injury in rats pretreated with L-NAME. These observations suggest that nitric oxide is somehow involved in the early disturbances of SCEP and contribute to the later pathophysiology of spinal cord injury.

Evaluation of traumatic spinal cord edema using evoked potentials recorded from the spinal epidural space: An experimental study in the rat

Spinal cord evoked potentials (SCEP) elicited by simultaneous distal tibial and sural nerve stimulation were continuously recorded from the epidural space at the T 9 and T 12 levels of urethane anaesthetized rats before and after a unilateral incision (about 3 mm deep and 5 mm long) in the right dorsal horn of the T 10–11 segments. The changes in SCEP were correlated with the increase in spinal cord water content measured 5 h after injury. In addition, the influence of serotonin (5-HT) in mediating such changes was explored using a pharmacological approach. The changes in SCEP immediately after injury correlated well with development of spinal cord edema measured 5 h after injury. Thus, the maximal negative peak (MNP) amplitude of SCEP decreased by an average of 64.0% immediately after injury and the water content of the spinal cord was increased from 71.6% (controls) to 77.6% 5 h after injury. Pretreatment with p-CPA (a serotonin synthesis inhibitor) prevented the initial decrease of the MNP amplitude and also the increase of water content (72.5%). On the other hand, pretreatment with cyproheptadine (a 5-HT 2 receptor antagonist) enhanced both the initial decrease of the MNP amplitude as well as the increase of water content (81.3%). The results show a good correlation between changes of SCEP immediately after injury and the magnitude of spinal cord edema ( r = 0.9) measured 5 h after injury. The findings reveal a major role of serotonin in mediating early changes of SCEP and later development of spinal cord edema and demonstrate a prognostic value of early SCEP recordings in predicting the final outcome of traumatic spinal cord injuries.