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PubMed1998

Clinical outcomes of cervical spinal cord injuries without radiographic evidence of trauma.

We investigated 33 cervical spinal cord injury patients (25 males and eight females) without bony injury. Patients whose neurologic recovery had reached a plateau and who had evidence on imaging of persistent spinal cord compression were considered candidates for surgical decompression. When imaging did not show spinal cord compression or patients were maintaining a good neurologic recovery from the early days after injury, we pursued conservative treatment. Age at injury varied from 20 to 76 years (mean, 55.6). Average follow-up was 31 months. Twelve patients were treated conservatively (Group 1). Groups 2 and 3 had surgery. Group 2 (14 cases) had multi-level compression of spinal cord due to pre-existing cervical spine conditions such as ossification of posterior longitudinal ligament, cervical canal stenosis, and cervical spondylosis. Group 3 (7 cases) patients existed single-level compression of spinal cord by cervical disc herniations or spondylosis. We evaluated clinical results according to the Frankel classification, the American Spinal Injury Association (ASIA) scales and Japanese Orthopaedic Association (JOA) scores. Overall improvement of JOA and ASIA scores after treatment was 56.3 +/- 35.5% and 67.1 +/- 38.0%, respectively. Patients in Group 1 showed very good recovery after conservative treatment, with improvement of JOA and ASIA scores being 70.4 +/- 40.2% and 77.4 +/- 34.2%, respectively. The average interval between injury and operation was 4.3 +/- 4.4 months. The improvement of the surgically treated patients (Groups 2 and 3) in JOA and ASIA score was 48.2 +/- 30.7% and 61.2 +/- 39.6% respectively. We obtained good neurological recovery after operation, with significantly more improvement in Group 3 than in Group 2. No significant neurologic recovery had occurred preoperatively in these groups. In such patients operative intervention is essential for neurologic recovery.

Adult↗
PubMed2004

The dynamics of axolemmal disruption in guinea pig spinal cord following compression.

Membrane damage has been postulated as a critical factor in mediating axonal degeneration in brain and spinal cord trauma. Despite compelling evidence of membrane disruption as a result of physical insults in both in vivo and in vitro studies, the dynamics of such damage over the time post injury in in vivo studies has not been well documented. Using a well-characterized in vivo guinea pig spinal cord compression model and horseradish peroxidase exclusion assay, we have documented significant membrane disruption at 1 hr, 3 days, and 7 days following injury. Furthermore, the membrane damage was found to spread laterally 10 mm beyond the center of original compression site in both rostral and caudal directions. A second-degree polynomial fit of the measured data predicts a bilateral spread of approximately 20-21 mm of membrane disruption from the epicenter of injury over a period of about 20 days. Thus, this study shows that membrane damage exists days, and possibly weeks, after spinal cord trauma in live guinea pigs. This provides the evidence necessary to investigate the role of membrane damage in triggering axonal deterioration in the future. Furthermore, this study has also revealed a long therapeutical window for membrane repair and functional enhancement following traumatic injury in the central nervous system.

Animals↗
PubMed1999

Epidural Bilharzioma mansoni compressing the spinal cord: case report.

A case of an epidural Bilharzioma mansoni (epidural granuloma due to Schistosoma mansoni) compressing the spinal cord at T11-T12 is presented. The patient, a 20-year old African man, started complaining of recurrent back pain since 1993 and became paraparetic in 1996. The myelography showed a complete block at T12 and the CT scan showed a mass at T11-T12 compressing the spinal cord. Through a bilateral laminectomy of T 10, T11 and T12, the bilharzioma was completely removed. The histopathology and the laboratory tests confirmed the diagnosis of granuloma due to Schistosoma mansoni. The patient recovered completely and was seen last time more than one year after surgery. Not a similar case has been found in the literature and the authors presume that this is the first case ever successfully treated by surgery and chemotherapy and reported in the world literature.

Adult↗
PubMed2001

Beneficial effects of nitric oxide synthase inhibition on the recovery of neurological function after spinal cord injury in rats.

We have demonstrated recently that treatment with N(G)-monomethyl-L-arginine (L-NMMA) accelerates electrophysiological recovery after transient spinal cord ischaemia in anaesthetized cats. To determine whether nitric oxide synthase (NOS) inhibition in the acute phase of spinal cord injury results in better functional recovery in the chronic phase, we evaluated the influence of L-NMMA on the time course of changes of neurological function and the histopathological changes after spinal cord compression in rats. Experimental spinal cord injury was produced in anaesthetized rats by short-term (5 min) compression with a thread placed around the spinal cord at T13. The recovery of motor function was assessed by a treadmill test 10, 20 and 30 days after spinal cord compression. The latency of potentials evoked by hindlimb stimulation was measured at the funiculus posterior at C1 10 days after the spinal cord injury in anaesthetized rats. Histological examinations were also performed at the same time. The compression-induced spinal cord injury resulted in motor dysfunction of hindlimbs, an increase in the latency of the evoked potentials and neuronal degeneration in funiculus posterior at T13. Repeated administration of L-NMMA for 1 day significantly accelerated the recovery of the motor function, shortened the latency of the evoked potentials and attenuated the myelin vacuolization in the spinal cord. These beneficial effects of L-NMMA on neurological function and histopathological changes were abolished by coadministration of L- but not D-arginine. These results suggest that NOS inhibition during the early stage of spinal cord injury has beneficial effects on the recovery of neurological function and the histopathological changes in the chronic stage.

Animals↗
PubMed1989

Blocking weight-induced spinal cord injury in rats: effects of TRH or naloxone on motor function recovery and spinal cord blood flow.

The ability of thyrotropin releasing hormone (TRH) or naloxone to reduce the motor function deficit and to improve the spinal cord blood flow (SCBF) was investigated in a rat spinal cord compression injury model. Spinal cord injury was induced by compression for 5 min with a load of 35 g on a 2.2 x 5.0 mm sized compression plate causing a transient paraparesis. One group of animals was given TRH, one group naloxone and one group saline alone. Each drug was administered intravenously as a bolus dose of 2 mg/kg 60 min after injury followed by a continuous infusion of 2 mg/kg/h for 4 h. The motor performance was assessed daily on the inclined plane until Day 4, when SCBF was measured with the 14C-iodoantipyrine autoradiographic method. It was found that neither TRH nor naloxone had promoted motor function recovery or affected SCBF 4 days after spinal cord injury.

Animals↗
PubMed1988

Myelopathy due to epidural varicose veins of the cervicothoracic junction. Case report.

A 30-year-old man presented with a subacute course of myelopathic signs and symptoms. Magnetic resonance imaging demonstrated an epidural mass lesion of the spinal canal at the cervicothoracic junction causing compression of the spinal cord. Laminectomy with resection of this lesion revealed a large varix with acute and chronic thrombus. Postoperatively, an improvement in neurological function occurred. Spinal epidural varicosities have been reported as an etiological factor in lumbar and sacral radiculopathies. This is the first reported case of spinal cord compression in association with spinal epidural varices. The diagnosis, pathophysiology, and management of this disorder are presented.

Adult↗
PubMed1992

Suggested MRI criteria for surgical decompression in acute spinal cord injury. Preliminary observations.

The effect of spinal cord compression identified with magnetic resonance imaging (MRI), on neurological prognosis, was retrospectively evaluated in 36 patients with acute spinal cord injury. Of the 21 patients without cord compression, 16 had potentially reversible injury (normal spinal cord or cord oedema), all having functional recovery. Of the 15 patients with cord compression, 3 had operative decompression. In the 12 patients who did not undergo surgery, the degree of recovery was directly related to the magnitude of spinal cord compression, only one of the patients with moderate or marked cord compression having useful motor function at follow up. In contrast, the 3 patients with surgical decompression had at least 2 grades of improvement, all having functional recovery. These findings raise the possibility that MRI may be used to identify a patient group who will benefit from surgical decompression. A numerical index is proposed to prospectively identify patients for surgical decompression, and further studies are underway to evaluate this.

Adolescent↗
PubMed1980

Spinal cord energy metabolism following compression trauma to the feline spinal cord.

The purpose of this study was to determine the spinal cord metabolic state for 24 hours after compression trauma to the feline spinal cord. Cats were anesthetized with pentobarbital and injured by placing a 190-gm weight on the spinal cord for 5 minutes. Biochemical analysis of the injured segment revealed a significant depletion in the levels of adenosine triphosphate (ATP), phosphocreatine (P-creatine), and total adenylates for the entire 24-hour recovery period. Glucose levels initially declined, but by 1 hour had normalized, and at 8 and 24 hours were significantly supranormal. The lactate/pyruvate ratio and tissue lactate concentrations increased four and five and half times, respectively, for the first 4 hours after injury. Between 8 and 24 hours, lactate levels remained elevated, whereas the lactate/pyruvate ratio declined to contol levels as the result of a significant rise in the tissue pyruvate concentration. This sequence of metabolic changes suggested that metabolism was probably not homogeneous throughout the injured segment, and that tissue metabolic rate was depressed for the initial 4 hours after trauma then increased in metabolically active tissue for the remainder of the 24-hour recovery period. This model of spinal cord trauma results in a severe, prolonged ischemia and metabolic injury to the affected tissue. Whether these metabolic changes results from or cause the tissue damage and irreversible paraplegia associated with this type of spinal cord injury remains to be determined.

Adenosine Monophosphate↗
PubMed2005

Methylprednisolone inhibits production of interleukin-1beta and interleukin-6 in the spinal cord following compression injury in rats.

Interleukin-1beta (IL-1beta) and interleukin-6 (IL-6) are major inflammatory cytokines produced after spinal cord injury (SCI). This study sought to evaluate the effects of methylprednisolone (MP) on IL-1beta and IL-6 protein in spinal cord tissue following SCI. Halothane-anesthetized, female Sprague-Dawley rats weighing (280-320 g) underwent laminectomy at T7-T8. No lesions were produced in animals in the saline control and MP control groups. SCI was induced by temporary placement of an aneurysm clip at T7-T8, with a closing pressure of 55 g at the spinal level of T7-T8, resulting in spinal cord compression for one minute. Animals with SCI were treated with MP (30 mg/kg sc) or an equal volume of saline. IL-1beta and IL-6 spinal cord protein were measured by enzyme-linked immunosorbent assays (ELISA). Data were summarized as mean +/- SD and compared by two-way analysis of variance (ANOVA). IL-1beta and IL-6 levels were elevated in the SCI + Saline animals (P < 0.01) compared with saline control, MP control, and SCI + MP-treated animals. The rise in IL-1beta and IL-6 levels after SCI was blunted after administration of MP, suggesting an interaction between glucocorticosteroids and the cytokine cascade after spinal cord trauma. Further evaluation of the effects of MP on the cytokine cascade may be important in assessing whether or not the anti-inflammatory effects of glucocorticosteroids confer neuroprotection after SCI.

Animals↗
PubMed1986

Cystic necrosis of the spinal cord in compressive cervical myelopathy: demonstration by iopamidol CT-myelography.

Seven consecutive patients with compressive cervical myelopathy were studied with standard water-soluble contrast myelography and immediate CT followed by delayed CT of the spinal canal at 10 to 12 hr. Every case demonstrated findings suggestive of necrosis and/or cavitation of the central portions of the spinal cord on the delayed CT study. Two types of abnormalities were visualized in the form of delayed collections of contrast media inside the cord: bilateral enhancement, a double-barreled "snake-eyes" appearance at or near the level of compression (consistent with central gray matter necrosis and/or cavitation--local syringomyelia ex-vacuo); and longitudinally oriented, "pencil-shaped" central enhancement of variable length distant from the level of compression (consistent either with an enlarged central canal--hydromyelia ex-vacuo--or with necrosis and/or cavitation extending craniad and caudad from the area of maximal compression and located in or near the anterior portion of the dorsal columns--distant syringomyelia ex-vacuo). These findings, supported by previous reports of autopsy specimens, may explain in part: the frequent discrepancy between the levels of maximal cervical compression and the variable neurologic signs; and the frequent lack of improvement in clinical signs after surgical decompression of the spinal cord at this late stage of the illness. We believe similar intramedullary lesions may be present in other cases of chronic compression of varying etiology at any location within the spinal cord.

Adult↗
PubMed2001

A correlation between magnetic resonance imaging and electrophysiological findings in cervical spondylotic myelopathy.

STUDY DESIGN: Correlation between compressed spinal cords on magnetic resonance imaging (MRI) and electrophysiological findings in cervical spondylotic myelopathy patients. OBJECTIVE: To clarify the correlation between spinal-cord-evoked potentials and MRI measurements of compressed spinal cords in patients with cervical spondylotic myelopathy. SUMMARY OF BACKGROUND DATA: Compression of the spinal cord does not always cause clinical symptoms and it is difficult to infer the degree of dysfunction of the spinal cord from MRI findings. METHODS: Seventeen patients with cervical spondylotic myelopathy were examined with MRI and spinal-cord-evoked potentials before surgery. Using abnormality in spinal-cord-evoked potentials as indicators of spinal cord morphology, spinal-cord transverse area and compression ratios (central and 1/4-lateral) were measured on T1-weighted axial imaging. The correlations between these dimensions and electrophysiological findings were investigated. RESULTS: The mean preoperative transverse area of the spinal cord was 47.13 mm2. The mean preoperative central compression ratio of the spinal cord was 34.4%. The mean preoperative 1/4-lateral compression ratio of the spinal cord was 27.5%. A correlation (Spearman r=0.65, P < 0.01) was observed between the 1/4-lateral compression ratio of the spinal cord and the amplitude ratio of spinal-cord-evoked potentials after electric stimulation of the brain (Br(E)-SCEPs). CONCLUSIONS: The preoperative 1/4-lateral compression ratio of the spinal cord was found to reflect the degree of dysfunction of the corticospinal tracts.

Adult↗
PubMedDate not supplied

Ossification of posterior longitudinal ligaments: evaluation with MRI.

Ossification of the posterior longitudinal ligament is a special subcategory of degenerative disease responsible for compression of the spinal cord. On MR images, T2-weighted sequences are the most effective to evaluate both spinal cord compression due to the ossification and abnormal signal intensity of the cord. Although ossification of the ligaments is well demonstrated on CT and plain radiographs, MRI noninvasively provides useful information about the degree and extent of spinal cord compression, as well as the character of the ossification.

Diagnosis, Differential↗
PubMed1984

Intraoperative ultrasonic evaluation of spinal cord motion.

The spinal canals of 11 patients with various pathological conditions, both benign and malignant, were examined intraoperatively using real-time ultrasonography. The spinal cords in eight of these patients with lesions causing cord compression were seen to oscillate rhythmically over each mass with a frequency corresponding to the patient's arterial pulsations. The majority of the observed motion was transmitted or extrinsically induced from compression of the anterior spinal artery. In one case, after resection of an anterior cervical neurofibroma, these oscillations diminished markedly. Spinal cord motion, as described, has important implications for neurosurgery, since it contradicts the previously held belief that oscillations of the spinal cord or dura mater imply a "free" or noncompressed spinal cord. Furthermore, spinal cord motion may play a role in the degradation of computerized tomography images of the cord, since these movements are maximized at the areas with the most severe pathology.

Adult↗
PubMed2003

Upregulation of phospholipase D1 in the spinal cords of rats with clip compression injury.

This study examined phospholipase D 1 (PLD1) expression in the central nervous system following clip compression spinal cord injury (SCI) in Sprague-Dawley rats. After inducing SCI with a vascular clip, the expression of PLD1 in the affected spinal cord was analyzed by Western blot and immunohistochemistry. Western blot analysis showed that the expression of PLD1 gradually increased in the spinal cord on days 0.5, 1, 2, and 4 post injury. Immunohistochemistry showed that some cells, including neurons, astrocytes, and some inflammatory cells, were positive for PLD1 in the lesions at days 1 and 2 post injury. At day 4, the number of PLD1-positive cells in SCI lesions increased, largely matching the increases in ED1-positive macrophages and glial fibrillary acidic protein-positive astrocytes. At this time, macrophages expressed proliferating cell nuclear antigen in addition to PLD1. These results suggest that PLD1 expression is increased in injured spinal cords, and might be involved in the activation and proliferation of macrophages and astrocytes in SCI.

Animals↗
PubMed2005

Stretch-associated injury in cervical spondylotic myelopathy: new concept and review.

The simple pathoanatomic concept that a narrowed spinal canal causes compression of the enclosed cord, leading to local tissue ischemia, injury, and neurological impairment, fails to explain the entire spectrum of clinical findings observed in cervical spondylotic myelopathy. A growing body of evidence indicates that spondylotic narrowing of the spinal canal and abnormal or excessive motion of the cervical spine results in increased strain and shear forces that cause localized axonal injury within the spinal cord. During normal motion, significant axial strains occur in the cervical spinal cord. At the cervicothoracic junction, where flexion is greatest, the spinal cord stretches 24% of its length. This causes local spinal cord strain. In the presence of pathological displacement, strain can exceed the material properties of the spinal cord and cause transient or permanent neurological injury. Stretch-associated injury is now widely accepted as the principal etiological factor of myelopathy in experimental models of neural injury, tethered cord syndrome, and diffuse axonal injury. Axonal injury reproducibly occurs at sites of maximal tensile loading in a well-defined sequence of intracellular events: myelin stretch injury, altered axolemmal permeability, calcium entry, cytoskeletal collapse, compaction of neurofilaments and microtubules, disruption of anterograde axonal transport, accumulation of organelles, axon retraction bulb formation, and secondary axotomy. Stretch and shear forces generated within the spinal cord seem to be important factors in the pathogenesis of cervical spondylotic myelopathy.

Biomechanical Phenomena↗
PubMed1995

MRI findings in patients with a cervical spinal cord injury who do not show radiographic evidence of a fracture or dislocation.

We investigated the usefulness of magnetic resonance imaging (MRI) in assessing cervical spinal cord injury in patients where there was no evidence of bone injury on radiographs, and examined the relationship between the MRI findings and the clinical prognosis of this injury. MRI allowed us to confirm directly the cause and severity of spinal cord compression in 30 of 31 cases. The patients with severe spinal cord compression demonstrated by MRI showed poor neurological improvement. In regard to the signal changes in the spinal cord, the patients who showed no signal change on T1- and T2-weighted images had a better prognosis. MRI is a very useful non-invasive adjunctive imaging modality for diagnosis of this injury and for the evaluation of the compressed spinal cord. It also demonstrates potential in predicting neurological recovery.

Adult↗
PubMed1983

[An evaluation of decompressive laminectomy in metastatic spinal cord tumors].

The results of consecutive cases of decompressive laminectomy for spinal cord compression from spinal metastatic tumor were reviewed. In a series of 65 patients undergoing decompressive laminectomy, the postoperative survival was 8.3 months with 60 patients. Twenty-three per cent of the group was able to ambulate for at least some period postoperatively. Paralysis had developed with great rapidity in the half of the patients who were unable to walk prior to operation. For early diagnosis and effective removal of these lesions this treatment should be taken before when signs of cord compression are evident, and especially before the patient loses his ability to walk.

Adolescent↗