Spinal Cord Potentials Research Articles

Spinal function monitoring by evoked spinal cord potentials in aortic aneurysm surgery

Evoked spinal cord potentials (ESCPs) were monitored in 12 patients who underwent repair of thoracoabdominal aortic aneurysm with a high risk of spinal ischemia. A pair of bipolar catheter electrodes were introduced into the epidural space, one at the level of the C5-T2 vertebrae and the other at the level of T11-L2. Conductive mixed ESCP in seven patients, conductive sensory ESCP in one patient, and segmental descending ESCP in three patients were observed by applying a rectangular electric current to one of each pair of epidural electrodes and recording through the other. Segmental ESCP in response to posterior tibial nerve stimulation was observed in one patient. Following aortic cross-clamping, the I wave of conductive mixed ESCPs gradually decreased in amplitude with latency prolongation in five of the seven patients and disappeared in one of these five; transient augmentation of amplitude was observed before eventual decline in four of these five patients. The N wave of segmental descending ESCP subsequently flattened in two of the three patients and the N1 wave of segmental ESCP in the one patient. Three of the four patients in whom the ESCPs disappeared during aorta clamping recovered the ESCPs after declamping and showed no neurological disorders postoperatively. Intraoperative ESCP monitoring appears to be useful to detect spinal cord ischemia in the early stage and to alert surgeons and anesthesiologists so that timely resuscitative steps can be taken.

Auditory P3 event related potentials (ERP) and brainstem auditory evoked responses (BAER) after spinal cord injury in humans.

Previous studies have observed altered somatotopic sensory fields after experimental deafferentation in animals as well as enhanced somatosensory evoked potentials and altered cortical motor pathways following spinal cord injury (SCI) in humans. These observations indicate that cortical reorganization may occur subsequent to SCI. In earlier work, we have observed attenuated amplitudes for both tactile P3 and auditory N1/P2 orienting event-related potentials (ERP) in spinal cord injured groups. These results suggest that the reorganization process may have functional perceptual and cognitive consequences. In an effort to determine if deafferentation affects the P3 ERP using stimuli other than somatosensory, we measured brain activity from central recording sites during an auditory "oddball" task. Additionally, we obtained brainstem auditory evoked responses (BAER) in order to assess subcortical primary auditory pathways as well. Results show that the SCI groups produced significantly attenuated N1/P2 complexes and P3 when compared to controls. Also, the quadriplegic group exhibited increased latencies of the P3 at frontal and central sites. There were no differences between groups in BAER results. These findings suggest that primary subcortical auditory information processing stages remain intact after SCI although later stages may be significantly altered.

Spinal function monitoring by evoked spinal cord potentials in aortic aneurysm surgery

Spinal function monitoring by evoked spinal cord potentials in aortic aneurysm surgery

Spinal cord potential recordings from the extradural space during scoliosis surgery

For monitoring spinal cord functions during corrective surgery of scoliosis, we have recorded percutaneously from the posterior extradural space at the C5-7 levels the ascending conducted spinal cord potentials (ASCP) in response to extradural stimulation of the cauda equina in 134 patients. The ASCP consists of three spike-like components (C1, C2 and C3) followed by slow components. The extradurally recorded ASCP were not affected by anaesthetic agents. There were no significant differential effects of spinal distractions on each of the three spike potentials. There were no post-operative neurological abnormalities in patients whose ASCP showed no changes, amplitude increases, amplitude decreases of less than 50% or latency increases (> 0.2 ms) during spinal manipulations (no false negatives, but some false positives). Five patients who suffered postoperative neurological damage exhibited more than 50% changes in amplitude of the ASCP during surgery. All these neurological sequelae occurred in the first 80 patients. In the last 54 patients, in whom the distraction forces on the spine were controlled rapidly by observation of the amplitude changes in ASCP, there were no postoperative neurological abnormalities, except for one patient in whom an accidental spinal cord injury was produced by a hook. The results suggest that the distraction force on the spine must be reduced immediately when the amplitudes of the ASCP decrease by more than 50% of control values with or without latency increases.

Vocational Potential and Spinal Cord Injuries - A Review and Evaluation

The purpose of this paper is to review the vocational potential of spinal cord injured persons. The results of 17 recent (1976-1991) studies were reviewed. A diversity of study outcomes was indicated and the return to work rates varied from a low of 13% to a high of 69%. A total of 3568 subjects participated in the 17 studies and an estimated 56% of these were described specifically as paraplegics, 44% quadriplegics. Sample sizes within the reports ranged from small ethnographic studies of 15 to large scale follow-up surveys of 760. The results of these independent studies were combined. Overall, 1441 or 40.3% of all the 3568 subjects sampled in the 17 studies returned to work post-injury. For subjects who were followed-up less than five years post-injury, the average return to work rate was 37.9%; for subjects who were followed up at periods exceeding five years post-injury, the return to work rate was higher at 48.6%. From the methodological point of view, some standard measures of outcome are required. It was concluded that the results of these 17 studies are encouraging and indicate the potential of persons with a range of spinal cord injuries.

Changes of Evoked Action Potentials and Histology of the Spinal Cord, and Hind Limb Dysfunction in Spinal Cord Ischemia of Cats

The electrophysiological, neurological, and neuropathological correlates of the spinal cord ischemia induced by the aortic cross-clamping of cats were studied with the goal of developing the reliable evoked spinal cord potentials (ESCPs) for the monitoring of spinal cord ischemia. The five types of ESCPs were elicited as follows; descending ESCPs recorded from the L2 and L5 vertebral levels, vertex motor evoked potential from the L2 vertebral level, ascending ESCP from the T1 vertebral level, and segmental ESCP after sciatic nerve stimulation. The late negative waves of both descending ESCP from L5 and segmental ESCP were susceptible to ischemia. The descending ESCP from L5 was not influenced by peripheral nerve ischemia or reflected ischemia in the whole spinal cord. Therefore, the late negative wave of the descending ESCP from L5 served as the most reliable index for spinal cord ischemia. When aortic clamping was continued for > or = 30 min after the disappearance of the late negative wave of descending ESCP from L5, the amplitude recovery of this wave decreased to 25%, resulting in paraplegia. Histologically, the posterior horn of the gray matter in the lumbar enlargement was the most vulnerable to ischemia.

Clinical application of evoked spinal cord potentials elicited by direct stimulation of the cord during temporary occlusion of the thoracic aorta

Evoked spinal cord potentials elicited by direct stimulation of the cord were used to monitor spinal cord ischemia in 68 patients undergoing temporary occlusion of the thoracic aorta (29 thoracic nondissecting aortic aneurysms, 9 nondissecting thoracoabdominal aneurysms, and 30 dissecting aneurysms). "Immediate" postoperative paraplegia developed in three patients and "immediate" paraparesis developed in one, whereas "delayed" paraplegia developed in two others. During aortic crossclamping, four response patterns of the spinal cord potentials were obtained: (1) no change (n = 53), (2) change with return (n = 10), (3) change with inconsistent return (n = 2), and (4) change without return (n = 3). Neurologic complications occurred in 2%, 0%, 100% of these groups, respectively. Delayed paraplegia developed on the second postoperative day in only one patient with a false-negative result, and the potentials correlated well with this patient's clinical neurologic recovery. The aortic crossclamp time was significantly longer in the patients with "change with inconsistent return" and "change without return" than in the other two groups (p < 0.01). Femoral artery pressure and the cardiopulmonary bypass flow rate were also significantly lower in these groups than in the other two groups (p < 0.02 and p < 0.01, respectively). We conclude that intraoperative monitoring of direct spinal cord responses is useful for the early detection of spinal cord ischemia for assessing the efficacy of surgical countermeasures.

Erb's point stimulation produces slow positive potentials in the human lumbar spinal cord.

Evoked spinal cord potentials (SCPs) were recorded from the posterior epidural space (PES) at the cervical and lumbrosacral enlargements in response to electrical stimulation of the brachial plexus at Erb's point in 17 chronic pain patients. Erb's point stimulation produced slow positive potentials (heterosegmental slow positive potentials, HSPs) in the PES at the lumbrosacral enlargement in all 13 subjects without spinal cord lesions but not in 4 subjects with spinal cord lesions. The HSP1 with a central peak latency of 21 +/- 2 ms (mean +/- SE) was recorded at the stimulus intensity up to two to three times the threshold strength (T) of the initially positive spike (P1) of the segmental SCP, which was simultaneously recorded from the PES at the cervical enlargement. At the stimulus intensity of more than 3T, another slow positive potential (HSP2) with central peak latency of 71 +/- 6 ms was recorded. These slow positive potentials (HSP1 and HSP2) might be produced by a feedback loop via supraspinal structures, presumably primary afferent depolarizations, in comparison to the HSPs of our previous studies in the rat. Slow negative potentials were sometimes noted before (5 of 13) and/or after (2 of 13) the HSP1. These slow negative potentials probably reflect the activities of dorsal horn neurons producing the HSP1 and HSP2, respectively, also elicited by a feedback loop via supraspinal structures.

Effects of systemic cooling and rewarming on the evoked spinal cord potentials and local spinal cord blood flow in dogs.

Changes in evoked spinal cord potential (ESCP) and in local spinal cord blood flow (local SCBF) were measured simultaneously in eight dogs in the course of systemic cooling and rewarming using a water mattress. PaCO2 was maintained at 35-40 mm Hg (temperature-uncorrected values) by adjusting ventilatory volume every 1 degree C change of esophageal temperature under N2O (60%)-O2-isoflurane (1.15%) anesthesia. Local SCBF and arterial blood pressure decreased and ESCP latencies increased linearly with the decrease in body temperature to 23-24 degrees C. The conductive ESCPs (non-synaptic components) showed temporary augmentation in amplitude before eventual decrease under cooling. These showed a tendency to return to the precooling baselines after the initiation of rewarming. These results demonstrate that conductive ESCPs could be available for intraoperative monitoring of spinal function under hypothermia down to 23-24 degrees C.

Conduction pathways and generators of magnetic evoked spinal cord potentials: a study in monkeys

Evoked spinal cord potentials (ESCPs) following transcranial magnetic stimulation werer recorded from the spinal cord in monkeys anesthetized with ketamine. Isopotential maps of the earlier negative deflection of the magnetic ESCP (N 1 wave) revealed a distribution of negative field potentials, the maximum of which were located within the medial dorsolateral funiculus, which corresponds to the dorsolateral corticospinal tracts. The N 1 wave of the magnetic ESCP had the same latency as the D-wave of the electrical ESCP elicited by either direct cortical or transcranial electrical stimulation. We assumed that the N 1 wave was generated by direct excitation of pyramidal axons. Isopotential maps of the waves that followed the N 1 peak (waves N 2, N 3, N 4, and N 5) of the magnetic ESCP showed a negative field potential distribution, the maximum of which was at the ventromedial funiculus as well as within the medial dorsolateral funiculus. Later waves of magnetic ESCP were suggested to reflect not only the dorsal corticospinal tracts but also the ventromedial spinal cord function.

Limitation by gabapentin of high frequency action potential firing by mouse central neurons in cell culture

The investigational anticonvulsant drug, gabapentin (GP; 1-(aminomethyl) cyclohexaneacetic acid) limited repetitive firing of sodium-dependent action potentials of mouse spinal cord and neocortical neurons in monolayer dissociated cell culture. The effect developed slowly over time with sustained exposure. The IC 50 was 1.3 × 10 −4M for exposure times ⩾ 60 s, 1.9 × 10 −5M for 10–60 min, and 4.0 × 10 −6M for 12–48 h. Hyperpolarization restored sustained firing in the continuing presence of GP. Blockade of action potential firing by GP was frequency (use)-dependent. After preincubation with 2.9 × 10 −5 M GP (5 μg/ml), trains of brief stimuli at ⩾ 50 Hz elicited fewer action potentials than in control solution. Also, at 150 Hz, maximal rate of rise of action potentials decreased progressively with repetitive firing in GP-containing, but not control, solution. After overnight incubation in 2.9× 10 −5 M GP, the absolute refractory period was prolonged from 2.4 ± 0.6 ms in control solution ( n = 11) to 4.7 ± ms ( n = 10; P = 0.02 vs. control), and complete recovery from inactivation was prolonged from 8.0 ± 1.3 ms to 17.0 ± 2.6 ms ( P < 0.001 vs. control). These findings suggest that GP may alter function of voltage-activated sodium channels, but the mechanism is unproven and may be indirect. Limitation of firing was observed in ⩾ 50% of neurons at concentrations in the range of those found in plasma and cerebrospinal fluid of patients treated successfully with GP. These results suggest that limiting the rate of firing of sodium-dependent action potentials may contribute to the anticonvulsant efficacy of gabapentin.

Spinal epidural oxygen partial pressure and evoked spinal cord potential in relation to the severity of spinal ischemia during cross-clamping of the thoracic aorta.

Experiments were undertaken to determine the relationship between evoked spinal cord potential (ESP) and the partial pressure of oxygen in tissue in the epidural space (E-pO2) during aortic clamping. Eighteen adult mongrel dogs were studied as follows. In group I (n = 6), the descending thoracic aorta was clamped partially at the proximal site for 15 min to maintain the distal arterial pressure at 60, 40, and 20 mmHg consecutively at 15 min intervals. In group II (n = 6), the descending thoracic aorta was clamped proximally for 30 min. In group III (n = 6), the descending thoracic aorta was cross-clamped at proximal and distal sites for 30 min. Postoperative complete paraplegia was observed in 4 of 6 dogs in group III, but none in group II. The change in ESP with aorta cross-clamping was very mild in groups I and II. Transient increases and decreases in the ESP amplitude were observed in group III. The decrease of E-pO2 correlated well with the distal arterial pressure, and a rapid return to baseline of the E-pO2 was observed after declamping. The E-pO2 changed in response to spinal ischemia more rapidly than did ESP in all groups. The critical level of E-pO2 was 50 mmHg or a 40% decrease from baseline. Because the ESP reflects spinal function and the E-pO2 reflects spinal blood pressure, we propose that combined recording of ESP and E-pO2 would improve spinal monitoring during thoracic aortic surgery.

An experimental study on spinal cord ischemia during cross-clamping of the thoracic aorta: the monitoring of spinal cord ischemia with motor evoked potential by transcranial stimulation of the cerebral cortex in dogs.

The usefulness of spinal motor evoked potential by transcranial stimulation of the motor cortex (MEPT) in detecting spinal ischemia and predicting postoperative neurological dysfunction was evaluated using a model of spinal ischemia. Group 1 was comprised of 11 dogs used for measuring the basic wave form of spinal MEPT. The normal spinal MEPT response curve consists of two major peaks: peak I and peak II. The latency of peak I and peak II at T13-L1 was 6.0 +/- 0.6 and 7.1 +/- 0.6 msec, and the amplitude, 3.3 +/- 1.6 and 6.1 +/- 2.6 microV, respectively. Group 2 was comprised of six animals subjected to spinal ischemia, in which a time-related deterioration of the MEPT as well as evoked spinal cord potential (ESP) was demonstrated. The time taken until the loss of peak I and peak II was 19.2 +/- 5.3 and 21.7 +/- 6.2 min, respectively, while the time taken until the loss of ESP was 36.7 +/- 14.0 min. In group 3, comprised of seven animals, the aorta was unclamped and the animals were allowed to recover when the spinal MEPT had disappeared. Four had paraparesis immediately after the operation, two had a normal gait, one died, and one developed spastic paraplegia after 24 h. We concluded that the change in spinal MEPT during spinal ischemia occurred earlier than the change in ESP, and that the loss of MEPT suggested irreversible spinal cord damage.

Thienyl-GABA derivatives as specific baclofen agonists in the rat and cat spinal cord in vivo

The depression of the amplitude of extracellularly recorded monosynaptic excitatory field potentials in the lumbar spinal cord of pentobarbitone anaesthetised rats and cats by three thienyl derivatives of GABA: 4-amino-3-(2-thienyl)-butanoic acid; 4-amino-3-(2-thienyl-5-methyl)-butanoic acid and 4-amino-3-(2-thienyl-5-chloro)-butanoic acid was reversibly blocked by the (−)-baclofen antagonist 3-aminopropyl-diethoxymethyl-phosphinic acid (CGP 35348). These compounds, of which the most potent, the 5-chloro derivative, was weaker than (−)-baclofen, thus activate baclofen receptors in the cat and rat spinal cord.

Intraoperative monitoring of evoked spinal cord potentials directly recorded from the dural surface during spinal operation — In surgical cases of cervical spondylosis and spinal cord tumor

Intraoperative monitoring of evoked spinal cord potentials directly recorded from the dural surface during spinal operation — In surgical cases of cervical spondylosis and spinal cord tumor

Changes of the segmental evoked spinal cord potential (S-ESCP) with reference to numbness of the hand, in cervical segmental myelopathy

Changes of the segmental evoked spinal cord potential (S-ESCP) with reference to numbness of the hand, in cervical segmental myelopathy

Substance P and NMDA receptor-mediated slow potentials in neonatal rat spinal cord: age-related changes

Slow ventral root potentials (slow VRP's) recorded from 1- to 5-day-old rat spinal cords are implicated in nociception, but there is controversy over their origin and persistence in the adult. The present study investigated changes in the role of substance P and NMDA receptors in slow VRP generation during the postnatal period (1–21 days). Through 9 days, dorsal root stimulation elicits slow VRP's with typical peak amplitudes at 3–4 s, decay time constants of 18–20 s, and durations > 20 s. After 11 days, peak amplitude shortens to < 1 s, decay time constant 4–5 s, and duration < 10 s. At 1–6 days, slow VRP's are sensitive to the NMDA receptor antagonist APV and the substance P antagonists apantide and CP 96,345. After 11 days, APV sensitivity is retained, but spantide sensitivity and ability of substance P to evoke a response are diminished. Abbreviated slow VRP's in post-11-day spinal cords appear to correspond to the early APV-sensitive component of long-duration slow VRP's in younger animals. Attempts to restore long-duration slow VRP's in 12- to 14-day-old rat cords by blocking various inhibitory mechanisms were not successful. The results suggest that a substance P response, some of which is mediated by NK1 receptors, is lost with maturation of the cord. Either a developmental role played by substance P changes with maturity, or the motor neurons of the isolated post-11-day cord lose the capacity to sustain large long-duration plateau potentials.

An in vitro investigation of the action of lamotrigine on neuronal voltage-activated sodium channels

Lamotrigine (LTG), 6-(2,3-dichlorophenyl)-1,2,4-triazine-3,5-diamine, is a novel antiepileptic drug structurally unrelated to the major anticonvulsants in current use. Previous studies of LTG in rodents revealed efficacy in maximal electroshock test, pentylenetetrazol test and kindling models of seizures suggesting potential utility in the treatment of partial and generalized (tonic-clonic) seizures. In the present study, LTG was found to block sustained repetitive firing of sodium-dependent action potentials in mouse spinal cord cultured neurons and inhibit [ 3H]batrachotoxinin A 20-α-benzoate binding in rat brain synaptosomes suggesting a direct interaction with voltage-activated sodium channels.

Long duration ventral root potentials in the neonatal rat spinal cord in vitro; the effects of ionotropic and metabotropic excitatory amino acid receptor antagonists

Long duration, primary afferent evoked ventral root potentials (VRP's) have been recorded in vitro from hemisected spinal cords prepared from 8–12-day-old rat pups. Single shock stimulation of a dorsal root at stimulus strengths sufficient to recruit C/group IV afferent fibres evoked a long duration (11.9±1.2 s) ipsilateral VRP in all preparations. This long duration VRP consisted of two components, (i) a slow wave, time to peak 137.0±5.1 ms, the amplitude of which was reduced to 8.7% of mean control value in the presence of the N- methyl- d-aspartate (NMDA) antagonist d-AP5 (40 μM), (ii) a prolonged wave with a time to peak of 2.0±0.2 s which was partially resistant to d-AP5 (40 μM). Both the slow and the prolonged waves were unaffected following superfusion with tthe metabotropic excitatory amino acid (EAA) receptor antagonist l-AP3 (100–200 μM). Low frequency (1–10 Hz) repetitive stimulation (20s duration) of high threshold dorsal root afferents evoked a temporal summation of synaptic activity which generated a progressively depolarizing VRP. This cumulative VRP was graded with frequency of stimulation (0.89 ± 0.13 to 1.25 ± 0.19 mV). The cumulative VRP was followed by a post-stimulus depolarization which outlasted the period of repetitive stimulation by tens of seconds (47.6 ± 8.4 to 91.2 ± 19.9 s). In the presence of AP5 the amplitude of the cumulative VRP was depressed to 54.5 ± 11.5% of control values when low frequency (1.0 Hz) stimulation was used. The proportion of the cumulative VRP resistant to d-AP5 increased as the frequency of stimulation was increased to 10 Hz. The decay time of the post-stimulus depolarization was unaffected by AP5. Neither the amplitude nor the post-stimulus depolarization of the cumulative VRP was affected by 200 μM l-AP3. It is suggested that both an AP5 sensitive and AP5 insensitive potential contribute to the long duration VRP evoked in the neonatal rat spinal cord following single shock high threshold afferent stimulation. Moreover, the AP5 insensitive prolonged depolarization is manifest following sustained low frequency stimuli and higher frequency inputs.

Study of experimental cervical spondylotic myelopathy.

Most cervical spondylotic myelopathy cases show insidious onset. Experimental cervical spondylotic myelopathy models were made using cats to analyze advancing patterns of myelopathy in the spinal cord and to identify the most responsible factor. Spinal cord compression was applied anteriorly using one screw through the C5 vertebral body or three screws through the C4, C5, and C6 vertebral bodies. Every few weeks, the screws were turned approximately 1 mm at a time up to approximately 50% of the spinal canal. At more than 6 months after final compression, limb function and evoked spinal cord potentials were evaluated. Thereafter, histologic examinations were performed. the single compression group showed normal limb function, but the multiple compression group showed sluggish gait. Histologically, mild neuronal decrease in the gray matter was noticeable in the single compression group. Conversely, the multiple compression group showed severe changes in the gray matter and significant changes in the posterior and anterior columns. There was a correlation between the evoked spinal cord potentials and histologic changes. It was clear that multiple compressions to the spinal cord caused more severe deterioration functionally and electrophysiologically as well as histologically than a single compression.