Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to produce syringomyelia, localized arachnoiditis was created in adult New Zealand albino rabbits and Wistar rats by the injection of kaolin into the thoracic spinal subarachnoid space and incision of the dura mater of the thoracic spinal cord. The rabbits and rats were divided into 3 groups; the control group, dural incision group (DG) and kaolin injection group (KG). Each rabbit was sacrificed at 4, 8, 12 and 16 weeks after the operation. Each rat was sacrificed at 8 and 16 weeks after the operation. Cavity formation in the cord of all rabbits was examined by ultrasound. All animals were perfused with 10% neutral beffered formalin at 150 cm H2O pressure, and histological examination was performed with Luxol fast blue (LFB) and hematoxylin and eosin (H&E) stains. Results obtained: (1) Cavity formation was noted in 6 of 16 DG of rabbit (37.5%), 5 of 16 KG of rabbit (31.2%) and 2 of 9 KG of rat (22.2%) with histological verification. With use of ultrasound, cavity was noted in 3 of 16 DG rabbits (12.5%) and 2 of 16 KG rabbits (18.8%). (2) Cavity formation was present in the cord adjacent to the marked adhesive arachnoiditis both in rabbits and in rats. (3) Cavity was noted in the ischemic area. (4) In 2 rabbits in which kaolin encircled whole surface of the spinal cord, hydromyelia was formed communicating with enlarged central canal caudad from the kaolin subarachnoid block. (5) Histological examination showed obliteration or narrowing of lumen of the small pial vessels involved in the adhesive arachnoiditis. In the cord parenchyma adjacent to the arachnoiditis, multiple spots of demyelination due secondary to ischemia demonstrated by LFB stain were noted. On the other hand, in the cord with the pia-arachnoid remained uninvolved, no demyelination was observed. (6) Localized adhesive arachnoiditis consisted of proliferation of fibrous tissue, lymphocytic infiltration and obliterating processes of small pial vessels involved in it. These data suggest that the cavitation within the cord would be induced by the ischemia, and hydromyelia would be produced by the pressure dissociation between the spinal subarachnoid space and the central canal.
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PMID:[Experimental syringomyelia in rabbits and rats after localized spinal arachnoiditis]. 129 32

The cauda equina syndrome is an uncommon and poorly understood complication of ankylosing spondylitis. The clinical and radiologic findings in five patients with this syndrome are described. Typical findings include cutaneous sensory impairment of the lower limbs and perineum with sphincter disturbances. Motor impairment occurs less frequently, and associated pain is an inconstant feature. Enlargement of the caudal sac and dorsal arachnoid diverticula that erode the lamina and spinous processes are characteristic myelographic and computed tomographic findings. The pathogenesis of the cauda equina syndrome in ankylosing spondylitis remains unknown but may be due to demyelination, post-irradiation ischemia, or compression from spinal arachnoiditis.
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PMID:Cauda equina syndrome complicating ankylosing spondylitis. 232 76

The authors review the clinical course of 29 patients who underwent syringosubarachnoid shunting for syringomyelia. Twenty-two patients presented hindbrain-related syringomyelia; seven patients had non-hindbrain-related syringomyelia secondary to trauma (four cases) and to spinal arachnoiditis (three cases). The surgical technique is described in detail. All patients showed postoperative deflation or collapse of the syrinx at follow-up magnetic resonance imaging evaluation. Symptoms stabilized in 17 cases (59%); 9 cases (31%) showed improvement in the neurological function; 3 cases (10%) presented delayed neurological deterioration, probably owing to spinal cord ischemia.
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PMID:Surgical treatment of syringomyelia: favorable results with syringosubarachnoid shunting. 247 14

Twenty-five patients with suspected spinal cord neoplasms were studied with high-field-strength magnetic resonance (MR) imaging (1.5 T) before and after administration of gadolinium diethylenetriamine-pentaacetic acid (DTPA) (gadopentetate dimeglumine). Five patients had enhancing, nonneoplastic lesions, including spinal dural arteriovenous fistulas (AVFs), cord infarction, and chronic arachnoiditis. Fifteen patients had proved spinal cord neoplasms, 13 intramedullary and two extramedullary. Four of the intramedullary tumors were detected only after Gd-DTPA administration; in five others, contrast material enhancement improved observer confidence. Gd-DTPA also demonstrated one dural AVF not detected on precontrast images. Regions of cord ischemia or infarction related to spinal dural AVF also enhanced in three patients. Advantages of Gd-DTPA include the demonstration of small isointense intramedullary tumors and the ability to permit differentiation of tumor from adjacent cord syrinx and solid tumor from postoperative gliosis and arachnoid scarring. Gd-DTPA enhancement is a useful adjunct to high-resolution MR imaging of the spinal cord.
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PMID:Intradural spinal cord lesions: Gd-DTPA-enhanced MR imaging. 290 1

Seven patients who received epidural anesthesia for gynecological (5 cases), cosmetic (1 case) or general surgery (1 case) developed spinal arachnoiditis leading to subarachnoid cyst in all 7 and cord cavitation in 5. MRI was useful to show the subarachnoid and intramedullary cysts, as well as to monitor lesion extent and progress. Associated MRI findings were a Chiari anomaly in one case, a tethered cord in another and spinal cord atrophy in a third. One patient refused surgery but improved spontaneously while the other six were treated by a shunting procedure, with a satisfactory outcome in three. Meningeal inflammation may have left scars which later induced ischemia and subsequent cavitation. Alternatively, CSF circulation blockade may have dilated the central spinal canal causing ischemia by compression, followed by myelomalacia and cavitation. Careful handling of this procedure is urged in order to avoid such severe complications.
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PMID:[Spinal arachnoiditis as a complication of peridural anesthesia]. 799 43

A 70-year-old man with prostatic cancer extending to the urinary bladder underwent transurethral resection of the bladder neck under spinal anesthesia and developed weakness of the proximal lower limbs a few hours after the procedure. The weakness persisted for several months. Because there were no local surgical complications (hematoma, infectious epiduritis, abscess) or bone metastases responsible for nerve root or spinal cord compression, a causal relation between the neurologic deficit and the spinal anesthesia was considered likely. Neurologic deficits are uncommon after spinal anesthesia and can be produced by complications of the surgical procedure (direct nerve injury, hematoma, abscess), arachnoiditis, neurotoxicity of disinfectants or of preservatives added to solutions of anesthetic drugs, or spinal cord ischemia. Precipitating factors for spinal cord ischemia include faulty patient position during the procedure, intraoperative arterial hypotension and injection of vasoconstricting agents.
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PMID:Proximal paraparesis following spinal anesthesia. 881 56

The neurological complications observed in 6 HIV negative intravenous drug users are reported. Four developed acute neuromuscular involvement in a lumbosacral or brachial distribution with rhabdomyolysis, myoglobinuria, hypovolemia, renal and hepatic failure in the 3 most severely affected patients. Despite evidence of immunologic abnormalities and especially presence of anti-heroin antibodies, we feel that causative mechanisms include mixed compression and ischemia with an underlying toxic myopathy, resulting in segmental myopathy with secondary compression of peripheral nerves. Two patients developed myelopathy with acute or chronic onset. The mechanisms were vascular with spinal cord infarction in the acute form and probably infectious with secondary compressive arachnoiditis in the chronic form. In these 2 patients with myelopathy, outcome was poor.
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PMID:[Peripheral nerve and spinal cord complication in intravenous heroin addiction]. 903 43

We reviewed the clinical and neuroradiological features in 16 patients with serious neurological complications of lumbar epidural anaesthesia. We observed acute, transient or permanent and delayed complications. Four patients had symptoms immediately after the procedure. One patient developed a subacute flaccid paraparesis. Two other patients had infectious spondylodiscitis at lumbar puncture level. Eight patients had a delayed progressive spastic paraparesis and were found to have subarachnoid cysts and irregularities of the surface of the spinal cord consistent with arachnoiditis; six of them had an extensive, complex syrinx within the cord. One patient had a severe lumbar polyradiculopathy, and MRI showed adhesive arachnoiditis involving the cauda equina. Although epidural anaesthesia is generally considered safe, rare but severe complications, such as radiculopathy, infectious disease, myelopathy from ischemia and arachnoiditis with a syrinx may occur. The patients with arachnoiditis had a relentless progression of the disease and a poor outcome: five are confined to a wheelchair, one is bedridden. Complications of epidural anaesthesia are easily recognised when they develop immediately; their relationship to the anaesthesia may be ignored or underestimated when they appear after a delay. Awareness of the possibility of delayed complications is important.
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PMID:Imaging and outcome in severe complications of lumbar epidural anaesthesia: report of 16 cases. 1099 61