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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↗
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↗
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↗
PubMed2026

Editor's Choice - Aquaporin-4: A Predictor and Therapeutic Target for Permanent Paraplegia after Endovascular Thoraco-abdominal Aortic Aneurysm Repair.

OBJECTIVE: Endovascular thoraco-abdominal aortic aneurysm (TAAA) repair can impair spinal cord perfusion, leading to paraplegia. The mechanisms driving this devastating complication are poorly understood. This study aimed to interrogate the cerebrospinal fluid (CSF) proteome in patients after TAAA repair to identify biomarkers that herald permanent paraplegia. It also aimed to investigate a potential therapeutic target identified by proteomics using an in vivo model of ischaemic spinal cord injury (iSCI). METHODS: CSF was collected for proteomic analysis from patients before and following TAAA repair. A differentially expressed protein identified in human paraplegic subjects was subsequently interrogated in a rodent model of iSCI. The protein composition of CSF was analysed using tandem mass tag proteomics. Neurological examinations were carried out by a blinded neurologist and T2 weighted magnetic resonance imaging (MRI) was used to measure spinal cord volume and oedema. A rodent model of iSCI was used to investigate a clinically relevant therapeutic target informed by proteomic findings. RESULTS: CSF analysis was taken from 37 patients, all of whom had aneurysm repair using a custom branched and or fenestrated device (median age 73.5 years, range 67 - 78 years; 27 men, ten women; Crawford classification: six type I, 11 type II, 15 type III, three type IV, and two type V). Five patients remained permanently paraplegic and seven recovered from transient paraplegia. The CSF of patients who remained paraplegic contained approximately fourfold more aquaporin-4 (AQP4) (41.8 &#xb1; 19.2 ng/mL, n = 5) than those who recovered from paraplegia (10.8 &#xb1; 1.3 ng/mL, n = 7; p = .005) or did not develop paraplegia (10.8 &#xb1; 1.2 ng/mL, n = 25; p = .004). Permanently paraplegic patients had CSF AQP4 levels > 15 ng/mL and this was associated with greater cord oedema on T2 weighted MRI (1.77 &#xb1; 0.19 vs. 1.03 &#xb1; 0.36; p = .032). In a rodent model of iSCI, AQP4 inhibition preserved spinal neurons and glia in the dorsal horn and intermediate zones of white matter (p = .004) and protected against ischaemia induced paraplegia (p < .001). CONCLUSION: The AQP4 level in the CSF of a patient represents a prognostic marker of permanent paraplegia after TAAA repair and highlights a novel therapeutic target. These findings represent a conceptual advance in the management of iSCI.

Paraplegia↗
PubMed2003

Paraplegia differentially increases arterial blood pressure related cardiovascular disease risk factors in normotensive and hypertensive rats.

Older individuals (>50 years of age) are increasingly sustaining spinal cord injuries (SCI) and often have pre-existing medical conditions, including hypertension. Furthermore, the life expectancy of individuals with paraplegia has increased to near that of able-bodied individuals. Thus, chronic diseases associated with aging (e.g. hypertension) are increasing in this population. We tested the hypothesis that paraplegia differentially increases blood pressure related cardiovascular disease (BP-CVD) risk factors in normotensive (Wistar Kyoto rat, WKY) and spontaneously hypertensive rats (SHR). To test this hypothesis, intact and paraplegic SHR and WKY rats were chronically instrumented for recording BP-CVD risk factors over 7 weeks. Paraplegia in both the SHR and WKY rats increased heart rates (27 and 22% in SHR and WKY, respectively), heart rate loads (425 and 323% in SHR and WKY, respectively), the standard deviation of systolic (15 and 23% in SHR and WKY, respectively) and diastolic blood pressure (15 and 13% in SHR and WKY, respectively) and reduced activity (-70 and -57% in SHR and WKY, respectively). Paraplegia in the WKY rats reduced systolic (-4%) and diastolic (-5%) blood pressures while systolic and diastolic loads were not significantly different. In sharp contrast, paraplegia in the SHR increased systolic (6%) and diastolic (5%) blood pressures as well as systolic (41%) and diastolic loads (9%). These data demonstrate that paraplegia increased BP-CVD risk factors in normotensive and hypertensive rats. Importantly, the impact of paraplegia on BP-CVD risk factors was greater in the SHR.

Animals↗
PubMed1985

Energy expenditure in patients with low-, mid-, or high-thoracic paraplegia using Scott-Craig knee-ankle-foot orthoses.

Renewed interest in ambulation in patients with paraplegia prompted us to measure the energy expenditure (kcal/kg per min) during standing and ambulating with the Scott-Craig orthosis in nine patients who had low-, mid-, or high-thoracic paraplegia. Energy expenditure during standing and during ambulation with a walker was similar for patients with all levels of paraplegia. In patients with high-thoracic paraplegia, energy efficiency was significantly less (P less than 0.05) than that for patients with mid- or low-thoracic paraplegia, whose efficiency levels were similar. In patients with low-thoracic paraplegia, the only patients who could perform swing-through gait patterns, energy efficiency was increased because of increased velocity. Our data do not support the concept of denying, on the basis of the level of the lesion alone, young, otherwise healthy, well-motivated patients with thoracic paraplegia the opportunity of using Scott-Craig orthoses to supplement wheelchair mobility and activities of daily living.

Adolescent↗