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.

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.

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.

Effect of 4-aminopyridine in acute spinal cord injury.

BACKGROUND: The demyelination process has been proven to be an important factor contributing to long-term sensory and motor impairments after spinal cord injury (SCI). The loss of myelin promotes exposure of K+ channels in internodal region of the damaged myelinated axons leading to K+ efflux into the neurons with subsequent blockage of action potentials. The potassium channel blocker 4-aminopyridine (4-AP) has been effective in restoring some sensory and motor impairment in incomplete SCI patients. The effect of this compound given immediately after an acute injury is not known. The objective of this study was to determine if blockage of K+ ions efflux immediately after an acute SCI would improve neuronal conduction in this model of injury. METHODS: Cortical somatosensory evoked potentials (SSEPs) were recorded before and after a weight-induced compression injury of 120 grams, and were monitored up to 5 hours postinjury. A randomized treatment was initiated with administration of either vehicle or 4-AP. All 4-AP treatments were given as intravenous bolus injections of 1.0, 0.5, and 0.3 mg/kg at 1, 2, and 3 hours after the trauma. RESULTS: The SSEPs were abolished immediately after the injury in all control and treated animals. Both groups showed spontaneous recovery of the SSEPs at the rate of 44.5% for the 4-AP treated and nontreated groups at the second hour postinjury. This recovery rate remained the same for both groups at the end of the experiments. CONCLUSIONS: Based on the recovery of the SSEPs, our data indicate that early administration of 4-AP lacks any beneficial effect on axonal function during acute stage of spinal cord injury.

Stereotactic surgery in the management of intracranial disorders.

Fifty-six stereotactic procedures (thirty-eight stereotactic biopsies, 13 stereotactic craniotomies, and 5 implantations of intracranial catheters) were performed on 54 patients at the University of Missouri between 1990 and 1994. In 89.5% of cases a definitive diagnosis was made by stereotactic biopsy with a major complication rate of 2.6%, rates comparable to other published series. Stereotactic craniotomy was associated with no mortality and minimal morbidity. Stereotactic surgery is a safe and effective technique that improves the management of many intracranial disorders.

Effect of 21-aminosteroid pretreatment in compression trauma to the spinal cord.

The present work was performed to establish whether pre-injury administration of the 21-Aminosteroid, U-74389F, is beneficial for treatment of acute spinal cord trauma in rats, as it has been demonstrated that the bolus administration of the same compound one hour after injury facilitates the return of the spinal cord function as measured by electrophysiological recordings in this compression animal model of spinal cord trauma. Cortical somatosensory evoked potentials (CSSEPs) were recorded as an indicator of spinal cord function before and after a severe compression injury. Vital signs and the CSSEPs were monitored up to five hours post-injury. U-4389F treatment was given as a single injection (15 mg kg-1) one hour prior to the injury which was followed by a continuous infusion (3 mg kg-1h-1) during the procedure. The CSSEPs were abolished immediately after this injury both, in the untreated and treated animal groups. The majority of the treated animals (80%) demonstrated recovery of the CSSEPs within the second hour post-injury. The control group showed 40% recovery at this time period. At five hours post-injury, recovery rates were 47% and 87% for control and treated groups respectively. We conclude that the administration of the 21-Aminosteroid, U74389F, one hour prior to spinal cord injury facilitates the return of spinal cord function as measured by CSSEPs in a compression rat model of acute spinal cord trauma, supporting and verifying our previous experiences using the same compound as i.v. bolus injections one, two and three hours after the trauma, respectively.

Monitoring of motor tracts with spinal cord stimulation.

STUDY DESIGN: Sensory- and motor-evoked potentials were recorded after high thoracic (T2) epidural electrical stimulation of the spinal cord. Under general anesthesia, 22 cats underwent single or repetitive spinal cord stimulation. OBJECTIVES: Sensory-evoked potentials were recorded after antidromic activation of the posterior column sensory fibers at lower electrical intensities (< 5 V). Motor tract activation was accomplished by recording the ventral root and muscle action potential using single pulse stimulation (> 50 V). METHODS: Sensory-evoked potentials were recorded from the lumbar spinal cord (n = 20), dorsal root (n = 80), and peroneal nerve (n = 40). Motor-evoked potentials were recorded from the ventral root (n = 40) and the hindlimb musculature (n = 10). RESULTS: The lumbar spinal-evoked response resisted lesioning and showed a minimal change after a spinal cord hemisection. Dorsal rhizotomy abolished the ipsilateral peroneal nerve action potential, indicating antidromic activation of afferent fibers. Motor responses did not change after the dorsal rhizotomy, suggesting involvement of nonsensory pathways. CONCLUSIONS: These findings indicate that spinal cord stimulation activates sensory and motor tracts that can be recorded at various sites along the central or the peripheral nervous system.

Spinal cord injury without radiographic abnormality and Chiari malformation.

Spinal cord injury without radiographic abnormality and asymptomatic Chiari I malformation have an unusual coincidence. A young boy who had recently fallen from his porch was transferred to the neurosurgery service with a high cervical central cord syndrome. Careful study demonstrated no radiographic abnormality and, although the patient was previously quite well, magnetic resonance imaging revealed Chiari I malformation. Although expectedly uncommon, reports of three other similar cases support a less than independent relationship between these two processes. All four children, each aged 2 years, were premorbidly asymptomatic and were playing when they fell from low elevations; two were on a couch. All were evaluated by primary authorities 12 to 48 hours before definitive admission, and all had normal plain film examinations. Three of the four children suffered injuries in flexion, the fourth in extension. Three realized a 5-minute to 3-hour delay before the onset of symptoms, and three suffered gradual progression of deficit. Magnetic resonance imaging was the most commonly applied and productive diagnostic medium, demonstrating cerebellar ectopia in three of three cases. Two children were surgically treated, and all achieved at least a functional outcome. Similarities among these cases support a common mechanism of injury, and indicate careful counseling in children with asymptomatic Chiari I malformation and consideration of operative decompression in those children with progressive neurological injury and deficit.

Therapeutic value of 21-aminosteroid U74389F in acute spinal cord injury.

The effect of bolus injections of 21-aminosteroid U74389F after an acute spinal cord compression trauma in rats was studied. Cortical somatosensory evoked potentials (CSEPs) were recorded before and after a weight-induced injury of 120 g and monitored up to five hours post-injury. All U74389F treatments were given as i.v. bolus injections of 15, 7.5, and 3.75 mg kg-1 at 1, 2, 3 h after the trauma, respectively. The CSEPs were abolished immediately after the injury in the control and treated animals. The majority of the treated animals (88.8%) demonstrated a return of the CSEPs within the second hour post-injury. In contrast, the animals in the control group showed only 44.4% recovery at this time period. At three hours post-injury, U74389F-treated animals (n = 18) showed a full recovery (100%) while the recovery rate remained at 44.4% for the control animals. We conclude that the bolus administration of U74389F one hour after injury facilitates the return of the spinal cord function as measured by the CSEPs in this compression model of acute spinal cord trauma.

Evaluation of the calcium channel antagonist nimodipine after experimental spinal cord injury.

The cortical somatosensory evoked potentials (CSEPs) were recorded to determine if the administration of nimodipine improves axonal function after spinal cord injury. Animals receiving a 52 g compression injury (a moderately severe injury) for 5 minutes were randomly allocated to one of five treatment groups. Each group was given an infusion of one of the following nimodipine regiments over 2 hours, commencing 1 hour before compression: placebo (n = 20), 0.5 micrograms/kg (n = 10), 0.25 micrograms/kg (n = 20), 0.125 micrograms/kg (n = 10), and 0.25 micrograms/kg + Hetstarch (n = 10). In the control group, 65% of animals lost the CSEPs immediately after the injury with almost all (95%) of these regaining the CSEPs within 15 minutes after decompression of the spinal cord. In the treated groups, the rate of the CSEP loss was highest in the 0.5 micrograms/kg group. This group also had the lowest CSEP recovery. The proportion of the CSEP loss was essentially the same for the other nimodipine-treated groups, although it seemed that there was an increasing number of nonresponses with increasing the nimodipine dose. Our data indicate lack of any beneficial effects of nimodipine on axonal function as measured by evoked activities in experimental spinal cord injury.

Motor-evoked potential changes during hypoxic hypoxia.

Motor-evoked potentials (MEPs) from forearm muscles were recorded in response to single-shock electrical stimulation of motor cortex of rats (n = 15) under pentobarbital anesthesia and controlled room air ventilation. In addition, electroencephalograms (EEGs) were recorded for all animals. Following baseline MEP recording in room air (21% O2), animals were subjected to graded hypoxia of either 15.75%, 10.5%, or 5.25% oxygen for 10 minutes, then followed by room air ventilation for 15 minutes. The mean baseline latency, amplitude, and duration of the evoked muscle response were 4.3 +/- 0.4 mseconds, 556 +/- 476 microV, and 9.6 +/- 2.3 mseconds, respectively. At moderate hypoxia (15.75%), the latency was 4.2 +/- 0.5 mseconds and the amplitude and the duration were 530 +/- 356 microV (n = 14), and 9.5 +/- 2.2 mseconds, (n = 14). These values did not deviate significantly from baseline (p > 0.56). Only one animal lost MEPs at the 15.75% hypoxia level. At 10.5% hypoxia, 27% of animals (n = 4) lost MEP within minutes. In the remaining animals (n = 11), there was a trend toward a prolongation of latency and a decrease of both amplitude and duration. All animals lost MEPs under extreme hypoxia (5.25%) within 2 minutes. No change was seen in the EEG recording until the level of extreme hypoxia was reached. The loss of MEPs at this level of hypoxia was concurrent with the loss of EEGs. We conclude that hypoxia effects MEPs in experimental animals.

Osteoma of the internal auditory canal.

The use of MRI for the evaluation of lesions in the internal auditory canal presents a potential pitfall in the diagnosis of bony lesions of the IAC, because bone is poorly visualized with this method of imaging. The presence of marrow in an osteoma might aid in its detection, since fat in the marrow has a bright signal intensity of T1-weighted imaging. Computed tomography remains the imaging modality of choice for bony lesions of the temporal bone. We demonstrate a case of IAC osteoma in which surgical removal resulted in improvement of symptoms. The gross and microscopic appearance of the IAC osteoma in this case is similar to the characteristic findings of osteomas of the EAC. This suggests that the criteria applied to osteomas and exostoses of the EAC may also be used to differentiate bony lesions of the IAC.

Dissociation of somatosensory and motor evoked potentials in a patient with an intramedullary spinal tumor.

We describe a patient with an intramedullary spinal tumor who demonstrated postoperative improvement of motor and sensory function despite the lack of somatosensory evoked potentials (SSEPs) before and after intraoperative monitoring. The motor system was evaluated by direct spinal cord stimulation across the tumor bed. The resultant evoked compound muscle action potentials and compound nerve activities were normal. Although there is sufficient clinical evidence that SSEPs are sensitive to posterior and posterolateral ischemic insults of the spinal cord, the technique should be employed with an awareness of its limitations in monitoring the descending tracts which have a different blood supply and occupy more anterior locations in the spinal cord.

"Backfiring" in spinal cord monitoring. High thoracic spinal cord stimulation evokes sciatic response by antidromic sensory pathway conduction, not motor tract conduction.

Spinal cord stimulation has been advocated as an alternative to motor cortex stimulation for motor tract activation. To test this theory, evoked responses were recorded from lumbar spinal cord (L2; n = 14), spinal roots (L4-L7; n = 112), peripheral nerves (sciatics; n = 28), and hind limb muscles (n = 28) after epidural stimulation of the T1-T2 segment of the spinal cord in dogs (n = 12), cats (n = 2), and monkeys (n = 2). The spinal response evoked by spinal cord stimulation was resistant to a dorsal hemisectioning (depth, 7-8 mm) of the midthoracic spinal cord. A minimal attenuation of latency and amplitude occurred with dorsal hemisectioning, suggesting signal transmission through descending or ascending pathways in the ventrolateral and ventral quadrants of the spinal cord. The sciatic nerve response was abolished by a dorsal column transection (depth, 3-4 mm) or ipsilateral lumbar dorsal rhizotomy (four dorsal roots). This shows that the evoked response recorded from the sciatic nerve in our animals was not travelling, as we expected, through the ventral roots, but rather was conducted antidromically through sensory fibers in dorsal roots.

Effect of graded hypoxia on cortical and spinal somatosensory evoked potentials.

Cortical somatosensory evoked potential (CSEP), spinal somatosensory evoked potential (SSEP), and electroencephalogram were recorded in rats under pentobarbital anesthesia. After baseline recordings in room air (21% O2), animals were subjected to a graded hypoxia at 15.75%, 10.5%, and 5.25% oxygen levels for 10 minutes. Each level of hypoxia was followed by a 15-minute reoxygenation period. With a moderate hypoxia (15.75% O2), measured latencies for the CSEP and the SSEP were not significantly different compared with baseline (p greater than 0.05). The CSEP amplitude showed a significant increase (p = 0.02) during reoxygenation after the moderate hypoxia. Change in the latency or amplitude of SSEP at 15.75% hypoxia or during the reoxygenation period was not significant compared with the room air (p greater than 0.05). No change in the electroencephalogram was noticed with the moderate hypoxia. At severe hypoxia (10.5% O2), 80% of the animals lost CSEP within 2 minutes. The loss of CSEP was concomitant with significant attenuation of the electroencephalogram waves. The SSEP was resistant to the severe hypoxia and was present in all animals. We concluded that hypoxia affects CSEP with the tendency to increase the amplitude at moderate hypoxia (15.75%) and loss of the latency and amplitude with severe (10.5%) and extreme (5.25%) hypoxia.

The effects of propofol anesthesia on transcortical electric evoked potentials in the rat.

The effects of halogenated anesthetic agents on somatosensory and motor evoked potentials (MEP) have been documented previously. Intravenous anesthetic propofol has not yet been used during MEP monitoring. This study investigates the effects of propofol on transcortical MEP in rats during bolus, infusion, and recovery conditions. After baseline MEP recordings, animals received a hetastarch bolus, followed by a propofol (10 mg/kg) bolus dose. A propofol infusion (10 mg/kg/h) and a hetastarch infusion were then begun. MEP recordings were obtained after the propofol bolus, during the infusion, and after a 30-minute recovery phase. Blood pressure readings remained stable. MEP onset latency increased, and amplitude decreased. Response duration diminished. All values returned towards the baseline during recovery. Our results show that the effects of propofol on MEPs are similar to its effects on somatosensory evoked potentials. Propofol seems to be a reasonable agent for use during intraoperative MEP monitoring and should be further investigated for use during spinal cord monitoring in humans.

Depressive effect of isoflurane anesthesia on motor evoked potentials.

The influence of the volatile anesthetic isoflurane (Forane) on motor evoked potentials was examined in rats. To record motor evoked potentials, single-shock electrical stimulation was delivered to the forelimb representation of the motor cortex. This resulted in elicitation of a compound muscle action potential from the contralateral extensor muscles. The effect of isoflurane was examined at various concentrations ranging from 0.2 to 1.5%. With increasing concentrations of isoflurane there was a progressive increase in onset latency of the compound muscle action potential and a decrease in peak-to-peak amplitude and duration. Latencies were significantly increased over baseline values for concentrations of isoflurane from 0.5 to 1.5% (P values were 0.001 to 0.007). For the amplitude and the duration, responses at 0.5 to 1.5% isoflurane were significantly lower than baseline (P values were 0.001 to 0.007). We conclude that isoflurane anesthesia significantly changes the muscle response evoked by motor cortex stimulation in experimental animals.