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Nontraumatic spinal cord compression can have very dramatic clinical presentations with rapid onset of symptoms and quickly ensuing paralysis. The manifestations may be much more subtle. This text will discuss the four most common causes of myelopathy, including spinal canal hemorrhage, spinal abscess, compression by tumor, and skeletal disease. Compressive lesions to the spinal cord from other than these etiologies are rare.
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Spinal cord blood flow (SCBF) was measured in 24 rhesus monkeys after injury to the cord produced by the inflatable circumferential extradural cuff technique. Measurement of regional blood flow in the white and gray matter of the cord in areas of 0.1 sq mm was achieved with the 14C-antipyrine autoradiographic technique and a scanning microscope photometer. After moderate cord injury (400 mm Hg pressure in the cuff maintained for 5 minutes), which produced paraplegia in 50% of animals and moderate to severe paresis in the other 50%, mean white matter SCBF was significantly decreased for up to 1 hour. White matter blood flow then rose to normal levels by 6 hours posttrauma and was significantly increased by 24 hours posttrauma. Gray matter SCBF was significantly decreased for the entire 24-hour period posttrauma. After severe cord injury (150 mm Hg pressure in the cuff maintained for 3 hours), which produced total paraplegia in almost all animals; SCBF in white and hours), which prodced total paraplegia in almost all animals, SCBF in white and gray matter was reduced to extremely low levels for 24 hours posttrauma. In addition, focal decreases in SCBF were seen in white and gray matter for considerable distances proximal and distal to the injury site. It is concluded that acute compression injury of the spinal cord is associated with long-lasting ischemia in the cord that increases in severity with the degree of injury.
Spinal cord compression is a common neurological emergency. The causes of spinal cord compression may include primary or (more frequently) metastatic tumor, infections, trauma, and vertebral or intervertebral disc disease. In most instances the underlying etiology is known or easily ascertained. We present here three recent cases in which patients presented with spinal cord compression and lytic bone lesions suggesting metastatic cancer. In these cases, vertebral osteomyelitis was found to be the cause.
Metastatic tumours of the bone system occur up to 60% in the spinal cord. The epidural spinal cord compression is also found by metastatic tumour, so patients with metastatic disease in this localisation carry a poor prognosis. From 1986 to 1988 35 patients with symptomatic spine metastasis are operated upon. 43% of these patients recover their capability of walking. 90% from the operated collective show a reduction of pain. The primary tumour is first found from cancer of the lung and second from the kidneys. The most common localisation of metastatic tumour is the thoracic spine. The ratio from male to female is 2:1. If the risk of operation and differential therapy is discussed, the decompression and tumour resection will be the first. The concept for postoperative mobilisation and therapy concludes the stabilisation of spinal cord with internal fixation. Treatment of metastatic tumours takes aim at the improvement of life quality.
Temporary compression of spinal cord was modelled in anesthetized cats. The degree of spinal disfunction was estimated by component analysis of far-field somatosensory EPs which were recorded along vertebral column and scalp. Even a weak and short-term compression of spinal cord's dorsal columns changed biopotentials' latencies, amplitudes and interpeak intervals. Usefulness of correlative analysis of interpeak intervals as an additional way of differential evaluation of spinal pathways conductivity, was shown.
The spinal evoked response obtained in cats at a site immediately rostral to the site of a graded spinal cord compression is described. They usually show an earlier decrease in amplitude than cortical SEP's and the appearance of a particular positive potential. The degree of reversibility after decompression is variable and is not correlated with histological damage.
Canine spinal cords were compressed by a cylindrical balloon placed in the T-13 epidural space and maintained at 160 mm Hg for one hour. Fifteen minutes after deflation, either local hypothermia or parenteral dexamethasone therapy was initiated. Local hypothermia (dorsal dura mater at 6 degrees C for four hours) was achieved with a miniature epidural heat exchanger which kept cooling fluid isolated from tissue. At seven weeks, the treated groups achieved motor ratings which were significantly superior to those of the untreated group. The untreated group were unable to walk, while both treated groups were able to do so.
Epidural spinal cord compression was produced in rats by injection of Walker 256 carcinoma cell suspension anterior to the T-12 or T-13 vertebral body. The tumor grows through the intervertebral foramina to compress the spinal cord and produce paraplegia in 3 to 4 weeks. The effect of several treatments upon clinical signs was assessed. Dexamethasone caused a significant but transient improvement in neurological function. Radiation therapy likewise improved neurological function, and was more effective when given by a high-dose protracted course than when given either in a single dose or a low-dose protracted course. Laminectomy was not helpful in relieving neurological symptoms. Dimethyl sulfoxide did not relieve neurological symptoms. Cyclophosphamide was most effective in relieving neurological symptoms, and most of the animals that were treated with that drug when they were severely weak but still able to move their hind limbs recovered fully. Some animals that were totally paraplegic when treatment began recovered function after radiation therapy or cyclophosphamide treatment, but recovery was better if treatment was started when animals could still move their hind limbs. This animal model appears to be a useful way of studying the treatment of human spinal cord compression produced by epidural neoplasms.
Spinal aneurysmal bone cyst is sufficiently rare for the authors to report this case with rapid evolution and development of paraplegia. Total removal was achieved, and clinical recovery remained complete six months after operation. The pathogenic, clinical, radiological, histological and therapeutic aspects are briefly reviewed and discussed.
A retrospective analysis of 59 patients with diffuse histiocytic and diffuse poorly differentiated lymphocytic lymphoma was performed to determine the incidence and characteristic features of patients developing spinal cord compression. Spinal cord compression occurred in 6 of 59 (10.2%) patients. All were females despite a 1:1 male: female ratio in the entire group. The mean age of females with spinal cord compression was significantly lower than the mean age of females with lymphoma without this complication. These findings suggest that young females with diffuse histiocytic or diffuse poorly differentiated lymphocytic lymphoma represent a subgroup at high risk for spinal cord compression.
A case of spinal cord compression, presumed to be due to a calcification in the arachnoid, is presented. Its relationship to a previous spinal subarachnoid haemorrhage is mentioned. The literature is reviewed and the relationship of this condition to spinal subarachnoid haemorrhage, previous myelogram, and spinal anaesthetic is stressed.
Spinal cord compression due to epidural metastases, and malignant pleural effusions are devastating complications of advanced cancer that can destroy the quality of a life that is already limited in quantity. Neither need do so. A diagnostic algorithm has been developed for each of these complications. Early diagnosis of cord compression can be accomplished by prompt myelography or magnetic resonance imaging of the affected area of the spine. A malignant pleural effusion, even one that initially appears cytologically negative, can be promptly diagnosed. Radiation and steroids are optimal therapy for most patients with cord compression, and few require surgery. Intrapleural bleomycin appears to be the most effective agent for pleurodesis.
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An aortic body tumour in a 7-year-old wire-haired fox terrier with hind limb ataxia is described. A metastatic lesion in the dorsal arch of the eighth thoracic vertebra caused compression of the spinal cord. Radiographic techniques are discussed that enabled the position and extent of the primary tumour and its metastasis to be defined and allowed a provisional diagnosis of chemodectoma.
We have developed an experimental model of spinal cord compression in rats. Tumor injected anterior to the T-12 vertebral body grows through the intervertebral foramina to compress the cord and produces paraplegia in 3 to 4 weeks. Evidence for vasogenic edema in spinal cord compressed by tumor includes increased water content, leakage of horseradish peroxidase into gray matter, and histologic evidence of edema. The vascular supply to the cord overlying the tumor appears to be compromised. Both spinal cord edema and clinical symptoms are lessened by treating symptomatic animals with dexamethasone.
Clinical interest in spinal compression and resultant paraplegia due to metastases has mounted in recent years. This has stimulated attention to the neuropathology of the condition. 14 cases of spinal cord compression due to vertebral metastases are compared with over 100 traumatic cases. In the traumatic lesions there is central haemorrhagic necrosis leading to cavitation and gliosis with nerve root regeneration in the late stages. In the metastatic cases, lesions are often peripheral, pie-shaped and are related to vascular factors. The neuropathology of cord necrosis due to metastatic spinal disease is therefore different from that caused by trauma. These observations have clinical importance in planning treatment.
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