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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↗

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↗

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↗

Advances in hereditary spastic paraplegia.

Hereditary spastic paraplegia refers to a group of clinically similar disorders whose primary feature is insidiously progressive lower extremity weakness and spasticity. Hereditary spastic paraplegia is genetically diverse: loci for autosomal recessive (chromosome 8p), autosomal dominant (chromosome 2p, 14q, and 15q), and x-linked hereditary spastic paraplegia have been identified. The existence of hereditary spastic paraplegia families for whom the disorder is unlinked to these loci indicates the existence of additional, as yet undiscovered, hereditary spastic paraplegia loci. Hereditary spastic paraplegia exhibits axonal degeneration that is maximal at the terminal portions of the longest central nervous system axons. Efforts to positionally clone the hereditary spastic paraplegia gene are in progress.

Humans↗

Diagnosis and treatment of spinal fractures combined with paraplegia and diaphragm injury.

OBJECTIVE: To study the mechanism and treatment principle of spinal fractures combined with paraplegia and diaphragm injury. METHODS: A total of 16 patients (14 males and 2 females, aged from 18 to 50 years) with spinal fractures combined with paraplegia and diaphragm injury, receiving emergency treatment and admitted to our hospital in the past 20 years, were retrospectively analyzed in this study. RESULTS: The injuries were caused by direct or indirect violence. Six cases were of fractures of cervical spine combined with paraplegia and diaphragm injury, 2 of fractures of thoracic vertebra combined with paraplegia and diaphragm injury, and 8 of thoracolumbar fractures combined with paraplegia and diaphragm injury. Six cases received non-operative treatment, but died finally. Ten cases received spine surgical treatment, of which 4 died and 6 were improved. The total mortality rate was 62.5%. CONCLUSIONS: Spinal fractures combined with paraplegia and diaphragm injury are one of the most severe traumas in departments of orthopaedics. Paraplegia can be found easily, but diaphragm injury is often neglected and missed. When a patient suffers from both of them, he is in danger of death. What measures should be taken to rescue the patient's life depends on the severity of the wounds.

Adolescent↗

Operative technique, paraplegia, and mortality after blunt traumatic aortic injury.

HYPOTHESIS: The use of mechanical circulatory support (MCS) during repair of traumatic aortic injuries is associated with a decreased incidence of postoperative paraplegia and mortality. DESIGN AND SETTING: Historical cohort study with contemporaneous but nonrandomized controls in a tertiary care hospital from July 1, 1988, through December 31, 1999. PATIENTS AND INTERVENTIONS: Consecutive cases undergoing operation for traumatic aortic injuries. Use of MCS (with or without systemic heparinization) determined by surgeon preference. MAIN OUTCOME MEASURES: Incidence of postoperative paraplegia and mortality. RESULTS: Twenty-two patients underwent repair of traumatic aortic injuries using MCS, resulting in no paraplegia but 4 deaths, 3 of them from cerebral ischemia. Thirteen patients had their traumatic aortic injuries repaired using a "clamp-and-sew" or passive shunt technique with no deaths but paraplegia in 2. Compared with an earlier report from our group from January 1, 1975, through June 30, 1988, the annual incidence of traumatic aortic injuries has decreased, whereas the age of patients and proportion of operations using MCS have increased. A review of the recent literature on traumatic aortic injuries reveals an average postoperative paraplegia incidence of 1% with MCS and 16% without MCS. Overall mortality is similar, but others have also reported cases of cerebral ischemia after aortic repair. CONCLUSIONS: The use of MCS during repair of traumatic aortic injuries is associated with a decreased incidence of postoperative paraplegia. The occasional occurrence of cerebral ischemia deserves further study.

Adolescent↗

Partial left heart bypass for thoracic aorta repair. Survival without paraplegia.

OBJECTIVE: Emergency repair of the torn descending thoracic aorta has been associated with an almost 15% incidence of paraplegia. The literature to date suggests that the incidence of paraplegia is not influenced by mechanical adjuncts to enhance distal aortic perfusion during cross-clamping and therefore, "clamp and sew" has been considered an acceptable technique. The purpose of the present study was to review our experience with repair of descending thoracic aortas using partial left heart bypass and to compare this favorable initial experience with the available data on the use of the heparinless centrifugal pump. DESIGN: A retrospective review of the routine use of partial left heart bypass in 16 consecutive patients with descending thoracic aorta disruptions. Results were compared with similar reports in the recent literature on trauma. SETTING: A level 1 trauma facility in the Denver, Colo, metropolitan area. PATIENTS: All patients with multisystem blunt trauma with a mean injury severity score of 36. INTERVENTION: Repair of the descending thoracic aorta disruption using partial left heart bypass with a heparinless centrifugal pump. MAIN OUTCOME MEASURES: Primary outcome measures were survival and paraplegia; other monitored variables included proximal and distal aortic pressure, flow rates, and oxygen transport. RESULTS: Among the 14 survivors (88%) there were no cases of paraplegia, and intraoperative hemodynamics and oxygen transport were well maintained with partial left heart bypass. This experience is added to the available reported data on the use of the centrifugal pump. In these additional 42 patients, the mortality rate was 7%, with no incidence of paraplegia. CONCLUSIONS: This collective experience failed to disclose a single case of paraplegia when partial left heart bypass was employed for repair of descending thoracic aorta. Moreover, the use of partial left heart bypass in this cohort of critically injured patients is associated with survival and perioperative morbidity rates comparable with the best recent reports of emergency thoracic aortic repair.

Abdominal Injuries↗

Genetic heterogeneity in inherited spastic paraplegia associated with epilepsy.

We have recently mapped a new rare form of spastic paraplegia complicated by bilateral cataracts, gastroesophageal reflux with persistent vomiting, and amyotrophy to chromosome 10q23.3-q24.2. This locus, named SPG9, is located in an interval spanning about 12 cM of genomic DNA, between markers D10S536 and D10S603, where different neurological disorders have been mapped. In particular, a gene for partial epilepsy has been assigned to a 3 cM interval between markers D10S185 and D10S577, which is completely included in the SPG9 critical region. A few families affected with spastic paraplegia and epilepsy have been reported; in the present study, we tested a pedigree with concurrence of spastic paraplegia, epilepsy, and mental retardation inherited as an autosomal dominant trait, using markers located in the SPG9 interval. Haplotype reconstruction excluded the linkage to 10q23.3-q24.2. In addition, the seven different loci so far reported to be associated with autosomal dominant pure forms of spastic paraplegia have been tested and excluded by linkage analysis and haplotype reconstruction, including SPG4 on chromosome 2p22-p21, where a familial form of spastic paraplegia associated with dementia and epilepsy has been mapped. These data confirm genetic heterogeneity in familial spastic paraplegia with epilepsy and suggest a specific locus for the family here analyzed.

DNA↗

Recovery from experimental paraplegia after levodopa administration.

In decompression sickness and during some surgical procedures, air emboli that form sometimes cause serious damage if the gas bubbles find their way to the vital organs. Paralysis of the spinal cord is one of the most serious manifestations induced by air emboli. Exposure to compression chambers is effective in air emboli treatment, but availability of chambers is inadequate and the treatment is lengthy. Until now there has been no fully effective injectable agent that can remedy the damage caused by air embolization. In this work levodopa was chosen as an injectable drug that might help to improve recovery from experimental paraplegia because of the reported effects of levodopa on muscle tone, spasticity and locomotion. To induce air emboli, the descending aorta of rats was chronically cannulated. Two weeks later, after full recovery from surgery, air was injected through the chronically implanted cannula into unanesthetized rats (0.35 ml of air per 100 g, during 4 sec). The paraplegia (paralysis of both hind legs) was manifested 2-10 minutes later. Only animals that had total paraplegia, without any sensation, were used in the experiments. Levodopa was administered 2 minutes after paraplegia was established. The levodopa treatment was repeated each day during one week. After six days, ten levodopa treated (intra-arterially) animals in a group of twelve and six levodopa treated (intraperitoneally) animals in a group of eight recovered completely from paraplegia. In control groups only three from thirteen (untreated), or two from twelve (solvent administration) animals recovered from paraplegia.

Animals↗

Traumatic aortic rupture: twenty-year metaanalysis of mortality and risk of paraplegia.

A metaanalysis of articles concerning the surgical management of acute traumatic rupture of the descending thoracic aorta published in the English-language literature between 1972 and July 1992 was performed. The overall mortality of 1,742 patients who arrived at the hospital alive was 32.0%, one-third died before surgical repair was started. Paraplegia was noted preoperatively in 2.6% of these hospitalized patients, and paraplegia complicated the surgical repair in 9.9% of 1,492 patients who reached the operating room in a relatively stable condition. Patients then were analyzed according to the surgical intervention used. Simple aortic cross-clamping (n = 443) was associated with a hospital mortality of 16.0% and incidence of paraplegia of 19.2%, despite lower average mean cross-clamp times (32 minutes; p < 0.01 versus passive or active methods of providing distal perfusion). In a subset of 290 patients in whom individual data were available, the cumulative risk of paraplegia was shown to increase substantially if the duration of aortic cross-clamping exceeded 30 minutes, but only when distal perfusion was not augmented (p < 0.00001). "Passive" perfusion shunts (n = 424) were associated with a mortality of 12.3%, and the incidence of paraplegia decreased to 11.1% (p < 0.001). However, shunts inserted from the apex of the left ventricle had a contradictory high 26.1% incidence of paraplegia compared with shunts from the ascending aorta (8.2%; p < 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗

Left heart bypass during descending thoracic aortic aneurysm repair does not reduce the incidence of paraplegia.

BACKGROUND: The preferred technique for spinal cord protection during surgical repair of descending thoracic aortic aneurysms (DTAAs) remains controversial. The purpose of this retrospective analysis was to determine if the use of left heart bypass (LHB) reduced the incidence of paraplegia in patients who underwent DTAA repair. METHODS: Over a 15-year period 387 consecutive patients underwent surgical repair of DTAAs using either the "clamp-and-sew" technique (341 patients, 88.1%) or distal aortic perfusion via a LHB circuit (46 patients, 11.9%). Data regarding patient characteristics, operative variables, and outcomes were retrieved from a prospectively maintained database. The impact of LHB on the frequency of paraplegia was determined using univariate and propensity score analyses. RESULTS: There were 17 operative deaths (4.4%) including 11 patients (2.8%) who died within 30 days. Paraplegia occurred in 10 patients (2.6%). On univariate analysis increasing age (p = 0.03), increasing aortic clamp time (p < 0.001), increasing red blood cell transfusion requirements (p = 0.01), and acute dissection (p = 0.03) were associated with increased incidence of paraplegia. Patients who received LHB had a similar incidence of paraplegia (2/46, 4%) compared with those treated without LHB (8/341, 2.3%; p = 0.3). Both matching and stratification propensity score analyses confirmed that LHB was not associated with reduced risk of paraplegia. CONCLUSIONS: On retrospective analysis the use of LHB during DTAA repair did not reduce the incidence of spinal cord injury. The "clamp-and-sew" technique remains an appropriate approach to DTAA repair.

Aorta, Thoracic↗

The value of motor evoked potentials in reducing paraplegia during thoracoabdominal aneurysm repair.

OBJECTIVE: Paraplegia after thoracoabdominal aortic aneurysm (TAAA) repair mainly occurs in patients with Crawford extent I and II. We assessed the impact of monitoring spinal cord integrity and the subsequent adjusted surgical maneuvers on neurologic outcome in repairs of type I and II TAAAs. METHODS: Surgical repair of TAAAs was performed in 112 consecutive patients with extent type I (n = 42) and type II (n = 70) aneurysms. The surgical protocol included cerebrospinal fluid drainage, moderate hypothermia, and left heart bypass with selective organ perfusion. Spinal cord function was assessed by means of monitoring motor evoked potentials (MEPs). Significant decreased MEPs always generated adjustments, including raising distal aortic and mean arterial pressure, reattachment of visible intercostal arteries, or endarterectomy of the excluded aortic segment with revascularization of back bleeding intercostal arteries. RESULTS: Motor evoked potential monitoring could be achieved in all patients. By maintaining a mean distal aortic pressure of 60 mm Hg, MEPs were adequate in 82% of patients. Increasing distal aortic pressure restored MEPs in all patients. In 19 patients (17%), MEPs decreased significantly during aortic cross-clamping because of critical spinal cord ischemia. MEPs returned in all patients after spinal cord blood flow was re-established except in three patients with type II TAAA in whom MEPs could not be restored, and absent MEPs at the end of the procedure corresponded with neurologic deficit. Delayed paraplegia developed in two patients owing to hemodynamic instability with insufficient mean arterial blood pressure to maintain adequate spinal cord perfusion. CONCLUSION: Monitoring MEPs is a highly reliable technique to assess spinal cord ischemia during TAAA repair. A surgical protocol including cerebrospinal fluid drainage, left heart bypass, and monitoring of MEPs can reduce the paraplegia rate significantly. Adjusted hemodynamic and surgical strategies induced by changes in MEPs could restore spinal cord ischemia in most patients, preventing early and late paraplegia in all type I patients. In type II patients, early paraplegia occurred in 4.2% and delayed neurologic deficit in 2.9%. Despite all available measures, complete prevention of paraplegia in type II aneurysms seems to be unrealistic.

Adult↗

Estimating group mortality and paraplegia rates after thoracoabdominal aortic aneurysm repair.

BACKGROUND: Most clinical studies regarding thoracoabdominal aortic aneurysm (TAAA) surgery are retrospective comparisons involving heterogeneous groups of patients. Risk models that evaluate susceptibility bias enhance interpretation of these intergroup comparisons. The purpose of this analysis was to derive group risk models for mortality and paraplegia after TAAA repair. METHODS: Data regarding 1,220 consecutive patients undergoing TAAA repair were analyzed via multiple logistic regression with stepwise model selection. Categorical preoperative risk factors that predicted 30-day mortality and paraplegia were used to develop risk models. RESULTS: Fifty-eight patients (4.8%) died within 30 days and 56 patients (4.6%) developed paraplegia or paraparesis. Predictors of mortality were rupture, renal insufficiency, symptomatic aneurysms, and Crawford extent II repairs. Extent of repair and acute presentation were predictors of paraplegia. The derived risk models estimated mortality and paraplegia rates that correlated well with actual frequencies reported in other contemporary series (regression slopes = 0.87 and 1.06, respectively). CONCLUSIONS: The derived risk models accurately estimate paraplegia and mortality rates in groups of patients. Prospective model validation will be required to confirm their accuracy.

Adolescent↗

Delayed paraplegia after thoracic and thoracoabdominal aneurysm repair: a continuing risk.

BACKGROUND: Paraplegia or paraparesis after otherwise successful thoracic or thoracoabdominal aortic reconstruction is a devastating complication for patient and physician. Interventions for its prevention have focused primarily on the intraoperative period. We have recently noted a significant incidence of delayed-onset neurologic deficit. METHODS: We reviewed our most recent 5-year experience with thoracic and thoracoabdominal reconstruction to examine the incidence of and potential contributors to delayed paraplegia or paraparesis. RESULTS: Between June 1996 and June 2001, 60 patients (29 men, 31 women) underwent repair of isolated thoracic (n = 26) or thoracoabdominal aortic aneurysm (Crawford I, n = 7; Crawford II, n = 14; Crawford III, n = 12; Crawford IV, n = 1) by the cardiac and vascular surgical services collaboratively. Repair was performed endovascularly in 6, and open with either circulatory arrest in 12, partial left heart bypass in 37, or partial femorofemoral bypass in 5. Operative mortality was 9.3% (5 of 54 patients) for open repair and 0% for endovascular repair. Paraplegia or paraparesis occurred in 6 (10%) patients of which 83.3% (5 of 6) were delayed in onset. All patients with delayed paraplegia or paraparesis had degenerative aneurysms of Crawford extent II (n = 3) or III (n = 2), had intraoperative left heart bypass, and had perioperative spinal drainage. Delayed paraplegia or paraparesis occurred up to 27 days postoperatively, and was associated with a documented episode of hypotension in 60% (3 of 5) of patients. CONCLUSIONS: Improvements in intraoperative management may have reduced immediate paraplegia or paraparesis among vulnerable patients only to leave them at risk of delayed-onset deficit. Postoperative care, including assiduous attention to avoidance of even transient hypotension, must be tailored to this patient population.

Adult↗

Recovery from paraplegia following aortic saddle embolism. Case report.

An aortic saddle embolus causing paraplegia is rare and even rarer is a documentation of neurological recovery from this event. A 47 year old male presented with absent pulsations in the lower limbs and paraplegia, both of sudden onset. He underwent immediate bilateral transfemoral embolectomy. The postoperative period was stormy. The paraplegia recovered over a period of 2 months and he could walk to his place of work after 6 months. The rare combination of saddle embolus and paraplegia is discussed. An attempt has been made to verify the hypothesis of Dickson et al which states that a low origin of the great radicular artery (GRA) below T12 level may be responsible for paraplegia when obstructed by a saddle embolus. We found the GRA arising at L2 vertebral level in this patient. Postoperative selective spinal arteriogram and magnetic resonance imaging (MRI) of the spinal cord showed a patent GRA and normal spinal cord structure respectively. Early surgical intervention in restoring the blood flow into the GRA may prevent severe histological changes hitherto responsible for nonrecovery from paraplegia in the earlier reports.

Aortic Diseases↗

Treatment and prognosis of patients with paraplegia or quadriplegia because of metastatic spinal cord compression in prostate cancer.

Metastatic spinal cord compression (MSCC) is a serious complication of metastatic prostate cancer (PCa). This study retrospectively evaluated patients who presented with paraplegia or quadriplegia because of MSCC of PCa. Of 847 patients with PCa who were treated between 1989 and 1998, 26 (3.1%) demonstrated paraplegia or quadriplegia because of MSCC. Characteristics, treatment efficacy, and prognosis of these patients were analyzed. In total, 15 cases became paraplegic despite androgen ablation therapy (Group I). Average time to paraplegia from initial hormonal treatment was 34 months. Out of nine cases who underwent radiation therapy (RT) to spinal lesions with/without chemotherapy, one patient became ambulatory. However, this patient subsequently had recurrent compression. Two cases had remission of paralysis. Two cases underwent laminectomy plus RT and in one case paralysis improved. MSCC was the first indication of PCa in 11 cases (Group II). Two cases underwent laminectomy plus hormone therapy and nine cases underwent hormone therapy alone. Four patients became ambulatory and two cases showed improved motor capacity. Average interval from paraplegia to death was 7.4 months in Group I and 27.1 months in Group II. However, there was no statistical difference in these two groups on disease-specific survival from the start of initial treatment. It is difficult to recover the ability to walk if paraplegia or quadriplegia occurs in PCa patients although decompression surgery plus hormone therapy seemed to impair the prognosis. Stage M1 patients with paraplegia had survival rates as good as stage M1 patients without paralysis. This should encourage an aggressive treatment approach. However, for patients with hormone-independent disease there seems to be no effective treatment and prognosis is poor.

Adenocarcinoma↗

The serum lipoprotein profile in veterans with paraplegia: the relationship to nutritional factors and body mass index.

Individuals with spinal cord injury have a shortened life expectancy, with coronary heart disease as a leading cause of death. Identifying potentially reversible risk factors would be expected to be of value in the long-term care of the person with a spinal cord injury. We addressed the relationships among diet, body mass index, and serum lipid levels in 28 veterans with paraplegia compared to 52 age-matched ambulatory veteran controls. There are no significant differences in body mass index or in total caloric, saturated fat, or cholesterol intake between those with paraplegia and the control group. The serum HDL cholesterol level is significantly lower in those with paraplegia compared to the control group (35 +/- 2 vs 49 +/- 2 mg/dL). There are no significant differences noted in serum total cholesterol, LDL cholesterol, or triglycerides between the groups. Total caloric intake decreases significantly with age in the control subjects but not in the subjects with paraplegia. Inverse correlations are found between serum HDL cholesterol and serum triglycerides levels both in those with paraplegia (r = -0.54, p less than 0.005) and in the controls (r = -0.42, p less than 0.001). In our group of subjects with paraplegia, serum lipid levels appear to be independent of dietary intake and body weight.

Adult↗

Paraplegia associated with epidural anesthesia.

Spinal anesthesia has lost its popularity among physicians due to rare occurrences of paraplegia that have precipitated lawsuits, with staggering judgments in favor of claimants. Epidural block has now become a popular alternative because some believe it cannot cause paraplegia; however, paraplegia is as prevalent after induction of epidural anesthesia as after spinal anesthesia. Arachnoiditis has been incriminated as the causative agent when paraplegia has followed spinal anesthesia. Arachnoiditis is also a causative factor when paraplegia follows epidural block. Cord compression and anterior spinal artery syndrome have also been associated with paraplegia after epidural block though they have not been a problem with spinal block.

Adult↗