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Daipayan Guha, Benjamin Davidson, Mustafa Nadi, Naif M. Alotaibi, Michael G. Fehlings, Fred Gentili, Taufik A. Valiante, Charles H. Tator, Michael Tymianski, Abhijit Guha and Gelareh Zadeh


A surgical series of 201 benign and malignant peripheral nerve sheath tumors (PNSTs) was assessed to characterize the anatomical and clinical presentation of tumors and identify predictors of neurological outcome, recurrence, and extent of resection.


All surgically treated PNSTs from the Division of Neurosurgery at Toronto Western Hospital from 1993 to 2010 were reviewed retrospectively. Data were collected on patient demographics, clinical presentation, surgical technique, extent of resection, postoperative neurological outcomes, and recurrence.


One hundred seventy-five patients with 201 tumors had adequate follow-up for analysis. There were 182 benign and 19 malignant PNSTs. Of the benign lesions, 133 were schwannomas, 21 of which were associated with a diagnosis of schwannomatosis. There were 49 neurofibromas, and 26 were associated with neurofibromatosis Type 1 (NF1). Patients presenting with schwannomas were significantly older than those with neurofibromas. Schwannomas were more readily resected than neurofibromas, with the extent of resection of the former influenced by tumor location. Patients with benign PNSTs typically presented with a painful mass and less frequently with motor deficits. The likelihood of worsened postoperative motor function was decreased in patients with fully resected tumors or preoperative deficits. Recurrence of schwannomas and neurofibromas were seen more frequently in patients diagnosed with NF3 and NF1, respectively. Subtotal resection was associated with the increased recurrence of all benign lesions.


Outcomes following resection of benign PNSTs depend on tumor histopathology, tumor location, and genetic predisposition syndrome. Gross-total resection should be attempted for benign lesions where possible. The management of malignant PNSTs remains challenging, requiring a multimodal approach.

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Rajiv Midha, Catherine A. Munro, Paul D. Dalton, Charles H. Tator and Molly S. Shoichet

Object. The authors' long-term goal is repair of peripheral nerve injuries by using synthetic nerve guidance devices that improve both regeneration and functional outcome relative to an autograft. They report the in vitro processing and in vivo application of synthetic hydrogel tubes that are filled with collagen gel impregnated with growth factors.

Methods. Poly(2-hydroxyethyl methacrylate-co-methyl methacrylate) (PHEMA-MMA) porous 12-mm-long tubes with an inner diameter of 1.3 mm and an outer diameter of 1.8 mm were used to repair surgically created 10-mm gaps in the rat sciatic nerve. The inner lumen of the tubes was filled with collagen matrix alone or matrix supplemented with either neurotropin-3 at 1 µg/ml, brain-derived neurotrophic factor at 1 µg/ml, or acidic fibroblast growth factor (FGF-1) at 1 or 10 µg/ml. Nerve regeneration through the growth factor—enhanced tubes was assessed at 8 weeks after repair by histomorphometric analysis at the midgraft level and in the nerve distal to the tube repair. The tubes were biostable and biocompatible, and supported nerve regeneration in more than 90% of cases. Nerve regeneration was improved in tubes in which growth factors were added, compared with empty tubes and those containing collagen gel alone (negative controls). Tubes filled with 10 µg/ml of FGF-1 dispersed in collagen demonstrated regeneration comparable to autografts (positive controls) and showed significantly better regeneration than the other groups.

Conclusions. The PHEMA-MMA tubes augmented with FGF-1 in their lumens appear to be a promising alternative to autografts for repair of nerve injuries. Studies are in progress to assess the long-term biocompatibility of these implants and to enhance regeneration further.

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R. Loch Macdonald, Michael G. Fehlings, Charles H. Tator, Andres Lozano, J. Ross Fleming, Fred Gentili, Mark Bernstein, M. Chris Wallace and Ronald R. Tasker

✓ This study was conducted to determine the safety and efficacy of multilevel anterior cervical corpectomy and stabilization using fibular allograft in patients with cervical myelopathy. Thirty-six patients underwent this procedure for cervical myelopathy caused by spondylosis (20 patients), ossified posterior longitudinal ligament (four patients), trauma (one patient), or a combination of lesions (11 patients). The mean age (± standard deviation) of the patients was 58 ± 10 years and 30 of the patients were men. The mean duration of symptoms before surgery was 30 ± 6 months and 11 patients had undergone previous surgery. Prior to surgery, the mean Nurick grade of the myelopathy was 3.1 ± 1.4. Seventeen patients also had cervicobrachial pain. Four vertebrae were removed in six patients, three in 19, and two in 11 patients. Instrumentation was used in 15 cases. The operative mortality rate was 3% (one patient) and two patients died 2 months postoperatively. Postoperative complications included early graft displacement requiring reoperation (three patients), transient dysphagia (two patients), cerebrospinal fluid leak treated by lumbar drainage (three patients), myocardial infarction (two patients), and late graft fracture (one patient). One patient developed transient worsening of myelopathy and three developed new, temporary radiculopathies. All patients achieved stable bone union and the mean Nurick grade at an average of 31 6 20 months (range 0–79 months) postoperatively was 2.4 ± 1.6 (p < 0.05, t-test). Cervicobrachial pain improved in 10 (59%) of the 17 patients who had preoperative pain and myelopathy improved at least one grade in 17 patients (47%; p < 0.05). Twenty-six surviving patients (72%) were followed for more than 24 months and stable, osseous union occurred in 97%. These results show that extensive, multilevel anterior decompression and stabilization using fibular allograft can be achieved with a perioperative mortality and major morbidity rate of 22% and with significant improvement in pain and myelopathy.

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Charles H. Tator and Izumi Koyanagi

✓ Vascular injury plays an important role in the primary and secondary injury mechanisms that cause damage to the acutely traumatized spinal cord. To understand the pathophysiology of human spinal cord injury, the authors investigated the vascular system in three uninjured human spinal cords using silicone rubber microangiography and analyzed the histological findings related to vascular injury in nine acutely traumatized human spinal cords obtained at autopsy. The interval from spinal cord injury to death ranged from 20 minutes to 9 months. The microangiograms of the uninjured human cervical cords demonstrated new information about the sulcal arterial system and the pial arteries. The centrifugal sulcal arterial system was found to supply all of the anterior gray matter, the anterior half of the posterior gray matter, approximately the inner half of the anterior and lateral white columns, and the anterior half of the posterior white columns. Traumatized spinal cord specimens in the acute stage (3–5 days postinjury) showed severe hemorrhages predominantly in the gray matter, but also in the white matter. The white matter surrounding the hemorrhagic gray matter showed a variety of lesions, including decreased staining, disrupted myelin, and axonal and periaxonal swelling. The white matter lesions extended far from the injury site, especially in the posterior columns. There was no evidence of complete occlusion of any of the larger arteries, including the anterior and posterior spinal arteries and the sulcal arteries. However, occluded intramedullary veins were identified in the degenerated posterior white columns. In the chronic stage (3–9 months postinjury), the injured segments showed major tissue loss with large cavitations, whereas both rostral and caudal remote sites showed well-demarcated necrotic areas indicative of infarction mainly in the posterior white columns. Obstruction of small intramedullary arteries and veins by the initial mechanical stress or secondary injury mechanisms most likely produced these extensive white matter lesions. Our studies implicate damage to the anterior sulcal arteries in causing the hemorrhagic necrosis and subsequent central myelomalacia at the injury site in acute spinal cord injury in humans.

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R. John Hurlbert, Charles H. Tator and Elizabeth Theriault

✓ Electrical stimulation of the mammalian central nervous system (CNS) can result in extensive destruction of tissue unless applied within specific stimulation parameters. Classically, unbalanced or monopolar currents have been avoided in order to minimize these harmful effects. However, direct current (DC) fields have recently been proposed for the treatment of spinal cord injury. Until now, no rigorous analysis has been made of the safety of these fields in the mammalian CNS. The purpose of this study was to determine the amount of chronically applied DC current that can be tolerated by the normal rodent spinal cord stimulated with metal disc electrodes.

Thirty-five normal rats underwent implantation of DC stimulating devices and were allowed to recover for a period of 2 to 12 weeks. The stimulators delivered constant currents of 0 to 50 µA through two disc-shaped platinum/iridium electrodes positioned extradurally at the C-7 and T-3 levels. Following sacrifice of the animals, serial 8-µm cross sections of the spinal cord at the electrode sites were examined microscopically. Evidence of demyelination presumed due to the physical presence of the rostral electrode was seen in animals from most groups including control animals. Pathological changes directly attributable to the applied fields were seen with current as low as 3 µA. It was concluded that DC's of 3 µA or more are harmful to the mammalian CNS with this method of stimulation. In addition, the data suggest that the maximum current density tolerated by the rodent spinal cord is in the order of 75 µA/sq cm. These findings have important implications for the use of chronic DC stimulation in the mammalian CNS.

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Luis F. Pitty and Charles H. Tator

✓ Hypoglossal-facial nerve anastomosis is one of the procedures frequently performed to restore function after facial palsy secondary to surgery for removal of cerebellopontine angle tumors. The published results of hypoglossal-facial nerve anastomosis have been variable, and there are still questions about the indications, timing, and surgical techniques for this procedure. The goals of the present retrospective analysis of 22 cases of hypoglossal-facial nerve anastomosis were to assess the extent of the functional recovery and to analyze the factors affecting this recovery.

The 22 cases of complete facial palsy were gleaned from a series of 245 cases of cerebellopontine angle tumors treated surgically by one of the authors. Twenty patients had an acoustic neuroma (average size 3.5 cm), one patient had a petrous meningioma, and one patient had a facial neuroma. The average age of the patients was 47.3 years (range 19 to 69 years). The average interval from tumor surgery to hypoglossal-facial nerve anastomosis was 6.4 months (range 12 days to 17 months), and the average follow-up period after the procedure was 65 months.

The results were graded as good, fair, poor, or failure according to a new method of classifying facial nerve function after hypoglossal-facial nerve anastomosis. The results were good in 14 cases (63.6%), fair in three (13.6%), and poor in four (18.2%); one (4.5%) was a failure. Good and fair results occurred with higher frequency in younger patients who were operated on within shorter intervals, although these relationships were not statistically significant. There were no surgical complications. Good or fair results were achieved in 17 (77.3%) of the 22 cases, and thus hypoglossal-facial nerve anastomosis is considered an effective procedure for most patients with facial palsy after surgery for cerebellopontine angle tumors.

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R. John Hurlbert, Charles H. Tator, Michael G. Fehlings, Greg Niznik and R. Dean Linden

✓ Although the assessment of spinal cord function by electrophysiological techniques has become important in both clinical and research environments, current monitoring methods do not completely evaluate all tracts in the spinal cord. Somatosensory and motor evoked potentials primarily reflect dorsal column and pyramidal tract integrity, respectively, but do not directly assess the status of the ventral funiculus. The present study was undertaken to evaluate the use of evoked potentials, elicited by direct cerebellar stimulation, in monitoring the ventral component of the rodent spinal cord. Twenty-nine rats underwent epidural anodal stimulation directly over the cerebellar cortex, with recording of evoked responses from the lower thoracic spinal cord, both sciatic nerves, and/or both gastrocnemius muscles. Stimulation parameters were varied to establish normative characteristics. The pathways conducting these “posterior fossa evoked potentials” were determined after creation of various lesions of the cervical spinal cord.

The evoked potential recorded from the thoracic spinal cord consisted of five positive (P1 to P5) and five negative (N1 to N5) peaks. The average conduction velocity (± standard deviation) of the earliest wave (P1) was 53 ± 4 m/sec, with a latency of 1.24 ± 0.10 msec. The other components followed within 4 msec from stimulus onset. Unilateral cerebellar stimulation resulted in bilateral sciatic nerve and gastrocnemius muscle responses; there were no significant differences (p > 0.05) in the thresholds, amplitudes, or latencies of these responses elicited by right- versus left-sided stimulation. Recordings performed following creation of selective lesions of the cervical cord indicated that the thoracic response was carried primarily in the ventral funiculus while the sciatic and gastrocnemius responses were mediated through the dorsal half of the spinal cord. It is concluded that the posterior fossa evoked potential has research value as a method of monitoring pathways within the ventral spinal cord of the rat, and should be useful in the study of spinal cord injury.

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Charles H. Tator and Michael G. Fehlings

✓ In patients with spinal cord injury, the primary or mechanical trauma seldom causes total transection, even though the functional loss may be complete. In addition, biochemical and pathological changes in the cord may worsen after injury. To explain these phenomena, the concept of the secondary injury has evolved for which numerous pathophysiological mechanisms have been postulated. This paper reviews the concept of secondary injury with special emphasis on vascular mechanisms. Evidence is presented to support the theory of secondary injury and the hypothesis that a key mechanism is posttraumatic ischemia with resultant infarction of the spinal cord. Evidence for the role of vascular mechanisms has been obtained from a variety of models of acute spinal cord injury in several species. Many different angiographic methods have been used for assessing microcirculation of the cord and for measuring spinal cord blood flow after trauma. With these techniques, the major systemic and local vascular effects of acute spinal cord injury have been identified and implicated in the etiology of secondary injury.

The systemic effects of acute spinal cord injury include hypotension and reduced cardiac output. The local effects include loss of autoregulation in the injured segment of the spinal cord and a marked reduction of the microcirculation in both gray and white matter, especially in hemorrhagic regions and in adjacent zones. The microcirculatory loss extends for a considerable distance proximal and distal to the site of injury. Many studies have shown a dose-dependent reduction of spinal cord blood flow varying with the severity of injury, and a reduction of spinal cord blood flow which worsens with time after injury. The functional deficits due to acute spinal cord injury have been measured electrophysiologically with techniques such as motor and somatosensory evoked potentials and have been found proportional to the degree of posttraumatic ischemia. The histological effects include early hemorrhagic necrosis leading to major infarction at the injury site.

These posttraumatic vascular effects can be treated. Systemic normotension can be restored with volume expansion or vasopressors, and spinal cord blood flow can be improved with dopamine, steroids, nimodipine, or volume expansion. The combination of nimodipine and volume expansion improves posttraumatic spinal cord blood flow and spinal cord function measured by evoked potentials. These results provide strong evidence that posttraumatic ischemia is an important secondary mechanism of injury, and that it can be counteracted.