Origin of motor evoked potentials in the rat.
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Biomedical subjects
Publications and source records attributed to C H Tator.
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Most cervical spine injuries are due to motor vehicle accidents. Proper extrication of the victims is vital; the ideal device should be easily assembled and applied, should facilitate removal of victims from automobile seats without changing the body's position, must not hinder airway access or the performance of cardiopulmonary resuscitation, must accommodate all types of patients, including children and obese or pregnant patients, and must completely immobilize the patient, especially if hyperextension is suspected. Current methods of immobilization, such as the use of a soft collar and sandbags, allow neck extension; the short board protects against extension but interferes with airway access. Newer devices are discussed in this article. Injuries of the upper cervical spine are less common but more serious than those of the lower portion and usually involve the vertebral arch. Radiologic examination of the first and second cervical vertebrae and the seventh cervical and first thoracic vertebrae should be emphasized. If lateral and anteroposterior views do not reveal abnormal findings and injury is still suspected, oblique views and computed or conventional tomography should be used. Cervical spinal cord injuries can be minimized or prevented if proper early management is applied.
An accurate neurophysiological technique that is able to monitor both the sensory and motor tracts of the spinal cord is required to assess patients with injury or other lesions of the cord, and for the evaluation of experimental studies of cord injury. We have recorded and characterized the motor and somatosensory evoked potentials (MEPs and SSEPs) from 20 normal rats and from 16 rats with cord lesions. MEPs were elicited by applying constant current anodal stimuli to the sensorimotor cortex (SMC) with the responses recorded from microelectrodes in the spinal cord at T10 (MEP-C) and from a bipolar electrode placed on the contralateral sciatic nerve (MEP-N). SSEPs were elicited by stimulating the sciatic nerve and were recorded from the cord at T10 and the contralateral SMC. The MEP-C consisted of an initial D wave (mean latency 1.21 +/- 0.12 msec and 4 subsequent I waves, 11-14). The D wave was elicited at stimulation frequencies exceeding 100 Hz. The initial positive wave of the MEP-N (mean latency 3.09 +/- 0.19 msec) was followed by several slower components which were attenuated by repetition rates exceeding 8.2 Hz. The grand mean SSEP consisted of 7 peaks. Sectioning of the dorsal columns abolished the SSEP but spared the MEP. Complete cord transection abolished both the MEP and SSEP. These experiments demonstrate that the combined recording of MEPs and SSEPs is an accurate and easily performed method of monitoring the functional integrity of the rat cord, and suggest that this technique would be of value in patients, especially those undergoing operative treatment of spinal lesions.
Intracranial pressure was increased in 59 rats by inflating a subdural balloon to a total mass volume of 0.3 ml. The increase in intracranial pressure ranged from 75 to greater than 500 mm Hg. With few exceptions, mean arterial pressure increased to as high as 227 mm Hg during the increase in intracranial pressure. Significant increases in plasma catecholamines, major electrocardiographic changes and a considerably shortened survival time were observed only in the rats that demonstrated an increase in mean arterial pressure greater than 50 mm Hg. A perfusion study with liquid silicone rubber (Microfil) revealed dilated irregular myocardial vessels with areas of focal constriction consistent with microvascular spasm. Histologic examination of the myocardium revealed widespread patches of contraction band necrosis and occasional contraction bands in the smooth muscle media of large coronary arteries. These observations suggest that myocardial damage after suddenly increased intracranial pressure resulted both from exposure to toxic levels of catecholamines and from myocardial reperfusion. Extension of these studies to humans suggests that a detailed assessment of myocardial function should be performed in victims of severe brain injury. Myocardial dysfunction may be a major determinant of the patient's prognosis or may render the heart unsuitable for transplantation.
The surgical results in 40 patients with syringomyelia, treated with a syringosubarachnoid shunt or other procedures are reviewed. The principal indication for surgery was that of significant neurological deterioration. There were 12 patients with idiopathic syringomyelia without tonsillar ectopia, 12 with an associated Chiari malformation, 11 with post-traumatic syringomyelia and five patients with spinal arachnoiditis. There were 38 syringosubarachnoid shunts performed in 35 patients, and an excellent or good result was achieved in 26 patients (74.3%). In terms of the type of syringomyelia, the best results were obtained in the idiopathic group without tonsillar ectopia and in the post-traumatic group. A short duration of pre-operative symptoms favoured a better outcome, and in our opinion, early surgical treatment is indicated for all patients with neurological deterioration. All eight patients in whom a posterior fossa decompression was performed as the initial surgical procedure required a second operation, either a syringosubarachnoid or syringoperitoneal shunt to achieve neurological improvement or stabilization. Thus, the syringosubarachnoid shunt is an effective therapeutic modality for patients with syringomyelia, particularly for the idiopathic and post-traumatic groups. More than one surgical procedure may be required to achieve cessation of deterioration. Overall, excellent or good results were achieved in 29 (72.5%) of the 40 patients.
Techniques used to monitor the function of the seventh and eighth cranial nerves during acoustic neuroma and other posterior fossa surgery are reviewed. The auditory brainstem response (ABR), electrocochleogram (ECochG) and direct recording from the auditory nerve (CNAP) were compared. The best technique is the ECochG, although in many cases, the CNAP should be used as a back-up technique. The CNAP is especially useful for the identification of the auditory nerve. Both can provide real-time feedback on the physiological integrity of the auditory nerve. The ABR may be helpful in monitoring brainstem function. For some procedures, optimal monitoring requires the combined recording of all three techniques. Monopolar constant-voltage intracranial stimulation of the facial nerve is helpful for the identification and preservation of the facial nerve. Audio monitoring of spontaneous electromyographic activity provides real-time feedback on the effect of surgical manipulation of the nerve. Monitoring of ephaptic transmission in the facial nerve during microvascular decompression for hemifacial spasm aids in the identification of the offending vessel.
An unusual case of sphenoethmoidal sinusitis complicated by cavernous sinus thrombosis, meningitis and pontine and cerebellar infarction is described. The patient presented with advanced intracranial complications which in retrospect caused delay in recognition and treatment of the underlying sphenoethmoidal sinusitis. Surgical drainage of the sinusitis was ultimately required. The pathogenesis of these complications is discussed, and the topic of sphenoid sinusitis reviewed in order to emphasize the numerous neurological manifestations of this disease.
The effects of acute head injury or subarachnoid hemorrhage on the cardiovascular system (CVS) are well known, but data are lacking on the effects of acute spinal cord injury (SCI) on the CVS. The clip compression SCI rat model was used to measure changes in the mean systemic arterial pressure (mSAP), cardiac output (CO), heart rate (HR), total peripheral resistance (TPR), and central venous pressure (CVP) after SCI. Three groups of five animals each were anesthetized with chloralose-urethane: one group underwent only the surgical procedures including laminectomy, and the other two received either a 2.3- or 53.0-gm injury at the T1 spinal cord segment for 1 minute. The CO was measured using the thermodilution technique. CVS parameters were measured before injury, and then at designated times for 135 minutes after SCI. Analysis of variance and paired t-test with significance at p = 0.05 were used for analysis. There were no CVS changes as a result of anesthesia, operative time, or laminectomy alone. Cardiovascular system (CVS) changes occurred after the 2.3- and 53.0-gm. injuries but were significantly different only in the 53.0-gm injured animals. In this group mSAP increased from a preinjury value of 105 +/- 8 mm Hg to 178 +/- 11 mm Hg as a result of SCI, followed by a prolonged period of hypotension (46 +/- 15 mm Hg) lasting until 135 min post SCI. The CO after SCI also decreased from 394 +/- 22 to 218 +/- 29 ml/min/kg with the TPR reaching a minimal level at 45 min post SCI (265 +/- 23 to 213 +/- 29 mm Hg/ml/min gm wt), after which it returned to preinjury values. There were no significant changes in the CVP in either group. In the 53.0-gm group significant bradycardia (492 +/- 7 to 356 +/- 44 beats/min) was observed by 45 min and continued to decrease until 135 min after SCI. Thus the CVS showed two major alterations after severe SCI: post-traumatic hypotension, and a parallel decline in CO. There were no major changes in TPR, HR, or CVP, although HR ultimately declined. These findings suggest that the decline in CO was not entirely due to decreased sympathetic tone, but may also have resulted from direct myocardial injury, similar to that demonstrated after head injury or subarachnoid hemorrhage.
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Two cases of progressive myelopathy occurring years after incomplete cervical spinal cord injury are presented. In both patients, the clinical features, as well as the "bull's-eye" appearance of the delayed computerized tomography (CT) myelography study and the circumscribed low density of the magnetic resonance image, were consistent with posttraumatic syringomyelia, but surgical exploration including intra-operative spinal sonography failed to reveal a syrinx. Although arachnoiditis was present in both patients, the striking abnormality found at surgery was the softened appearance and the microcystic degeneration of the cord. The microcystic spinal cord degeneration found in these cases represents a previously undescribed cause of late deterioration after spinal cord injury that may mimic the clinical, CT-myelographic, and magnetic resonance features of posttraumatic syringomyelia.
Recent work has indicated that direct-current (DC) fields may promote recovery after acute spinal cord injury. In the present experiments, the therapeutic value of an applied DC field was studied in 40 rats with clip compression injuries of the cord at C7-T1. The rats were randomly allocated to one of four groups including 10 rats each: two groups received a 17-gm cord injury and two groups a 53-gm injury. One group at each injury severity received implantation of a treatment (14 microA) DC stimulator and the other group a control (0 microA) stimulator. Clinical neurological function was assessed weekly by the inclined-plane technique. At 8 weeks after injury, motor and somatosensory evoked potentials (MEP's and SSEP's) were recorded, and the axonal tracer horseradish peroxidase (HRP) was introduced into the cord at T-6. The total number of HRP-labeled cells was counted in every sixth coronal section through the brain stem and motor cortex. All outcome parameters were assessed blindly. In the 17-gm group, there were no significant differences in any outcome measure between control and treated rats. In contrast, in the 53-gm group, the inclined-plane scores, the amplitude of the MEP's, and the number of labeled cells in the red nucleus, raphé nuclei, and vestibular nuclei were greater in treated than in control rats. These data strongly indicate that an applied DC field can produce functional neurological and anatomical improvement in rats with acute spinal cord injuries.
This paper describes an objective, quantifiable technique for assaying the degree of severity of spinal cord injury. Twenty-one rats underwent a C7-T1 laminectomy: 12 received a C8 spinal cord clip compression injury with forces of either 2.3, 16.9 or 53.0 g; 4 had cord transection at C8, and 5 had no cord lesion. Postoperative clinical neurological assessment was performed by the inclined plane method. At 4 weeks, the spinal cord-injured rats underwent a T10 transection and insertion of a Gelfoam pledget impregnated with horseradish peroxidase (HRP). HRP was similarly administered to 9 normal rats. Longitudinal sections of the spinal cord encompassing the injury site were stained with Luxol fast blue, and coronal sections from the cerebrum and midbrain were processed for HRP reactivity with tetramethylbenzidine. Labelled corticospinal and rubrospinal neurons were counted in every 6th section to derive a cortical score (CS) and a red nucleus score (RNS) for each animal. The CS reflected the extent of the pathological changes at the site of cord injury and the ln CS decreased linearly with increasing injury severity (P less than 0.0001). In contrast, the RNS was only reduced in animals with severe (53.0 g) cord injuries (P less than 0.0006). The degree of preservation of the dorsal columns including the corticospinal tracts at the injury site correlated with the CS, whereas the RNS was related to the degree of preservation of the lateral columns. Counts of rubrospinal neurons, but not corticospinal neurons, correlated closely (r = 0.96, P less than 0.001) with the inclined plane results, suggesting the importance of non-pyramidal tracts in controlling gross motor function. Thus, counting corticospinal and rubrospinal neurons is an objective, reliable test of the severity of experimental spinal cord injury.
A multi-disciplinary approach is described for the development of a microcomputer based on-line data collection system for blood flow experiments. Well designed software provides a flexible approach to data collection, which is particularly suited to blood flow research laboratories. The choice of well supported hardware ensures ease of development with minimum time and cost.
Long-term regenerative changes and pathological effects after acute compression injury of the spinal cord were studied in rats. Twenty adult female Wistar rats underwent cord injury by the extradural clip compression technique at T6-7. Following injury, extradural electrodes attached to receiver-stimulators that were implanted subcutaneously were placed proximal and distal to the injury site. The animals were maintained in cages with electromagnetic fields created by encircling antennae. The control animals were in a field adjusted to a frequency below the sensitive frequency range of the receiver-stimulators so that they received no spinal cord stimulation. After 15-20 weeks of continuous spinal cord stimulation, histological sections of the cords were assessed and scored blindly for pathological changes including magnitude and extent of cord injury, and cystic cavitation, and for regenerative changes including proliferation of axons, Schwann cells and ependymal cells, and formation of myelin. In all 20 animals, there was a complete absence of normal cord tissue at the injury site, and cystic cavitation was frequently present at the injury site and beyond. Extensive regenerative changes were seen in all animals including regeneration of axons, Schwann cells and ependymal cells, and formation of myelin. Statistical analysis did not show a significant difference between treatment and control groups.
The therapeutic value of electrical stimulation of the spinal cord was studied in rats injured by acute compression of the spinal cord. Twenty adult Wistar rats underwent cord compression at T6-7 by the extradural clip compression technique at a force of 125 g for 1 minute. After injury and group randomization, stimulating electrodes were placed extradurally, proximal and distal to the injury site, and attached to a small, implantable receiver-stimulator. The receiver was secured to the paraspinal muscles and implanted subcutaneously, overlying the thoracic spine. The animals were maintained in specially designed cages with encircling antennae attached to radio frequency transmitters. The 10 treatment animals were subjected to a 460-kHz electromagnetic field, pulsed at a frequency of 10 Hz. The receivers converted the pulsed radio frequency into square-wave pulses at the cord electrodes (width 1 ms, frequency 10 Hz). The 10 control animals were exposed to a similar field but with a frequency below the range of the tuned receiver, and therefore they did not receive the square-wave pulse. Clinical recovery was assessed by the inclined plane technique which measures the maximum angle of inclination attained without falling. After 15 weeks of continuous spinal cord stimulation, the inclined plane performance was not significantly different between the two groups (treatment group mean, 44.4 +/- 5.4; control group mean, 41.7 +/- 7.9). This is the first experimental study of the effect of long-term continuous electrical stimulation on spinal cord recovery in mammals. The methods required and the technical aspects involved in achieving continuous stimulation, and the guidelines for future study of this modality are discussed.
The role of surgery in the management of acute spinal cord or cauda equina injuries remains controversial. The present study analyzed ten admission features and three outcome variables in 208 patients treated in an Acute Spinal Cord Injury Unit, 116 (56%) of whom underwent at least one spinal operation. The surgical and non-surgical groups showed no significant differences in the following seven clinical features: age, sex, distance travelled to the Unit, time interval between trauma and admission, type of accident, severity of injuries to the spinal cord, and severity of associated injuries. However, the two groups showed significant differences in level and type of vertebral column injury, and in the frequency of pre-existing spinal abnormalities. These differences were due to management policies which selected certain injuries for surgical or non-surgical treatment. One-third of the operative procedures were performed primarily for neural decompression, one-third primarily for reduction of bony structures and one-third for fusion. However, 95% of the operative patients had a fusion at the initial operation. Operative treatment was associated with a lower overall mortality rate (6.1%) than non-operative (15.2%), despite a higher frequency of thrombo-embolic complications in the surgical group. Overall, there was no difference between operated and non-operated patients in length of stay or neurological recovery. Surgical management of patients with acute spinal cord injury appears safe in terms of mortality rate and neurological recovery, but it has not been proven to improve the latter.
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The value of decompression after spinal cord injury in patients is still an unresolved issue. It has previously been shown in our laboratory that functional recovery in rats after cord compression varied with both the force and time until decompression. However, the longest duration studied was only 15 minutes, which is far less than that usually encountered in clinical practice, and therefore, the present study was undertaken to determine the value of decompression after more prolonged periods of compression. A factorially designed experiment with five rats per cell was used with the clip compression injury model. Forces of 2.3, 16.9 or 53.0 gms were applied at C7-T1 until decompression was performed after 15, 60, 120, or 240 minutes of compression. Functional recovery was assessed weekly for 8 weeks using the inclined plane technique. Maximum and minimum performance limits were established in normal rats and rats with cord transection, respectively. Univariate analysis and multiple comparison tests were used to analyse the data. The major determinant of recovery was the force of the injury. For example, the animals injured by the 2.3 gm clip performed significantly better than those injured at higher forces for all times until decompression (p less than 0.0001), and there was a significant difference in recovery between the groups injured by the 16.9 and 53.0 gm clips, although only for the 15 minutes until decompression group (p less than 0.05). The time until decompression also affected recovery, but only for the lighter compression forces (2.3 and 16.9 gm). For example, animals decompressed after 60 minutes of 2.3 gm compression recovered significantly better than those decompressed after 240 minutes (p less than 0.05). Thus, if the initial injury force is small, decompression is beneficial even after prolonged injury.