Images in clinical medicine. Epidural lipomatosis causing spinal cord compression.
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Experiments were conducted to determine the therapeutic value of subarachnoid perfusion of the traumatized dog spinal cord with the fluorocarbon, Fluosol-DA (20%). Control dogs without lesions, but which had durotomy, subarachnoid catheter placement, and saline irrigation for 4 hours, did not have any residual neurological deficit. A series of 41 dogs underwent an acute spinal cord compression using an epidural balloon inflated to a pressure of 160 mm Hg and maintained for 1 hour. Treatment included durotomy only (11 dogs), durotomy with saline perfusion at room temperature (15 dogs), and durotomy with oxygenated Fluosol-DA perfusion at room temperature (15 dogs). The dogs underwent daily grading of neurological status for a 60-day period. Dogs undergoing perfusion of the spinal cord with either saline or oxygenated Fluosol-DA had significantly improved motor recovery (p less than 0.004) compared with dogs undergoing durotomy only. Perfusion with oxygenated Fluosol-DA resulted in significantly better motor recovery (p less than 0.05) than did perfusion with normal saline. Microscopic examination of the traumatized spinal cords failed to reveal a substantial difference between the three groups. However, dogs with better functional results tended to have less destruction of the white matter. Hemorrhagic necrosis of the central gray matter was consistently observed in all traumatized spinal cords.
OBJECTIVE AND IMPORTANCE: Castleman's disease is a rare lymphoproliferative disorder most often found in the mediastinum. Localized forms are usually benign, whereas multicentric forms may be aggressive. We report a patient with Castleman's disease who presented with spinal cord compression, and we review previously published cases of Castleman's disease involving the central nervous system. To our knowledge, this is only the second case of Castleman's disease presenting as a spinal epidural mass with cord compression. CLINICAL PRESENTATION: A 44-year-old otherwise healthy woman presented acutely with difficulty walking. Examination revealed mild myelopathy in her legs. Magnetic resonance imaging revealed a posterior epidural mass compressing the thoracic spinal cord at T3-T5. INTERVENTION: Thoracic laminectomy and gross total resection of the lesion were performed. Pathological examination of the lesion identified the hyaline-vascular type of Castleman's disease. The patient's symptoms resolved postoperatively. CONCLUSION: Castleman's disease presenting as a spinal epidural mass lesion with cord compression is rare. Surgical treatment can result in an excellent outcome.
In order to investigate the mechanism of delayed progressive or secondary neuronal damage after the spinal cord injury, we developed a mild-compression injury model in the rat thoracic spinal cord. Our compression device consists of a soft silicone point of contact to the dura, in order to prevent violent injury that may cause axonal tears or hemorrhages in the spinal cord. Since rats often assume a 'standing' posture, i.e. raising head with lifting their fore-limbs, damage to the thoracic spinal cord was evaluated by measuring the frequency of 'standing', which effectively indicates hind limb function. Twenty-four hours after compression by a 20 g weight for 10 or 20 min, the standing frequency of the injured rat was almost the same as that of sham animals that underwent laminectomy without compression. However, the standing frequency decreased with time; the frequency of standing at 72 h was approximately 30-50% that of sham animals. In the compressed spinal cord tissue, microglial cells, detected by lectin staining, proliferated with time. An enormous amount of microglia was observed at 48 and 72 h after compression, although only a small amount of cells were positive to lectin staining at 24 h after the compression. These results suggest that our mild-compression spinal cord injury model showed late-onset or delayed neuronal damage that may be related to pathological microglia proliferation.
A patient undergoing regular haemodialysis for chronic renal insufficiency developed neck pain followed by progressive spinal cord compression due to subluxation at the level C3-4. Decompression, laminectomy and osteosynthesis led to an almost complete recovery. A review of all the histological specimens suggested that hyperparathyroidism and not amyloidosis caused the vertebral destruction.
We report on a 19-year-old man with a spinal cord compression secondary to granulocytic sarcoma (GS) as the initial presentation of a chronic myelogenous leukemia (CML). Blastic crisis developed two months later. According to our case report and to the literature, the diagnosis of GS could predict a rapid progression to blastic phase.
Breast cancer is the most common cause of metastatic epidural spinal cord compression (SCC) in women, and this condition results in significant neurologic dysfunction and morbidity. Prior studies of patients with suspected SCC did not employ multivariate analysis techniques, often included persons with a wide variety of malignancies, and generally focused on identifying associated neurologic and radiologic features. We therefore conducted a study examining a more comprehensive set of potential clinical risk factors in breast cancer patients with suspected SCC. We retrospectively analysed 123 episodes of suspected SCC among 93 breast cancer patients evaluated by spine computed tomography (CT) scanning. Multiple logistic regression analysis was employed to identify independent predictors of SCC. Clinically significant metastatic epidural cancer was defined as thecal sac compression (TSC), which occurred in 33 episodes (27%). Four independent predictors of TSC were identified and included oncologic features (known bone metastases > or = 2 years, metastatic disease at initial diagnosis) in addition to neurologic and radiologic features (objective weakness, vertebral compression fracture on spine radiograph). These four predictors stratified episodes into subgroups with widely varying risks of TSC, ranging from 12% (0 risk factors) to 85% (> or = 3 risk factors). These results suggest that the evaluation of breast cancer patients with suspected SCC should include clinical information about their disease course in addition to neurologic examination and prior imaging studies. If confirmed, these predictors may help clinicians assess risk in this patient population.
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