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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A new applicability of the suppressive Nauta impregnation method was tested allowing the detailed mapping of early neuronal damage expressed in the form of somatodendritic argyrophilia. Two spinal cord ischemia-reperfusion models of rabbit and dog, a model of canine global brain ischemia-reperfusion, involving cardiac arrest followed by resuscitation, and a canine spinal cord compression-decompression model were used. Early phases of neuronal damage are characterized by conspicuous somatodendritic argyrophilia permitting an exact evaluation of acute neuronal damage according to soma size, dendritic ramifications and localization of the affected neuronal neuronal pool. By its high sensitivity to somatodendritic damage the suppressive Nauta method appears to be a valuable neuropathological technique.
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PMID:A new applicability of the suppressive Nauta method in the early phase of neuronal damage. 794 5

To permit long-term measurement of time-dependent changes in levels of dialyzable drugs and transmitters in the spinal intrathecal (i.t.) space of the unanesthetized rat, we developed a dialysis catheter for chronic placement. This was accomplished by constructing a loop probe 9 cm in length from 0.3-mm-diameter dialysis tubing that was made impermeable except for the distal loop. This loop catheter was readily inserted though an incision in the cisternal membrane and passed to the lumbar enlargement. The ends of the catheter were then externalized on the top of the head. To permit i.t. injections, an additional i.t. catheter could also be inserted simultaneously by the same route. For dialysis, an external end of the loop catheter was connected to a syringe pump and perfused with artificial CSF (10 microliters/min) and the out flow collected. A series of studies were performed to demonstrate the characteristics and utility of this technique. (1) Stability of resting release: glutamate and glucose concentrations in spinal dialysate showed no significant changes from 3 to 10 days after implantation. (2) Spinal cord ischemia: ischemia induced by aortic occlusion or cardiac arrest evoked a time dependent increase in retrieved glutamate. (3) Spinal cord compression caused a time-dependent glutamate, aspartate and PGE2 increase. (4) Noxious afferent stimulation induced by the injection of formalin into the hindpaw resulted in a rapid and transient increase in dialysate glutamate concentration. (5) Direct activation of spinal excitatory amino acids receptors by i.t. injection of kainic acid (1 microgram) evoked a significant increase in aspartate and taurine. (6) Continuous delivery of spinal opiate (alfentanil) via dialysis resulted in a maintained, concentration dependent elevation in the thermal escape latencies in the unanesthetized rat. The loop dialysis catheter provides a robust experimental tool for studying time dependent changes in the concentration of diffusible substances in spinal CSF over an extended post-implantation interval and allows comparison of these changes with concurrently assessed behavioral indices.
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PMID:The spinal loop dialysis catheter: characterization of use in the unanesthetized rat. 875 84

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

We evaluated in rats, the effect of moderate hypothermia (30-31 degrees C) on extracellular levels of amino acids, with special emphasis on the excitatory amino acids (EAAs) glutamate and aspartate, lactate and pyruvate, after severe spinal cord compression. A laminectomy of Th7 and Th8 was made. A probe was inserted in a dorsal horn and microdialysis was performed for 1.5 h before and 4 h after applying severe compression for 5 min. Dialysate samples were collected at intervals of 10 min and analyzed by high-performance liquid chromatography. In normothermic (37.5 degrees C) animals there was a several-fold rise of glutamate that peaked in the first 10 min fraction after trauma. Hypothermic animals showed a similar increase after trauma, which was statistically significant until 20 min after injury. The level of glutamate was significantly higher in hypothermic animals from 20 to 70 min after injury, compared with normothermic animals. Aspartate also showed a marked increase following injury. The peak concentration was similar for both groups, whereas recovery was delayed in hypothermic animals. There was no significant difference between the normothermic and hypothermic animals for arginine, taurine, alanine, glutamine, histadine, glycine, threonine, tyrosine, and asparagine. No significant effect of hypothermia on lactate or lactate/pyruvate was noted. However, the mean level of lactate tended to be lower and recovery was quicker in hypothermic animals. The results of the present study suggest that moderate hypothermia does not attenuate extracellular accumulation of EAAs or markedly improve energy metabolism in our model. Instead, our findings raise the possibility that moderate hypothermia prolongs the duration of glutamate receptor overactivation. Since hypothermia effectively attenuates glutamate release in CNS and spinal cord ischemia models our results suggest different mechanisms of extracellular accumulation of EAAs in ischemia and trauma.
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PMID:Effects of moderate hypothermia on extracellular lactic acid and amino acids after severe compression injury of rat spinal cord. 904 12

Systemic hypothermia has neuroprotective effects in experimental models of central nervous system ischemia caused by vascular occlusions. The present study addresses the question as to whether systemic hypothermia can influence the extravasation of plasma proteins following severe spinal cord compression trauma using immunohistochemistry to identify the plasma proteins albumin, fibrinogen and fibronectin. Fifteen rats were assigned to one of three groups and received either thoracic (T) laminectomy or severe spinal cord compression trauma of the T8-9 segment. One group comprised laminectomized animals without compression trauma submitted to a hypothermic procedure in which the core temperature was reduced from 38 degrees to 30 degrees C. The two trauma groups were either submitted to the same hypothermic procedure or kept normothermic during the corresponding time. All animals were killed 24 h following the surgical procedure. The normothermic and hypothermic trauma groups had indications of marked extravasation of albumin, fibrinogen and fibronectin at the site of the injury (T8-9). There was also pronounced extravasation in the cranial and caudal peri-injury zones (T7 and T10) of normothermic injured rats but, with few exceptions, not in the hypothermic ones with the same degree of compression. By measuring the cross-sectional area of the peri-injury zones we found in the hypothermic trauma group a significant reduction of the expansion compared with that present in normothermic injured rats. Our study thus indicates that hypothermia reduces the extravasation of the plasma proteins albumin, fibrinogen and fibronectin following spinal cord compression in the rat. Such a reduction may contribute to neuroprotective effects exerted by hypothermia.
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PMID:Systemic hypothermia following compression injury of rat spinal cord: reduction of plasma protein extravasation demonstrated by immunohistochemistry. 1041 96

Systemic hypothermia exerts neuroprotective effects following trauma and ischemia caused by vascular occlusion in the brain. In the spinal cord similar effects have been demonstrated following ischemia after aortic occlusion. We have previously presented protective effects on several morphological parameters in the early period after the injury, using an established spinal cord compression injury model and systemic hypothermia. In the present study we have evaluated the effects on motor function following severe spinal cord compression trauma and treatment with moderate systemic hypothermia. Thirty Sprague Dawley rats were randomized into three groups: In group 1 (n = 4), the animals underwent a hypothermic procedure, including a 2 h hypothermic period with a body temperature of 30 degrees C, following the initial laminectomy. In group 2 (n = 12) a 50 g compression was applied to the spinal cords for 5 min, after which the animals were kept under normothermic anesthesia for 3 h. In group 3 (n = 14), the animals underwent the same trauma procedure as in group 2 and the same hypothermic procedure as in group 1. The animals were allowed to survive for 14 days, during which the motor function was recorded. This degree of trauma results in a non-reversible paraplegia, and the addition of systemic hypothermia as described above did not alter the neurological recovery as measured by two different methods of recording the motor function up to two weeks after injury. All animals survived in group 1. However, the mortality rates in group 2 were 25% and in group 3, 50%, respectively, which mirrors the severity of the trauma. The application of systemic hypothermia and the lack of experimental therapeutic success highlight the difficulties of transferring experimental beneficial neuroprotective effects to a clinically useful treatment method. In this experimental set-up the effects of the severe primary injury may overshadow the effects of the secondary injury mechanisms, which limits the therapeutic possibilities of systemic hypothermic treatment.
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PMID:Motor function changes in the rat following severe spinal cord injury. Does treatment with moderate systemic hypothermia improve functional outcome? 1089 65

The primary objective of this study was to investigate the effects of topical L-arginine and Ng-nitro-L-arginine methyl ester vs the role of ischemia in contributing to secondary injury after experimental acute spinal cord trauma. Twenty-six rabbits were submitted to spinal cord compression at the T7/8 level. The animals were divided into three groups: no applied drug (n=6), L-arginine (n=10), and Ng-nitro-L-arginine methyl ester (n=10). L-arginine was topically administered at a dose of 10 micromol (1.742 mg) per kg immediately after acute spinal cord injury. Ng-nitro-L-arginine methyl ester was applied topically at a dose of 10 pmol (10 mg/kg) immediately after acute spinal cord injury. Cortical somatosensory evoked potentials were recorded before injury and 1 min, 15 min, 30 min, and 60 min after injury. Physiological parameters were followed before, during, and I h post injury. Light and electron microscopic analysis was performed in all of the groups. In contrast to group 1, the edema of perineural, axoplasm, or surrounding tissue, the thickening of walls of the arterioles and venules, and the degeneration in myelinated axons in groups 2 and 3 were well observed. However, no differences between group 2 and group 3 occurred.
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PMID:The effects of topical L-arginine and Ng-nitro-L-arginine methyl ester after experimental acute spinal cord injury. A light and electron microscopic study. 1213 33

Osteoporosis is the most common contributing factor of spinal fractures, which characteristically are not generally known to produce spinal cord compression symptoms. Recently, an increasing number of medical reports have implicated osteoporotic fractures as a cause of serious neurological deficit and painful disabling spinal deformities. This has been corroborated by the present authors as well. These complications are only amenable to surgical management, requiring instrumentation. Instrumenting an osteoporotic spine, although a challenging task, can be accomplished if certain guidelines for surgical techniques are respected. Neurological deficits respond equally well to an anterior or posterior decompression, provided this is coupled with multisegmental fixation of the construct. With the steady increase in the elderly population, it is anticipated that the spine surgeon will face serious complications of osteoporotic spines more frequently. With regard to surgery, however, excellent correction of deformities can be achieved, by combining anterior and posterior approaches. Paget's disease of bone (PD) is a non-hormonal osteometabolic disorder and the spine is the second most commonly affected site. About one-third of patients with spinal involvement exhibit symptoms of clinical stenosis. In only 12-24% of patients with PD of the spine is back pain attributed solely to PD, while in the majority of patients, back pain is either arthritic in nature or a combination of a pagetic process and coexisting arthritis. In this context, one must be certain before attributing low back pain to PD exclusively, and antipagetic medical treatment alone may be ineffective. Neural element dysfunction may be attributed to compressive myelopathy by pagetic bone overgrowth, pagetic intraspinal soft tissue overgrowth, ossification of epidural fat, platybasia, spontaneous bleeding, sarcomatous degeneration and vertebral fracture or subluxation. Neural dysfunction can also result from spinal ischemia when blood is diverted by the so-called "arterial steal syndrome". Because the effectiveness of pharmacologic treatment for pagetic spinal stenosis has been clearly demonstrated, surgical decompression should only be instituted after failure of antipagetic medical treatment. Surgery is indicated as a primary treatment when neural compression is secondary to pathologic fractures, dislocations, spontaneous epidural hematoma, syringomyelia, platybasia, or sarcomatous transformation. Five classes of drugs are available for the treatment of PD. Bisphosphonates are the most popular antipagetic drug and several forms have been investigated.
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PMID:Principles of management of osteometabolic disorders affecting the aging spine. 1450 19

Spinal epidural abscess (SEA) is a neurological emergency that requires urgent diagnosis and treatment. We report 2 patients with SEA, in whom, on neuropathological examination, the neurological signs were found to be caused by spinal cord ischemia due to thrombosis of leptomeningeal vessels and compression of spinal arteries, respectively, while evidence of spinal cord compression was absent. Clinicians and neuropathologists should be aware of the variable mechanisms underlying the neurological involvement in SEA. Absence of spinal cord compression by the abscess may hamper early diagnosis and treatment.
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PMID:Myelopathy due to spinal epidural abscess without cord compression: a diagnostic pitfall. 1520 Feb 87

The rapid development of paraparesis or tetraparesis combined with a bilateral sensory deficit that has a clearly defined rostral border and bladder dysfunction are the principal features of acute transverse myelopathy. Acute partial transverse myelopathy is far much more frequent: its symptoms are asymmetric, sometimes unilateral, and sensory deficit may predominate. An urgent MRI is required to exclude acute spinal cord compression. Diagnosis of ischemic acute transverse myelopathy includes the following elements: sudden onset, neurologic symptoms compatible with infarction in the anterior spinal artery area (by far the most frequent location for spinal cord infarction), and presence of a specific cause of spinal cord ischemia. In all other cases where it is difficult to distinguish spinal cord infarction from myelitis, analysis of the cerebrospinal fluid is essential. Most cases of inflammatory acute transverse myelopathy can be linked to a defined cause. Multiple sclerosis is a major cause of partial acute transverse myelopathy. MRI lesions are usually small, located in the lateral or posterior part of the spinal cord. Diagnostic elements include multiple lesions of multifocal demyelination on the cerebral MRI, oligoclonal bands in the cerebrospinal fluid, and the absence of clinical or laboratory abnormalities that suggest systemic disease. Neuromyelitis optica, also known as Devic's disease, has often been considered a variant form of multiple sclerosis. Recent immunologic studies confirm the hypothesis that it is a distinct entity. Infectious transverse acute myelitis is often of viral origin. It may result from direct viral stress but more frequently follows immunologically-mediated indirect stress. This acute parainfectious myelitis, like postvaccinal myelitis, may be considered as a spinal single-focus form of acute disseminated encephalomyelitis (ADEM). It is important to distinguish the latter from an initial episode of multiple sclerosis, because their prognosis and treatment differ.
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PMID:[Acute transverse myelopathy: inflammatory or ischemic?]. 1609 12


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