Search Results

You are looking at 1 - 10 of 150 items for

  • Author or Editor: Michael Fehlings x
Clear All Modify Search
Full access

Charles H. Tator and Michael G. Fehlings

In this paper the authors review the clinical trials of neuroprotection that have been performed for the treatment of acute spinal cord injury (SCI). The biological rationale for the selection of each treatment modality is discussed with reference to current knowledge of the principles in the management of acute SCI as well as the primary and secondary injury mechanisms identified by experimental and clinical studies of the pathophysiology of acute SCI. The trials are evaluated with regard to the availability and use of accurate clinical outcome measures, and the methodologies of the trials are critically evaluated with an emphasis on prospective randomized controlled studies. A detailed description and critical analysis are provided of the results of the 10 clinical trials conducted to date in which a randomized prospective controlled design has been used. The issue of the therapeutic time window in acute SCI is discussed. To date, methylprednisolone is the only effective neuroprotective agent that has been established for use in human SCI, and the only therapeutic time window established in human SCI is a maximum trauma-to-treatment time of 8 hours.

Restricted access

Gwen Schwartz and Michael G. Fehlings

Object. Persistent activation of voltage-sensitive Na+ channels is associated with cellular toxicity and may contribute to the degeneration of neural tissue following traumatic brain and spinal cord injury (SCI). Pharmacological blockade of these channels can attenuate secondary pathophysiology and reduce functional deficits acutely.

Methods. To determine the therapeutic effects of Na+ channel blockers on long-term tissue sparing and functional neurological recovery after traumatic SCI, the authors injected Wistar rats intraperitoneally with riluzole (5 mg/kg), phenytoin (30 mg/kg), CNS5546A, a novel Na+ channel blocker (15 mg/kg), or vehicle (2-HPβCD; 5 mg/kg) 15 minutes after induction of compressive SCI at C7—T1.

Functional neurological recovery of coordinated hindlimb function and strength, assessed 1 week postinjury and weekly thereafter for 6 weeks, was significantly enhanced in animals treated with riluzole compared with the other treatment groups. Seven weeks postinjury the preservation of residual tissue and integrity of descending axons were determined with digital morphometrical and fluorescent histochemical analysis. All three Na+ channel blockers significantly enhanced residual tissue area at the injury epicenter compared with control. Riluzole significantly reduced tissue loss in rostrocaudal regions surrounding the epicenter, with overall sparing of gray matter and selective sparing of white matter. Also, counts of red nuclei neurons retrogradely labeled with fluorogold introduced caudal to the injury site were significantly increased in the riluzole group.

Conclusions. Systemic Na+ channel blockers, in particular riluzole, can confer significant neuroprotection after in vivo SCI and result in behavioral recovery and sparing of both gray and white matter.

Restricted access

Michael G. Fehlings and Charles H. Tator

Object. The authors conducted an evidence-based review of the literature to evaluate critically the rationale and indications for and the timing of decompressive surgery for the treatment of acute, nonpenetrating spinal cord injury (SCI).

Methods. The experimental and clinical literature concerning the role of, and the biological rationale for, surgical decompression for acute SCI was reviewed. Clinical studies of nonoperative management of SCI were also examined for comparative purposes. Evidence from clinical trials was categorized as Class I (well-conducted randomized prospective trials), Class II (well-designed comparative clinical studies), or Class III (retrospective studies).

Examination of studies in which animal models of SCI were used consistently demonstrated a beneficial effect of early decompressive surgery, although it is difficult to apply these data directly to the clinical setting. The clinical studies provided suggestive (Class III and limited Class II) evidence that decompressive procedures improve neurological recovery after SCI. However, no clear consensus can be inferred from the literature as to the optimum timing for decompressive surgery. Many authors have advocated delayed treatment to avoid medical complications, although good evidence from recent Class II trials indicates that early decompressive surgery can be performed safely without causing added morbidity or mortality.

Conclusions. There is biological evidence from experimental studies in animals that early decompressive surgery may improve neurological recovery after SCI, although the relevant interventional timing in humans remains unclear. To date, the role of surgical decompression in patients with SCI is only supported by Class III and limited Class II evidence. Accordingly, decompressive surgery for SCI can only be considered a practice option. Furthermore, analysis of the literature does not allow definite conclusions to be drawn regarding appropriate timing of intervention. Hence, there is a need to conduct well-designed experimental and clinical studies of the timing and neurological results of decompressive surgery for the treatment of acute SCI.

Restricted access

Editorial

The safety of percutaneous vertebroplasty and kyphoplasty

Michael G. Fehlings

Full access

Michael G. Fehlings and Charles H. Tator

The authors conducted an evidence-based review of the literature to evaluate critically the rationale and indications for and the timing of decompressive surgery for the treatment of acute, nonpenetrating spinal cord injury (SCI).

The experimental and clinical literature concerning the role of, and the biological rationale for surgical decompression for acute SCI was reviewed. Clinical studies of nonoperative management of SCI were also examined for comparative purposes. Evidence from clinical trials was categorized as Class I (well-conducted randomized prospective trials), Class II (well-designed comparative clinical studies), or Class III (retrospective studies).

Studies in which animal models of SCI were used consistently demonstrated a beneficial effect of early surgical decompression, although it is difficult to apply these data directly to the clinical setting. The clinical studies provided suggestive (Class III and limited Class II) evidence that decompressive procedures improve neurological recovery after SCI. However, no clear consensus can be inferred from the literature as to the optimum timing of decompressive surgery. Many authors have advocated delayed treatment to avoid medical complications, although there is good evidence from recent Class II trials that early decompressive surgery can be performed safely without added morbidity or mortality.

There is biological evidence from experimental studies in animals that early surgical decompression may improve neurological recovery after SCI, although the relevant interventional timing in humans remains unclear. To date, the role of surgical decompression in patients with SCI is only supported by Class III and limited Class II evidence. Accordingly, decompressive surgery for SCI can only be considered a practice option. Furthermore, analysis of the literature does not allow definite conclusions to be drawn regarding appropriate timing of intervention. Hence, there is a need to conduct well-designed experimental and clinical studies of the timing and neurological results of surgical decompression for the treatment of acute SCI.

Restricted access

Michael G. Fehlings and William S. Tucker

✓ 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.

Restricted access

Michael G. Fehlings

Restricted access

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.

Full access

W. Bradley Jacobs and Michael G. Fehlings

✓ Ankylosing spondylitis (AS) is a chronic inflammatory rheumatic disease that primarily affects the vertebral column and sacroiliac joints. Over time, the disease process promotes extensive remodeling of the spinal axis via ligamentous ossification, vertebral joint fusion, osteoporosis, and kyphosis. These pathological changes result in a weakened vertebral column with increased susceptibility to fractures and spinal cord injury (SCI). Spinal cord injury is often exacerbated by the highly unstable nature of vertebral column fractures in AS. A high incidence of missed fractures in the ankylosed spine as well as an increased incidence of spinal epidural hematoma also worsens the severity of SCI. Spinal cord injury in AS is a complex problem associated with high morbidity and mortality rates, which can be attributed to the severity of the injury, associated medical comorbidities, and the advanced age of most patients with AS who suffer an SCI. In this paper the authors outline the factors that increase the incidence of vertebral column fractures and SCI in AS and discuss the management of SCI in patients with AS. Primary prevention strategies for SCI in patients with AS are outlined as well.

Restricted access

Jefferson R. Wilson, David W. Cadotte and Michael G. Fehlings

Object

The object of this study was to identify, by means of a systematic review of the literature, the acute clinical predictors of neurological outcome, functional outcome, and survival after traumatic spinal cord injury (SCI).

Methods

A comprehensive computerized literature review search was performed, using MEDLINE, PubMed, EMBASE, CINAHL, and the Cochrane Database of Systematic Reviews. Selected articles were classified according to their level of evidence. Articles were then stratified into one of 3 domains depending on whether the primary focus was clinical prediction of 1) neurological outcome, 2) functional status, or 3) survival. For each study selected, clinical predictors related to patient demographic characteristics, injury mechanism, or neurological examination findings were extracted, and the individual relationship to outcome was defined.

Results

The initial search resulted in 376 citations. After application of the inclusion and exclusion criteria and study review, 51 relevant articles were identified and graded. Of these, 25 provided predictors for neurological outcome, 22 for functional outcome, and 15 for survival, with several of the articles providing information on more than one type of outcome. All of the included studies were designated as providing Class I, II, or III levels of evidence. The severity of neurological injury (as measured by admission Americal Spinal Injury Association Impairment Scale grade, Frankel grade, or injury completeness), level of injury, and the presence of a zone of partial preservation were consistent predictors of neurological outcome. Severity of neurological injury, level of injury, reflex pattern, and age were consistent predictors of functional outcome. Finally, severity of neurological injury, level of injury, age, and the presence of multisystem trauma seen with higher-energy injury mechanisms were consistent predictors of survival.

Conclusions

On the basis on this review, the authors have identified a constellation of acute clinical features that may help to define an individual's profile for recovery and survival after SCI. This study will help to facilitate communication in the clinical realm and assist in classifying subsets of patients within future clinical studies.