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✓ A case of a cavernous hemangioma located within Meckel's cave and involving the gasserian ganglion is described in a patient presenting with facial pain and a trigeminal nerve deficit. Although these lesions have been reported to occur in the middle fossa, this is believed to be the first case of such a vascular malformation arising solely from within Meckel's cave.

✓ 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 µA) DC stimulator and the other group a control (0 µA) 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.

✓ There is evidence that posttraumatic ischemia is important in the pathogenesis of acute spinal cord injury (SCI). In the present study spinal cord blood flow (SCBF), measured by the hydrogen clearance technique, and motor and somatosensory evoked potentials (MEP and SSEP) were recorded to evaluate whether the administration of nimodipine and dextran 40, alone or in combination, could increase posttraumatic SCBF and improve axonal function in the cord after acute SCI. Thirty rats received a 53-gm clip compression injury on the cord at T-1 and were then randomly and blindly allocated to one of six treatment groups (five rats in each). Each group was given an intravenous infusion of one of the following over 1 hour, commencing 1 hour after SCI: placebo and saline; placebo and dextran 40; nimodipine 0.02 mg/kg and saline; nimodipine 0.02 mg/kg and dextran 40; nimodipine 0.05 mg/kg and saline; and nimodipine 0.05 mg/kg and dextran 40.

The preinjury physiological parameters, including the SCBF at T-1 (mean ± standard error of the mean: 56.84 ± 4.51 ml/100 gm/min), were not significantly different (p > 0.05) among the treatment groups. Following SCI, there was a significant decrease in the SCBF at T-1 (24.55 ± 2.99 ml/100 gm/min; p < 0.0001) as well as significant changes in the MEP recorded from the spinal cord (MEP-C) (p < 0.0001), the MEP recorded from the sciatic nerve (MEP-N) (p < 0.0001), and the SSEP (p < 0.002). Only the combination of nimodipine 0.02 mg/kg and dextran 40 increased the SCBF at T-1 (43.69 ± 6.09 ml/100 gm/min; p < 0.003) and improved the MEP-C (p < 0.0001), MEP-N (p < 0.04), and SSEP (p < 0.002) following SCI. With this combination, the changes in SCBF were significantly related to improvement in axonal function in the motor tracts (p < 0.0001) and somatosensory tracts (p < 0.0001) of the cord. This study provides quantitative evidence that an increase in posttraumatic SCBF can significantly improve the function of injured spinal cord axons, and strongly implicates posttraumatic ischemia in the pathogenesis of acute SCI.

✓ 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.

✓ 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.

✓ Lhermitte-Duclos disease is a rare lesion characterized by enlarged cerebellar folia containing abnormal ganglion cells. This case report describes a 51-year-old woman who was initially misdiagnosed as having adult-onset aqueductal stenosis. There were no abnormal findings on computerized tomography (CT), but subsequent magnetic resonance (MR) imaging showed a midline cerebellar lesion extending to the brain stem. This is a unique case of Lhermitte-Duclos disease arising within the cerebellar vermis. The characteristic feature of an enlarged cerebellar hemisphere is absent on CT scans; thus MR imaging is needed to confirm the diagnosis. If diagnosed late, this generally benign lesion becomes difficult to resect totally and has a poorer prognosis. Only two reports have mentioned the MR imaging characteristics of Lhermitte-Duclos disease; both described only T₂-weighted images. This case illustrates the full spectrum of MR imaging features of this disease. Both T₁- and T₂-weighted studies showed enlarged cerebellar folia within the lesion. The T₁-weighted image showed a mixed iso- and hypodense signal and the T₂-weighted image a homogeneously increased signal; with gadolinium administration the lesion did not enhance. The latter feature supports the theory that this disease is a hamartoma rather than a tumor.

✓ Although posterior plates are increasingly used to manage cervical spinal instability, long-term follow-up evaluation of patients with a critical analysis of efficacy and complications has not been reported. The authors have retrospectively analyzed the outcome in 44 consecutive patients (37 males and seven females, age range 16 to 80 years) treated with posterior cervical plates. The indications for instrumentation were instability due to trauma in 42 cases, tumor in one, and infection in one. In four patients the follow-up period was limited to 3, 5, 11, and 16 months. Two patients died of chronic medical problems 4 and 9 months after treatment. The remaining 38 patients were followed from 2 to 6 years (mean 46 months). One motion segment was stabilized in 23 patients using two-hole plates; two motion segments were stabilized in the other 21 patients using three-hole plates. In the majority of patients (37 cases), supplemental bone grafting was not used. Patients were immobilized postoperatively in a Philadelphia collar. Solid arthrodesis was achieved in 39 (93%) of 42 patients. Three patients required revision of the cervical plating: in one patient with a C-5 burst fracture, two-hole plates were applied at C5–6 and progressive kyphosis mandated anterior fusion; the second patient required posterior wiring due to screw pull-out resulting from a technical error in screw insertion; the third patient, who refused to wear an orthosis postoperatively, also developed screw pull-out. In two patients who went on to spinal fusion, there was an increase in sagittal kyphosis (6° and 8°) without clinical sequelae. Screw loosening was noted in five patients, involving eight (3.8%) of the 210 lateral mass screws; this complication resulted in instrumentation failure or increased kyphosis in three cases. There were two superficial infections.

This analysis indicates that posterior cervical plating is highly effective; at long-term follow-up review the cervical spine was successfully stabilized in 93% of cases. Plate failure was related to faulty screw placement, failure to include sufficient motion segments, and noncompliance with postoperative orthoses. Halo vest immobilization was unnecessary and supplemental bone grafting was generally not required for recent trauma.

✓ 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.