Continuous somatosensory evoked potentials monitoring is highly sensitive to intraoperative occlusion of iliac artery during anterior lumbar interbody fusion: case report.

We report a case of thrombotic occlusion of the left common iliac artery during an L5-S1 anterior interbody fusion exposed via a retroperitoneal approach. The loss of distal blood flow was detected by loss of cortical and peripheral somatosensory evoked potentials on the left lower extremity. Restoration of the blood flow resulted in gradual return of evoked potentials of the involved extremity. The neurophysiological and pulse oximetry monitoring of the lower extremities are extremely sensitive for an early detection of thrombotic occlusions and vascular complications.

Cortical localization of external urethral sphincter activation by transcranial electrical stimulation.

PURPOSE: Repetitive transcranial electrical stimulation (rTES) was used to activate descending output to the external urethral sphincter muscle. METHODS: Motor evoked potentials (MEPs) were recorded from external urethral sphincter (EUS), and anterior tibial (TA) muscles following high voltage rTES in 9 consecutive patients undergoing spine surgery. Anesthesia was achieved by continuous propofol/narcotic infusion without paralytic agents. Anodal cortical stimulation was delivered at C4/C3, C2/C1, and Cz/Fz locations in each patient. Latency and amplitude of the MEP was measured and compared for each bipolar stimulation montage. RESULTS: The mean latency was 20.24 +/- 1.3 msec. for Cz/Fz; 20.19 +/- 1.1 msec. for C4/C3 and 20.19 +/- 1.1 msec. for C2/C1. Statistical analysis showed no significant difference in latency between the three sites (F(2,15) = 0.004; p > 0.05). The mean amplitude was 37.14 +/- 24.3 microV for Cz/Fz; 113.33 +/- 100.6 microV for C4/C3; and 85 +/- 73.9 microV for C2/C1. A significant difference between the amplitudes at three sites was observed (F(2,8) = 5.2; p < 0.05). The amplitude at C4/C3 was significantly greater than amplitude at CzlFz (t (8) = 3.08; p < 0.05), but data did not give enough evidence to believe that difference between amplitudes for site C4/C3 & C2/C1 was significant (p > 0.05). CONCLUSIONS: This study shows that the intraoperative MEP monitoring of the EUS is a feasible method. Furthermore, activation of descending axonal outflow to the EUS muscle is best achieved by cortical stimulation directed from C4 to C3 or C2 to C1 points.

Transcranial stimulation parameters to elicit motor evoked potentials.

PURPOSE: We studied effectiveness of single, paired, and repetitive transcranial electrical stimulation to activate motor cortex in patients during spine surgery. METHODS: In ten consented patients, the latency and amplitude of the muscle action potential from abductor pollicis brevis muscle after cortical stimulation was measured. RESULTS: The number of responses evoked by double (pair) pulse stimulation was significantly higher than that evoked by single pulse (p = 0.0191). A similar finding was obtained between the repetitive and single pulse stimulation (p = 0.0001). The repetitive stimulation was more effective than the double pulse stimulation (p = 0.0253). An increase of interstimulus interval (ISI), between pulses, from 1-3 msec did not significantly alter latency (p > 0.05) or amplitude (p > 0.05) with the double pulse or repetitive stimulations. The latency or amplitude did not significantly change with varying number of electrical pulses from 3-9. CONCLUSIONS: This study shows that the intraoperative repetitive transcranial stimulation is the most effective method to activate descending motor tracts under anesthesia.

Sensory and motor evoked potentials findings in patients with thoracic outlet syndrome.

OBJECTIVE: Diagnostic utility of somatosensory and motor evoked potentials in two patients with neurogenic and vascular thoracic outlet syndrome (TOS) were investigated. MATERIALS AND METHODS: In two female patients with progressive weakness and sensory disturbance of the arms, mixed nerve somatosensory evoked potentials (SSEP), and motor evoked potentials (MEP) were tested before and after dynamic position of the affected arm. RESULTS: The cortical and cervical (C7) ulnar SSEPs demonstrated no change in latency of major peaks at rest and after abduction of the shoulder. A slight diminishment of cortical amplitude was noted in the first patient after the dynamic position of the arm. The MEPs demonstrated significant drop in amplitude after dynamic position of the arm in both cases signifying neurovascular compression during elevation of the affected arm. No change in MEP latency was noted. The MEP amplitude completely returned to normal after repositioning the arm. CONCLUSIONS: Evoked potential studies are helpful in the diagnosis of neurogenic or vascular TOS. Reduced amplitude of MEP occurs after elevation of the arm above the head which improves after normal position of the arm.

Cervical myelopathy due to chronic vitamin B12 deficiency or herniated cervical disc or both.

OBJECTIVE: A female patient with diagnosis of combined system degeneration due to vitamin B12 deficiency and multi-level cervical disc herniation underwent a comprehensive neurophysiologic tests. MATERIALS AND METHODS: Central conduction time (CCT) was calculated after recording of the SSEPs from cervical, brainstem, and parietal sensory cortex to peripheral stimulation. RESULTS: The CCT between the lower cervical spine and brainstem was 3.63 msec and 3.41 msec for left and right side. All values were within the normal range. The visual EPs and brain-stem auditory EPs were also normal. The MR imaging of the cervical region was remarkable for multi-level degenerative changes as well as osteophyte formation at C4-7 segments causing canal stenosis. CONCLUSIONS: It is possible that her symptoms are related to two separate chronic problems. The first is history of B12 deficiency, causing a subacute systems degeneration syndrome. The second is evidence of a cervical spondylotic myelopathy.

Diagnostic utility of somatosensory and motor evoked potentials in a patient with thoracic outlet syndrome.

OBJECTIVE: To evaluate the utility of somatosensory and motor evoked potentials in the diagnosis of neurogenic thoracic outlet syndrome (TOS). MATERIALS AND METHODS: In a female patient with progressive weakness and sensory disturbance, ulnar nerve somatosensory evoked potentials (SSEP), and intraoperative motor evoked potential (MEP) were performed. RESULTS: The SSEPs demonstrated no significant change in latency of major peaks at rest and after abduction of the shoulder. Diminishment of amplitude was noted after dynamic position of the arm. The MEPs demonstrated no significant change in latency after dynamic position. Diminishment of amplitude was noted after the dynamic position. The amplitude returned to normal after repositioning the arm. CONCLUSIONS: Electrophysiologic study is helpful in the diagnosis of neurogenic TOS. Reduced amplitude of cortical SSEP and myogenic MEP is expected during dynamic position of the affected arm.

Psychogenic paraplegia in a patient with normal electrophysiologic findings.

STUDY DESIGN: A case report of psychogenic paraplegia following a motor vehicle accident was clinically diagnosed using median (MN) and posterior tibial nerves (PTN) somatosensory evoked potentials (SSEPs). OBJECTIVE: To report an unusual case of paraplegia in spite of normal electrophysiological and non-compromising radiographic spine findings. SUMMARY OF BACKGROUND DATA: Conversion disorder with motor system symptoms or deficit is a subtype which includes symptoms such as impaired motor coordination or balance, paraplegia, muscle weakness, difficulty in swallowing, and urinary retention. METHODS: The SSEPs were performed by each PTN at the ankle region behind the medial malleolus or the MN at the wrist using square wave pulses in 15 mA intensity. The SSEPs revealed well-developed somatosensory peaks for all extremities. RESULTS: Well-resolved MN-SSEPs were seen with stimulation of either arm. The principal peaks of N20 and P22 were 17 and 21 ms for both upper extremities. The principal peaks of P37 and N45 were 35 and 46 ms for both lower extremities. No side-to-side latency difference was noted. The MRI scan finding was a non-displaced L1 fracture without spinal canal compromise. CONCLUSIONS: In spite of an apparent paraplegia, contradictory clinical findings, normal neurophysiologic tests, and normal neuroradiologic findings are positive criteria for paraplegia/quadriplegia with psychogenic etiology.

Effects of methylprednisolone and MK-801 on functional recovery after experimental chronic spinal cord injury.

STUDY DESIGN: An experimental study was conducted to evaluate the effects of methylprednisolone and MK-801 after the compressive injury of spinal cord in rats. OBJECTIVES: To investigate the effect of methylprednisolone and non-competitive NMDA antagonist MK-801 in long-term functional outcome after spinal cord injury (SCI). METHODS: A randomized group A of Sprague-Dawley rats were treated with MK-801 (1.0 mg/kg, n=10; Group A) after a compression injury. A group of methylprednisolone (MP)-treated (30 mg/kg, n=10; Group B) and non-treated animals (n=9; Group C) were included for comparison. The functional motor outcome such as inclined plane (IP), toe spreading reflex (TSR), and modified Tarlov scale (TS) were measured in each animal at regular time points up to 8 weeks post-treatment. Histologically the injury site was scored in four groups and immunohistochemically Wallerian Degeneration (WD), astrocytosis and expression of beta-amyloid protein was identified. RESULTS: In examining the IP data, no significant difference was recognized between the group means (P-value>0.5). For the TSR, there were no differences in the group responses. For the TS, the differences were not statistically significant. Only group B showed significance in cavitation scores compared to group A (P>0.0094), WD was significantly different than group C (P>0.03), astrocytosis was significantly higher than group A (P>0.001) and modest presence of beta-amyloid protein. CONCLUSION: Our data indicate that one time bolus administration of MK-801 lacks any significant effect on axonal function in chronically injured rats. Daily bolus administration of MP at 30 mg/kg also did not ensure a better functional outcome. Immunohistochemically we have been able to show significant differences in WD, astrocytosis and small insignificant changes in beta-amyloid protein.

Balloon device for experimental graded spinal cord compression in the rat.

We have developed a balloon device that creates reproducible graded compression of the rat spinal cord. It uses a modified Camino intracranial pressure monitor bolt with a small latex balloon attached to the tip. The device is affixed to the spinous processes of two cervicothoracic vertebrae and positioned directly over an exposed segment of spinal cord. Ten compression balloons were tested and revealed reproducible pressure transmission at expansion volumes from 0.12 to 0.34 cc. Reversible graded spinal cord compression was verified by monitoring cortical somatosensory and motor evoked potentials before, during, and after cord compression. The pathophysiologic changes occurring with graded compression and the effect of therapeutic interventions can be studied in a rat model.

Influence of isoflurane anesthesia on motor evoked potentials elicited by transcortical, brainstem, and spinal root stimulation.

Electrical stimulation over the motor cortex, base of the skull, and cervical spine motor roots was performed in 9 male rats (410 +/- 86 g) before and after induction with isoflurane at 1 MAC concentration. The mean latency and amplitude of descending spinal evoked potential (DSEP) from spinal cord and motor evoked potentials (MEPs) from forearm muscles obtained after motor cortex, brainstem, and cervical root stimulations were calculated and compared. The electrical current intensity to elicit the MEPs after cortical, brainstem, and spinal roots stimulation were 23.4 +/- 7.6, 7.0 +/- 3.1, and 1.4 +/- 0.8 mA, respectively. The brainstem stimulation activated descending motor pathways with a latency midway between that produced by electrical stimulation over the motor cortex, and by electrical stimulation over the cervical enlargements. The latency difference between cortical (8.8 +/- 3.2 msec) and brainstem (5.7 +/- 1.2 msec) stimulation was 3.1 +/- 2.3 msec in all forearm extensor muscles. The latency difference between cervical (3.6 +/- 0.9 msec) and brainstem stimulation (5.7 +/- 1.2 msec) was 2.3 +/- 1.1 msec for the same muscles, suggesting the brainstem stimulation activates the descending motor neurons at the level of cervical-medullary junction. The amplitudes were 189 +/- 141, 672 +/- 354, and 765 +/- 389 microV for cortical, brainstem, and cervical root stimulations. The inhalation anesthesia isoflurane at 1 MAC (1.2%) completely abolished the cortical and brainstem MEPs within minutes, while the MEPs elicited by direct stimulation of the cervical spinal roots remained unchanged. Our results indicate synaptic-dependent MEPs elicited at motor cortex or brainstem levels are highly sensitive to isoflurane anesthesia.

Effect of 4-aminopyridine and single-dose methylprednisolone on functional recovery after a chronic spinal cord injury.

The demyelination process is an important factor contributing to long term sensory and motor impairments after spinal cord injury (SCI). Exposure of axonal K+ channels after demyelination may contribute to blockage of action potentials across the injury site. A K+ channel blocker, 4-aminopyridine (4-AP), has been effective in restoring some sensory and motor impairment in incomplete SCI patients. The long-term effect of this compound in chronic model of SCI is not known. In this study, after a compression injury of 50 grams in rats, a randomized treatment was initiated 3 weeks after the initial injury which was followed by daily administration of 4-AP at 2 mg/kg (n = 8), 4 mg/kg (n = 8), and 6 mg/kg (n = 8) for 4 weeks. A group of methylprednisolone (MP)-treated (30 mg/kg, n = 8) and non-treated animals (n = 8) were included for comparison. The functional motor outcome was measured in each animal at regular time points up to 4 weeks post-treatment. All animals receiving 6 mg/kg developed generalized seizure and were excluded from the study. In the other animal groups, analysis of the behavioral outcome and neuro-pathological changes were essentially similar and did not show any significant effect of treatment. Our data indicate that daily administration of 4-AP, over 4 weeks of treatment period, lacks any significant effect on axonal function in chronically injured rats. This could be due to (a) lack of significant numbers of demyelinated axons which could improve the functional outcome and (b) a treatment regimen that was not adequate to contribute to a better functional outcome. One time bolus-administration of MP at 30 mg/kg also did not ensure a better functional outcome.

Experience with transcranial magnetic stimulation in evaluation of spinal cord injury.

Nine subjects (seven male, two female) underwent transcranial magnetic stimulation (TMS) toward the evaluation of spinal cord injury (SCI). The evaluation of SCI with TMS tended to support clinical findings. Those subjects with clinically complete injuries demonstrated no evoked muscle response below the level of injury. Those subjects with clinically incomplete injuries showed trends toward prolonged evoked muscle latencies on the weaker side. Facilitation tended to enhance distal muscle responses. With incomplete spinal injury, the facilitation maneuver allowed the recording of weak muscle responses as well as those otherwise not present at rest. Maximum anal sphincter contraction also helped facilitate muscle responses and tended to impart less noise in the recordings. Facilitation failed, however to produce a response in those subjects with clinically complete injuries. No subject experienced adverse effects during the study. TMS promises to be an effective tool for the evaluation of SCI.

Experience with transcranial magnetic stimulation in cortical mapping.

Seventeen subjects underwent transcranial magnetic stimulation (TMS) toward cortical mapping. Cortical mapping produced scalp representations of five upper extremity muscles, and their spatial orientation tended to support an expected anatomic pattern. Muscle map locations and map areas showed trends across musical skill and hand dominance, as well. No subject experienced adverse effects during the study. TMS promises to be an effective tool for noninvasive cortical mapping.

Pretreatment with NMDA receptor antagonist MK801 improves neurophysiological outcome after an acute spinal cord injury.

The post-traumatic release of excitatory amino acids (EAA) and their actions on N-methyl-D-aspartate (NMDA) receptors plays a major role in the spinal cord secondary injury process. The neuronal damage caused by the release of EAA may be reduced by NMDA-receptor channel blockers. To investigate the involvement of NMDA receptors in spinal cord injury (SCI), we pretreated animals with the noncompetitive NMDA antagonist MK801 (1.0 mg kg-1) before a compressive acute SCI. Pretreated animals with MK801 significantly (p = 0.038) improved the recovery of function as measured by evoked potential activities. Morphologically, specimens from rats treated with MK801 were characterized by milder and more localized hemorrhage in the gray matter. Immunohistochemical staining for glial fibrillary acidic protein (GFAP) and neurofilament (NF) histochemistry showed leakage of these antigens in traumatized cord while characteristic staining of astrocytes and neurons and their processes was observed in morphologically preserved tissue. The loss of NF immunoreactivity was reduced by MK801 treatment.

The effects of taxol, methylprednisolone, and 4-aminopyridine in compressive spinal cord injury: a qualitative experimental study.

BACKGROUND: Taxol is a diterpene alkaloid that stimulates tubulin production in cells. It may be effective in preserving the cytoskeleton of spinal cord axons after injury. METHODS: Thirty-nine rats were submitted to spinal cord compression. The animals were divided into three groups that received taxol (18.75 mg/m2), methylprednisolone (30 mg/kg), or 4-aminopyridine (1 mg/kg). Taxol was administered as one dose immediately after injury and two additional doses on days 14 and 21. Methylprednisolone was given as a single injection immediately postinjury. Four-aminopyridine was administered on days 25, 26, and 27. A group of nine injured animals served as a control without any treatment. Evoked potentials were recorded before, during, and 4 weeks postinjury. Behavioral tests were measured to evaluate recovery of motor function. RESULTS: The taxol and methylprednisolone-treated animals demonstrated a significant improvement in comparison with the control group. No functional improvement was found at 1 mg/kg treatment of 4-aminopyridine in rats. CONCLUSIONS: We conclude that taxol and methylprednisolone given shortly after the compression injury improve functional outcome after an incomplete spinal cord injury.

Radiofrequency as a lesioning model in experimental spinal cord injury.

Many models have been developed to study spinal cord injury (SCI), such as cryogenic lesioning, hot water injury, scalpel lesioning, compressive trauma using clips, electromechanical devices, extradural cuffs, and weight-drop techniques. In this study, the radiofrequency (RF) lesion was used for inducing an experimental SCI in cats. The neuropathology was correlated with the MRI. In this model, 4 cats were injured at the thoracic spinal cord (T11-T12) with a lesion of 65 degrees C for 1 min using a micromanipulated penetrating RF electrode. The MRI of the lesions after 2, 3, 5, and 6 weeks post-injury as well as the correlative histological changes were obtained. The RF-induced lesion was discrete with little spreading across the spinal cord. There was a good correlation between the histopathology findings and the MRI. We conclude that experimental RF lesioning of the spinal cord can produce a consistent lesion with predictable histopathological changes in experimental animals. A 65 degree C injury for 1 min induced a clinical picture of an incomplete SCI. The RF lesioning should be considered as a new model to study SCI, particularly those with a penetrating component.

Suppression of spinal and cortical somatosensory evoked potentials by desflurane anesthesia.

The effect of the volatile anesthetic desflurane on spinal and cortical somatosensory evoked potentials (SEPs) was examined in 11 Sprague-Dawley male rats. Platinum recording electrodes were placed stereotactically over the left somatosensory cortex and dorsal midline of the T11-12 spinal cord while the right posterior tibial nerve was stimulated at twice motor threshold. The effect of desflurane was examined at various concentrations ranging from 0.7 to 11.4% (2 MAC). Mean arterial blood pressure (MAP) decreased (p = 0.001) progressively with increasing end-tidal desflurane concentrations. Concentrations of 1.4% (1/4 MAC) and 2.8% (1/2 MAC) did not significantly affect the spinal SEP (SSEP) amplitude or the latency. With higher concentrations, there was a progressive decrease in amplitude of the cortical SEPs (CSEPs; p = 0.002) and SSEPs (p = 0.008). However, CSEP and SSEP latencies did not change. At 5.7% (1 MAC), three animals (33%) lost CSEPs while SSEPs remained intact. At 11.4% (2 MAC), the CSEPs were lost in all animals. Only one rat lost the SSEPs at the 2 MAC concentration of desflurane, indicating the resistance of the SSEPs to desflurane anesthesia. We conclude that desflurane anesthesia significantly alters the amplitude of SSEPs and CSEPs without a significant change in the peak latency.

Neurophysiological evidence of spared upper motor neurons after spinal cord injury.

Fourteen cats were subjected to a moderate (100 gm-cm; n = 7) or a severe (600 gm-cm; n = 7) spinal cord injury at the C4-C5 level using a weight drop technique. Somatosensory evoked potentials (SSEPs) were recorded after stimulation of the median nerve in the forearm. The SSEPs were measured in each animal before and after the injury. Motor evoked potentials (MEPs) were recorded from forearm extensor muscles after transcranial magnetic stimulation of the motor cortex. The SSEPs and The MEPs were measured in each animal before and after the injury under ketamine-based anesthesia. After the moderate injury (n = 7), 83% of the animals (6/7) maintained the SSEPs and 100% (7/7) maintained the MEPs. Postoperatively, only one animal who lost the SSEPs post-injury became tetraplegic. The remainder were neurologically intact. In the severely injured animals (n = 7), 5/7 of animals lost SSEPs and subsequently became tetraplegic. The MEPS were maintained in 3/5 (60%) of these tetraplegic animals. Two of seven animals (40%) in this group did not lose SSEPs or MEPs and recovered with no clinical deficit. Our data show a good correlation between the presence of SSEPs and functional recovery in the injured groups. The presence of MEPs in 3/5 (60%) of the tetraplegic animals may imply the existence of functionally active motor fibers after severe spinal trauma.

Effect of desflurane anesthesia on transcortical motor evoked potentials.

The effect of the volatile anesthetic desflurane on motor evoked potentials was examined in male rats. Animals underwent cortical stimulation using small platinum ball stimulating electrodes secured on the motor cortex. To record evoked compound muscle action potentials (CMAPs), single-shock electrical stimulation was delivered to the forelimb representation of the motor cortex. Muscle responses were readily obtained in the contralateral extensor muscles. The effect of desflurane was examined at various concentrations ranging from 0.7 to 11.4%. With increasing concentrations of desflurane, there was a progressive decrease in the CMAP amplitude and systemic blood pressure over the baseline values. This decrease became statistically significant (p = 0.0078) at 5.7% [1 maximum alveolar concentration (MAC)] concentration of desflurane. Although there was a decrease in heart rate, the results were not statistically significant (p = 0.03). No significant difference in the onset latency or the duration of the CMAP was noted at different concentrations of the anesthetic. We conclude that desflurane anesthesia significantly alters the amplitude of the muscle response evoked by motor cortex stimulation in experimental animals.

Origin of muscle action potentials evoked by transcranial magnetic stimulation in cats.

We studied the effects of transcranial magnetic stimulation on ipsilateral and contralateral forelimb extensor muscles in anesthetized cats. A magnetic stimulator, operating at 100% intensity, was used through a circular coil, which was placed tangentially over the midline scalp. Bilateral activation of extensor muscles was readily obtained in all animals. The onset latencies were 7.3 +/- 1.1 and 7.07 +/- 0.8 msec for the contralateral and ipsilateral muscles, respectively. The amplitude of muscle response was unstable in magnitude, nevertheless, it did not show any significant difference between the two sides. The latency of response for ipsilateral and contralateral muscles was similar, which suggests simultaneous activation of motor pathways servicing forelimb muscles. Lesioning or ablation of the motor cortex and decerebration at mid-colliculi level did not abolish the evoked responses elicited at high intensity magnetic stimulation. Stereotactic electrical stimulation of the vestibular nuclei complex was performed, and satisfactory ipsilateral motor responses were obtained. Subsequently, a stereotactic radiofrequency lesion was made at the vestibular nuclei complex, with morphological confirmation. After this lesion, the motor evoked potentials (MEPs) were significantly diminished in amplitude. This finding strongly suggests that the generator of the MEPs resides in the brainstem, mainly at the vestibular nuclei complex.