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M G Fehlings

Publications and source records attributed to M G Fehlings.

At least 73 records · Page 4Linked to original sources
PubMed1995

Role of sodium in the pathophysiology of secondary spinal cord injury.

STUDY DESIGN: Experimental study using an in vitro model of compressive injury to isolated adult rat dorsal column axons. OBJECTIVES: To examine the role of extracellular Na+ (Na+e) in mediating secondary injury to spinal cord axons after compressive trauma. The mechanisms of intracellular sodium entry were examined using ion substitution techniques and pharmacologic blockers. SUMMARY OF BACKGROUND DATA: There is evidence that intracellular Na+ entry potentiates hypoxic-ischemic cell death by causing cytotoxic cell swelling, intracellular acidosis, and gating of Ca++ entry through reverse activation of the Na(+)-Ca++ exchanger. In the present study, we have examined the role of Na+e in the pathophysiology of spinal cord injury. METHODS: Dorsal column segments isolated from the thoracic cord of adult rats (n = 40) were pinned in a recording chamber and superfused with oxygenated Ringer's solution. Extracellular field potentials were recorded from glass microelectrodes (150 mmol KCl; 5-10 mol). Injury was accomplished in vitro by compression with a modified aneurysm clip (closing force, 2 g) for 15 seconds. The effect of zero Na+e (equimolar substitution with NMDG+), the Na(+)-H+ exchange blocker amiloride, the Na+ channel blocker procaine, and the Na(+)-Ca++ exchanger blocker benzamil on CAP recovery after compressive injury were assessed. RESULTS: Pretreatment with zero Na+, amiloride and procaine conferred significant neuroprotection (P < 0.05). In contrast, the NCE blocker benzamil was ineffective in attenuation secondary injury. CONCLUSIONS: Reduction of extracellular Na+, inhibition of the Na(+)-H+ exchanger or blockade of voltage gated Na+ channels is neuroprotective after spinal cord injury. The mechanism of Na(+)-associated cytotocity does not involve reverse gating of the Na(+)-Ca++ exchanger.

Action Potentials↗
PubMed1995

Assessment of axonal dysfunction in an in vitro model of acute compressive injury to adult rat spinal cord axons.

An in vitro model of spinal cord injury was developed to study the pathophysiology of posttraumatic axonal dysfunction. A 25 mm length of thoracic spinal cord was removed from the adult male rat (n = 27). A dorsal column segment was isolated and pinned in a recording chamber and superfused with oxygenated (95% O2/5% CO2) Ringer. The cord was stimulated with a bipolar electrode, while two point responses were recorded extracellularly. Injury was accomplished by compression with a modified aneurysm clip which applied a 2 g force for 15 s. With injury the compound action potential (CAP) amplitude decreased to 53.7 +/- 5.4% (P < 0.001), while the latency increased to 115.6 +/- 3.1% (P < 0.0025) of control values. The absolute refractory period increased with injury from 1.7 +/- 0.1 ms to 2.1 +/- 0.1 ms (P < 0.05). The infusion of 5 mM 4-aminopyridine (4-AP), a blocker of voltage-sensitive 'fast' K channels confined to internodal regions, resulted in broadening of the CAP of injured axons to 114.9 +/- 3.1% of control (P < 0.05). Ultrastructural analysis of the injured dorsal column segments revealed marked axonal and myelin pathology, including considerable myelin disruption. In conclusion, we have developed and characterized an in vitro model of mammalian spinal cord injury which simulates many of the features of in vivo trauma. Injured axons display characteristic changes in physiological function including a shift in refractory period and high frequency conduction failure. The ultrastructural data and response of injured axons to 4-AP suggest that myelin disruption with exposure of 'fast' K+ channels contributes to posttraumatic axonal dysfunction.

4-Aminopyridine↗
PubMed1995

The relationships among the severity of spinal cord injury, residual neurological function, axon counts, and counts of retrogradely labeled neurons after experimental spinal cord injury.

Substantial residual neurological function may persist after spinal cord injury (SCI) with survival of as few as 5-10% of the original number of axons. A detailed understanding of the relationships among the severity of injury, the number and origin of surviving axons at the injury site, and the extent of neurological recovery after SCI is of importance in understanding the pathophysiology of SCI and in designing treatment strategies. In the present study, these relationships were examined in rats with graded severity of clip compression injury of the cord at T1. The rats were randomly assigned to one of the following injury groups (n = 5 each): normal (laminectomy only), 2-, 18-, 30-, 50-, and 98-g clip injuries. Neurological function was assessed by the inclined plane method and by the modified Tarlov technique. A morphometric assessment of axons at the injury site was performed by a computer-assisted line sampling technique. The origin of descending axons at the injury site was determined by retrograde labeling with horseradish peroxidase. The inclined plane scores varied as a negative linear function of the closing force of the clip used to inflict SCI (r = -0.93; P < 0.0001). The mean axon count was 367,000 +/- 59,000 in normal rats and decreased as a negative exponential function of injury force (r = -0.92; P < 0.0001). As well, SCI caused preferential destruction of large axons as reflected by the change in mean axon diameter from 1.74 +/- 0.06 microns in normal cords to 1.46 +/- 0.04 microns in injured cords (pooled mean for all injuries).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

C1-C2 posterior cervical fusion: long-term evaluation of results and efficacy.

Posterior wiring techniques are the most commonly used methods of achieving C1-C2 arthrodesis. Recently, transarticular screw fixation and interlaminar clamping have been advocated to achieve more secure fixation. A retrospective review of patients undergoing C1-C2 fusion for nonneoplastic disease was undertaken at the University of Toronto Hospital, with the aim of determining the long-term outcome of the selected procedures. Thirty-two patients underwent 36 procedures from 1986 to 1992, with a mean follow-up of 4.7 +/- 2.2 years (range, 2.0-8.0 yr). The most common disease processes were odontoid fracture (18 patients), transverse atlantal ligament injury (5 patients), os odontoideum (5 patients), and rheumatoid C1-C2 instability (3 patients). Thirty-one Gallie fusions, one Brooks-Jenkins fusion, two transarticular screw fusions, and two Halifax clamp applications were performed. Six (19%) of Gallie/Brooks-Jenkins fusions failed. These occurred with os odontoideum (three patients), Type II odontoid fracture (two patients), and transverse atlantal ligament injury (one patient). All transarticular screw and Halifax clamp procedures resulted in successful fusions. Two procedures (6%) resulted in new neurological deficit; both of these patients underwent posterior wiring for os odontoideum. This study suggests that Type II odontoid fractures may be successfully managed by a posterior wiring technique alone. Rheumatoid C1-C2 instability may be managed by posterior wiring supplemented with halo immobilization. Transarticular screw fixation has several potential advantages as a technique for C1-C2 arthrodesis and, in particular, may be appropriate for os odontoideum that had a high failure rate (75%) with conventional posterior wiring, even when this was supplemented with halo bracing.

Adolescent↗
PubMed1995

Microdiskectomy for lumbar disk herniation: a review of 100 cases.

One hundred patients who underwent microlumbar diskectomy over 5 years were retrospectively reviewed. L4-5 and L5-S1 were compared to determine whether a patient's post-surgical outcome is related to the level where a herniation has occurred. Overall results included 70 excellent, 19 good, 2 fair, and 9 poor. Statistical analysis showed that neither the level involved, length of follow-up, nor degree of manual labor predicted outcome. Older patients and females tended to fare worse, but the trends were not significant. Three recurrent herniations occurred, 1 in the L4-L5 group and 2 in the L5-S1 group. No variable predicted recurrence.

Adult↗
PubMed1994

Lhermitte-Duclos disease mimicking adult-onset aqueductal stenosis. Case report.

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.

Cerebellar Neoplasms↗
PubMed1994

Posterior plates in the management of cervical instability: long-term results in 44 patients.

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 degrees and 8 degrees) 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.

Adolescent↗
PubMed1993

Occipitocervical fusion with a five-millimeter malleable rod and segmental fixation.

Although occipitocervical fusion is frequently used for instability of the upper cervical spine and the occipitocervical articulation, most currently used techniques have one or more of the following disadvantages: the necessity for sublaminar wires, the use of occipital screws, a fixed angle of instrumentation, or the necessity for routine postoperative halo immobilization. Moreover, many reported techniques are associated with a high rate of nonunion or instrumentation failure. We present our experience with a technically simple method of obtaining rigid occipitocervical arthrodesis using a 5-mm malleable rod that is fixed to the skull by a pair of wires passed through four suboccipital burr holes. Segmental spinal fixation is achieved with Wisconsin interspinous wires and is occasionally supplemented with sublaminar wires. Supplemental autogenous bone graft is used in all cases. A cervical collar is routinely used for postoperative immobilization. The results of treatment were retrospectively reviewed in 16 patients with an average age of 49.4 years (range, 9-69). Mean follow-up was 24 months (range, 12-36 mo). The indication for fusion was instability of the occiput-C1-C2 complex as a result of Chiari malformation, rheumatoid disease, skull base tumor resection, basilar invagination, ankylosing spondylitis, Down's syndrome, cervical laminectomy, and trauma. The average number of levels fused was 5.4 (range, O-C3 to O-T3). Successful occipitocervical arthrodesis was achieved in all but one of the surviving patients. The single patient with a pseudarthrosis was successfully managed with supplemental bone grafting and halo immobilization. There were two deaths from medical complications in chronically ill patients. Other complications included one postoperative instrumentation loosening, one myocardial infarction, and one superficial occipital decubitus. In conclusion, rodding and segmental interspinous wiring is an effective, technically simple method of obtaining rigid occipitocervical fixation, which obviates the need for bulky orthoses.

Adolescent↗
PubMed1993

Deep cerebral venous system thrombosis: case report.

A 38-year-old woman with thrombosis of the deep cerebral venous system, presumed to be secondary to the use of the oral contraceptive pill, is reported. The use of cerebral angiography and magnetic resonance imaging in establishing the diagnosis and management strategies is discussed. It is concluded that magnetic resonance imaging is an appropriate investigative modality for diagnosis and therapeutic decision making, and that, as with superficial cerebral dural sinus and venous thrombosis, anticoagulation is a safe and effective therapy.

Adult↗
PubMed1992

The effect of direct current field polarity on recovery after acute experimental spinal cord injury.

Recent evidence indicates that direct current (DC) fields promote recovery of acutely injured central and peripheral nervous system axons. The polarity of the applied DC field may play an important role in modulating these effects. In the present study, the effect of DC field polarity on recovery of injured spinal cord axons was examined anatomically, electrophysiologically and behaviourly in a rat model. After a 53 g clip compression injury of the cord at T1, 30 adult rats were randomly and blindly allocated to one of three groups (n = 10 each): one group received implantation of a DC stimulator (14 microA) with the cathode caudal to the injury site; the second group received implantation of a similar stimulator with the cathode rostral to the injury site; and the third group received a sham (O microA) stimulator. Clinical neurological function was assessed by the inclined plane technique and axonal function was assessed by motor- and somatosensory-evoked potentials (MEP and SSEP). A quantitative assessment of axonal integrity was performed by counting neurons in the brain retrogradely labelled by the axonal tracer horseradish peroxidase (HRP) and by counting axons at the injury site. The inclined plane scores (P less than 0.0001), MEP amplitude (P less than 0.02), counts of neurons retrogradely labelled by HRP (P less than 0.0001), and axon counts at the injury site (P less than 0.01) were significantly greater in the group treated with a DC field with the cathode caudal to the lesion than in the other two groups. Conversely, the cathode rostral DC field caused a decrease in the number of neurons retrogradely labelled by HRP (P less than 0.05) compared to the sham and cathode caudal groups. These data confirm our previous finding that DC fields promote recovery of acutely injured spinal cord axons. Furthermore, the polarity of the applied field is of critical importance to this effect.

Animals↗
PubMed1992

Evoked potentials from direct cerebellar stimulation for monitoring of the rodent spinal cord.

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 greater than 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.

Animals↗
PubMed1992

Syringomyelia as a complication of tuberculous meningitis.

Tuberculous meningitis may rarely be followed by the development of syringomyelia despite appropriate chemotherapy. In the present paper, we report a case of tuberculous meningitis in a 23-year-old Vietnamese male complicated by a rapidly progressive myelopathy due to granulomatous arachnoiditis which culminated in the development of a syrinx. The relevant literature is reviewed. The present case supports the hypothesis that vasculitic thrombosis of spinal cord vessels leading to ischemic myelomalacia is the mechanism causing postinflammatory syringomyelia.

Adult↗
PubMed1991

The association between polycystic kidney disease and cerebral aneurysms.

Rupture of cerebral aneurysms is an important cause of morbidity and mortality in patients with adult polycystic kidney disease (PKD). In the present paper, we review the literature regarding the association of cerebral aneurysms and PKD and emphasize, by means of a case report, the importance of familial clustering of aneurysms in patients with PKD. We conclude that the prevalence of intracranial aneurysms in patients with PKD approaches 40% and is likely significantly higher in patients with PKD and a positive family history for cerebral aneurysm. We recommend that screening cerebral angiography be strongly considered in all patients with PKD and a family history of cerebral aneurysm or subarachnoid hemorrhage.

Cerebral Angiography↗
PubMed1991

Review of the secondary injury theory of acute spinal cord trauma with emphasis on vascular mechanisms.

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.

Animals↗
PubMed1991

The electrophysiological assessment of the pyramidal and non-pyramidal tracts of the spinal cord of rats.

The present paper summarizes our experience with the use of motor evoked potentials (MEP) and cerebellar evoked potentials (CEP) to assess the physiological integrity of the motor tracts of the spinal cord in a rat model. The MEP elicited by intracortical microstimulation of motor cortex reflected activity only in the pyramidal tracts; in contrast the MEP obtained by extradural cortical stimulation with a macroelectrode also reflected activity in a number of non-pyramidal pathways including the lateral vestibulospinal and rubrospinal tracts. The CEP was principally conducted in ventral spinal cord tracts and may reflect direct activation of brainstem nuclei. Data are presented which correlate the relationship between the MEP and axonal integrity after cord injury.

Animals↗
PubMed1989

The effect of nimodipine and dextran on axonal function and blood flow following experimental spinal cord injury.

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 greater than 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 less than 0.0001) as well as significant changes in the MEP recorded from the spinal cord (MEP-C) (p less than 0.0001), the MEP recorded from the sciatic nerve (MEP-N) (p less than 0.0001), and the SSEP (p less than 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 less than 0.003) and improved the MEP-C (p less than 0.0001), MEP-N (p less than 0.04), and SSEP (p less than 0.002) following SCI. With this combination, the changes in SCBF were significantly related to improvement in axonal function in the motor tracts (p less than 0.0001) and somatosensory tracts (p less than 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.

Animals↗
PubMed1989

Effect of a direct current field on axons after experimental spinal cord injury.

There is evidence that direct current (DC) stimulation promotes neurologic recovery in spinal cord injury. The authors conducted a morphometric analysis of axons at the site of spinal cord injury in adult rats treated with a DC field. Ten rats received a 17-g and 15 rats a 53-g clip compression injury and were treated with either a sham (control) or a functioning DC stimulator for 8 weeks. Five normal rats were also assessed. There was a significant relation (p less than 0.0001) between the severity of injury and the number of axons at the injury site. After the 17-g injury, there was no significant difference in the number of axons between control and treated rats. However, after the 53-g injury, there were significantly (p less than 0.05) more axons in treated than control rats. Both degrees of injury caused preferential destruction of large-calibre axons. Subsequent analysis showed that the axon diameter of treated rats with 17-g or 53-g injury was significantly greater (p less than 0.05) than that of control rats with 17-g or 53-g injury. These data, for the first time, show that the application of a DC field increases the number and calibre of axons at the site of a spinal cord injury and enhances the survival or regrowth of axons following spinal cord injury in the rat.

Animals↗