PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Paraplegia”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1991

Surgery for progressive Pott's paraplegia (tuberculous paraplegia)

This is a study of 20 patients who had surgical intervention for Pott's paraplegia at the Hacettepe University Neurosurgery Department, Ankara. All patients were admitted with progressive paraparesis. Eleven patients had vertebrectomies, 5 laminectomies and in 4 patients costo-transversectomies were performed. The follow-up period ranged from 1 to 10 years. Thirteen patients were found to be normal at follow-up examinations (65%). In 4 patients there was some improvement in their neurological status, and the others had no improvement.

Adult↗
PubMed1996

Hereditary spastic paraplegia: advances in genetic research. Hereditary Spastic Paraplegia Working group.

Hereditary spastic paraplegia (HSP) is a diverse group of inherited disorders characterized by progressive lower-extremity spasticity and weakness. Insight into the genetic basis of these disorders is expanding rapidly. Uncomplicated autosomal dominant, autosomal recessive, and X-linked HSP are genetically heterogeneous: different genes cause clinically indistinguishable disorders. A locus for autosomal recessive HSP is on chromosome 8q. Loci for autosomal dominant HSP have been identified on chromosomes 2p, 14q, and 15q. One locus (Xq22) has been identified for X-linked, uncomplicated HSP and shown to be due to a proteolipoprotein gene mutation in one family. The existence of HSP families for whom these loci are excluded indicates the existence of additional, as yet unidentified HSP loci. There is marked clinical similarity among HSP families linked to each of these loci, suggesting that gene products from HSP loci may participate in a common biochemical cascade, which, if disturbed, results in axonal degeneration that is maximal at the ends of the longest CNS axons. Identifying the single gene defects that cause HSPs distal axonopathy may provide insight into factors responsible for development and maintenance of axonal integrity. We review clinical, genetic, and pathologic features of HSP and present differential diagnosis and diagnostic criteria of this important group of disorders. We discuss polymorphic microsatellite markers useful for genetic linkage analysis and genetic counseling in HSP.

Adolescent↗
PubMedDate not supplied

Experimental study of paraplegia caused by spinal tumors: an animal model of spinal tumors created by transplantation of VX2 carcinoma.

BACKGROUND: Little is known about the mechanism of the paraplegia produced by metastatic spinal tumors, although the quality of life of patients with paraplegia caused by malignant tumors depends to a great extent on treatment of the paraplegia. We previously established an experimental model of malignant femoral tumors by transplanting VX2 carcinoma into the femur, and we have reported the efficacy of chemical embolic therapy, radiotherapy and hyperthermal therapy in treating the tumors in the model. PURPOSE: The purpose of the present study was to establish an animal model of metastatic spinal tumors by transplanting VX2 carcinoma into a pedicle and to analyze the mechanism of the paraplegia produced by metastatic spinal tumors. STUDY DESIGN: An experimental study. METHODS: VX2 carcinoma that had been successively transplanted to the thigh muscles of Japanese White rabbits in the Department of Orthopaedic Surgery of Kyorin University School of Medicine was used. The third lumbar vertebra of 37 healthy rabbits was exposed, and a piece of VX2 carcinoma was transplanted into a hole created in the pedicle with an air drill after transplantation. The animals were examined every other day. As soon as paraplegia developed, the animals were sacrificed, and the axial localization of the tumor was evaluated based on the surgical staging of the spinal tumor (SSST classification by Tomita). Roentgenographic, histological and angiographic studies were also performed. RESULTS: Twenty-two rabbits (60%) had paraplegia at the time of the final examination. Seventeen of them had complete paraplegia, and the other five had incomplete paraplegia. The average interval until incomplete paraplegia developed was 18.4+/-4.3 days, and the average interval until complete paraplegia developed was 30.0+/-4.3 days. The average proportion of the diameter of the spinal canal occupied by the tumor was 37.2+/-4.9% in the incomplete cases, and 70.6% in the complete cases. The radiographs revealed an osteolytic area in the pedicle and posterior border of the third lumbar vertebra in the rabbits with complete paraplegia, but no osteolytic areas were detected in the rabbits with incomplete paraplegia. According to the SSST classification, the lesions of all of the rabbits with paraplegia were classified as stage IV. Pathological studies revealed that the spinal cord generally exhibited degenerative change, especially at the site of tumor compression. No tumor cells had invaded the spinal cord. Microangiography showed a marked reduction in blood vessels in the gray matter of the spinal cord in the complete paraplegia in comparison with incomplete paraplegia. CONCLUSION: Our method succeeded in establishing a model of metastatic spinal tumors, because the natural history of the disease, including the anatomical location of the tumors and the imaging findings, was similar to the natural history in clinical cases. This model was useful for elucidating the pathogenetic mechanism of the paraplegia caused by metastatic spinal tumors.

Animals↗
PubMed2002

Interventions for reversing delayed-onset postoperative paraplegia after thoracic aortic reconstruction.

BACKGROUND: Delayed postoperative paraplegia is a recognized complication of thoracic (TAA) or thoracoabdominal aortic aneurysm (TAAA) repair. The purpose of this study was to evaluate the effectiveness of interventions to treat delayed-onset paraplegia. METHODS: Between January 1, 2000 and August 31, 2001, 99 patients underwent surgical repair of TAA, Crawford type I, II, or III TAAA. Standard intraoperative management included distal aortic perfusion and cerebrospinal fluid (CSF) drainage unless contraindicated. Therapeutic interventions to treat delayed paraplegia included lumbar CSF drainage and vasopressor therapy. RESULTS: Three of the 99 patients had paraplegia upon awakening. Delayed-onset paraplegia occurred in 8 patients, 2 of whom had recurrent episodes. In those 8 patients, the initial episode occurred at a median of 21.6 hours (range 6.4 to 110.0 hours) after surgery and the second episode averaged 176 hours after surgery. At the onset of paraplegia, the average mean arterial pressure was 74 mm Hg and CSF pressure was 14 mm Hg. Three of the 8 patients had a functioning CSF catheter at the onset and the other 5 patients had catheters subsequently placed. Therapeutic interventions increased blood pressure to a mean arterial pressure of 95 mm Hg and decreased CSF pressure to 10 mm Hg. Five of the 8 patients with delayed-onset paraplegia made a full neurologic recovery and 3 had partial recovery. CONCLUSIONS: Patients with delayed-onset paraplegia had an increased chance of recovery as compared with those patients in whom paraplegia was diagnosed upon emergence from anesthesia. Acute interventions directed to increase spinal cord perfusion by increasing systemic blood pressure and decreasing CSF pressure were effective for the reversal of delayed onset of paraplegia after TAA or TAAA repair, resulting in an overall 3% incidence of permanent paraplegia and 3% incidence of residual paraparesis.

Aged↗
PubMed1986

Cross-clamping of the thoracic aorta. Influence of aortic shunts, laminectomy, papaverine, calcium channel blocker, allopurinol, and superoxide dismutase on spinal cord blood flow and paraplegia in baboons.

There is a high incidence of paraplegia associated with thoracic aortic cross-clamping, even when cardiopulmonary bypass or shunts are used. In 56 adult baboons, spinal cord blood flow (SCBF), vascular anatomy, and paraplegia rates were evaluated. Tissue blood flow was measured by radioactive microspheres. Various procedures were used to increase SCBF and to prevent ischemia-reperfusion injury. It was found that the rate of paraplegia was inversely correlated with neural tissue ischemia (SCBF) and directly correlated with reperfusion hyperemia. Two methods completely prevented paraplegia. These two methods were a thoracic shunt with occlusion of the infrarenal aorta or cerebrospinal fluid drainage plus intrathecal papaverine injection, both of which were associated with an increased SCBF. Furthermore, papaverine dilated the anterior spinal artery (ASA) (p = 0.007) and increased the blood flow through the lower ASA. Whereas procedures utilizing a calcium channel blocker (flunarizine), allopurinol, superoxide dismutase (SOD), laminectomy alone, and a thoracoabdominal shunt not perfusing the arteria radicularis magna (ARM) all failed to prevent paraplegia, allopurinol (p = 0.026) and SOD (p = 0.004) did prevent gastric stress lesions, indicating that their failure to prevent paraplegia was not due to a lack of activity. Of great clinical interest is that, if a shunt is used and the ARM is perfused, infrarenal aortic cross-clamping increases SCBF, thus preventing paraplegia. Intrathecal application of papaverine proved to be even more effective in increasing SCBF and also completely prevented paraplegia. As this is a safer procedure than the insertion of shunts, this is the method of choice for the prevention of paraplegia associated with thoracic aortic cross-clamping. The preliminary trial using intrathecal papaverine in human beings has thus far shown no adverse side effects from the drug, and no paraplegia has occurred.

Allopurinol↗
PubMed2005

Evidence for an exaggerated postprandial lipemia in chronic paraplegia.

BACKGROUND/OBJECTIVE: Excessive delay in triglyceride (TG) metabolism after ingestion of dietary fat represents a significant cardiovascular disease (CVD) risk. The objective of this study was to compare the postprandial lipemic responses of individuals with paraplegia with those of healthy nondisabled individuals. METHODS: The ability of 3 recreationally active individuals with paraplegia having normal fasting TG (mean = 103 mg/dL) to metabolize TG after ingestion of a high-fat test meal was compared with a previously published cohort of 21 recreationally active individuals without paraplegia (TG mean = 86 mg/dL) who underwent identical testing. The subjects with paraplegia had venous blood taken under fasting conditions, and then ingested a milkshake containing premium ice cream blended with heavy whipping cream (approximately 92% of calories from fat). Additional blood samples were obtained at 2, 4, and 6 hours after ingestion. The area under the curve (AUC) for TG clearance for both subject groups was measured with an area planimeter. RESULTS: TG uptake for both groups was almost identical for the first 2 hours after ingestion. At 4 and 6 hours after ingestion, the TG levels were 50 and 35 mg/dL higher, respectively, in subjects with paraplegia than in nondisabled subjects. When corrected for small baseline differences in TG concentrations (16 mg/dL), the AUC was 46.5% greater for the group with paraplegia than in the nondisabled group. A near mirror association across time was observed between postprandial serum high-density lipoprotein cholesterol (HDL-C) and TG levels in subjects with paraplegia. CONCLUSION: This case series finds an exaggerated postprandial lipemia (PPL) in persons with paraplegia with normal fasting TGs. This finding is the first evidence, in a small population, of an unreported potential CVD risk in persons with paraplegia.

Adult↗
PubMed1994

Spinal cord protection in the absence of collateral circulation: meta-analysis of mortality and paraplegia.

A meta-analysis of paraplegia complicating aortic surgery on patients having neither intercostal nor spinal collaterals, epitomized by patients with acute traumatic aortic rupture, was done. Index Medicus and Medline were searched for all suitable English publications between 1972 and 1992. New paraplegia occurred in 9.9% of 1492 patients who underwent surgery. However, 19.2% of patients undergoing surgery with only simple aortic cross-clamping developed paraplegia, in contrast to 6.1% if distal aortic perfusion was augmented by either "passive" or "active" methods (p < 0.00001). The risk of paraplegia increased progressively as cross-clamp times lengthened if simple aortic cross-clamping was used (p < 0.00001), but only once did the cross-clamp time exceed 30 minutes (p < 0.05). Paraplegia occurred in 8.2% of patients with "passive" shunts from the ascending aorta (p < 0.001 vs simple cross-clamping). Shunts from the left ventricular apex, however, had an incidence of paraplegia of 26.1% and, therefore, did not decrease the risk of paraplegia. "Active" augmentation of distal perfusion had the lowest risk of paraplegia: 2.3% (p < 0.00001 vs simple cross-clamping or "passive" shunts). Mortality, however, was higher in these potentially polytraumatized patients when they were perfused distally using methods requiring full systemic heparinization (18.2%), compared to mortality with methods not requiring heparin (11.9%; p < 0.01). In conclusion, simple aortic cross-clamping has a high risk of paraplegia if the cross-clamp time extends beyond 30 minutes. "Active" modalities of augmenting distal perfusion provide optimal spinal protection.

Aorta, Thoracic↗
PubMed2000

Ischemic preconditioning protects against paraplegia after transient aortic occlusion in the rat.

BACKGROUND: Paraplegia can result from operations requiring transient occlusion of the thoracic aorta. A rat model of paraplegia with the characteristics of delayed paraplegia and transient ischemic dysfunction was developed to determine whether ischemic preconditioning (IPC) improved neurologic outcome. METHODS: Rats underwent balloon occlusion of the upper descending thoracic aorta. One group (2 minute IPC, n = 19) underwent 2 minutes of IPC and a second group (5 minute IPC, n = 19) had 5 minutes of IPC 48 hours before 10 minutes of occlusion. The control group (n = 31) had no IPC prior to 10 minutes of occlusion. RESULTS: Paraplegia occurred in 68% of the control animals (21 of 31 paraplegic: 6 delayed and 15 immediate paraplegia). Both the 2-minute IPC and 5-minute IPC groups had a decreased incidence of paraplegia when compared to controls (32%, p = 0.011 and 26%, p = 0.009, respectively). CONCLUSIONS: A rat model of spinal cord ischemia demonstrating both delayed paraplegia and transient ischemic dysfunction was characterized. Both 2-minute and 5-minute periods of IPC were found to protect against paraplegia.

Animals↗