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The intradural spinal spread from operated primary carcinomas of the breast is discussed considering our own case and the literature. The identical localization of the intradural spinal metastases at the junction of the cervical to the thoracic spine in all three known cases is striking.
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This study was conducted to induce chronic spinal cord compression myelopathy in rabbits. The L5 lumbar lamina was cut partially in 70 rabbits, and bone morphogenetic protein (BMP) was implanted on the ligamentum flavum in 35 of them. In the BMP group, new bone formed on the dorsal side of the spinal canal and flattened the spinal cord in an anteroposterior direction. No pathological changes were detected in the intramedullary tissues by light microscopic examination. In rabbits it is possible to induce compression of the cord by using BMP, although sufficient cord compression to induce myelopathy was not achieved.
We evaluated in a rat model of severe spinal cord compression the effect of the 21-aminosteroid tirilazad on extracellular levels of energy metabolites and amino acids, until 3 h after injury. The compound was given i.v. 30 min before injury (3 mg/kg) and hourly thereafter (1.5 mg/kg). The findings were compared with previously reported effects of methylprednisolone. Both treated and untreated rats with spinal cord compression showed, at 10 min after injury, a five- to sixfold elevation of extracellular lactate above the preinjury level. There was no significant difference for lactate, pyruvate or lactate/pyruvate ratio between the treated and untreated injured groups at any time point after trauma. Glutamate was significantly elevated both in treated and untreated injured rats for 20 min after trauma. The mean glutamate level was lower in animals treated with 21-aminosteroid. However, there was no statistically significant difference between the treated and untreated rats at any time after trauma. There was no statistically significant difference between the groups for aspartate, serine, glutamine, histidine, glycine, threonine, taurine, alanine and tyrosine. In conclusion our findings indicate that, in the injured spinal cord, methylprednisolone and the 21-aminosteroid have differences and similarities, regarding their effects on energy and amino acid metabolism. The lowering of the lactate and arginine levels early after trauma seen with methylprednisolone pretreatment was absent after 21-aminosteroid pretreatment. However, the mean extracellular level of glutamate was lower with both methylprednisolone and 21-aminosteroid after injury, although the difference was not statistically significant between treated and untreated rats.
OBJECTIVE: To study the relation of compressive spinal cord changes in morphology with postoperative results. METHODS: 114 cases of operative patients were divided in to three groups: ossification of posterior longitudinal ligament (OPLL), cervical spondylotic myelopathy (CSM), and cervical intervertebral disc herination. The spinal cord plane and to the compressive ratio in the most heavily pressed position were measured according to the JOA record. RESULTS: The compressive ratio and the plane were not corelated with clinical history. The spinal cord plane was positively corelated with the recovery rate. CONCLUSIONS: The preoperative spinal cord plane in OPLL and CSM is mostly corelated with the recovery rate.
OBJECT: It is known that the spinal cord can sustain traumatic injury without associated injury of the spinal column in some conditions, such as a flexible spinal column or preexisting narrowed spinal canal. The purpose of this study was to characterize the clinical features and to understand the mechanisms in cases of acute cervical cord injury in which fracture or dislocation of the cervical spine has not occurred. METHODS: Eighty-nine patients who sustained an acute cervical cord injury were treated in our hospitals between 1990 and 1998. In 42 patients (47%) no bone injuries of the cervical spine were demonstrated, and this group was retrospectively analyzed. There were 35 men and seven women, aged 19 to 81 years (mean 58.9 years). The initial neurological examination indicated complete injury in five patients, whereas incomplete injury was demonstrated in 37. In the majority of the patients (90%) the authors found degenerative changes of the cervical spine such as spondylosis (22 cases) or ossification of the posterior longitudinal ligament (16 cases). The mean sagittal diameter of the cervical spinal canal, as measured on computerized tomography scans, was significantly narrower than that obtained in the control patients. Magnetic resonance (MR) imaging revealed spinal cord compression in 93% and paravertebral soft-tissue injuries in 58% of the patients. CONCLUSIONS: Degenerative changes of the cervical spine and developmental narrowing of the spinal canal are important preexisting factors. In the acute stage MR imaging is useful to understand the level and mechanisms of spinal cord injury. The fact that a significant number of the patients were found to have spinal cord compression despite the absence of bone injuries of the spinal column indicates that future investigations into surgical treatment of this type of injury are necessary.
The authors report a case of cauda equina compression by intradural hydatid cyst. An 18-year-old man presented with paraparesis and sphincter dysfunction. MRI showed an intradural cystic lesion extending from L1 to L2 with low signal intensity on T1 and high signal intensity on T2. The cyst was removed after laminectomy and opening of the dural sac. Histological and parasitic examinations confirmed a diagnosis of hydatid cyst. The patient improved progressively after surgery. The similar 22 cases of intradural extramedullary hydatid disease reported in the literature were reviewed. All spinal areas were involved, with a predilection for the thoracic region. Neurological complications were usual with rapid spinal cord compression in this rare form of hydatid disease. The treatment was by surgery with a favourable outcome compared to the classic hydatid cyst of the spine.
We performed myelography in chin-up position during neck flexion in 20 patients with juvenile muscular atrophy of unilateral upper extremity, and we also performed CT-myelography in rotational position during neck flexion in 15 of them. In this disease, in which posterior lower cervical dural wall shifts anteriorly and compresses the spinal cord during neck flexion, we found that the anterior dural shift and cord compression became lessened by making chin-up without changing the position of neck flexion. By measuring the posterior dural length from foramen magnum to C6 vertebra on the profile of myelogram in neutral and neck flexion posture, we found that the posterior lower cervical dural wall of this disease was less extensible during neck flexion than that of control cases. On CT-myelogram the spinal cord compression of muscularly atrophic side increased by the neck rotation to the non-atrophic side during neck flexion, which is the position of maximum extension of posterior dural wall. The spinal cord compression decreased by the rotation to the atrophic side. We think that the low extensibility and asymmetry of posterior lower cervical dural wall may be the cause of this disease and its laterality may be relevant to unilaterality of this disease. These findings could also explain the efficacy of cervical immobilization by using cervical coller.
The authors conducted a study in which they applied the spinal cord compression-decompression model in rabbits to investigate the morphological changes and histopathological findings in the deformed spinal cord over a long-term period after performing decompressive surgery. Throughout the experimental period, mangnetic resonance (MR) images were obtained frequently; after obtaining a final MR image, the spinal cord was dissected and underwent histological examination. Immediately after decompressive surgery, axial T1-wieighted MR imaging revealed an increase in the cross-sectional area of the spinal cord during the 1st and 2nd weeks. The spinal cord area achieved a peak at an average of 5.9 weeks after decompressive surgery, when it displayed isointensity on T1- and high-intensity on T2-weighted images. The main histological findings were spongy changes in the white matter, which persisted for 4 months postsurgery. There was a significant correlation between the presurgical spinal cord area and the postsurgical decreased number of motor neuron cells. Based on the MR imaging and histopathological studies, although the deformed spinal cord that underwent compression for 3 months was immediately restored morphologically after decompressive surgery, the change in quality in the spinal cord persisted at least 4 months.
OBJECTIVE: Gabexate mesilate is a synthetic protease inhibitor capable of inhibiting both coagulation and cytokine production by monocytes. To investigate whether gabexate mesilate is useful for the prevention of posttraumatic spinal cord injury, we examined its effect on compression trauma-induced spinal cord injury in rats. DESIGN: Prospective, randomized, blinded, controlled study. SETTING: Research laboratory at a university medical center. SUBJECTS: Male Wistar rats weighing 300 to 350 g. INTERVENTIONS: Spinal cord injury was induced by applying a 20-g weight extradurally to the spinal cord at the level of the 12th thoracic vertebra for 20 mins. Spinal cord injury was evaluated by assessing the motor function of the rats 24 hrs posttrauma. The accumulation of leukocytes and histologic changes in the injured spinal cord tissue also were examined. Rats received gabexate mesilate (10 or 20 mg/kg i.p.) 30 mins before or after the compressive trauma. The effects of heparin or an inactive derivative of activated factor X (a selective inhibitor of thrombin generation) on compressive trauma-induced spinal cord injury also were examined. Leukocytopenia was induced by the administration of nitrogen mustard. MEASUREMENTS AND MAIN RESULTS: The motor disturbances observed following traumatic spinal cord compression, evaluated by Tarlov's score, and the accumulation of leukocytes in the injured tissue, evaluated by measuring tissue myeloperoxidase activity, were markedly reduced by leukocyte depletion induced by nitrogen mustard and by pre- or posttreatment of animals with gabexate mesilate. Neither heparin nor the inactive derivative of activated factor X prevented the motor disturbances and the accumulation of leukocytes. Histologic examination demonstrated that intramedullary hemorrhages observed 24 hrs after trauma at the 12th thoracic vertebra were significantly attenuated by nitrogen mustard-induced leukocytopenia and the administration of gabexate mesilate. CONCLUSIONS: The compression trauma-induced spinal cord injury demonstrated by this model was mainly mediated by leukocytes. Gabexate mesilate prevented spinal cord injury not by inhibiting coagulation, but by inhibiting the activation of leukocytes.
Twenty-one patients with universal syndesmophytosis due to ankylosing spondylitis were identified in a consecutive series of 1578 patients with acute spine and spinal cord injuries. They were predominantly male, older than spinal cord-injured patients in general, and most were injured by falls. Approximately one-half were managed by halo-vest immobilization alone with good clinical and radiological outcomes. The remainder required surgery either for recurrent dislocation or for spinal cord compression associated with neurological deterioration. Extradural hematoma, a recognized cause of spinal cord compression in ankylosing spondylitis patients with spinal fractures, was encountered in two patients. Herniated intervertebral disc as a cause of spinal cord compression in ankylosing spondylitis does not appear to have been previously reported and was recognized three times in the present series, once in association with extradural hematoma. The pathology of ankylosing spondylitis is such that the nucleus pulposus tends to be spared, allowing disc herniation to occur in the heavily ossified spine. In virtually all patients, satisfactory correction of the flexion deformity could be safely accomplished following spinal fracture. It is concluded that fracture/dislocations of the cervical spine should be managed initially by halo-vest immobilization, without prior traction and with careful incremental correction of flexion deformity. Decompression is performed as required for extradural hematoma or intervertebral disc herniation, and internal fixation is carried out for recurrent dislocation.
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Magnetic resonance imaging (MRI) has enabled us to see the spinal intramedullary pathology as differences in signal intensity. Intramedullary high intensity lesions were observed on T2-weighted MRI in patients with cervical spondylotic myelopathy (20.0%) and ossification of the posterior longitudinal ligament (OPLL) of the cervical spine (25.7%). The frequency of this findings was proportional to the clinical severity of myelopathy and degree of spinal cord compression. The pathophysiological basis of such signal abnormality was presumed to vary from acute edema to chronic myelomalacia. The intramedullary lesion on MRI is considered to be the main site of lesion responsible for the neurological symptom because of a good correlation between the neurological level and high intensity level. We found from nine autopsy cases of OPLL that there are distinct differences in severity and extent of pathological changes between the spinal cord with a boomerang-shaped cross-section and that with a triangular-shaped cross-section. In the boomerang-shaped cases, major pathological changes were restricted to the gray matter and the white matter was relatively well preserved. Secondary wallerian degeneration was restricted to the fasciclus cuneatus the fibers of which were derived from the affected segments. In the cases of a triangular shape, pathological changes were more severe, both white and gray matter were involved. There were severe pathological changes over more than one segment, and both descending degeneration of the lateral pyramidal tracts and ascending degeneration of the posterior column, including the fasciclus gracilis, were observed. In conclusion, it is clinically very important to understand the pathological basis of the compressed spinal cord on neuroimages.
Macrophage migration inhibitory factor (MIF) is a multipotential protein that acts as a pro-inflammatory cytokine, pituitary hormone, immunoregulator, and mitogen. To elucidate function of MIF in spinal cord injury, we examined expression of MIF after compression-induced spinal cord injury using Northern blot analysis, in situ hybridization and immunohistochemistry. The MIF mRNA was up-regulated in injured spinal cord, peaking 3 days after injury shown by Northern blot analysis. In situ hybridization revealed up-regulation of MIF in microglia accumulating in the lesion epicenter 3 days after injury and astrocytes around the cystic cavity 1 week after injury. Double staining showed co-localization of MIF and tomato lectin in the lesioned site, indicating that microglia accumulating to the lesion epicenter express MIF. The time course of MIF expression is different from that of previous reports about cytokine expression peaking at earlier time points; thus, it is unlikely that MIF acts as a pro-inflammatory factor in the present study. The MIF may contribute to proliferation of astrocytes around the lesioned site in spinal cord injury because of its cell proliferation-promoting property.
The authors reported two cases of vertebral haemangiomas with spinal cord compression. The first case deteriorated during her pregnancy. Plain radiography of the thoracic spine gave the hint for the diagnosis and computed axial tomography showed the lesion. She was treated via surgical removal with minimal improvement of her paraparesis. The second case was diagnosed after operation because there was no abnormality over the relevant vertebra and the myelogram demonstrated an extradural mass lesion compressing the lower thoracic spinal cord. The patient improved satisfactorily after total removal of the tumour. Both surgical specimens were classical pictures of haemangiomas histologically.
Intervertebral disc disease (IVDD) is a common problem encountered in veterinary practice. The primary goal in treating animals with IVDD should be to relieve nerve root and spinal cord compression, thereby retaining or regaining normal neurologic function. Methods of nonsurgical management include corticosteroid medication, nonsteroidal anti-inflammatory drugs, acupuncture therapy, and chemonucleolysis. Each one of these modalities have their own inherent advantages and disadvantages that should be considered before instituting therapy.
A 78-year-old woman developed an osteoporotic fracture of L2 followed two months later by spinal cord compression. Imaging study findings suggested a malignancy but a biopsy showed osteonecrosis, of which there was no evidence on the imaging studies. Osteonecrosis may be the cause of neurologic compromise associated with osteoporotic vertebral fractures.